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Validated All-in-One™ qPCR Primer for TP53(NM_001276697.3) Search again
Product ID:
HQP162219
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
BCC7, BMFS5, LFS1, P53, TRP53
Gene Description:
tumor protein p53
Target Gene Accession:
NM_001276697.3(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Summary
This gene encodes tumor protein p53, which responds to diverse cellular stresses to regulate target genes that induce cell cycle arrest, apoptosis, senescence, DNA repair, or changes in metabolism. p53 protein is expressed at low level in normal cells and at a high level in a variety of transformed cell lines, where it's believed to contribute to transformation and malignancy. p53 is a DNA-binding protein containing transcription activation, DNA-binding, and oligomerization domains. It is postulated to bind to a p53-binding site and activate expression of downstream genes that inhibit growth and/or invasion, and thus function as a tumor suppressor. Mutants of p53 that frequently occur in a number of different human cancers fail to bind the consensus DNA binding site, and hence cause the loss of tumor suppressor activity.
Gene References into function
- There was a differential upregulation of p53-responsive genes by genotoxic stress in hematopoietic cells containing wild-type p53 (MOLT-4) or a mutant p53 with a codon 161 mutation (U266).
- Binding to the p53 binding sites of the Mdm2 promoter alleviates the requirement for p53 C-terminal activation.
- P72R polymorphism in human papillomavirus associated premalignant laryngeal neoplasm
- phosphorylation of p53 was rapidly induced in human fibroblasts upon exposure of cells to hydrogen peroxide (H(2)O(2))
- A loss of wild-type p53 gene function and consequent p53 overexpression in gastric carcinomas may be involved in early stages of tumor progression.
- protein stability measured by hydrogen exchange
- Restoration of wt-p53 activity in Hep3B leads to sensitiveness to chemotherapeutic agents because of the decrease of p-glycoprotein expression.
- differentiation status of the tumor was found for the p53 aberration but not for CD95 expression.
- No association was found between the p53 codon 72 polymorphism and rheumatoid arthritis.
- interactions with DNA in solution using time lapse atomic force microscopy
- Mutations of p53 gene were present in 24% (5 of 21) of the evaluable cases, all of them overexpressing p53 in the majority of tumor cells.
- Tissue samples from 42 ulcerative colitis patients were evaluated for p53 alterations by immunohistochemistry, loss of heterozygosity analysis, polymerase chain reaction-single-strand conformation polymorphism and direct sequencing.
- WOX1/p53 has a potential role as a signaling complex in mitochondrial apoptosis.
- different genotype combinations of p53 and GSTM1 increase the risk of developing specific histological subtypes of NSCLC.
- DNA-PK and p53 may form a sensor complex that detects the disruption of DNA replication caused by nucleoside analogue incorporation and may subsequently signal for apoptosis.
- Expression of Id helix-loop-helix proteins in colorectal adenocarcinoma correlates with p53 expression and mitotic index.
- We show a novel alternative pathway of apoptosis in human primary cells that is mediated by transcriptionally dependent decreases in p53 and c-Myc and decreases in p21.
- pH-sensitive molecular defect of p53 (R337H)suggests that pH-dependent p53 dysfunction is the molecular basis for cases of adrenocortical carcinoma in Brazilian children
- New mutations of p53 identified by SSCP in acute myeloid leukemia cell lines. Loss of p53 is not the decisive event causing tumor cells to proliferate in vitro without externally added growth factors.
- To determine whether genotoxic stress regulates DNA binding by p53 in vivo, we have performed quantitative chromatin immunoprecipitation (ChIP) assays on tumor and normal cell lines containing wild-type p53
- A lower invasiveness and shorter survival was seen in tumors with a TP53 mutation
- higher expression in childhood leukemias with poor prognosis compared to long-term survivors
- Mutation pattern included base substitution (point mutation, G-->T, T-->G) and frame-shift mutation (base insertion and base loss).
- acetylation of p53 activates transcription through recruitment of coactivators/histone acetyltransferases
- role in inducing CD95 gene expression in endothelial cells exposed to doxorubicin
- P53 protein overexpression is an early event in esophageal carcinogenesis and useful biomarkers for early detection.
- P53 protein expression and intratumoral microvessel density (IMVD) can be considered as a biological indicator of malignant potential in brain astrocytoma.
- These results demonstrate that butyrate inhibited the growth of breast cancer cells in a P53-independent manner.
- protein inhibitor of activated Stat1 (PIAS1) interacts with the tetramerization and C-terminal regulatory domains of p53 in yeast two-hybrid analyses
- Telomerase activity in microdissected human breast cancer tissues: association with p53, p21 and outcome
- TP53-mutated tumors need fewer additional genetic alterations to develop metastases in primary head and neck tumors compared with TP53 wild-type primary tumors.
- systematic automated analysis of the effects of p53 mutations on the structure of the core domain of the protein
- IkappaBalpha x p53 complex plays an important role in responses involving growth regulation, apoptosis, and hypoxic stress
- These results suggest that p53 might modulate the repair of DNA adducts generated from the human bladder carcinogen ABP in its target human uroepithelial cells.
- nuclear mutant p53 protein is expressed in early precancerous stages suggesting this is an early change in NSCLC tumorigenesis; may be a potential marker for development of NSCLC
- biogenesis in vitro to determine how wild type and mutant forms form hetero-oligomers
- Polymorphism at p53 codon 72: A striking reduction in Pro/Pro allele frequency has been found in HPV positive cases, indicating Arg/Arg genotype to be more susceptible to HPV infection and oral carcinogenesis
- p53, activated by NF-kappa B, is essential for H(2)O(2)-induced apoptosis in glioma cells
- Repression of hepatocyte nuclear factor 4alpha tumor suppressor p53: involvement of the ligand-binding domain and histone deacetylase activity
- p53 expression was an independent parameter related to a poor prognosis in diffuse large B cell non-Hodgkin's lymphomas.
- The temperature sensitive mutant p53-143ala extends in vitro life span, promotes errors in DNA replication and impairs DNA repair in normal human oral keratinocytes.
- TSG101 expression in gynecological tumors: relationship to cyclin D1, cyclin E, p53 and p16 proteins.
- inhibition by TP53 of G2 phase checkpoint abrogation and radiosensitization induced by PD0166285
- MDMX post-translational processing may be regulated by p53
- A link between the p53 germ line polymorphisms and white blood cells apoptosis in lung cancer patients
- role in regulating growth-promoting gene IEX-1
- Transactivation-deficient Delta TA-p73 inhibits p53 by direct competition for DNA binding: implications for tumorigenesis.
- aberrent expresion correlates with VEGF and IL-8 mRNA expression and neoangiogenesis in non-small-cell lung cancer
- Curcumin induces apoptosis in human breast cancer cells through p53-dependent Bax induction.
- effect of phosphorylation on structure and fold of transactivation domain
- overexpression may be marker of radioresistance in head and neck cancer
- p53 binds telomeric single strand overhangs and t-loop junctions in vitro
- the presence or absence of wild-type p53, may be an important determinant of response to antiangiogenic therapy
- Immunostaining of p53 accumulation in families with multiple glioma pts showed that p53 alterations are as common in familial as in sporadic gliomas.Germline p53 mutations in exons 4-10 were not found.
- Targeted inactivation of p53 in human cells does not result in aneuploidy.
- Human tumor suppressor ARF impedes S-phase progression independent of p53.
- Under severe hypoxic conditions p53 protein accumulates only in S phase; this correlates with replication arrest. Inhibition of ATR kinase activity substantially reduces hypoxia-induced phosphorylation of p53 protein on ser 15 as well as p53 accumulation
- NO induces the accumulation of transcriptionally active p53 in a variety of cell types and NO signaling to p53 does not require ataxia telangiectasia-mutated (ATM), poly(ADP-ribose) polymerase 1, or the ARF tumor suppressor protein
- We investigated three common sequence variants in TP53 and p21 for possible associations with the risk of breast cancer and with various phenotypic features of this disease
- phosphorylation at multiple sites by ATM in response to ionizing radiation
- The low-molecular-weight compound PRIMA-1 restored sequence-specific DNA binding and the active conformation to mutant p53 proteins in vitro and in living cells.
- role for IGF-I in the regulation of the MDM2/p53/p21 signaling pathway during DNA damage
- p53 contributes to the reversible, growth factor-dependent arrest of quiescence
- The first direct demonstration of p53 mutations in pleuropulmonary blastomas (PPB)suggests p53 inactivation can occur as a nonrandom genetic change involving the pathogenesis and outcome of PPB.
- minor role of exon 5-9 among Sudanese breast cancer patients
- Squamous cell carcinoma of the head and neck shows a high incidence of p53 tumor suppressor gene alterations; the latter therefore appears to play an important role in the pathogenesis and progression of such neoplasms.
- SN2 DNA-alkylating agent-induced phosphorylation of p53 increases its DNA-binding properties to cause an increased expression of p21 that may play a role in cell cycle arrest and/or apoptosis of human colon cancer cells HCT-116.
- SV40 large T antigen associates with a cellular phosphoprotein, p53, in virus-transformed cells.Monoclonal antibodies, PAb1101, PAb1102 and PAb1103 define at least two non-overlapping determinants on human p53.
- Involvement of TP53 in apoptosis induced in human lymphoblastoid cells by fast neutrons
- role in inhibiting p63 activity
- Resveratrol enhances the expression of non-steroidal anti-inflammatory drug-activated gene (NAG-1) by increasing the expression of p53
- review on mutations in brain neoplasms
- Wild-type and mutated presenilins 2 trigger p53-dependent apoptosis and down-regulate presenilin 1 expression in HEK293 human cells and in murine neurons
- Interaction between bcl-2 and P53 in neoplastic progression of basal cell carcinoma of the head and neck
- A senescence rescue screen identifies BCL6 as an inhibitor of anti-proliferative p19(ARF)-p53 signaling
- role in the regulation of ceramide biosynthesis
- binding and activation of PIG3 promotoer via a pentanucleotide microsatellite sequence
- expression has an independent effect on prediction of survival, progression, and development of metastasis in transitional cell bladder carcinoma
- Akt enhances Mdm2-mediated ubiquitination and degradation of p53.
- Deubiquitination of p53 by HAUSP is an important pathway for p53 stabilization
- description of a novel MDM2 binding interface in p53 that plays a regulatory role in MDM2-dependent ubiquitination of p53
- Results indicate that loss of RAR-beta expression and accumulation of p 53 and Ki67 proteins may serve as biomarkers for early identification of esophageal cancer in the high-risk populations.
- inverse relationship seen between HPV infection and p53 positivity suggests loss of p53 function in cervical cancer, either by binding to E6 oncoprotein of HPV or by mutation in p53
- mutations in p53 gene can lead to enhanced chemoresistance; p53 gene may serve as a marker for NSCLC response to chemotherapy
- not very likely that TP53 mutations are involved in the etiology of meningiomas
- Apoptotic index (includes nick-end labeling) and bcl-2 do not correlate with key clinical data (prognosis and blood counts at diagnosis) in patients with myelodysplastic syndrome, while p53 protein levels do.
- Peg3/Pw1 is a mediator between p53 and Bax in DNA damage-induced neuronal death
- Characterization of the p53-rescue drug CP-31398 in vitro and in living cells
- p53 and recombination intermediates: role of tetramerization at DNA junctions in complex formation and exonucleolytic degradation.
- Evaluation of relationship between chromosome 22 and p53 gene alterations and the subtype of meningiomas by the interphase-FISH technique.
- expression of apoptosis-regulating proteins p53, Bcl-2, and Bax in primary resected esophageal squamous cell carcinoma
- Expression of p53 and bcl-2 proteins in acute leukemias: an immunocytochemical study
- MDMX, when exceedingly overexpressed, inhibits MDM2-mediated p53 degradation by competing with MDM2 for p53 binding
- Mutation of human thioredoxin reductase 1 promotes p53-dependent gene expression
- p53 mutational pathway may favor selection for ErbB2 gene amplification during tumor progression in breast cancer
- high level of p53 protein in cPNETs measured by immunostaining intensity associated with poor patient survival
- expression in pelvic lymph nodes and primary tumors in early stage cervical carcinomas
- p53 expression and vascular density in colon cancer
- the lack of correlation between p73 or p63 and p53 expression in head and neck squamous carcinoma suggests an independent and/or compensatory functional role
- P53 mediates ceramide-induced apoptosis in SKN-SH cells
- C-terminus of p53 is required for G(2) arrest.
- summarize the current understanding of post-translational modifications and their effect on conformation-based functional relationship between Mdm2 and p53
- Genetic status of cell cycle regulators in squamous cell carcinoma of the oesophagus: the CDKN2A (p16(INK4a) and p14(ARF) ) and p53 genes are major targets for inactivation.
- VEGF and p53 are highly expressed in esophageal carcinomas
- These results suggest that p53 is vulnerable to free radical-mediated oxidation at cysteine residues.
- These results demonstrate direct activation of the human DDB2 gene by p53. The corresponding region in the mouse DDB2 gene shared significant sequence identity with the human gene but was deficient for p53 binding and transcriptional activation.
- Identification of a novel mouse gene, mRTVP-1, as a p53 target gene. The mRTVP-1 protein has 255 amino acids and differs from the human RTVP-1 protein by two short in-frame deletions of two and nine amino acids. (mRTVP-1)
- P53 protein accumulation may be responsible for gastric carcinogenesis and tumor aggressiveness of gastric cancer in northern China.
- pathogenesis of nasopharyngeal carcinoma in children may involve EBV infection leading to LMP-1 expression and p53 overexpression
- Expression of mitotic spindle checkpoint protein hsMAD1 correlates with cellular proliferation and is activated by a gain-of-function p53 mutant.
- cyclin K is targeted for transcription by p53
- O-phospho-L-tyrosine protects TP53 wild-type cells against ionizing radiation
- A HLA-A2 restricted human CTL line recognizes a novel tumor cell expressed p53 epitope
- disrupted p53/BAX pathway is associated with a poor clinical outcome in UICC III tumors
- Prognostic significance of p53 mutations in colon cancer at the population level
- mtCLIC/CLIC4, an organellular chloride channel protein, is increased by DNA damage and participates in the apoptotic response to p53.
- p53 protein overexpression was noted in 59% of T-cell ltymphoblastic lymphoma cases and was correlaed with higher rate of relapse
- Mutations for basal cell carcinoma (BCC), were screened in 15 cases of sporadic BCCs that developed in sun-exposed skin region in a Korean population
- placental transforming growth factor-beta as an important downstream mediator of DNA damage signaling and a transcriptional target of p53 (PTGF-beta)
- Resistance to p53-mediated growth suppression in human ovarian cancer cells retain endogenous wild-type p53.
- p53 protein transport in hepatoma cells with VP22
- DN-p73 is activated after DNA damage in a p53-dependent manner to regulate p53-induced cell cycle arrest.
- Refolding and structural characterization of the human p53 tumor suppressor protein.
- Redox state of tumor suppressor p53 regulates its sequence-specific DNA binding in DNA-damaged cells by cysteine 277.
- Interactions between p53, hMSH2-hMSH6 and HMG I(Y) on Holliday junctions and bulged bases
- Induction of gene amplification is a gain-of-function phenotype of mutant p53 proteins.
- were not able to confirm that the TP53 polymorphism at exon 4 increases the susceptibility to be infected by HPV or to develop high-grade intra-epithelial lesion of the cervix
- p53 negatively regulates intestinal immunity by delaying mucosal T cell cycling
- Changes of NF-kB, p53, Bcl-2 and caspase in apoptosis induced by JTE-522 in human gastric adenocarcinoma cell line AGS cells: role of reactive oxygen species.
- The point mutation of p53 gene exon7 in hepatocellular carcinoma from Anhui Province, a non HCC prevalent area in China.
- reacts with glycogen synthase kinase-3beta after DNA damage
- Deregulated c-Myc partially disabled the p53-mediated DNA damage response
- Recognition of DNA by p53 core domain and location of intermolecular contacts of cooperative binding.
- TP53 arginine/arginine genotype could represent a potential risk factor for the development of squamous cell carcinoma in renal transplant recipients
- Perturbations of chromosome 17 in general and the p53 locus in particular occur frequently in severe/late stage endometriosis.
- polymorphism in codon 72 and risk of head and neck neoplasms
- UVB-mediated activation of p38 mitogen-activated protein kinase enhances resistance of normal human keratinocytes to apoptosis by stabilizing cytoplasmic p53.
- Coexpression of P-glycoprotein, Ets-1, and p53 in oral carcinoma is associated with poor prognosis
- use of p53MH algorithm in detection of p53-responsive genes
- A two-stage, p16(INK4A)- and p53-dependent keratinocyte senescence mechanism that limits replicative potential independent of telomere status.
- recombinant p53 binds to BLM and WRN helicases and attenuates their ability to unwind synthetic Holliday junctions in vitro
- Nucleophosmin (NPM) interacts directly with p53, regulates the increase in stability and transcriptional activation of p53 after different types of stress, and induces p53-dependent premature senescence on overexpression in diploid fibroblasts
- RNA polymerase III transcription can be derepressed by mutations that compromise p53 function in tumours and Li-Fraumeni syndrome. Substitution R175H, the most common mutation in cancers, converts p53 from a pol III repressor to an activator.
- UV-induced DNA damage in epidermal KCs triggers p53 activation and apoptosis. Lack of activation in aging KCs and psoriatic Regulation of apoptosis by p53 in UV-irradiated human epidermis, psoriatic plaques and senescent keratinocytes
- Anoxia induces macrophage inhibitory cytokine-1 (MIC-1) in glioblastoma cells independently of p53 and HIF-1.The macrophage inhibitory cytokine-1 (MIC-1) gene was identified as a most prominent p53 target gene upon gene expression profiling.
- Sequential extension of proliferative lifespan in human fibroblasts is induced by over-expression of CDK4 or 6 and loss of p53 function.
- Human p14(ARF)-mediated cell cycle arrest strictly depends on intact p53 signaling pathways.
- A cytoplasmic accumulation of wild-type p53 in human primary glioblastomas correlates with GFAP and vimentin expression. Cytoplasmic p53 is inactive in growth suppression.
- A new germline p53 mutation was found associated with a choroid plexus papilloma. The 7-BP insertion in exon 5 causes a frameshift from 161-182 and affected transactivation but not apoptosis induction.
- identified executioner caspase-6 as a transcriptional target of p53. The mechanism involves DNA binding by p53 to the third intron of the caspase-6 gene and transactivation.
- Mutations in APC, Kirsten-ras, and p53--alternative genetic pathways to colorectal cancer. The most common combination of mutations was p53 and APC (27.1%), whereas mutations in both p53 and K-ras were extremely rare.
- Novel gain of function activity of p53 mutants: activation of the dUTPase gene expression leading to resistance to 5-fluorouracil.
- Adenovirus encoding HIV-1 Vpr activates caspase 9 and induces apoptotic cell death in both p53 positive and negative human tumor cell lines.
- role in adriamycin-induced senescence in breast tumor cells
- persistence of induced levels of ROS in normal diploid human cells for 1 month after X-ray exposure and the role of TP53 in this oxidant response
- Genetic signature of oligoastrocytomas correlates with tumor location and denotes distinct molecular subsets.
- role of tyrosine phosphorylation of Mdm2 by c-abl in p53 regulation
- binding sites of 53BP1
- mutations in epithelial ovarian cancer
- mutations in rheumatoid arthritis synovium
- two sequence motifs from HIF-1alpha bind to the DNA-binding site of p53
- An identical single nucleotide deletion within the C/EBP-like site of the promoter in 2 OF 18 Li-Fraumeni families. This site is not utilized in the wild type TP53 promoter and mutation of this site in LFS/LFL does not have a functional effect.
- Expression of this molecule and its correlation with prognostic markers in patients with head and neck tumors
- p53 status is an important modulator of nitric oxide-induced mutagenesis and apoptosis, and suggest that level of the Apaf-1 ans XIAP proteins are regulated by p53
- Data suggest a model in which p53 directly recruits a TRRAP/acetyltransferase complex to the mdm2 gene to activate transcription. In addition, this study defines a novel mechanism utilized by the p53 tumor suppressor to regulate gene expression.
- These data indicate a novel p53-dependent mechanism in which cell stress mobilizes nucleolin for transient replication inhibition and DNA repair.
- Syncytia from cells expressing the HIV-1 Env gene fused with cells expressing CD4/CXCR4 undergo apoptosis after nuclear translocation of mTOR, mTOR-mediated p53 phosphorylation, p53-dependent Bax upregulation & mitochondrial death pathway activation.
- enhanced microtubule-dependent trafficking and p53 nuclear accumulation by suppression of microtubule dynamics
- Inactivation of p21WAF1 sensitizes cells to apoptosis via an increase of both p14ARF and this protein and an alteration of the Bax/Bcl-2 ratio
- CARF is co-regulated with ARF and cooperates with it in activating p53
- GSH plays a vital role in the protection of tri- and perchloroethylene-induced oxidative stress & apoptosis, which may be mediated through a p53-dependent pathway.
- These results demonstrate that overexpression of Activating transcription factor 3 (ATF3) suppresses tumor necrosis factor-alpha-induced cell death of HUVECs, at least in part, through down-regulating the transcription of p53 gene.
- MDMX-mediated regulation of p53 activity during development.
- p53 represses TauT and is involved in renal development and apoptosis.
- Relationship between p53 codon 72 polymorphism and susceptibility to sunburn and skin cancer.
- p53 is acetylated by tumor necrosis factor alpha, then p53 attenuates its trans-activation by depleting CREB binding protein in rheumatoid synoviocytes
- Hypophosphorylation of Mdm2 augments p53 stability.
- Human wild-type p53 inhibits homologous recombination between substrates for conservative HR & for gene deletions. Non-homologus end-joining was downregulated after p53 expression. p53 mutations at codon 281, 273, 248, 175, or 143 disrupted DSB repair.
- Vascular endothelial growth factor (VEGF) expression correlates with p53 and ki-67 expressions in tongue squamous cell carcinoma.
- Genetic alterations of INK4alpha/ARF locus and p53 are observed in human hepatocellular carcinoma.
- MYCL1, FHIT, SPARC, p16(INK4) and TP53 genes associated to lung cancer in idiopathic pulmoary fibrosis
- Mutations in exons 4-10 of the p53 gene in acute myeloid leukemia patients screened in an epidemiologic study in Brazil were found to correlate with poor prognosis and to occur at frequencies similar to those reported for Northern America and Europe.
- The lack of Bcl2 accompanied by p53 overexpression affects the distribution of cells among the cell cycle phases and modifies the sensitivity to cytotoxic drugs and the type of cell death.
- In response to irradiation, the amount of p53 protein synthesized in patients with AT and NBS was significantly lower than that in normal cells.
- Wild-type p53 protein conformation is stabilized upon CP-31398 exposure.
- Efficient repair of bulky anti-BPDE DNA adducts from non-transcribed DNA strand requires functional p53 but not p21(waf1/cip1) and pRb.
- E1B-55K-anchored proteome is linked to polyubiquitination of p53 in vitro
- p53 was detected more frequently in CIN I compared with CIN II/III and invasive carcinoma
- Affects relative biological effectiveness of light ions in human tumoural cell lines.
- The suppression of STK15 oncogenic activity by p53 might be explained by the finding that p53 inhibited STK15 kinase activity via direct interaction with the latter's Aurora box. This revealed a novel mechanism for the tumor suppressor function of p53.
- The candidate tumor suppressor ING1b can stabilize p53 by disrupting the regulation of p53 by MDM2.
- Cellular effects of CPT-11 on colon carcinoma cells: dependence on p53 and hMLH1 status.
- TP53 mutations in breast cancer tumors of patients from Rio de Janeiro, Brazil: association with risk factors and tumor characteristics.
- bcl-2/Jh lymphomas show molecular heterogeneity and that bcl-6 and p53 mutations may be acquired during the evolution of such lymphomas
- A case-control study showed that polymorphism in codon 72 of the p53 gene was not a cervico-uterine cancer risk factor in Mexico.
- p53 proteasomal degradation is regulated by NADPH quinone oxidoreductase 1 and independent of MDM2 and ubiquitin
- p53 controls global nucleotide excision repair of low levels of structurally diverse benzo(g)chrysene-DNA adducts in human fibroblasts.
- studies define a novel p53-survivin signaling pathway activated by DNA damage that results in down-regulation of survivin, cell cycle arrest, and apoptosis
- Immunohistochemical expression of this protein in squamous cell carcinomas from immunosuppressed renal transplant recipients and immunocompetent individuals
- CD27 and CD40 co-stimulatory signals regulated the p53-amplified apoptotic pathway in B cells through the inhibition of p53-independent apoptotic pathway primarily induced by BCR ligation
- Purification, crystallization and preliminary X-ray analysis of the BRCT domains of human 53BP1 bound to the p53 tumour suppressor
- Results indicate that full-length p53 is a modular protein consisting of defined structured and unstructured regions, which may allow the physiological interaction of p53 with a multitude of partner proteins and the regulation of its turnover.
- p53 activation is inhibited by MDMX, which is transported to the cell nucleus with or without p53 upon DNA damage
- These findings suggest that impairment of transcriptionally active p53 in response to replication blockade is not a general phenomenon.
- p53 activates ATF3 in human tumor cells
- role in enhancing MUC2 mRNA expression
- there are high frequencies of somatic mutations in TP53 (encoding tumor protein p53) in breast neoplastic epithelium and stroma
- P53 overexpression in transitional-cell carcinoma of the kidney pelvis and ureter correlated with tumor-dependent death (p<0.001), tumor proliferation & disease progression, but not histologic grade.
- Results describe the thermodynamic and kinetic-binding parameters for the interaction between MDM2 and p53 proteins.
- Two peptide epitopes on Mdm2 oncoprotein affect this protein's degradation.
- By inhibiting p21(Cip1) expression Myc favours the initiation of apoptosis, thereby influencing the outcome of a p53 response in favour of cell death
- role in regulating expression of 67-kDa laminin receptor precursor 37LRP
- role in mediating cell cycle arrest in Rb(-/-) Saos2 cells
- regulation of function by Pin1 during DNA damage
- hepatitis B virus X protein on the regulation of cell-cycle control depending on the status of cellular p53
- insulin inhibits TNF-alpha-dependent cell killing, induction of p53, p21 and apoptosis in a human cervical carcinoma cell line
- azurin, tumor suppressor protein p53, and regression of cancer
- ultraviolet rays increase the specificity of CK2 for p53 at the expense of other cellular CK2 substrates and leading to an overall increase in p53 serine 392 phosphorylation
- The prolyl isomerase Pin1 is a regulator of p53 in genotoxic response
- following stress-induced phosphorylation, p53 needs to form a complex with Pin1 and to undergo a conformational change to fulfil its biological roles
- Data suggest that securin is a p53 target gene and may play a role in p53-mediated cellular response to DNA damage.
- role in inducing cyclooxygenase 2 and in counteracting mutagen-induced apoptosis
- The major lipid peroxidation product, trans-4-hydroxy-2-nonenal, preferentially forms DNA adducts at codon 249 of human p53 gene, a mutational hotspot in hepatocellular carcinoma. 4-HNE may cause human cancers with mutations at codon 249 of p53 gene.
- IRF-1 and the tumour suppressor protein p53 are coordinately up-regulated during the response to DNA damage in an ATM-dependent manner.
- Lung-specific expression of human point mutant p53-273H (under the SP-C promoter) is associated with a high frequency of lung adenocarcinoma in transgenic mice. This mutation is frequent in human lung tumors.
- acetylation of the C-terminal domain is sufficient to abrogate its ubiquitination by Mdm2
- One major function of p53 acetylation is to promote p53 stability by preventing MDM2-dependent ubiquitylation, while recruitment of HDAC1 by MDM2 promotes p53 degradation by removing these acetyl groups
- p53 is regulated by Kruppel-like factor 4 during G1/S cell cycle arrest in response to DNA damage
- heat shock stabilization by phosphorylation and heat shock protein 90 binding
- p53 as a sensor of transcriptional integrity
- description of the role of ionic interactions in the stability of the p53 tetramer and of heterotetramers of the protein scaffold
- Role of p53 domains in binding to supercoiled DNA
- p53 positivity has been found only in part of the HGD cases and moreover a number of HGD with low or absent p53 scores has been found associated with high proliferation indices independently of the clinical evolution.
- Many genes are affected by TP53 gene dosage for their expression. We report several candidate genes as potential downstream targets of p53 in nonstressed cells. Among them, CSPG2 is validated as being directly transactivated by p53.
- inactivation of p53 is an important cause of aberrant accumulation of beta-catenin in cancer cells
- Interacts with WT1 in insulin-like growth factor-I receptor gene regulation
- p53 mutations are a later event in vulvar carcinoma
- Results suggest that intrinsic DNA binding affinity and p53 protein levels are important contributors to p53-induced differential transactivation.
- TP53 mutations could be a useful prognostic indicator in precancerous oral lesions.
- The p53 overexpression was an important factor in the process of carcinogenesis of elder women with cervical cancer and a predictive indicator for lymph node status.
- expression of telomerase genes (hTR, hTRT) and apoptosis related genes (p53, bcl-2) in mammary atypical ductal hyperplasia
- abnormal expressions of COX-2, p53, PCNA, and nm23 associate with malignant potential, lymph node metastasis and clinical stage, and they might therefore play a role in development of gastric cancer
- Data suggest that naturally occurring genetic variability at p53 gene explains part of the inter-individual difference in the in vitro susceptibility to a chemotherapeutic drug.
- estradiol induces variations of p53 protein levels in epithelial cancer-derived cell lines from the reproductive tract in vitro; this may be related with status p53 and/or presence of E6/E7 from human papillomavirus [review]
- Cancerous hyper-mutagenesis in p53 genes is possibly associated with transcriptional bypass of DNA lesions.
- p53 has a role in T-cell protein tyrosine phosphatase-induced apoptosis in a human tumor cell line.
- TP53 has a role in aortal endothelial cell aging
- expressed in biopsies from children with Langerhans cell histiocytosis
- P53 directly inhibits expression of the T cell growth factor (IL-2) in activated T cells.
- Expression or this protein does not predict outcome in colorectal cancer patients.
- p53 mediates DNA damaging drug-induced apoptosis by increasing its levels in the nucleus, thus inducing its transcription targets p21(Waf1/Cip1) and MDM2
- Loss of p53 function leads to myeloma cell progression and resistant phenotype through bcl-2-related mechanisms.
- p53 has a role in cyclin D1-induced death signalling and causes caspase activation controlled by Bcl-2
- Thus, the accumulation of mutant p53 in tumor cells may contribute to tumorigenesis by inhibiting stress-inducible kinase pathways.
- DNA repair of the gene region in two human bladder carcinoma cell lines
- Status of gene affect and nature of chromosome damage seen in human skin fibroblasts after gamma irradiation beyond the G1-phase checkpoint but prior to the G2-phase checkpoint
- role of gene in the complexity of the mechanisms of initiation and maintenance of DNA damage-induced G2-phase arrest and subsequent G1-phase arres
- A selective growth advantage for cells carrying a type of TP53 mutation seen in breast carcinomas when the mutation resides on Arg72 allele. These are not seen in colorectal neoplasms.
- There is some evidence that p53 is involved in the regulation of XPE DDB2 or XPC.
- p53 protein was analyzed in ovarian tumor samples and p53 exons were analyzed using SSCP and immunohistochemistry. 52% of tumors stained positive for p53; there was no correlation with telomerase activity based on p53 staining.
- The relationships and interactions between p53, Rb and bcl-2 immunostaining, clinical parameters and response to cisplatin-based chemotherapy were evaluated in the present study.
- investigated whether Tat might alter p53 acetylation and p53-responsive transcription; results allude to mechanism where the HIV-1 trans-activator might impair tumor suppressor functions favoring establishment of neoplasia in AIDS
- the persistence of p53 overexpression after Bacillus Calmette-Guerin intravesical therapy is predictive of progression in patients treated for carcinoma in situ
- Analysis of BRCA1, TP53, and TSG101 germline mutations in German breast and/or ovarian cancer families.
- Ubiquitination and degradation of p53 are largely controlled by Mdm2, an oncogenic E3 ligase.
- Results describe the relationship between Helicobacter pylori (H.pylori) infection and the expressions of the p53, Rb, c-myc, bcl-2 and hTERT mRNA in a series of diseases from chronic gastritis to gastric cancer.
- p53 plays an important role in PP2C alpha-directed cell cycle arrest and apoptosis
- beta-catenin, p53 and PCNA may play important roles in the carcinogenesis of colorectal adenoma.
- pivotal role of NO in the induction of cellular stress and the activation of a p53 response pathway during chronic inflammation
- basal expression of p53 plays a functional role in a glucocorticoid receptor-mediated response regulating the expression of p21(Waf1/Cip1) via a mechanism that is suppressed by PP5 and associated with the phosphorylation of p53 at Ser-15
- the data demonstrate that wild-type p53 in cytoplasm, in its noninduced state, is functional; it displays intrinsic 3'-->5' exonuclease activity
- Mutated-p53 (Asp281His), in head & neck cancer cells prevents cell death from DNA damage. This probably accumulates genetic alterations and accelerates the malignant progression of the cells by DNA damaging therapy.
- The presence of E-cadherin mutations can significantly alter the accumulation of the apoptosis-regulating p53 protein, whereas no correlation with the p53 mutation status or with Ki-67 staining was observed.
- This protein and p73 interact with CTF2 and regulate HMG1 gene expression.
- Data show that aspirin decreases endothelial cell proliferation through cell cycle arrest mediated by enhanced p53 expression.
- Simulated sunlight and benzo[a]pyrene diol epoxide induced mutagenesis in the human p53 gene
- Selection pressures of TP53 mutation and microenvironmental location influence epidermal growth factor receptor gene amplification in human glioblastomas.
- P53 genes from South African esophageal squamous cell carcinoma patients showed: 2 mutations (G>A, codon 331; G>T, donor splice site) in exon 9,4 polymorphisms in intron 3 (16 bp duplication) & exon 4 (C>A, codon 34; G>C, codon 36; G>C, codon 72).
- role of binding to mdm2 protein in p53 regulation
- The complement inhibitor CD59 and the lymphocyte function-associated antigen-3 (LFA-3, CD58) genes possess functional binding sites for the p53 tumor suppressor protein.
- Haplotype structure of TP53 locus in Indian population and possible association with head and neck cancer.
- Expression of p53 in primary central nervous system diffuse large B-cell lymphoma may be a prognostic marker for poor overall survival.
- Data show that activated protein C directly prevents apoptosis in hypoxic human brain endothelium through transcriptionally dependent inhibition of tumor suppressor protein p53.
- Expression of p53R2, newly p53 target in oral normal epithelium, epithelial dysplasia and squamous cell carcinoma.
- in cell lines containing inducible versions of alleles encoding the Pro72 and Arg72 variants, and in cells with endogenous p53, the Arg72 variant induces apoptosis markedly better than does the Pro72 variant
- mutation analysis of this gene in a case of familial endometriosis
- Differential expression of genes induced by resveratrol in LNCaP cells: P53-mediated molecular targets.
- mediation of apoptotic response in colorectal cancer cells by PUMA
- TP53 rearrangements in families with the Li-Fraumeni syndrome reveals a complete deletion of the TP53 gene
- Methylation of CpG and CCWGG motifs in the promoter of TP53 could represent a novel mechanism leading to functional impairment of this tumor suppressor gene in ALL.
- Through a combination of induced p53 aggregation and diminished site-specific DNA binding activity, Zn2+ loss may represent a significant inactivation pathway for p53 in the cell.
- Mdm2-mediated p53 ubiquitination is suppressed by HIF-1 alpha, which blocks Mdm2-mediated nuclear export of p53
- These results indicate that p53 and BLM functionally interact during resolution of stalled DNA replication forks and provide insight into the mechanism of genomic fidelity maintenance by these nuclear proteins.
- VEGF expression plays a role in promoting angiogenesis in invasive ductal carcinoma of the breast, and p53 is likely to be involved in regulating VEGF expression.
- increased p53 and Ki-67 expression in varying grades of urothelial dysplasia of bladder
- Comparative study in the expression of p53, EGFR, TGF-alpha, and cyclin D1 in verrucous carcinoma, verrucous hyperplasia, and squamous cell carcinoma of head and neck region.
- Mutation of p53 gene endows gliomas with an angiogenic phenotype by reducing thrombospondin-1 production as well as enhancing the angiogenesis inducers in the early phase of malignant progression.
- Germline mutations of this protein exist in a cohort with childhood sarcoma: sex differences in cancer risk.
- CP-31398-mediated stabilization of p53 may result from reduced ubiquitination, leading to high levels of transcriptionally active p53.
- Delayed activation of p53 occurrs in the progeny of irradiated cells.
- Wild-type p53 regulates human ribonucleotide reductase by protein-protein interaction with p53R2 as well as hRRM2 subunits.
- results indicate HPV 16E6 may have multiple modes of interaction with E6AP and that assembly of p53 containing complexes for targeted degradation by E6AP may occur in more than one way
- p53 induction and activation of DDR1 kinase counteract p53-mediated apoptosis and influence p53 regulation through a positive feedback loop.
- the p53 tetramerization domain can be converted from the soluble native state to amyloid-like fibrils under certain conditions
- ING1 expression is frequently associated with Adenocarcinoma of the esophagogastric junction tumorigenesis, further supporting its role as a tumor suppressor gene, and ING1 expression is independent of p53 status
- study establishes poly(ADP-ribose) polymerase-1 as a critical regulator of the protein p53 response to DNA damage
- mutations induce loss of DNA methylation and amplification of the TROP1 gene
- modulation of level by cyclin G via a negative feedback reglation
- there is a relationship between the p53 pathway and the ubiquitin-mediated degradation of mitotic cyclins and possible cross-talk between the G2-DNA damage checkpoint and the mitotic checkpoint
- activates ICAM-1 (CD54) expression in an NF-kappaB-independent manner
- deacetylase HDAC1 acts as an antagonist of the tumor suppressor p53 in the regulation of the cyclin-dependent kinase inhibitor p21
- We probe the significance of mitochondrial p53 and show that tumor-derived transactivation-deficient mutants of p53 concomitantly lose the ability to interact with BclXL and promote cytochrome c release.
- p53 protein can directly induce permeabilization of the outer mitochondrial membrane by forming complexes with the protective BclXL and Bcl2 proteins, resulting in cytochrome c release
- Patients with tumors who also showed overexpression of p53 had a significantly inferior response to chemotherapy compared with the patients with p53-negative tumors
- this gene regulates the matastasis suppressor gene Nm23 in cultured tumor cells.
- Bcl-2 constitutively suppresses aptoptosis dependent on this protein in colorectal cancer cells.
- Fas-mediated apoptosis is dependent on wild-type p53 status in human cancer cells expressing a temperature-sensitive p53 mutant alanine-143.
- During apoptosis, p53 activates transcription of PAC1 by binding to a palindromic site in the PAC1 promoter
- Codon 249 mutation in exon 7 of this gene in plasma DNA may be a new early diagnostic marker of hepatocellular carcinoma in Qidong risk area, China.
- p53 and c-fos are significantly overexpressed in thyroid cancer patients, indicating their role in the genetic mechanisms leading to thyroid tumorigenesis
- the expression of p53 is very probably involved in the regulation of leukemic hematopoiesis and that the inhibition of p53 expression could modulate the proliferation of leukemic cells.
- generation of the polyubiquitinated forms of p53 that are targeted for proteasome degradation requires the intrinsic ubiquitin ligase activities of MDM2 and p300
- a transcriptional switch from P(0)-/P(2)- to P(1)-initiated p53 mRNA could be an important mechanism by which cells regulate p53 expression
- Modified DNA is recognized by "latent" and "active" protein p53.
- p53 mutations reflected histological progression in Barrett's patients with p53 mutations found in 30% of metaplasia patients (P=0.4) and low-grade dysplasia patients (P=0.33).
- This additivism, where doxorubicin acts via p53 expression and vinorelbine through p38 MAP KINASE activation, may contribute to the high clinical response rate when the two drugs are used together in the treatment of breast cancer.
- half-life (t(1/2)) of the unfolding of highly destabilized mutants
- central and carboxy-terminal regions are essential for interaction and complex formation with PARP-1
- Mutant p53 can delay growth arrest in senescing fibroblasts without reducing p21(WAF1) expression.
- Mutations in PTEN/MMAC1 gene correlated inversely with an altered p53 status.
- tp53 has a role in recruitment of nucleotide excision repair factors XPC and TFIIH to DNA damage
- deacetylated p53 can transactivate the p21Waf1 gene
- Mutations of p53 gene are associated features of aggressive phenotype of transitional cell carcinomas but do not seem to offer additional prognostic information.
- immunohistochemistry and PCR-SSCP analysis of p53 are useful for pathological discrimination between UC-associated neoplasia and inflammatory regenerative epithelium; may contribute to accurate endoscopic detection of UC-associated neoplasia
- The capability of p53 to activate transcription was used to develope a new assay that permits rapid determination of the status of p53 in cancer cell lines of different origin.
- Results showed significant differences in the expression patterns among p53-null. wild-type p53, and p53 mutants A138T, C141Y, R158L, G245C, and R248Q samples. We also report here the first found p53 mutant-triggered alternative splicing.
- p53 mutants mediate the AI growth of LNCaP cells in an AR-independent fashion, and that both Akt and Bcl-2 are not involved in this process.
- overexpression of p53 protein is observed in recurrent respiratory papillomatosis
- in progeria, the premature ageing phenotype does not arise from an enhanced p53 response.
- This gene is mutated in breast cancer.
- p53 accumulation and loss of bax expression influence the acquisition of a malignant phenotype but seem to have no further impact on tumor progression.
- This protein is required for the Nuclear localization of Y-box factor YB1.
- expression of p21/CDKN1A is necessary and sufficient for the negative regulation of gene expression by p53
- p53 exhibited no statistical correlation with survival and disease-free survival.
- p29ING4 and p28ING5 may be significant modulators of p53 function.
- p53 interacts with hRAD51 and hRAD54, and directly modulates homologous recombination.
- p53 is regulated by hGTSE-1 during apoptosis control after DNA damage in S and G2 phases
- p53 and p73alpha have roles in cell migration
- The detected pattern of the p53/ bcl-2 ratio in hypertrophic actinic keratosis suggests important role for another gene: the proapoptotic gene bax.
- Results showed that mutations in the p53 gene were frequently detected in in recurrent hepatocellular carcinoma.
- results demonstrated significant positive staining of p53 in the salivary tumorigenic tissue but not in the surrounding non-tumorigenic tissue, pointing to a biological role in the tumorigenic process
- GgA transition in codon 175 of the p53 gene as a potential marker of colon cancer progression
- No somatic mutations were identified in either TP53 or KRAS, indicating that disregulation of these genes is not required for leiomyomas development
- Data show that the 249(Ser) p53 mutation in plasma is strongly associated with hepatocellular carcinoma (HCC).
- p53-induced apoptosis inhibited by activated Notch1
- p53 mutations and/or protein overexpression are a predictor of reduced postoperative survival after surgical resection of esophageal adenocarcinomas. p53 may be a clinically useful molecular marker for stratifying patients in clinical trials
- The detection of mutant p53 protein in hepatocellular cancer is corellated with clinicopathologic parameters and incidence of the liver neoplasms in Turkey.
- p53 is inactivated by leukemic protein MLL-ELL
- Results obtained in breast carcinoma cell lines indicate that no clear-cut linear relationship exists between the p53 mutational status and the extent of its respective mRNA and protein expression.
- p53mt249 stimulates IGF-II dependent IGF-IR signaling by upregulating the expression of both ligand (IGF-II) and receptor (IGF-IR) through an autocrine and/or paracrine loop
- P53-negative AsPC-1 cells are resistant to p53-mediated apoptosis.
- Cooperation of two mutant p53 alleles contributes to Fas resistance of prostate carcinoma cells.
- role in mediating upregulation of CD95 gene expression upon genotoxic treatment in human breast tumor cells
- Gene-profiling experiments of breast cancer cells infected with wt p53 revealed both MASPIN and desmocollin 3 (DSC3) to be p53-target genes, even though both genes are silenced in association with aberrant cytosine methylation of their promoters
- Here we showed that 361 out of 1501 p53 responsive genes contained p53 consensus DNA-binding sequence(s) in their regulatory region, approximately 80% of which were repressed by p53
- The restoration of wild-type p53 expression and function in human autologous lung carcinoma IGR-Heu cells results in a significant potentiation of target cell susceptibility to cytotoxic T cell-mediated lysis.
- p53 may play important role in transition from intraductal papillary-mucinous tumor of the pancreas adenoma to carcinoma in situ
- Correlates with invasiveness including vascular permeation, grade of cellular differentiation, incomplete capsule and multinodular lesions. More recurrence. May also influence disease recurrence interval and survival time.
- p53-dependent apoptosis triggered by fast neutrons in lymphoid cells requires caspase 8-mediated BID cleavage
- p53 represses cyclin D1 transcription through down regulation of Bcl-3 and inducing increased association of the p52 NF-kappaB subunit with histone deacetylase 1
- In carcinoma in situ tumors, p53 expression is not associated with clinical outcome.
- p53 is recruited into the PML nuclear bodies by PML along with chk2
- Caffeine induces cell cycle arrest and apoptosis in association with activation of p53 by a novel pathway to phosphorylate the Ser-15 residue and induction of phosphorylation of cdc 2 in leukemic cells with normal p53.
- p53 has different modes of high affinity DNA binding which are related to its tumor suppressor functions
- study showed that polymorphism at codon 72 of TP53 gene is not associated with an increased susceptibility to cervical disease and/or HPV infection in the Argentine women population
- TP53 mutation frequently occurs in higher stages of bladder tumours
- p53 mutations in exon 7 might be associated with increased radiosensitivity in certain SCLC & NSCLC human lung cancer cell lines. No correlation concerning mutations in separate exons & response towards different chemotherapeutic agents could be found.
- p53 must be dephosphorylated on serine residues during N-alpha-tosyl-L-phenylalanyl chloromethyl ketone-induced apoptosis
- Inhibition of p53 causes ubiquitination and down-regulation, through increased degradation, of the IGF-1R in human malignant melanoma cells. By sequestering Mdm2 in the cell nuclei, the level of p53 may indirectly influence the expression of IGF-1R.
- The 3' UTR of p53 was found to be a target of the RNA-binding protein HuR in a UVC-dependent manner in vitro and in vivo.
- molecular interactions of p53 within the N-terminal domain are not required to restrain DNA recombination, but might contribute to the genome stabilizing function
- low incidence for actinic damage, basal cell and squamous cell carcinoma as documented in vitiligo could well reside in a protective function of up-regulated wild-type p53.
- P-53 over-expression can occur in initial stages of HCV-related liver disease.
- findings suggest that the Pro/Pro genotype of p53 codon 72 played a role in prostate cancer susceptibility in a Japanese population; the Pro allele did not appear to worsen such clinical parameters as clinical stage or pathological grade
- types of mutations in sinonasal NK/T cell lymphoma in northeast district of China
- Comprehensive site-directed mutagenesis technique & a yeast-based functional assay were used to construct, express, & evaluate 2,314 p53 mutants representing all possible AA substitutions caused by a point mutation throughout the protein.
- a novel p53-dependent mechanism in the PPARgamma ligand-mediated inhibition of cholangiocarcinoma growth and suggest a potential therapeutic role of PPARgamma ligands in the treatment of human cholangiocarcinoma.
- Hepatitis B virus X protein in liver cells down-regulates the expression of PTEN and activates AKT and affects p53-mediated transcription of PTEN.
- This protein interacts with TFAM and helps regulate DNA damage.
- Expression of apoptosis-inductive genes were increased by X-ray irradiation in squamous cell carcinoma cells(SAS) with wild-type p53, but not in SAS cells expressing mutated p53. Radiation sensitivity may come from expression of apoptosis-related genes.
- p21 is highly correlated with p73 expression irrespective of the p53 mutation status in human esophageal cancers
- TP53INP1s and HIPK2 could be partners in regulating p53 activity.
- potential improvement of the International Prognostic Scoring System by the addition of molecular analysis to the system, with particular reference to the configuration of the TP53 gene
- hepatitis C virus core protein induces p53-dependent gene expression of TAP1 protein and MHC class I upregulation in liver cells and thus impairs NK cell cytotoxicity
- P53 protein expression in quiescent vascular smooth muscle cells [VSMCs] is paradoxically increased by application of a growth stimulus. Through mediation of p21WAF1/CIP1 and Bax, induced p53 protein negatively regulates the growth of dividing VSMCs
- TP53 is regulated by superoxide dismutase 1 in human cells
- transcription of the p53 gene is induced by IFN-alpha/beta, accompanied by an increase in p53 protein level, contributing to tumour suppression and critical for antiviral defence
- p53 has a differential role in effecting G(2) arrest in response to topoisomerase II inhibitors, depending upon the mechanisms of action of the inhibitors tested.
- Data describe the correlation between inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 activities and p53 gene status in head and neck squamous cell carcinomas in vivo and in vitro.
- p53 has a pivotal role in apoptosis in the erythroid lineage development
- Fibrillar aggregates of the p53 core domain contribute to the loss of function of p53 and seed the accumulation of conformationally altered protein in some cancerous cells.
- Zinc deficiency caused an increase in p53 protein expression.
- tp53 may negatively control the MAKP pathway via MKP1
- the p53 gene polymorphism may associate with NPC susceptibility in Thai population, particularly the Pro/Pro genotype carriers with age of >40 years.
- Epigallocatechin-3-gallate-induced stabilization of p53 caused an upregulation in its transcriptional activity, thereby resulting in activation of its downstream targets p21/WAF1 and Bax.
- there is a mitotic checkpoint wherein p53-dependent activation of Snk/Plk2 prevents mitotic catastrophe following spindle damage
- p53 mutation [p53(R273H)], is frequently found in human cancers.
- p53 mutations, in stromal cells can increase stromal-derived support of leukemia growth. Increased synthesis of pro-angiogenic cytokines, such as VEGF, may constitute one possible pathway by which this process is mediated.
- role of p53 gene in the biophysics and biology in murine erythroleukemia cell line with the goal of understanding the influence of this tumor suppressor gene on the deformability and metastasis of tumor cells
- HIPK2-mediated enhancement of p53-dependent transcription, p53 serine 46 phosphorylation and the antiproliferative function of HIPK2 strictly rely on the presence of PML.
- Mutation of p53 is significantly associated with gain of 20q, 13q, and 8q and loss of 18q in colorectal adenocarcinoma.
- Functional mutants of the sequence-specific transcription factor p53 and implications for master genes of diversity.
- The p53 genotype distribution was markedly different between the ovarian mucinous cystadenocarcinomas and serous papillary cystadenocarcinomas with respect to homozygosity of both Arg and Pro.
- p53-induced apoptosis does not occur through the induction of CD95/CD95L expression
- Ligase dead mutants of Mdm2 did not act in a dominant negative manner to reactivate p53 and they are not oncogenes in human mammary epithelial cells.
- A shift from one p53 intron 2 genotype in the blood to another genotype in the tissue may be a prognostic factor in ovarian cancer patients.
- P53 mutation predicts the failure of intravesical adriamycin instillation in transitional cell carcinoma of the bladder.
- p53 alteration is an independent and significant indicator to predict unfavorable prognosis in patients with unresectable non-small cell lung cancer.
- The p53 tumor suppressor pathway is disrupted in most oral squamous cell carcinomas at the cellular levels, due to either an abnormality in p53 itself or loss of expression of p53 regulatory factors.
- p53 is involved in the progression of anal cancer and its expression increases from early in the development of pre-invasive anal lesions.
- HSU94788 may not be the wild-type p53 sequence. AF136270 and AF135120 may be the correct wild-type intron 7 sequences.
- findings suggest a novel mechanism of MLH1 in the induction p53 and apoptosis by inhibiting RNA polymerase II-dependent transcription on damaged DNA templates
- colocalization of a nonshuttling p53 with MDM2 either in the nucleus or in the cytoplasm is sufficient for MDM2-induced p53 polyubiquitination but not degradation.
- combination of protein p53 induction and ionizing radiation activate the proliferating cell nuclear antigen gene
- Radiation induced increased expression of p53. Ionizing radiation induces p53-dependent cell apoptosis in bladder cancer cells with wt- p53 but not in those with mutated p53.
- the greater severity of TP53-mutant B-CLLs compared with ATM-mutant B-CLLs is consistent with the additive effect of defective apoptotic and elevated survival responses after DNA damage in these tumors
- hyperoxia activates the ATR-Chk1 pathway and phosphorylates p53 at multiple sites in an ATM-independent manner, which is different from other forms of oxidative stress such as H2O2 or UV light.
- p53 has a role in transactivation of the Fas gene during radiation-induced Fas sensitization in prostate cancer cells
- Our results indicate that both p73 and p63 may be involved in the development of human buccal squamous-cell carcinoma, perhaps in concert with p53.
- Defect of spindle checkpoint gene Mad2 and mutation of p53 gene are involved mainly in colorectal carcinogenesis, and cancer/normal tissue ratio >2 is associated with prognosis of colorectal cancer.
- inactivation of p53 in osteosarcomas directly by mutation versus indirectly by HDM2 amplification may have different cellular consequences with respect to the stability of the genome
- p53 gene mutations might be a main causal factor for carcinogenesis for gynecological neoplasms.
- p53-induced transcription is inhibited by SINK-homologous serine-threonine kinase
- Plays a role in breast cancer in conjunction with BRCA1.
- The N-terminal domain of p53 is natively unfolded
- Inhibition of COX-2 in colon cancer cell lines by celecoxib increases the nuclear localization of active p53.
- tp53 has a role in apoptosis along with noxa protein in human tumor cells
- TP53-mediated transcription is induced by prohibitin in human tumor cells through enhanced recruitment to promoters
- Results identify a 22-mer peptide derived from the p53 core domain (peptide 14), which inhibits p53-specific DNA binding, and may prevent inappropriately-triggered apoptosis in normal tissues.
- p53 is not required for LKB1-induced apoptosis in pancreatic neoplasms
- identification of defect in response pathway induced by de novo purine synthesis inhibition
- VHL-mediated p53 upregulation may contribute to pVHL's tumor suppressive functions in renal cell carcinoma
- p53 activity is regulated by 14-3-3 sigma
- The poor prognosis associated with p53-null mutation is independent of the mutation mechanism in ovarian cancer survival.
- role of glycogen synthase kinase-3beta in binding and promoting action of p53
- adenovirus 2 E1B-55K protein blocks p53 as a transcriptional repressor protein of the survivin and the MAP4 promoters
- The immunodetection of both p53 and bcl-2 proteins in squamous cell carcinoma of the uterine cervix can be used as an independent diagnostic marker for cervical cancer associated with HPV infection.
- p53 and c-Myc expression may have a role in regulation of telomerase activity in ovarian tumours
- x-ray crystallography of mutant human p53 core domain
- there may be a p53-dependent regulatory pathway of the maspin protein in human cancer
- p53 inactivation caused by HPV infection may play a role in the pathogenesis of colon cancer
- Alterations in p53 are a common event in advanced epithelial ovarian cancer. A mutation in p53, but not overexpression of p53, is associated with a short-term survival benefit.
- p53 post-translational modification has a role in p53 inactivation in malignant epithelial cells with mdm2 gene amplification
- small airway epithelial cells expressing a p53 mutant alleles were able to inhibit endogenous p53 activity; only one allele, 248W demonstrated a markedly increased ability to facilitate E1B 55-kilodalton protein-deficient adenovirus (ONYX-015) replicatio
- Daxx significantly augmented p53-mediated transcription and the Adenovirus E1B 55-kDa protein eliminated this effect.
- PTEN inhibits MDM2 and protects p53 through both p13k/Akt-dependent and -independent pathways in ALL.
- Data suggest that both before and after UV irradiation, DDB2 directly regulates p53 levels, while DDB2 expression is itself regulated by p53.
- Cloning and characterization of a novel gene PDRG that is differentially regulated by p53 and ultraviolet radiation
- value of this tumor marker regarding relapse, metastasis and death in resectable non-small cell lung cancer
- ING1 has a subtle antiproliferative effect even in the absence of p53, and ING1b enhances the DNA damage responses through p53-dependent and -independent mechanisms.
- Nitric oxide depletion reduces the presence of p53-DNA complexes after cisplatin treatment.
- DeltaN-p63-alpha mediates the silencing of its own promoter thereby altering the pattern of p53-target gene expression.
- Out of 110 cases of oral carcinoma, 40 (36%) were p53 positive; p53 over-expression may be involved in only a certain proportion of oral carcinomas
- Activation of p53 reduces binding and relieves transcriptional repression of the Dnmt1gene, whereas loss of p53, a frequent, early event in tumorigenesis, may significantly contribute to aberrant genomic methylation.
- UV-induced activation of p53R2 transcription and binding of p53R2 to hRRM1 to form RR holoenzyme are impaired in the p53-mutant cell line PC3.
- Loss of p53, directly or indirectly, perturbs the normal regulation of phosphorylation of serine 10 in histone H3.
- Data show that growth arrested keratinocytes may resist ultraviolet-light induced apoptosis by inactivating the pro-apoptotic function of p53.
- p53 inhibits transcriptional activation of invasion gene thromboxane synthase mediated by the proto-oncogenic factor ets-1.
- Histone deacetylase inhibitors can induce Gadd45 through its promoter without the need for functional p53, and Oct-1 and NF-Y concertedly participate in Trichostatin A-induced activation of the gadd45 promoter.
- Resveratrol caused a dose-dependent increase in intracellular p53 and p21(WAF1/CIP1) levels.
- High p53 protein level is associated with advanced TNM stage and positive nodal status of squamous cell carcinoma of hypopharyngeal cancer
- The antiproliferative properties conjugated linoleic acids are a function their ability to elicit a p53 response that leads to the accumulation of pRb and cell growth arrest.
- P53 transcriptional activity is inhibited by MDM-2 overexpression, which blocks UV-induced cell cycle arrest and apoptosis
- The positive expression rates of p21 and p53 proteins were 75.0% and 57.3% respectively in pancreatic carcinoma, which were significantly different from those in the normal tissue (P<0.05). p21 and p53 proteins were positively correlated (P<0.05).
- increase in intracellular reactive oxygen species (ROS) associated with the magnitude of p53 protein expression correlated with the induction of either senescence or apoptosis in both normal and cancer cells
- proline-directed acetylation of p53 is a post-DNA binding event
- L11 functions as a negative regulator of HDM2 and there might exist in vivo an L11-HDM2-p53 pathway for monitoring ribosomal integrity
- p53 is an important mediators of chemoresistance in ovarian cancer cells.
- Tumor cells with wild-type p53 activity exhibited up-regulation of surface CD95 after ionizing irradiation.
- The presence of wild-type p53 increased survival of prostate carcinoma cells after fractionated exposure to radiation.
- p53 mutations are an infrequent event in nasopharyngeal carcinoma in Spanish patients
- p53 is part of the survival pathway induced by integrin alpha4beta1 ligation and has a role in B-cell chronic lymphocytic leukemia drug resistance
- cloned and characterized a p53 consensus element located within the first intron of the TRAIL-R3 gene
- p53 gene mutation is an independent predictor of poor prognosis in colorectal cancers
- In adenocarcinomas, no statistically significant correlation was found between K-ras mutational status and p21WAF1/CIP1 and p53 expression.
- p53 expression and certain apoptosis markers correlate with survival in thymic neuroendocrine tumors.
- p53 mutants showed increased binding to NQO1, which can explain their resistance to dicoumarol-induced degradation, as NQO1 has an important role in stabilizing hot-spot p53 mutant proteins in cancer
- We thus identified ik3-2 as a proapoptotic factor involved in both p53-mediated and p53-independent apoptotic pathways.
- Crucial role of p53 C-terminal phosphorylation in the regulation of its DNA-binding activity.
- MNNG induces apoptosis in lymphoblastoid cells by activating the p53-dependent Fas receptor-driven pathway.
- hHR23 binds to polyubiquitylated p53 via its carboxyl-terminal ubiquitin-associated (Uba) domain shielding p53 from deubiquitylation
- cytoplasmic sequestration of p53 by the E1B 55-kDa protein plays an important role in restricting p53 activities in human osteosarcoma cells
- p53 is required for sensitization to TRAIL
- bcl-2 may inhibit cell death at multiple points downstream of p53 activation
- epidemiological study suggests a role for p53PIN3 in tumorigenesis
- Bulgarian patients with invasive breast cancer screned for p53 gene mutations registered a 33.33% frequency of mutations.
- Association association between lack of response to 5-fluorouracil and mitomycin and mutations affecting the L2/L3 domains of the p53 protein.
- p53 protein was estimated by immunohistochemistry of beta-catenin and p53 proteins in colorecta mucinous carcinoma.
- Results suggest that progression of esophageal squamous cell carcinoma is controlled by a p53-dependent pathway.
- P53 mutation and LOH on chromosome 17 were found together only in glioblastomas, suggested that these genetic changes may accumulate during astrocytoma progression.
- A novel germline mutation in p53 gene was found in a patient with Li-Fraumeni syndrome.
- a correlation between focal p53 immunostaining in primary primary prostate cancers and cancer recurrence after radical prostatectomy
- Aberrant HPLC chromatographies were found in tumor tissues, while their normal-adjacent counterparts running in parallel showed a normal shape.
- both HPV infection and p53 gene abnormalities may contribute to Bilharzial bladder carcinogenesis in an independent way
- results show that low levels of Mdm2 activity induce monoubiquitination and nuclear export of p53, whereas high levels promote p53's polyubiquitination and nuclear degradation
- in subjects over 50, p53 Arg/Arg genotype is associated with increased risk of cutaneous melanoma as compared to genotypes Arg/Pro or Pro/Pro
- Abnormality of the p53 pathway was detected in cervix cancer and in CINs.
- TP53 mutations develop in non-neoplastic epithelial lesions of the vulva, lichen sclerosus and squamous hyperplasia and are intrinsic to the clonal evolution that leads to squamous cell carcinoma of the vulva.
- Adenovirus-p53 induces the expression of a variety of proapoptotic genes and that lack of induction in one of these genes does not block Ad/p53-mediated cell killing in human lung cancer cells.
- TP53 mutations were associated with high-stage, high-grade urothelial carcinomas of the bladder.
- The p21 upregulation followed the p53 phosphorylation process in irradiated MOLT-4 ce
- Study indicate that the coexistence of p53 protein accumulation and HER2 overexpression is a strong prognostic molecular marker in breast cancer.
- Review outlines uses of adenoviruses in brain tumor therapy by examining clinical trials of adenovirus-mediated p53 gene therapy and by reviewing the application of two conditionally replicative adenoviruses (CRAds) ONYX-015 and Delta 24 in brain tumors.
- The frequency of p53-positive patients is relatively low in T-ALL (29%) and B-CLL (16%). B-ALL, AML and CML patients revealed higher frequency of p53 protein.
- the p53 mutant p53R282del found in neuroblastoma cells is a non-functional mutant and has no dominant negative nature
- forced p53 gene expression is cytotoxic to human bladder cancer cells with either p53 mutant or wild-type background
- p53 basal transcription is regulated by down-regulation of protein kinase Cdelta
- expression of iNOS, P53 and Bax in the gallbladder wall
- cytoplasmic localization is stimulated my GTSE-1 expression
- Transcriptional activity depends on p53 and BRCA1: inability of the mutant suppressor to repress IGF-IR expression result in increased IGF-IR levels and IGF binding.
- results suggest that VEGF expression is involved in the promotion of angiogenesis in cervical neoplasia and that p53 is likely to be involved in the regulation of VEGF expression
- Expression of p53 protein can enhance proliferation of HCC cells and suppress apoptosis of HCC cells after transcatheter arterial chemoembolization
- Patient samples were stratified according to tobacco, alcohol consumption, and anatomic location of the tumor, but no statistically significant associations were obtained between the occurance of TP53 mutations and these lifestyle habits.
- p53 mutations are common among oral cavity cancers in the Brazilian population
- trp53 has a role in activation of the Fas/CD95 pathway
- Three novel TP53 mutations found in Russian breast cancer patients.
- O(6)MeG-triggered apoptosis in proliferating lymphocytes was preceded by a wave of double stranded breaks, which coincided with p53 and Fas receptor upregulation
- Upregulation of p14ARF paralleled with MDM2 inhibition contributes to p53 accumulation in the nucleus in radiation-treated breast cancer cells.
- Results suggest that apoptosis-associated speck-like protein (ASC) can function as an adaptor molecule for Bax and regulate a p53-Bax mitochondrial pathway of apoptosis.
- p53 induced apoptosis is inhibited by Bcl-xL in head and neck neoplasms
- complete loss of p53 is a prerequisite for collaborating with activated Ha-ras to promote bladder tumorigenesis
- TP53 polymorphisms were characterized in a cohort of 779 patients, of whom 342 cases had developed restenosis at six months post PTCA
- Results describe the structural effects of the R249S mutation in the DNA-binding core domain of the tumour suppressor protein p53.
- Downregulation of p16(INK4a) and loss of wild-type p53 expression occurs after escape from cell immortalization.
- TP53 inactivation is a major mechanism of HPV-related carcinogenesis in the oral cavity and oropharynx.
- inactivation of p53 is a protective mechanism utilized by cells to adapt to ER stress.
- effect of HCV core, NS3, NS5A and NS5B on cell proliferation is independent of p53 expression, and only HCV core protein induces the expression of both c-myc and p53
- v-Fos-stimulated invasion is independent of the pRb/p16(INK4a) and p53 tumor suppressor pathways and telomerase
- ATR-p53 pathway is suppressed in noncycling lymphocytes via ATR downregulation.
- Probably no association between TP53 polymorphism at codon 72, HPV infection and the etiology of cervical cancer in this population sample.
- Correlation between p53 accumulation and survival in bilharziasis associated bladder squamous cell carcinoma.
- The levels of p53 protein elevated in keloid, hypertrophic scar and white and hard hypertrophic scar
- PARP-1 overexpression counteracts DSB repair independently of its enzymatic activity and of poly(ADP-ribosyl)ation of p53 in particular, but synergizes with p53 in suppressing chromosomal rearrangements
- There was no correlation between human papillomavirus status and p53 overexpression in human oropharyngeal squamous cell carcinoma.
- Detection of P53 may be used as the screening marker for diagnosis of polycyclic aromatic hydrocarbons (PAHs)-related lung cancer related lung cancer, and may supplement the diagnostic value of conventional cytology.
- p53 might be involved in homologous recombination and/or checkpoint function by directly binding to DMC1 protein to repress genomic instability in meiotic germ cells
- basal p53 expression in WI38 human embryonic lung fibroblasts restricts growth rate and mediates density-dependent inhibition of growth and the associated G1 phase arrest of the cell cycle by affecting the density-dependent regulation of p16/INK4a.
- show that the Bcl-x(L) interaction surface on p53 involves the same region that is used by the protein to contact DNA. The p53-binding site on Bcl-x(L) is also defined.
- p53 disruption has a dramatic effect on how glioblastoma cells process topoisomerase I inhibitor-mediated DNA damage.
- levels of p53 are increased in three important brain tissues, i.e. frontal, parietal, and cerebellar cortices of autistic subjects, alluding to impaired apoptotic mechanisms in autism.
- TIAF1 and p53 functionally interact in regulating apoptosis, and TIAF1 is likely to participate in the nuclear translocation of activated p53.
- Results suggest that p53 degradation and inhibition of p14(ARF) signaling are independent functions of HPV16 E6, and that long-term proliferation of mammary epithelial cells requires inactivation of the p14(ARF)-p53 pathway.
- The ability to form unique amphipathic structures in both an aqueous cytosolic-like and a mixed organic membrane-mimetic solution environment may allow a p53 peptide from the mdm-2 binding domain to selectively and rapidly disrupt cancer cell membranes.
- Hepacivirus core protein modulates p53 transcription regulatory activity and post-translational modification.
- Loss of p21 and/or p53 might not predict for prognosis in oropharnyggeal squamous cell carcinoma.
- Acetylation of p53 in vivo may contribute, at least in part, to its transcriptional activation functions.
- p53 might play a protective role against cell damage induced by generation of intracellular ROS, through transcriptional activation of ALDH4
- p53 induced by ionizing radiation requires IFI16
- results suggest that microsatellite instability and p53 mutations are involved in tumor progression of dermatofibrosarcoma protuberans to fibrosarcoma as early and late events, respectively
- Low p53 expression attenuates HIF-1 transactivation by competing for p300. High p53 expression destroys the HIF-1alpha protein.Once p53 becomes activated under conditions of severe hypoxia/anoxia, it contributes to terminating HIF-1 responses.
- ChIP assays have shown that following radiation treatment the p21 and puma promoters, but not bax, have increased p53 binding. The presence of constitutive binding to putative p53 DNA binding sites in other genes was determined.
- combined expression of p53 and metallothionein did not improve the predictive value for recurrence compared to MT alone
- Hsp90-binding immunophilins link p53 to dynein during p53 transport to the nucleus
- p53 causes brain tumor regression by suppressing tumor proliferation and indirectly induces involution of tumor vessels by fostering unopposed activity of Ang-2 in an environment of diminishing VEGF.
- examination of expression of p53, p21, and phosphorylated p42/44 mitogen-activated protein kinase in human pulmonary arterial smooth muscle cells
- functions of p53 in regulating gene expression that play both synergistic and pleiotropic roles in p53-associated apoptosis
- the expression of DAP kinase, p19ARF, p53, and p21WAF1 was significantly down-regulated in the chronically HIV-1SF2-infected HUT78 T cells
- Overexpression of p53 is associated with the pathogenesis of urothelial cell carcinoma
- Data reveal that controlled MDM2 degradation is an important new step in p53 regulation.
- Results are not consistent with a high risk associated with TP53 codon 72 polymorphism in breast and in bladder cancers.
- Expression of this apoptosis-related protein may be a useful marker in cervix cancer development.
- Both survivors and nonsurvivors of fluorouracil treated rectal neoplasms show high P53 expression
- identified a global suppressor motif involving codons 235, 239, and 240
- HHV-6 has a mechanism for retaining p53 within the cytoplasm and protects the infected cells from apoptosis.
- Irinotecan resistant colorectal cancer lines are resistanst both in the presence or absence of p53.
- identification of one known and five new modulators of p53-dependent proliferation arrest, using an RNA interference library
- sustained inactivation of the p53 pathway by the HPV16 E6 protein is required for maintenance of the proliferative phenotype of HeLa cervical carcinoma cells
- The frequent presence of TP53 deletion detected in 48% of patients is surprising. It is generally thought that the aberration is found in 10-15% of clinical cases.
- Clinical course of B-CLL in group of patient with trisomy 12, trisomy 12 and TP53 deletion simultaneously is more aggressive compared to the course of disease of patients with no cytogenetic aberrations.
- the net deubiquitination of the various targets of HAUSP determines the steady-state level of p53
- Results identify a novel mechanism of p53-dependent apoptosis in which p53-mediated up-regulation of MnSOD and GPx, but not CAT, produces an imbalance in antioxidant enzymes and oxidative stress.
- These results have important implications regarding the mechanism of tumorigenesis involving missense p53 mutants or the N-terminally truncated isoforms.
- With respect to overexpressed p53 a significant difference was reached for complete remission rate (P = 0.01) and 5-year survival rate
- p53 induces a faster mobilization of Axin into the degradation complex thereby enhancing beta-catenin turnover as part of a protective mechanism against the development of cancer.
- p53 interacts with RNA via its C-terminal domain; oligomerization of p53 is significantly enhanced by disrupting this. Binding of RNA to p53 is involved in the mechanism of p53 latency.
- Phosphorylation of p53 on N-terminal serine residues is not required for increased transcription of most p53-responsive genes. Induction of p53 by p14ARF, with little phosphorylation, leads to substantial repression of genes with roles in proliferation.
- p53 activity and PIG3 gene function are uncoupled by UV-dependent alternative splicing through rapid proteolytic degradation
- A point mutation of p53 in a lung cancer patient simultaneously can elicit not only a humoral immune response against overexpressed p53 protein, but also a specific cytotoxic T lymphocyte response against the mutated epitope of p53 in the same patient.
- p53 codon 72 polymorphism may contribute to gastric cancer susceptibility
- The expression of p21 protein depends on p53 protein largely in normal gastric mucosa and dysplasia, but not in gastric carcinoma.
- p16INK4A, p14ARF, p53, and PCNA have roles in the progression of cervical neoplasia
- p53 induces NF-kappaB activation by an IkappaB kinase-independent mechanism involving phosphorylation of p65 by ribosomal S6 kinase 1
- These results are consistent with a model in which p53 and Mcl1 have opposing effects on mitochondrial apoptosis by interacting with, and modulating the activity of, the death effector Bak.
- Cyr61 activated the beta-catenin/TCF4 complex, which promoted the expression of c-myc and the latter induced expression of p53.
- Tumor-derived p53 mutants increase the cell growth rate. They cannot bind the wild-type p53 consensus sequence. The mutants have 'gain of function' properties. D281G transactivates asparagine synthetase & human telomerase reverse transcriptase promoters.
- role of pathway in regulating G1-S transition and apoptosis along with RFT
- These data suggest that nucleophosmin is an early responder to DNA damage that prevents premature activation of p53.
- p53-dependent BRCA1 nuclear export is induced by DNA damage
- Ceramide may function as a mediator of p53-independent apoptosis in human glioma cells.
- hNRAGE arrests cell growth through a p53 dependent pathway. hNRAGE also increases the p53 protein level as well as its phosphorylation (Ser392).
- results establish a direct functional link between p53 and human Rad51, and reveal that one of p53's functions in genome stabilization may be to prevent detrimental genome rearrangements promoted by Rad51
- TP53 mutation is common in early stage ovarian carcinomas of serous histology, with a mutation frequency comparable to that reported for advanced-stage ovarian tumors.
- p53-dependent apoptosis requires BOK and NOXA
- tumour-suppressor protein p53 is a COP1-interacting protein; COP1 is a critical negative regulator of p53
- Patients with cancer of the cardiac region had a significantly higher frequency of the Arg/Arg genotype than patients with chronic gastritis, duodenal ulcer, and noncardiac cancer.
- activation of the p53-p21WAF1 pathway and overexpression of cyclin D1 are induced during tumor cell differentiation by beta-catenin
- findings suggest that the tumor protein p53 codon 72 polymorphism is unlikely to be associated with endometriosis in Japanese women
- p53-dependent cell fate is determined by E1A-binding p300 nucleoprotein
- p53 codon 72 polymorphism contributes to a genetically determined variability in apoptotic susceptibility among old people and may have a role in myocardial ischaemia
- the N-terminal domain of PIAS1 interacts with DNA as well as p53
- new roles for several DNA damage response factors by demonstrating that they also participate in the oncogenic stress signaling pathway between E2F1 and p53
- mutated p53 has a role in human papillomavirus type 38-positive non-melanoma skin cancers
- Pifithrin-alpha inhibits p53 signaling after interaction of the tumor suppressor protein with hsp90 and its nuclear translocation
- mechanisms other than p53 may play a role in the regulation of bcl-2 expression in endometrial carcinoma
- survivin, p53, and bcl-2 are elevated in breast carcinoma but not ductal intraepithelial neoplasia
- WRN and TP53 perform different functions in a shared DNA damage response pathway.
- PCAF expression can be induced by wild-type p53
- unique mechanism for p53 regulation by the p65/RelA subunit of NF-kappaB.
- p53 protein increases in both neurons non-neuronal cells, including microglia, in HIV dementia. There may be a a novel role for p53 in the microglial response to gp120.
- BRCA1-BARD1 complexes act as an adaptor to mediate phosphorylation of p53, influencing G(1)/S cell cycle progression after DNA damage.
- thymidylate synthase and p53 have roles in regulating Fas-mediated apoptosis in response to antimetabolites
- 27.2% of hepatocellular carcinomas showed p53 alteration ,but only 1 of the tumors with p53 alteration was well differentiated.
- Evaluation of HIF-1alpha, p53 and p21 protein expression is a very useful and powerful indicator of sensitivity to chemotherapy and radiation resistasnce in human esophageal cancer.
- when p53 protein levels increase, it contributes to its own demise by up-regulating the transcription of S100B protein as part of a negative feedback loop
- p53 does not have a role in 14-3-3sigma/IGF-I receptor mediation of cell cycle progression
- suppression of p53-C277Y by RNAi reduced pig3 promoter activity, RNA, and protein expression
- nonagenarians and centenarians in good health have a statistically significant difference in the frequency of the GSTT1 deletion and the p53 genotypes when compared to younger controls; possible mechanisms for protection against aging are offered
- upon activation by DNA damage, wt p53 mediates an accelerated degradation of HIF-1alpha protein, resulting in reduced activation of CA9 transcription and, correspondingly, decreased levels of CAIX protein
- hMdmx is overexpressed in a significant percentage of various human tumors and amplified in 5% of primary breast tumors, all of which retained wild-type p53. iRNA-mediated reduction of hMdmx inhibited cell growth potential in a p53-dependent manner
- p53 is associated with the telomeric complex in alternative lengthening of telomeres (ALT) cells; inhibition of DNA synthesis in ALT cells by p53 requires intact specific DNA binding and suppression of recombination functions.
- Disruption of p53-p21/WAF1 cell cycle pathways contributes to tumor progression and worse clinical outcome of hepataocellular hepatoma.
- Glioma cells with functional p53 were relatively resistant to gamma-radiation, and ceramide may play an important role in caspase activation during gamma-radiation-induced apoptosis of glioma cells lacking functional p53.
- Relation between expression, DNA ploidy and human papillomavirus infection in cervical carcinoma.
- Results link p53 status with POLkappa expression and suggest that loss of p53 function may in part contribute to the observed POLkappa upregulation in human lung cancers.
- Activated p53 suppresses EZH2 expression, suggesting a further role for p53 in epigenetic regulation and in the maintenance of genetic stability.
- p53 codon 72 genotype does not influence CIN risk in the Taiwanese population
- No association between p53 status and overall survival in human glioma.
- Adenovirus infection does not need direct binding of E1B-55-kDa with p53 to inactivate p53, and forced p53 activity with consecutive apoptosis does not severely impair virus replication.
- Loss of heterozygosity at TP53.A (p53 gene exon 2-3) in 4 of 20(20%), at TP53.B (p53 gene exon 4) in 6 of 20(30%), and at TP53.G (p53 gene exon 11) in 0 of 20(0%) in hepatocellular carcinoma.
- P53 protein stimulates calmodulin 2 gene expression in 041 cells.
- observations identify hMutL proteins as regulators of p53 response and demonstrate for the first time a function of hMLH1-hPMS1 complex in controlling the DNA damage response
- FAK and Akt are activated in the attached fibroblast-populated collagen matrix whereas the p53 level is relatively low; matrix detachment downregulates FAK and Akt activity and induces p53.
- p53 and/or p21(WAF1/CIP1) genotype may influence the progression during gastric tumorigenesis.
- TP53 is ubiquitinated by topors
- in sensitive organs mitochondrial p53 accumulation in vivo occurs soon after a death stimulus
- p63 and p53 play a major role in the carcinogenesis of human esophageal squamous cells and in the growth of the carcinoma
- Results demonstrated a novel function of Ser(392) phosphorylation in regulating the oncogenic function of mutant p53.
- Regulation of cyclin E expression plays a role underlying numeral homeostasis of centrosomes in human bladder cancer cells and that deregulation of cyclin E expression, together with inactivation of p53, results in centrosome amplification.
- p53 acts upstream of Bax to promote antineoplastics mediated cell death in a proline-rich domain-dependent manner through both transcription-dependent and -independent mechanisms in human colon cancer HCT116 cells.
- A significant association between p53 gene Bam HI RFLP polymorphism and the infarction volume was found in patients with carotid atherothrombotic stroke from Moscow population.
- Ha-Ras(G12V) induced senescence regardless of p53 status and telomerase activation.
- Low-dose 5-aza-2'-deoxycytidine (DAC) induced enhancement of apoptosis mediated by Adenovirus-p53 infection, and ectopic overexpression of procaspase-9.
- activation of the DNA DSB checkpoint provides the selective pressure for the high frequency of p53 inactivation in human cancer [review]
- UbcH5B/C are E2s for Mdm2, which contribute to the maintenance of low levels of p53 and Mdm2 in unstressed cells; inhibition of p53 ubiquitination and degradation by targeting UbcH5B/C is not sufficient to up-regulate p53 transcriptional activity.
- Data suggest that geminin is required for suppressing overreplication in cells with wild-type or mutant p53 and that a G(2)/M checkpoint restricts the proliferation of cells with overreplicated DNA.
- hsp90beta is repressed by p53 in UV irradiation-induced apoptosis
- The coupled induction of iNOS and p53 upregulation in intrinsic renal cells of IgA nephropathy may be linked with both pro- and anti-apoptotic activities
- p53-induced apoptosis was investigated through quantitative proteomic profiling using comparative amino acid-coded tagging.
- analyses of statistical interactions between polymorphisms (p73 G4A, p53 Arg72Pro and p21 Ser31Arg polymorphisms) revealed the marginally significant risk of non-Hodgkin's lymphoma for interaction between p53 Arg72Pro and p73 G4A polymorphisms
- Tumorigenesis pathway independent of p53 dysfunction appears to exist in association with ulcerative colitis.
- YY1 regulates the transcriptional activity, acetylation, ubiquitination, and stability of p53 by inhibiting its interaction with the coactivator p300 and by enhancing its interaction with the negative regulator Mdm2.
- Cyclin D1, p53, and p21Waf1/Cip1 have roles in progression of serous epithelial ovarian cancer
- the inhibitory protein c-FLIP(L) is involved in resistance to CD95-mediated apoptosis in ovarian carcinoma cells with wild-type p53
- p53 activation is not necessary for up-regulation of NOXA in melanoma cells
- Serine 392 exerts important effects upon p53 stability via the inhibition of its nuclear export mechanism.
- the MDM2-L5-L11-L23 complex functions to inhibit MDM2-mediated p53 ubiquitination and thus activates p53
- the number of p53 gene alterations in low-grade central osteosarcomas is lower than that in conventional high-grade osteosarcomas.
- Tip60 plays a double role in the p53 pathway: under normal growth conditions, Tip60 contributes to maintain a basal pool of p53 by interfering with its degradation; following DNA damage, Tip60 functions as p53 co-activator
- NPM inhibits hypoxia-induced p53 phosphorylation at Ser-15 and interacts with p53 in hypoxic cells; hypoxia-driven cancer progression may require increased expression of NPM to suppress p53 activation and maintain cell survival
- These results reveal that ribosomal protein L23 is another regulator of the p53-MDM2 feedback regulation involved in cell growth.
- Data show that, when overexpressed, ribosomal protein L23 inhibits HDM2-induced p53 polyubiquitination and degradation and causes a p53-dependent cell cycle arrest.
- Radiation treatment in the presence of p53 C-terminal peptides is more effective for inducing p53 -mediated apoptosis than radiation treatment alone or p53 C-terminal peptide treatment alone in cancer cells.
- Review focuses on potency of p53 as an inducer of apoptosis and reasons for extraordinarily high frequency of p53 inactivation in tumors, and mechanisms of tumor cell sensitization to p53-induced apoptosis.
- Data show that the fundamental active unit of p53 appears to be the tetramer, which is induced by DNA binding.
- interaction of Ubc9 with p53 was regulated by phosphorylation of p53
- p53 plays a key role in luteinization of the primate ovarian follicle though the regulation of steroidogenic enzymes leading to progesterone synthesis.
- Data show that squamous cell carcinoma cells escape suspension-induced, p53-mediated anoikis by forming multicellular aggregates that use fibronectin survival signals mediated by integrin alpha(v) and focal adhesion kinase.
- SCN3B mediates a p53-dependent apoptotic pathway and may be a candidate for gene therapy combined with anticancer drugs.
- role in regulating survivin 2B
- Individuals carrying Arg allele compared to those with Pro allele have an increased risk for esophageal squamous cell carcinoma.
- Ras appears to attenuate p53 in SW480 cells by two independent regulatory mechanisms, the one leading to increased Mdm2-dependent p53 degradation and the other leading to a decrease in p53 transcription.
- Results describe the role of Daxx in modulating the apoptotic threshold and identify it as a possible integrating factor that coordinates the response of p53 family members.
- mechanism of p53 regulation originating through alternative splicing of the human p53 gene resulting in the expression of a novel p53 mRNA
- p53 gen mutation analysis may be useful in the follow-up of at-risk patients, and introduces new possibilities to analyse molecular markers before malignant lesions are clinically apparent.
- examined the binding of DNA in solution to a series of unmodified p53 constructs that lack various domains, and identified the residues of the C terminus that interact with the non-specific DNA
- Cyclin A1 methylation was inversely related to p53 mutational status in primary tumors, and forced expression of cyclin A1 resulted in robust induction of wild-type p53 in HNSCC cell lines.
- Anwuploidy of chromosomes 7, 8, 9, and 17 and of TP53 gene deletion and overexpression in intestinal mettaplasi samples from cancer-free patients.
- MDR functional phenotype could be associated with p53 mutation in the advanced stage of leukemias
- estimation of the sensitive positions to mutations in human p53 protein
- Protein tyrosine phosphatase 1-B levels increased with introduction of wt p53 and may be involved in the dephosphorylation of Janus kinase 2
- search for the factors interacting with NTH1 shows GST-NTH1 fusion protein precipitates proliferating cell nuclear antigen (PCNA) and p53 as well as XPG from human cell-free extracts
- Hsp90 chaperone activity is important for the transcriptional activity of genotypically wild-type p53
- Hsp90 is required to maintain the folded, active state of p53 by a reversible interaction
- Emerging evidence in this review discusses a key survival/death checkpoint in both peripheral and central neurons that involves the p53 tumor suppressor and its newly discovered family members, p73 and p63.
- STAG1, a novel transcriptional target for p53, mediates p53-dependent apoptosis, and might be a good candidate for next-generation gene therapy in cancer.
- herpesvirus saimiri (HVS) ORF73 binds both p53 and pRb in vitro and in vivo, colocalizes with p53 in T cells infected with HVS, and in cells overexpressing both ORF73 and p53, and adversely influences pRB/E2F and p53 transcriptional regulation
- p53 mutations were found in 70% of pancreatic adenocarcinoma cell lines and 33% of primary tumors. p53 missense mutations correlated with more frequenct metastases to all sites.
- repression of hTERT by endogenous p53 is mediated by p21 and E2F
- eIF5A may be a regulator of p53, and syntenin might regulate p53 by balancing the regulation of eIF5A signaling to p53 for apoptosis
- alterations in both p53 and p16ink4a can contribute to recessive dystrophic epidermolysis bullosa-associated squamous cell carcinoma
- NDRG1 is necessary but not sufficient for p53-mediated caspase activation and apoptosis
- describes that lactoferrin specifically transactivates the p53 tumor suppressor gene through the activation of nuclear factor-kappaB and consequently regulates p53-responsive oncogenes
- results suggest that SAP contributes to the execution of some p53 functions
- germline mutations in the TP53 gene in five index cases of German and Swiss origin with cancers typical of Li-Fraumeni syndrome
- The finding of different p53 gene mutations among multiple esophageal carcinoma lesions suggest further evidence of multicentric or field carcinogenesis of the human esophagus
- We conclude that overexpression of PKCdelta in human colon cancer cells induces multiple antineoplastic effects that depend on the activities of p21(Waf1/Cip1) and p53.
- solar UV rays in cause mutations in p53- specifically CC-->TT transitions- which lead to squamous cell carcinoma of the conjunctiva
- Genetic mutation analysis was performed and revealed a germline p53 mutation of CGT > CAT at codon 273
- TP53 does not have a role in the histologic response to chemotherapy in patients with osteosarcoma, but its mutation may be associated with disease progression
- p53 expression may have a role in progression of inflammatory breast cancer
- This study observes statistically significant differences on SNP rs2078486 and on haplotype CAC. These results demonstrated that TP53 might play a role in susceptibility to schizophrenia.
- PTIP facilitates ATM-mediated activation of p53 and promotes cellular resistance to ionizing radiation
- survivin can reduce the cell growth inhibition and apoptosis, and p53 elevates the p21 level, which may attenuate the cell death in the quercetin-treated human lung carcinoma cells
- Down-regulation of Cdc7 by small interfering RNA in a variety of tumor cell lines causes an abortive S phase, leading to cell death by either p53-independent apoptosis or aberrant mitosis.
- Upregulation of p53 protein is associated with breast disease
- proximal 5'-flanking region of the IKKalpha gene contains a functional promoter reciprocally regulated by p53 and ETS-1
- phosphorylation of p53 at Ser-215 by Aurora-A is a major mechanism to inactivate p53
- p53 phosphorylation on six major serine sites is not required for activation of p53 target genes or biological responses in vivo
- p53 protein expression is closely associated with decidual transformation indicates a novel role for this tumor suppressor in regulating human endometrial function.
- The p53 codon 72 gene polymorphism is not associated with the susceptibility of leiomyomas.
- E4orf6 uniquely utilizes two BC-box motifs for degradation of p53 and another target, Mre11
- In human osteosarcomas, hypermethylation of HIC1 is frequent only in tumors with p53 mutation
- sequestration of replication protein A by p53 at the sites of recombination is one means by which p53 can inhibit homologous recombination processes
- Decreased level of the phosphorylation is associated with basal cell carcinomas of skin
- A significant increase in p21, p53, and fas mRNA expression were reported in the proximal incompetent veins. The expression of p21 correlated with expression of p53. Fas overexpression did not correlate with p53 expression.
- low-dose radiation hypersensitivity is associated with p53-dependent apoptosis.
- increased expression is not an indicator of the presence of p53 gene mutations at exons 4-8 in hepatocellular carcinoma
- mutations in TP53 do not have a role in formation of human cerebral vascular malformations
- p53 antagonizes c-Myb by recruiting mSin3A to down-regulate specific Myb target genes
- IRF-1-p300 interface as an allosteric modifier of DNA-dependent acetylation of p53 at the p21 promoter
- Review. the role of p53 post-translational modifications in carcinogenesis and cancer prevention
- p53 may have important roles in the regulation of cytokinesis through controlling the transcription of PRC1
- Interaction with Brn-3a in sensory neurons may be critical for modulating p53-mediated gene expression and hence cell fate.
- Co-mutation of p53 and K-ras gene has neither synergic carcinogenesis-promoting effect, nor prognostic effect on rectal cancer.
- P53 is induced by Aluminum in neuron-like cells suggesting that the p53-dependent intrinsic pathway may be responsible for Aluminum-induced apoptosis.
- Data suggest that certain p53 mutations may have prognostic value in superficial bladder transitional cell carcinoma, even though they were not associated with other classic recurrence and tumor progression parameters.
- We propose that a major mechanism by which p53 maintains genome stability is the prevention of DSB accumulation at long-lived ssDNA regions in stalled-replication forks.
- VRK1 is the first step in a new pathway regulating p53 activity during cell proliferation
- p53, bcl-2 and telomerase have roles in progression of Egyptian breast cancer patients
- Twist-overexpressing MCF-7 cells displayed a deregulated p53 response to gamma-radiation and decreased regulation of downstream target genes
- role of Cul4A in the MDM2-mediated proteolysis of p53
- mutant p53s are likely to be distinct in terms of the extent to which each mechanism contributes to their gain-of-function phenotypes
- role in inducing EGR1 contributes to enhanced transformed properties and resistance to apoptosis
- COX-2-positive prostate cancer cells can have impaired p53 function even in the presence of wild-type p53 and that p53 activity can be restored in these cells via inhibition of COX-2 activity.
- Codon 72 of P53 genes may represent a risk factor for developing ovarian or endometrial neoplasms.
- Integrin alphav controls melanoma cell survival in 3D-collagen through a pathway involving p53 regulation of MEK1 signaling.
- p53 alterations commence as early as at the stage of benign and dysplastic nevi but there is no concordance between the frequent p53 protein expression and the rarity of both TP53 gene mutations in melanomas.
- protein kinase Calpha transcriptional repression via Sp1 by wild type p53 is involved in inhibition of multidrug resistance 1 P-glycoprotein phosphorylation
- Tax promotes cellular proliferation through activation of the NF-kappaB pathway while inhibiting the cell-cycle checkpoint and apoptotic function of the tumor suppressor gene p53 [review]
- downregulation of Cdc25C is mediated by p53 via two independent mechanisms, one involving direct binding to the cdc25C promoter
- The ability of p53 to bind and inactivate JNK, together with the activation of the p53 target genes related to cell cycle arrest and DNA damage repair, is responsible for its protection of cells against UV-induced apoptosis.
- maspin tumor suppressor expression is induced by p53 or TAp63gamma
- Interferon alpha-induced promyelocytic leukemia protein was unable to recruit p53 into nuclear bodies and its downregulation by RNA, Small Interfering did not alter CD95 expression
- p53 can directly induce Ipaf gene transcription, which contributes to p53-dependent apoptosis in at least some human cells
- in tumor cells lacking functional p53 and/or p21, p14(ARF) impaired mitotic entry and enforced a primarily cytoplasmic localization of p34(cdc2) that was associated with a decrease in p34(cdc2) kinase activity and reduced p34(cdc2) protein expression
- TP53 function closely influences the decision between apoptosis and growth arrest following Fatty acid synthase blockade
- p53-dependent loss of Fbxw7 leads to genetic instability by mechanisms that might involve the activation of Aurora-A, providing a rationale for the early occurrence of these mutations in human cancers
- p53 is an essential effector of PKCdelta in human colon cancer cells
- We conclude that (1) clinically achievable doses of ionizing radiation can trigger CDKN1A-dependent accelerated senescence in some human tumor cell lines that express wild-type TP53.
- an over-representation of the Pro allele of the p53 gene in women with idiopathic recurrent miscarriage gives support to the theory that p53 has a potential role during pregnancy.
- Cyclooxygexnase-2 in p53 wild-type cancer cells does not affect the cytoplasmic or nuclear levels of p53.
- p21WAF expression is induced by 5-Aza-CdR by demethylation of p73 leading to p53-independent apoptosis in myeloid leukemia
- Rad51 binds at a promiscuous, highly electrostatic binding site in p53
- LC8 binds to p53-binding protein 1 and mediates DNA damage-induced p53 nuclear accumulation
- cell lines that contain human tumor-derived temperature-sensitive p53 mutants show that Hsp90 is required for both stabilization and reactivation of mutated p53 at the permissive temperature
- Data show that 5-lipoxygenase activity increases during senescence-like growth arrest via a p53/p21-dependent pathway in both human and mouse embryo fibroblasts.
- The HIF-1alpha ODD domain binds weakly to the isolated p53 core domain but tightly to full-length p53 to give a complex of one HIF-1alpha ODD domain with a p53 dimer.
- Data suggest that MTBP differentially regulates the activity of MDM2 towards two of its most critical targets (itself and p53) and in doing so significantly contributes to MDM2-dependent p53 homeostasis in unstressed cells.
- Homozygosity for Pro of p53 Arg72Pro is potentially one of the genetic risk factors for hepatocarcinoma in a Chinese population.
- Tumor cell killing by autologous cytotoxic T lymphocytes can be enhanced by targeting degranulation-independent mechanisms via restoration of wild-type p53, a key determinant of apoptotic machinery regulation.
- Human papillomavirus infection and/or changes in p53 protein coexist in oral cavity papillomas.
- Mutated in choroid plexus carcinoma.
- that variations in TP53 and hCAD genes modulate the age of onset of Huntington disease .
- FADD/caspase-8 pathway induces apoptosis through p53 in human pre-malignant and malignant cells
- a productive human herpesvirus 6B infection suppresses T-cell proliferation concomitant with the phosphorylation and accumulation of p53
- DNMT1- and p53-mediated methylation of the survivin promoter, suggesting cooperation between p53 and DNMT1 in gene silencing.
- The mechanism of action of apigenin seems to involve p53, as it increased the levels of p53 and the p53-induced gene products p21WAF1/CIP1 and Bax.
- Epigallocatechin-3-gallate increased expression of tumor suppressor protein p53 in brest cancer cells.
- RAI3 is a cell growth-promoting gene and a novel P53 transcriptional target
- possible interplay between p53 C-terminal phosphorylation and acetylation, and they provide an additional mechanism for the control of the activity of p53 by Checkpoint kinase 1 and Checkpoint kinase 2
- mechanism by which p68 may act as a tumour cosuppressor in governing p53 transcriptional activity
- the promoter specificity plays an important role in selective activation of p53 DNA binding by c-Abl
- Data show that human papillomavirus E6 oncoprotein does not prevent p53 or p300 recruitment to the chromatin but inhibits p300-mediated acetylation on p53 and nucleosomal core histones.
- The results suggest that I3C represses cell proliferation through up-regulation of NAG-1 and that ATF3 may play a pivotal role in DIM-induced NAG-1 expression in human colorectal cancer cells.
- Plk3 is a RelA-NF-kappaB-regulated gene that induces apoptosis in both p53-dependent and -independent signaling pathways
- Rb and p53 have roles in progression of primary non-small cell lung carcinoma
- Ref-1 promotes association of dimers into tetramers, and de-stacking of higher oligomeric forms into the tetrameric form in vitro, thereby enhancing p53 binding to target DNA.
- Unique repressor domain resides in p53 at residues 90-116 whose activity can be modulated in the presence of 'differentiation therapy' and 'transcription therapy' agents.
- decreased cell-surface expression of Fas and resistance to Fas-mediated apoptosis may occur independently of loss of wt p53 expression in esophageal adenocarcinoma
- Structural analysis shows that the high stability of the Ser116Met modeled mutant is due to the preservation of the p53 core domain loop L1 conformation and the reduction of mobility in that region.
- p53 pathway mediates in part growth suppression by NaB and the p53 status may be an important determinant of chemosensitivity in HDI based cancer chemotherapy
- This study focused on the expression levels of Bcl-2 family regulators (anti-apoptotic Bcl-2 and Bcl-XL, pro-apoptotic Bcl-Xs and Bax), p53, and PCNA as a marker of proliferation, together with the evaluation of the level of apoptosis in human embryos.
- p14ARF induces p53-dependent cell cycle arrest but not apoptosis
- p53 might play a similar role in certain tissue stem cells and suppress the development of cancer stem cells [review]
- We found mutations in p53, K-ras, and BRAF genes in 35%, 30%, and 4% of tumors, respectively, and observed a minimal or no co-presence of these gene alterations.
- R273H removes an arginine involved in DNA binding, H168R and R249S induce substantial structural perturbation around the site
- Stress-induced activation of p53 in leukemia cells and normal lymphocytes requires mitochondrial activity and reactive oxygen species
- The homeodomain of Msx1 functions as a protein-protein interacting motif rather than a DNA-binding domain and is essential for stabilization, nuclear accumulation, and apoptotic function of wild-type p53.
- Taken together, these results suggest a novel function of COX-2 that inhibits DNA damage-induced apoptosis through direct regulation of p53 function.
- Phosphorylation of p53 plays a crucial role in detection and interaction with sites of DNA damage and unusual DNA structures.
- TP53 pathway is invslved in the carcinogenesis ofHepatic undifferentiated (embryonal) sarcoma.
- MUC1 regulates p53-responsive genes and thereby cell fate in the genotoxic stress response
- Activation domain 2 of p53 is required for induction of the proapoptotic target gene insulin-like growth factor binding protein 3 (IGFBP3) and p53 basic domain inhibits induction of this gene.
- Two cases of lymphomatoid palulosis with mutated p53 gene in biopsy showed no progression of disease in 5 yr follow up. May not play any significant role in the pathogenesis, progression or transformation of cutaneous CD30(+) lymphoproliferative diseases
- Atypical meningioma showed TP53 mutations and a 22q loss of heterozygosity (LOH), while glioblastoma showed epidermal growth factor receptor (EGFR) amplification and TP53 mutations.
- Expression of p53 is associated with NIH risk category, various pathological features, and clinical outcome, and may be independently prognostic for gastrointestinal stromal tumours.
- The p53 codon 72 polymorphism is unlikely to be related to HPV status and the onset of cervical cancer.
- Regulation of the nuclear export of hdm2 mRNA provides a mechanism whereby mitogen-stimulated cells avoid p53-dependent cell cycle arrest or apoptosis by maintaining the dynamic equilibrium of the Hdm2-p53 feedback loop
- Data showed that disabling of the p53 pathway was frequent event in oral carcinoma.
- an apoptosis-deficient Pro allele of the p53 gene may be related to psoriasis resistance to UV-based therapy
- p73, through HDM2, can oppose p53 tumor suppressor function and possibly contribute to tumorigenesis
- Quercetin and ellagic acid combined increase the activation of p53 and p21(cip1/waf1.
- DeltaNp73alpha not only acts as an inhibitor of p53/TAp73 functions in neuroblastoma tumors, but also cooperates with wt-p53 in playing a physiological role through the activation of BTG2TIS21/PC3 gene expression
- WR1065 specifically modulates a subset of p53 target genes in a colon carcinoma cell line, consistent with the observation that this agent elicits essentially p53-dependent, cell cycle arrest responses.
- Dehydroepiandrosterone increased the expression of p53 and p21 mRNAs.
- Specific silencing of p53 abrogated the antiviral effect of SD.IFN-beta, suggesting that the tumor suppressor is critically involved in antiviral defense mediated by intracellular IFN.
- blockade of pol II-mediated transcription induces p53 accumulation in mitochondria and is the critical factor for eliciting p53-dependent but transcription-independent apoptosis
- p53 protein expression in vivo does not correlate with the outcome of patients with primary in primary glioblastoma.
- association between genetic polymorphisms of GSTT1, p53 codon 72 and bladder cancer in southern Taiwan
- demonstrated that epigallocatechin-3-gallate activates growth arrest and apoptosis primarily via tumor suppressor p53-dependent pathway that involves the function of both p21 protein and Bax protein
- Data show that latent infection with Kaposi sarcoma-associated herpesvirus in B lymphocytes can be terminated by glycyrrhizic acid.
- TP53 deletion significantly associated with malignant transformation of breast papilloma, pointing to p53 role as a progression factor
- higher expression in atrophic oral lichen planus and patients with areca quid chewing
- The activation of the p53 pathway appears to be an effective approach in inhibiting tumor development.
- Limited activation of the PCNA promoter by p53 and its modified forms would restrict the amount of PCNA made available for DNA repair.
- p53 participates in a feedback mechanism with JNK to regulate the apoptotic process and is oppositely regulated by JNK1 and JNK2.
- Transactivation-dependent apoptosis does not always play a major role in p53-dependent apoptosis, indirectly supporting the importance role of the transactivation-independent mechanism.
- Mdm2 and mdmx prevent ASPP1 and ASPP2 from stimulating the apoptotic function of p53 by binding and inhibiting the transcriptional activity of p53.
- Effect of hibuscus polyphenol extracs in human gastric carcinoma cells is mediated via p53 signaling and p38 MAPK/FasL cascade pathway.
- Excision of nucleoside analogs from DNA by p53 protein suggests a potential cellular mechanism of resistance to inhibitors of human immunodeficiency virus type 1 reverse transcriptase
- A spontaneous increase of wild-type p53 occurring in ageing normal human MRC-5 fibroblasts is associated with irreversible reduction of proliferative potential.
- results provide a novel mechanism, by which p53 is stabilized in tumor cells, and they suggest that a mediator should exist between ubiquitinated p53 and proteasome, which may be defective in H1299 cells
- p53 is an effective repressor of snRNA gene transcription by RNA polymerases II and III.
- Loss or inactivation of p33(ING1b) normal function may be an important mechanism for the development of hepatocellular carcinoma retaining wild-type p53.
- the increased malignancy of cancer cells resulting from loss of p53 may be mediated, in part, through the choline phospholipid pathway
- data suggest that p53pSer15 plays a dual role in the functional interactions with early complexes of Rad51-dependent recombination and with BLM-associated surveillance and signalling complexes within distinct nuclear subcompartments
- l structure of the p53 binding domain of USP7 alone and bound to an EBNA1 peptide
- p53 was slightly increased in inverted follicular keratoses compared with inflammed or non-inflamed seborrheic keratoses.
- The p53 Pro allele is associated with an increased frequency of p53 mutations in non-small cell lung cancer.
- Colorectal cancers not expressing hMLH1 or hMSH2 may have distinct features from those expressing these mismatch repair proteins. p53 expression appears to be implicated in a compensatory pathway with mismatch repair proteins.
- Constitutive dephosphorylation at Ser 376 correlated with the nuclear accumulation of p53, but not with the transcriptional activity of the protein in glioma.
- TP53, CDKN1A, CDKN2A, and CDKN2B have roles in tumorigenesis in skin melanomas, but none of them is a main mutation target for melanoma tumorigenesis
- The coupled folding and binding of the p53 transactivation domain to the 70 kDa subunit of human replication protein A was investigated.
- DNA-damaging stresses showed a strong p53-dependent element in their responses, no discernible p53-dependent responses were triggered by the non-DNA-damaging stresses.
- TRR-Trx and APE/Ref-1 cooperate in the control of basal p53 activity, but not in its induction by DNA-damage.
- Proliferative inhibition of breast cancer cells by Velcade is associated with stabilization of p53.
- p53 may exert transcriptional upregulation effects on c-FLIP gene and more potent effects on promoting the degradation of c-FLIP protein
- p53, Bax, Bcl-2 and Mdm2 mRNA expression levels correlate with the malignant transformation of the uterine cervix
- Asymmetric self-renewal and immortal DNA strand cosegregation are regulated by the p53 cancer gene.
- Nuclear genetic polymorphisms related to oxidative stress or apoptosis may modify the age at onset of Leber's hereditary optic neuropathy (LHON).
- A potential association of P53 codon polymorphism was found with increased susceptibility to gastric cancer.
- protection of p53 from MDM2 by PTEN and the damage-induced activation of PTEN by phosphorylated p53 leads to the formation of an apoptotic amplification cycle in which p53 and PTEN coordinately increase cellular apoptosis
- The p53Arg allele was not associated with the development of cutaneous SCC
- Inactivating TP53 mutations were found in 55% of lethal metastatic pancreatic neoplasms.
- findings show that p53 plays a central role in the response of ARPE-19 cells to DNA damaging agents that act via different mechanisms. ARPE-19 cells with reduced p53 expression behave similar to tumor cell lines with mutated or non-functional p53.
- RB18A plays a central role to control p53wt and p53mut protein content and functions in cells through a loop of regulation, which involves MDM2
- Three point mutations of p53 gene were not predictive for tumor development in liver and renal transplantation patients.
- P73 may replace p53 in triggering not only apoptosis but also cell cycle arrest or DNA repair effectors in breast cancer cells.
- Analysis of expression levels of p21(waf1), as well as the activity of caspase-3 and caspase-8, allowed us to characterize some aspects of the arrest of PC-3 cells in G2 and the apoptotic response to oxidative stress in the absence of functional p53
- codon 47 polymorphism of p53 is functionally significant and may play a role in cancer risk, progression, and the efficacy of therapy
- abrogation of p53 functional activity can be a common feature of MLL fusion-mediated leukemogenesis
- FAK can suppress p53-mediated apoptosis and inhibit transcriptional activity of p53
- elevated levels of Myc counteract p53 activity in human tumor cells
- review of current knowledge about association of aneuploidy and p53
- role of p53 as a major pro-apoptotic factor in the pathogenesis of AIDS [review]
- review of the evidence for p53 as a participant in the responses of multiple CNS cell types to the presence of HIV and propose the hypothesis that HIV induced alterations in the CNS extracellular milieu converge at neuronal p53 activation
- expression of p53, MDM2, and p21Waf1 suggests a role for these oncoproteins in the regulation of endometrioma cell growth, but not in adenomyosis
- MdmX can affect post-translational modification and stability of Mdm2 and p53 activity through interaction with ARF
- The Aberrant expression of p53 Genes were determined in bone marrow samples of children with de novo B-lineage (n=170) and T-lineage (n=25) acute lymphoblastic leukemia (ALL).
- Ca2+ binding of human p53 tumor suppressor target peptide (residues 367-388) to rat S100B decreases the Ca2+ dissociation rate by approximately an order of magnitude.
- NLS domain of ING4 is essential for the binding of ING4 to p53 and the function of ING4 associated with p53
- spindle cell component of this case was genetically characterized by loss of heterozygosity (LOH) at a codon 234 of exon 7 of the p53 gene
- Many p53-defective tumors retain activity of the apoptosome, which is therefore a potential target for cancer chemotherapy. Inhibition of ACS may be a novel strategy to induce the death of p53-defective tumor cells
- TP53 mutation has only a limited role in the transformation of lymphoma to diffuse large B-cell lymphoma, exerting a heterogeneous influence upon phenotypic change. In contrast, dysregulation of MDM2 is frequent.
- p53 gene mutation may be an early event in esophageal carcinogenesis
- p35 reprter assays could not be ascribed to common dpible strand break-causing artifacts in standard genotoxicity screening.
- The combination of mutation with the codon 72 proline variant predicts poorer patient survival in non-small cell lung cancer.
- exposure-specific heterogeneity in inactivation of the TP53 pathway in bladder cancers
- Activated caspase-8 initiates the release of cytochrome c during thymoquine-induced apoptosis, thus offering a potential mechanism for TQ-induced apoptosis in p53-null HL-60 cancer cells.
- inhibition of transcriptional activity was caused by E1B-AP5
- overproduction of Mdm2, resulting from a naturally occurring SNP, inhibits chromatin-bound p53 from activating the transcription of its target genes.
- CHIP-induced degradation was observed for mutant and wild-type p53, which transiently associate with molecular chaperones Hsc70 and Hsp90 and can be diverted onto a degradation pathway through this association
- Pseudomonas aeruginosa azurin binds to tumor-suppressor protein p53
- Results indicate that the differential p53-regulated expression of survivin at different stages of the cell cycle results in different cellular outputs under the same apoptosis-inducer.
- The human gene in transgenic mice behaves like its murine ortholog in mouse hepatocarcinogenesis.
- In operable non-small lung cell cancers, there may be different relationship of this protein with paatient outcome.
- This meta-analysis produced evidence for interesting tumor site differences in the predictive value of TP53 mutation for survival benefit from 5FU chemotherapy.
- Specific TP53 mutations in L3 domain alone (only in DFS) or in combination with specific Ki-ras mutations at codon 13 are associated with a worse prognosis in sporadic Colorectal cancer.
- Study reports the first unequivocal case of a ganglioglioma harboring aberrant TP53 product that was expressed predominantly in the neuronal component.
- p53-specific serum antibodies are not associated with a history of skin carcinoma in renal transplant recipients and immunocompetent individuals.
- There is positive role for PI3K in p53 activation by anticancer agents, and suggest that the efficacy of PI3K inhibitors in cancer therapy may be greatly affected by the tumor p53 status.
- p53 is induced by urokinase in lung epithelial cells
- p53 not only can provide proapoptotic signals but also regulates a survival pathway influencing Mcl-1 and Bcl-x(L) levels
- in oral cancer cells the Ca(2+)- and cell cycle-dependent p53-S100A2 interaction might modulate proliferation
- Alterations of the TP53 gene occur not only as somatic mutations in human malignancies, but also as germline mutations in some cancer-prone families with Li-Fraumeni syndrome.
- p53 function was lost by TP53 germline mutation with the loss of a wild type allele induced by the chemotherapy against ovarian cancer, leading to the development of MDS.
- besides P53 alterations, mouse double minute 2 gene deregulation seems to be an important event in hepatocarcinogenesis
- The sequential accumulation of mutations in p53 drives the transition from normal epithelium through increasing adenomatous dysplasia to colorectal cancer.
- that wt-tumor protein p53 gene transfer inhibits interleukin 8 production and NF-kappaB transcription activity in cancer cells
- These results suggest that Chk2 regulates the transcription-independent mechanism of p53-mediated apoptosis by inducing stabilization of p53 in response to IR.
- Data show that the status of codon 72 polymorphism and p53 mutations can be used as a means for prediction of treatment response, although variables for each cancer type requires detailed evaluation.
- TrkA induces apoptosis of neuroblastoma cells and does so via a p53-dependent mechanism
- NPM inhibits ionizing irradiation-induced p53 transactivation, and interacts with p53 in hematopoietic cells.
- Mutations in proline 82 of p53 impair its activation by PIN1 and CHK2 in response to DNA damage.
- SAK repression by p53 is likely mediated through the recruitment of HDAC repressors, and SAK repression contributes to p53-induced apoptosis
- analysis of gain of function from a Li-Fraumeni TP53 mutation
- Taking p53 negativity in immunohistochemistry as evidence of a functional gene/protein, this extends the link between proliferation and apoptosis, hitherto observed only in cultured cells with functional p53, to a subset of solid tumours.
- a new T-->C point mutation was identified in intron 6 at position 13989 in a grade III medullary ductal breast carcinoma
- We propose that induction of NQO2 may relate to the observed increased expression of p53 that, in turn, contributes to the observed suppression of cell growth in both melanoma cell lines.
- Expression of p53 in renal carcinoma cells is independent of VHL.
- mutant p53 is reactivated and apoptosis is induced by maleimide analogs in human tumor cells
- p53-induced apoptosis may be important for efficient cell lysis and viral spread and that E1B-19K may neutralize the apoptotic activity of p53 at multiple levels
- inhibition in HTLV-1-transformed cells is regulated by activated AKT
- p53 polymorphism at codon 72 predicts the susceptibility to leiomyoma in a Caucasian population and may contribute to the pathogenesis of uterine leiomyoma.
- Results suggested that the loss of p53 expression in conjunction with the overexpression of p21(WAF1/CIP1) was a stronger predictor of survival benefit than either molecule alone in Japanese serous-type advanced ovarian cancer.
- The TP53 R337H mutation dramatically increases predisposition to childhood adrenocortical carcinoma (ACT) but not to other cancers, and explains the increased frequency of ACT observed in this geographic region.
- Activities of p53 are regulated during the cell cycle by E2F/p53 interactions; phosphorylation of p53 at Ser315 is required for this regulation.
- H pylori affect the p53 pattern in gastric mucosa when microsatellite system fails to work.
- Haplotype analysis also showed a significant association between TP53 and schizophrenia. These results provide further evidence that TP53 may play a role in the pathogenesis of schizophrenia.
- Differentiating human keratinocytes are deficient in p53 but they preserve global nucleotide excision repair as well as expression of genes encoding key DNA damage recognition proteins
- T-oligos transcriptionally down-regulate COX-2 expression in human skin via activation and up-regulation of p53, at least in part by inhibiting NFkappaB transcriptional activation
- A proteasome inhibitor, lactacystin, enhances TNFalpha cytotoxicity in p53-positive and -negative cells.
- p53 and p21 act in series in mediating cell cycle arrest. However, the two risk factors, p53 proline homozygosity and p21 arginine allele, although part of a common causal pathway, appear to act in a mutually exclusive manner.
- initiation of DNA replication is regulated by p53 through Cdc6 protein stability
- GSK3-dependent phosphorylation of Mdm2 regulates p53 abundance
- FGFR3 and Tp53 mutations do not appear to be associated with progression of T1G3 transitional bladder carcinomas
- Data may provide evidence to support the idea that p53 expression is related to multidrug resistance (MDR) in combination of 5-fluorouracil plus cisplatin therapy of gastric cancer cell lines.
- p53 undergoes ubiquitin-independent degradation by the 20S proteasomes and that this process is regulated by NAD(P)H quinone oxidoreductase 1 (NQO1) together with NADH [review]
- ATM directly activates p53 while activating a safe-lock mechanism to inactivate the negative regulators of p53, Mdm2, and Mdmx [review]
- p53 codon 72 alleles influence the response to anticancer drugs in cells from aged people by regulating the cell cycle inhibitor p21WAF1
- Ser15 phosphorylation is important in regulating the oncogenic function of mutant p53 apoptosis induction in the context of the NF-kappaB/IkappaB signaling pathway
- analysis of the role of HTLV I Tax in p53 inhibition in leukemia [review]
- ASPP2/(53BP2L) protein levels by proteasomal degradation modulates p53 apoptotic function
- mutant MYC proteins, by selectively disabling a p53-independent pathway, enable tumour cells to evade p53 action during lymphomagenesis
- Aberrant p53 expression appears to be a common event in both cutaneous and mucosal melanomas
- A significant correlation between YB-1 and PCNA-LI was found, but none was found between p53 expression and PCNA in lung cancer.
- first demonstration in human cancer cells that the p53 pathway can be suppressed by factors in the tumour-cell microenvironment
- p53 represses myelocytomatosis oncogene c-myc transcription through a mechanism that involves histone deacetylation
- repression of p53 expression by signal transducer and activator of transcription 3 is likely to have an important role in development of tumors
- uncoupling of the electrochemical gradient by increased manganese superoxide dismutase activity gives rise to p53 up-regulation
- ARF may regulate p53 acetylation and stability in part by inhibiting tripartite motif-containing 28-MDM2 binding
- polymorphic variants of p53 codon 72 are not clinically relevant for apoptosis induction or patient survival in B-type chronic lymphocytic leukemia
- These results suggest that the expression of eIF4E is reciprocally regulated by p53
- Data show that Topors enhances the conjugation of the small ubiquitin-like modifier 1 (SUMO-1) to p53 in vivo and in a reconstituted in vitro system.
- an aberrant p53 status was related to IL-8 expression in patients with non-small cell lung carcinoma
- evidence that in lung carcinomas, non-CpG methylation is frequently observed in certain GC rich regions of the p53 gene; evidence presented from the p53 mutation databases which corroborates the reported experimental results
- by binding to E6, Pitx2a interferes with E6/E6AP-mediated p53 degradation, leading to the accumulation of functional p53 protein in HeLa cells
- p53 isoforms can regulate p53 transcriptional activity.
- The p53 codon 72 Arg/Pro polymorphism is not associated with age of onset or severity of glaucoma.
- in nasopharyngeal carcinoma cells, SarCNU-induced apoptosis is p53-dependent while SarCNU-induced G2/M arrest is mediated by the cyclin B1-cdc-2 complex
- the p14ARF-p53-MDM2 pathway has a role in development of oral squamous cell carcinoma
- P53 is probably involved in the development of conjunctival and eyelid tumors due to its high rate of presence in both benign and malignant neoplasms of these organs.
- demonstrated that a tripartite nexus between Bcl-xL, cytoplasmic p53, and PUMA coordinates the nuclear and cytoplasmic p53 proapoptotic functions
- findings suggest that overexpression of EGFR in glioblastomas in Chinese patients may be associated closely with the patients age but not with the tumors' pathological pathway
- Transcriptionally active p53 is required for nuclear localization of Y-box-binding protein (YB1).
- p53-mdm2 binding is subtler than previously thought and involves global contacts such as multiple "non-contiguous" minimally structured motifs instead of being localized to one small helix mini-domain in p53 TAD
- redox cycling of anthracyclines and p53-dependent apoptosis in cancer cells requires thioredoxin
- Tumor suppressor molecule p53 maintains mitochondrial genetic stability through its ability to translocate to mitochondria and interact with mtDNA polymerase gamma (pol gamma) in response to mtDNA damage.
- PRIMA-1 could be considered in combination therapy with DNA-targeted agents for the treatment of breast cancer, especially for tumors with aberrant p53 function.
- HER-2/neu and p53 are likely to be involved in the regulation of COX-2 expression in invasive ductal carcinomas of the breast.
- mutant p53 suppresses the expression of the MSP (MST-1/HGFL) gene, encoding the ligand of the receptor tyrosine kinase RON, implicated in a variety of cellular responses
- Among women with p53 alterations, adjuvant radiotherapy substantially increased survival
- TP53 abnormalities are early and frequent events in the pathogenesis of gallbladder carcinoma, starting from chronic cholecystitis.
- p53 codon 72 genotypes are associated with the age of onset of colorectal carcinoma in a mismatch repair deficient background in a dose dependent manner
- Results indicated that p53 down-regulated the expression of MDM2 oncogene by binding specifically to P3 promoter region.
- Transient co-transfection of p53 family members showed that p53 and transactivating (TA)-p73, but not TA-p63, repress endogenous AFP transcription additively or independently.
- the p53 and MDM2 promoter polymorphisms do not appear to play a role on age of colorectal cancer onset in Lynch syndrome
- loss of nuclear p53 signal may have a role in cisplatin resistance in head and neck squamous cell carcinoma
- Trp/Met/Phe residues have roles in physical interactions of p53 with cellular proteins
- PARP activation and the concomitant reduction of Sir2alpha activity in failing hearts regulate the post-translational acetylation of p53
- pRB degradation involved in gastric tumor cell apoptosis is p53-independent
- WOX1 plays a critical role in conferring cellular sensitivity to apoptotic stress and Tyr33 phosphorylation in WOX1 is essential for binding and stabilizing Ser46-phosphorylated p53
- The data was obtained that establishes the contribution of the transcription-independent mitochondrial p53 pathway to apoptosis of primary cells in response to deregulated oncogenes.
- negative cross-talk between p53 and C/EBPbeta is likely to impact expression of their respective target genes
- Bcl-2 has a role in cell death, apoptosis, and cytochrome c release independent of p53
- TP53 mutations in BRCA1 mutation carriers do not appear to have a role in progression of ovarian neoplasms
- p53 may act as a DNA topology-modulating factor
- Results suggests that analysis of p53 codon 72 polymorphism may provide a simple predictive marker for selecting the right breast cancer patients to anthracycline-based neoadjuvant chemotherapy in clinical setting.
- In summary, the p53/p21 pathway is mainly responsible for GC-induced apoptosis, but the coordinated activation of the p53/p21 and p16 pathway is responsible for GC-induced endothelial cell senescence through a Rb-dependent mechanism.
- the p53-HDM2 interaction can be inhibited by a newly isolated hexylitaconic acid from the marine-derived fungus, Arthrinium
- Copper alters the conformation and transcriptional activity of TP53 in Hep G2 cells.
- Functional p53 can promote the adenovirus (Ad) lytic cycle
- BCL6 gene is a new p53 target, regulated through a p53 response element in B-cell lymphoma.
- 4-oxo-2-nonenal, a lipid peroxidation product is a potential trigger of the p53 pathway
- p53 expression in HBV or HCV cirrhotic liver are a rather late event in carcinogenesis and related to hepatocellular carcinoma grade
- overexpression of c-myc (p=0.038) related to poor survival whereas increased positivity for p53 predicted better survival (p=0.013).
- A role of Aurora-C in the development and progression of cancer especially in the presence of mutated p53.
- mutants of p53 may induce loss of drug sensitivity is via the NF-kappaB2 pathway
- analysis of p53 target genes by digital fluorescent differential display
- analysis of p53-regulated genes by the method of differential display
- p53 mutation was found in 28% of sporadic adenocarcinomas respectively and in 0% and 22% of the 9 HNPCC cases.
- The results showed that retroviral vector-mediated RNAi can substantially downregulate the expression of human p53 in 293-T cells.
- higher frequency of spicy food intake and use of unboiled well water may be risk factors of esophageal cancer via p53 mutations in China
- Both p53 and c-erbB-2 proteins appear to be involved at an early stage of malignization of pleomorphic adenoma
- Results demonstrate that p53 base mutations in combination with allelic imbalance do not predict survival or progression of colorectal cancer.
- TP53 expression may be a useful biomarker for assessing the risk of developing esophageal cancer.
- Transient transfection of hepatitis B virus into the SMMU-7721 cell line can enhance p53 expression and its effects on development of hepatocarcinoma
- p53 protein can regulate huntingtin expression at transcriptional level
- Results describe the opposite effect of ERK1/2 and JNK on p53-independent p21WAF1/CIP1 activation involved in the arsenic trioxide-induced human epidermoid carcinoma A431 cellular cytotoxicity.
- p53 protects the genome from oxidation by reactive oxygen species (ROS), a major cause of DNA damage and genetic instability.
- Genetic polymorphisms in cell cycle regulatory genes MDM2 and TP53 contribute to the risk of developing lung cancer.
- IFN-alpha plus IFN-gamma triggers apoptosis independent of p53 in HaCaT cells, and also demonstrate an unexpected survival role for p53 in human KCs as regards apoptotic responsiveness to cytokines
- The degree of acetylation regulates p53 nucleus-cytoplasm trafficking by neutralizing a lysine-dependent charge patch, which in turn, controls oligomerization-dependent p53 nuclear export.
- Loss of p53 function can lead to decreased hOgg1 repair activity.
- The current data collectively indicate that BaP induces apoptosis of Hepa1c1c7 cells via activation of p53-related signaling, which was, in part, regulated by p38 kinase.
- age dependent phosphorylation of p53 protein and deregulation of p53 gene has a role in the development of human vestibular schwannomas
- induction of transcription is mediated by HIC1 p53-responsive element
- We aimed to investigate the expression pattern of p53, Bcl-2 and C-Myc in colorectal cancer(CRC)tissues obtained from Egyptian colorectal cancer patients divided in two different groups, associated with and without Schistosoma mansoni.
- transglutaminase 2 (TG2) modification of p53 could be an additional mechanism whereby TG2 could facilitate apoptosis
- TFII-I is degraded in a p53-dependent manner and this degradation may contribute to p53-induced cell cycle arrest.
- p53 overexpression in esophageal cancer tissue is positively associated with the presence of the Arg allele of the p53 codon 72 polymorphism
- TAp63alpha may promote thyroid tumour progression by inactivating the tumour suppressor activity of p53.
- p33ING1b prominently enhances etoposide-induced apoptosis through p53-dependent pathways in human osteosarcoma cells.
- expression of p53 is essential for cytotoxic effect of cisplatin in human malignant glioblastoma cells, A172 and T98G, and introduction of apoptotic signal molecules, such as p53, will be beneficial to achieve chemosensitivity in malignant glioma
- DNA hypermethylation of p53 was detected in a quarter of the low-grade, low-stage transitional cell carcinomas(TCC) and undifferentiated small cell carcinomas, but only sporadically in squamous cell carcinomas, and was absent in high-grade, high-stage TC
- The P allele of the p53 R72P polymorphism has an increased risk for hepatocellular carcinoma in HbsAg-negative subjects, and exerts a synergistic influence on the risk for HCC when combined with HCC family history and the male gender.
- The experimental data suggest that the ANNEXIN A2 gene may relate to cellular apoptosis induced by p53 gene.
- These findings suggest that overexpression of Mdm2 can perturb a RB pathway regardless of the p53 gene status, promoting carcinogenesis.
- Overall, our findings indicate that FHL2 can also regulate p53 via a direct association with HIPK2.
- The signaling pathway for colonocyte apoptosis following toxin A exposure involves p38-dependent activation of p53 and subsequent induction of p21(WAF1/CIP1), resulting in cytochrome c release and caspase-3 activation through Bak induction.
- To investigate the prognostic and predictive relevance of p53 protein, Ki-67 antigen, MMP-2 and MMP-9 in patients with transitional cell carcinoma (TCC) of the upper urinary tract
- PPM1D promotes breast tumor growth both by inhibiting p53 activity and by enhancing steroid hormone receptor action
- Clear need in human melanoma cell lines to disrupt both RB and p53 pathways and recurrent mechanisms which play into the unique genetic vulnerabilities of this tumor type.
- Although SIRT1 deacetylates p53, this does not play a role in cell survival following DNA damage in certain cell lines and primary human mammary epithelial cells.
- The expression of bcl-2 and p53 represent biological characteristics of colorectal carcinomas.
- Our results indicate that chromatin alteration in interstitial chromosomal regions is the most likely cause of continuous activation of p53, which results in the induction of SLGA by ionizing radiation.
- Our results indicate that the TP53 P allele is associated with a worse prognosis (P=0.011) while P21 polymorphism genotypes did not reveal any statistically significant result (P>0.05).
- may contribute to the higher level of constitutive apoptosis in cultures of cytotrophoblasts compared to syncytiotrophoblasts
- These findings indicate that PKCdelta regulates p53 to induce apoptotic cell death in the cellular response to DNA damage.
- specific amino acid substitutions in hepatitis C virus NS3 impair p53 interaction and anti-apoptotic activity of NS3
- Mutation rate of p53 is not particularly high, but there is a significant risk that cancer cells will resist p53 retroviral gene therapy as a result of retroviral replication errors.
- Results illustrate a novel mechanism of the alteration of p53 function that is mediated by a cutaneous HPV type and support the role of HPV38 and deltaNp73 in human carcinogenesis.
- Tumours with FGFR3+/p53- phenotype seem to have a distinctive pathway in bladder tumorigenesis.
- TP53 gene mutations alone are not likely to represent a widely useful prognostic marker of the risk of progression to malignancy, at least not in Barrett's esophagus without dysplasia.
- P53 mutational analysis in 56 colorectal cancer cell lines
- BTG2 expression was found to be significantly reduced in a large proportion of human kidney and breast carcinomas, suggesting that BTG2 is a tumor suppressor that links p53 and Rb pathways in human tumorigenesis.
- there is a decrease in p53 apoptotic rate associated with the No Ins-72Pro haplotype in BRCA2 mutation carriers
- P53 interferes with the TAD-truncated p73alpha-mediated activation of NFkappaB.
- identification of a second binding site helps stabilize the interaction between HDM2 and p53 during p53 degradation
- the VEGF system is integrated into the p53 transcriptional network by an SNP in the flt-1 promoter
- Myc overexpression causes DNA damage in vivo and the ATM-dependent response to this damage is critical for p53 activation, apoptosis, and the suppression of tumor development
- Beta-interferon-induced senescence was more efficient in cells expressing either, p53, or constitutive allele of ERK2 or RasV12.
- Data suggest that, in the absence of DNA, the acetylation motif of p53 is in a cryptic state, but after DNA binding, allosteric effects mediate an exposure of the acetylation motif to allow DNA-dependent acetylation of the tetramer.
- indicate a novel translational control of p53 gene expression and activity
- co-expression of MT and p53 and their complex formation in tumor cells may be involved in regulation of apoptosis in these cells.
- WT p53, but not tumor-derived mutants, bind to BCL2 via the DNA binding domain and induce mitochondrial permeabilization.
- some isoforms of p63 serve as a pro-survival factor by up-regulating GPX2 to reduce the p53-dependent oxidative stress-induced apoptotic response
- These data provide evidence that in addition to the COOH-terminal residues, p53 may also be ubiquitinated at sites in the DNA-binding domain.
- TP53 mutations and cyclin-dependent kinase inhibitor 2A promoter methylation, but not alterations in the H-Ras and K-Ras genes, might be involved in the malignant progression of pleomorphic adenomas into carcinoma
- Polymorphisms in some insulin-related genes are associated with an increased risk of colon cancer with specific KRAS2 and TP53 mutations, implying a link between these genetic changes and specific mutational pathways in carcinogenesis.
- No deletions were found in the p53 gene of these MD tumor cell lines, truncations in the p53 ORFs observed in this study might result from alternative splicing of the p53 gene.
- PolH has a novel role in the DNA damage checkpoint, and a p53 target can modulate the DNA damage response and subsequently regulate p53 activation.
- molecular analysis of p53 haplo-insufficiency
- our data suggest that p53 N-terminal domain interacts with Bcl-Xl but the characteristic of the molecular interaction appears to be different from that of the DNA-binding domain of p53.
- phosphorylation of p53 by protein kinase c abolishes its interaction with Ki-1/57 in vitro
- the DNA-binding ability of the p53 protein was required for sequestration by human cytomegalovirus
- Mutations do not confer a growth advantage to somatic heterozygous clusters or maintenance turnover units.
- TP53 self-complementary surface for the association of core domains into dimers within the tetrameric complex was found.
- Tumor suppressor p53 structure was determined in solution using state-of-the-art isotopic labeling techniques and NMR spectroscopy to complement its crystal structure.
- interference with the p53/PUMA/Bax cascade is crucial for the antiapoptotic function of the viral E6 oncogene in HPV-positive cancer cells
- Trp53(72P) is more efficient than Trp53(72R) in specifically activating several Trp53-dependent DNA-repair target genes in several cellular systems.
- suppressing p53 function is an important component in the pro-proliferative role of ERalpha
- results indicate that KSHV vIRF1 comprehensively compromises an ATM/p53-mediated DNA damage response checkpoint by targeting both upstream ATM kinase and downstream p53 tumor suppressor
- N-terminal domain of USP7 binds two closely spaced 4-residue sites in both p53 and MDM2, falling between p53 residues 359-367 and MDM2 residues 147-159.
- This study demonstrated that p53 codon 72 Pro homozygosity is associated with a higher risk of developing hypopharyngeal cancer
- The expression rate of p53 was relatively high in small cell lung cancer without any prognostic significance.
- Logistic regression analysis showed p53 and COX-2 as dependent predictors in pancreatic carcinogenesis, and a reciprocal relationship to neoplastic progression between p53 and COX-2.
- Immunoreactivity of VEGF, p53 and ICAM-1 was found in epithelial, fibroblast and vascular endothelial cells.
- E6AP is extensively involved in the ubiquitin-mediated degradation of p53 (an HPV E6-dependent substrate) as a cellular E3 ubiquitin-protein ligase.
- an independent prognostic marker in stage III colrectal carcinoma
- p53 gene alterations may be involved in Balkan endemic nephropathy genetic pathways.
- Results show show that TP53 mutations identified by gene sequencing have an independent prognostic value in breast cancer and could have potential uses in clinical practice.
- Results suggest that the p53-VEGF pathway can regulate tumor angiogenesis in human gallbladder carcinoma.
- analysis of TP53 mutation pattern in radiation-induced sarcomas
- Results show that the TP53 R337H germline mutation predisposes to a larger spectrum of tumours.
- Increased risk of non-small cell lung cancer and frequency of somatic TP53 gene mutations in Pro72 carriers of TP53 Arg72Pro polymorphism
- Protein phoaphatase-1 directly dephosphorylates p53. This has as important an impact on its functions as phosphorylation does. One way PP-1 promotes cell survival is to dephosphorylate p53, & thus negatively regulate the p53-dependent death pathway.
- p53 inhibits protein synthesis in human lung carcinoma cells;The mechanism involves dephosphorylation and accumulation of the translational inhibitor 4E-BP1, and increased association of 4E-BP1 with initiation factor eIF4E.
- TP53 G-->T transversions associated with tobacco smoke carcinogens were most frequent (50%) in the intermediate location.
- No associations were observed with tp53.
- a novel function for p53 in the maintenance of Golgi complex integrity and for myosin VI in the p53-dependent prosurvival pathway.
- IRF3 induces cell growth inhibition and cellular senescence through activation of p53 tumor suppressor
- We suggest that p53 has a role in RAD51 clearance post DSB repair and that nucleoli might be sites of RAD51 protein degradation.
- caspase-6 and its cleavage of lamin A are critical in apoptotic signaling triggered by resveratrol in the colon carcinoma cells, which can be activated in the absence of Bax or p53
- Expression predicts response to anticancer drugs in advanced hepatocellular carcinoma.
- Data suggest that detection of mutated p53 could be a useful serological marker for diagnostic purposes.
- Findings support the hypothesis that p53 mutations are homogeneous throughout a tumor and may thus be a more useful diagnostic and prognostic indicator.
- Findings suggest TP53 allele combinations other than Arg/Arg may contribute to the risk of development of papillary thyroid cancer in individuals exposed to radiation during their late childhood, adolescence or in young adulthood.
- Alpha-tocopheryl succinate activates expression of DR4/DR5 in a p53-dependent manner and re-establishes sensitivity of resistant MM cells to TRAIL-mediated apoptosis.
- Two molecular dynamics simulations of the region E17-N29 of p53 (p53(17-29)) at different temperatures were performed for a total time of 0.2 micros, to study the conformational landscape of this region.
- Caspase-dependent cleavage of p53 resulting in the generation of four fragments, two of which lack a nuclear localization signal and consequently localize to cytosol; these translocate to mitochondria and induce membrane depolarization.
- STAT5 activation specifically cooperates with the loss of p53 function in B-cell lymphomagenesis
- p53 protein appears only in sporadic cases (6.6%) of severe colonic dysplasia
- analysis of p53 gene mutants in human breast cancer cell lines
- These findings suggest that the silencing of astrin induce a p53-dependent apoptosis and has an additive effect on paclitaxel treatment.
- CUL7 functions to promote cell growth through, in part, antagonizing the function of p53
- Telomere dysfunction in the absence of cell-cycle checkpoint protein p53 may explain the high frequency of alterations in chromosome numbers found in many solid tumors.
- results show that stabilizing peripheral structural motifs can greatly enhance the stability of the p53 core domain and therefore is likely to be a viable alternative in the development of stable p53
- 11 patients had TP53 mutations within the Barrett's epithelium.
- Cyclin dependent kinase 9, whose well-known substrate is RNA polymerase II, can also phosphorylate p53.
- findings of the present study indicate that p53 codon 72 arginine homozygous genotype may represent a genetic predisposing factor for colon cancer development
- p53 codon 72 polymorphisms do not serve as a susceptibility factor affecting the chances of miscarriage in an unselected population.
- While ATL patients carrying a wild-type p53 enter remission following treatment with AZT, those with a mutated p53 did not respond, and patients' disease relapse was associated with the selection of a tumor clone carrying mutated inactive p53.
- analysis of the role of p53 substrate conformation in controlling MDM2-dependent ubiquitination of p53 and identification of a link between substrate misfolding and susceptibility to ubiquitination
- concludes that(1) p53 binds RNA in vivo, (2) RNA binding by p53 is largely sequence-nonspecific in the yeast nucleus, (3) some structure-specific RNA binding by p53 cannot be ruled out, and (4) caution is required when interpreting results of RNA screens
- Myc and E2F1 engage the ATM signaling pathway to activate p53 and induce apoptosis [review]
- Fatty acid synthase (FAS) gene, encoding for a key enzyme involved in the biogenesis of membrane lipids in rapidly proliferating cells, is a conserved target of the p53 family throughout the evolution.
- analysis of a novel regulatory pathway for the expression of survivin under the control of KLF5 and p53
- Our data indicated that in MTX M cells, p53 is sequestered in the cytoplasm by a novel mechanism that abrogates p53 residual function.
- A Small Ras-like GTPase protein Ray was indicated to modulate p53 transcriptional activity of PRPK.
- Degradation of endogenous HIPK2 depends on the presence of a functional p53 protein.
- angiostatins K1-3, K1-4 and K1-4.5 mediate anti-angiogenesis in a process involvingp53, FasL, AKT and mRNA deregulation
- Authors report that the codon 72 polymorphism in the p53 gene may be a predictor of tamoxifen response, and that breast cancer patients lacking the pro72 allele might be candidates for other therapies.
- Variations in TP53 and BAX alleles are unrelated to the development of pemphigus foliaceus.
- binding of p53 serves to modify simian virus 40 large T antigen (SV40 LT) by targeting CREB binding protein and p300 binding to direct the acetylation of SV40 LT
- This study defines a new role for residues 53 and 54 of p53 in regulating transrepression and demonstrates that 25-26 and 53-54 work in the same pathway to induce apoptosis through gene repression.
- low doses of Taxol for 18 h determined the upregulation of p53 and p21 waf expression concomitantly with a decrease of the anti-apoptotic Bcl-2.
- DeltaNp63alpha would downregulate p53 in response to DNA damage.
- Findings not only identify mortalin as an upstream molecule of p53 but also provide evidence for the involvement of centrosomally localized p53 in the regulation of centrosome duplication.
- DNA fragmentation factor plays an important and P53-independent role in maintaining chromosome stability and suppressing tumor development.
- distribution of methylation sites and repetitive elements in silent and nonsense p53 mutations in cancers
- p90Rsk-mediated modulation of Hdm2 nuclear is linked to cytoplasmic shuttling with the diminished ability of p53 to regulate cell cycle checkpoints that ultimately leads to transformation
- HDM2 can selectively down-regulate the transcription function of p53 without either degrading p53 or affecting the interaction of p53 with target promoters
- Jab1 is required to remove post-translationally modified p53 in coordination with mdm2
- Alleles and smoking play a significant role in modified prostate cancer risk in this study population.
- Data show that nuclear accumulations of p53 and Mdm2 are accompanied by reductions in c-Abl and p300 in zinc-depleted human hepatoblastoma cells.
- Candidate p53-binding sites were identified in the AP-2alpha and AP-2gamma promoters and may mediate some of the downstream effects of p53 expression such as inhibition of proliferation
- Finds a corrrelation between the p53 codon 72 polymorphism and location of gastric cancer in Korea.
- p53 as a determinant of the response to oncogene inhibition
- Mutations in the p53 gene in bladder cancer may differ according to the presence or absence of certain DNA repair gene variants.
- Our comparison of binding by wild-type and mutant domains indicates the sequence specificity of BRCA1-p53 interaction.
- These results suggest that the tumor suppressor pVHL has an unexpected function to upregulate the tumor suppressor p53.
- In mammalian cells, translesion DNA synthesis (TLS) is controlled by the tumor suppressor p53, and by the cell cycle inhibitor p21 via its PCNA-interacting domain, to maintain a low mutagenic load at the price of reduced repair efficiency.
- serum p53 protein may have a role in hepatocellular carcinoma
- Immunohistochemical detection of TP53 expression is a biomarker of malignant progression in Barrett's oesophagus but sensitivity is too low to act as a criterion to inform endoscopic surveillance strategies.
- Data suggest that dose-dependent UV stabilization of p53 in cultured human cells undergoing apoptosis is mediated by poly(ADP-ribosyl)ation.
- p53 and NF-kappaB cooperate in upregulating Cox-2 expression, promoting cell survival in inflammatory precursor lesions.
- NF-kappaB-dependency of the platelet-activating factor -induced increase in VEGF expression is due to decreased p53 activity, which is reciprocally regulated by increased NF-kappaB activity.
- We demonstrated that p53 wild-type protein nuclei accumulation is associated with GEP protein expression in human HCC specimens, and GEP modulates p53 wild-type protein levels in vitro.
- p53 and c-erbB-2 may have independent role in carcinogenesis of gall bladder cancer
- Hghly modular role for the L1 loop in the recognition of specific DNA sequences, target transactivation, and apoptotic signaling by p53.
- in diffuse large B-cell lymphoma, molecular alterations in ice, bcl-2, c-myc and p53 are present in hematopoietic cells from bone marrow as well as in primitive hematopoietic progenitors
- NS3 plays an important role in the hepatocarcinogenesis of Hepatitis C virus by interacting differentially with p53 in an NS3 sequence-dependent manner.
- it is concluded that mutation of p53 & deletion of p16 might play important roles in the tumorigenesis of gliomas and it was significantly associated with the grade of tumor differentiation; P53 protein accumulation can indirectly reflect p53 mutation
- NKX3.1 engages cell cycle and cell death machinery via association with HDAC1, leading to increased p53 acetylation and half-life through MDM2-dependent mechanisms.
- The majority of the malignant thyroid cancers displayed aberrant expression of FHIT gene, concominant with p53 gene inactivation.
- VRK2 induces p53 stabilization by post-translational modification, largely due to threonine 18 phosphorylation in tumor cell lines.
- GAS41 plays a role in repressing the p53 tumor suppressor pathway during the normal cell cycle by a TIP60-independent mechanism.
- The activation of ATM/ATR/CHK signaling pathways contributes to this G2 checkpoint and highlight the interrelated roles of p14ARF and the Tip60 protein in the initiation of this DNA damage-signaling cascade.
- cell death induced by adenovirus/alpha-fetoprotein truncated Bid in hepatocellular carcinoma cells is via an apoptotic pathway that can be independent of p53 status
- PGE(2)-stimulated phosphoserine p53 abrogated DNA binding of c/EBPbeta dimers and c/EBPbeta/NF-kappaB p65 heterodimers.
- The multiple biological activities of p53 are orchestrated and deciphered by different "p53 cassettes," each containing combination patterns of posttranslational modifications and protein-protein interactions.
- p53 Arg72Pro may play a role in the early stages of colorectal neoplasia and possibly in progression to invasive disease, depending on site and sex
- decreased angiogenesis might account for reduced growth rate of tumor cells expressing the F134L p53 mutation
- The present paper aims to provide updated information on p53 regulation and function, with specific interest on its role in breast cancer.
- findings show that p53 modulates the balance between the utilization of respiratory and glycolytic pathways; identifed Synthesis of Cytochrome c Oxidase 2 (SCO2) as the downstream mediator of this effect
- Moreover, in the absence of overt apoptotic signals, the constitutive induction of AIF by p53 may underpin a cytoprotective maintenance role, based on the role of AIF in ensuring proper mitochondrial function.
- Loss of TP53 in chronic lymphocytic leukemia results from the absence of nearly the entire chromosome 17 p-arm due to translocations or isochromosome formations.
- HIPK2 cooperates with p53 in Gal-3 repression and that this cooperation requires HIPK2 kinase activity.
- presence of p53 in a transcription complex of NPM and Sp1 or NF-kappaB at the promoter of the MnSOD gene was verified. p53 interacts with Sp1 to suppress expression of the MnSOD gene.
- CD154 can sensitize leukemia cells to apoptosis via the c-Abl-dependent activation of p73 and mitigate the resistance of p53-deficient CLL cells to anticancer drug therapy.
- The DU145 cell line harbors a TS mutant of p53 and, in addition to being a widely used model of human prostate carcinoma, may also reveal new insights into p53 function due to the unique transcriptional properties of its TS phenotype.
- Existence of a feedback-loop between p53 and cdk9, pinpointing a novel mechanism by which p53 regulates the basal transcriptional machinery.
- Ability of calcitriol receptor to transcribe prostate derived factor in prostate cancer cells requires protein p53.
- Alterations in p53 levels arise from nucleolin binding to the p53 antagonist Hdm2
- Cdc25C may first be actived by polo-like kinase 1, and then its phosphatase activity makes p53 dephosphorylated at Ser15
- The tetrameric full-length mutated proteins had similar apparent melting temperatures to those of the individual domains, and the structural mutations lowered the melting temperature by similar amounts
- Eighteen mutations (12 missense, one nonsense, two deletions, three nucleotide substitutions at the level of the splice-junctions) and two polymorphisms were detected by FAMA in 17 patients with colorectal cancar.
- In 50 of the 66 primitive colorectal tumor cases at least one significant alteration was identified in Ki-Ras and/or TP53 and/or p16(INK4A) genes.
- measured the dynamics of the negative feedback loop between the tumor suppressor p53 and the oncogene Mdm2
- Stage B immunoproliferative small intestinal disease (IPSID) showed higher expression for bcl6 and p53 than stage A IPSID. bcl6 and p53 expressions correlated with a more advanced disease stage and aggressive tumour behavior.
- Metabolic activation of hormones can generate endogenous mutagens, and we demonstrate that estrone-quinone attenuates p53 function in human breast cancer cells.
- alteration of both p53 and PTCH genes is likely to play a role in radiation-induced basal cell carcinogenesis
- analysis of novel mechanisms for apoptosis induction by silibinin involving p53-caspase 2 activation and caspase-mediated cleavage of Cip1/p21
- Expressions of p53 proteins should be useful for determining the tumor properties, including prognosis, in patients with esophageal squamous cell carcinoma.
- ECT2 is negatively regulated by wild-type p53 but not tumor-derived mutant p53 or other p53 family members.
- Increased GEF-H1 expression contributes to the tumor progression phenotype associated with the p53 mutation.
- As the amount of p53 protein increases, there is a downregulation of the VRK1 protein level independent of its promoter.
- hCdc14A is differentially expressed in human cancer cells and can interact with both p53 and the Cdk1/cyclin B complex; it may play a role in carcinogenesis
- data indicate that a mutant p53 can contribute to the suppression of apoptosis in a human breast cancer cell line and suggest a rationale for the selection of p53 mutations early in tumorigenesis to suppress apoptosis in an emerging tumor
- the TP53 codon 72 polymorphism could be associated with susceptibility for adrenocortical cancer
- Sps1 affect cell viability upon ionizing radiation via modulation of p53 activity. Sps1 and its product selenophosphate might be involved in cancer prevention in a p53-dependent manner and could be applied to development of a novel cancer therapy.
- Polymorphism in the p53 gene at codon 72 revealed no significant association with the development of CAD or diabetes in Kuwait.
- p53-induced cell cycle arrest is a function of not only the transactivation of cell cycle inhibitors but also the repression of targets that regulate proliferation at several distinct phases of the cell cycle
- p53 not only plays a key role in the regulation of the topoisomerase I response to UV-C irradiation but also to treatment with colcemid
- The data implicate cyclin A1 as a downstream player in p53-dependent apoptosis and G2 arrest.
- L11, unlike L5 and L23, differentially regulates the levels of ubiquitinated p53
- Defective DNA mismatch repair and TP53 defects are common early events in carcinosarcoma tumorigenesis.
- Somatic chromosomal mutations, especially in exon 6 of Tp53 gene, among esophageal cancer patients of an ethnically homogenous population of Kashmir valley are closely related to continued exposure to various common dietary risk factors.
- Taken together, our present results strongly suggest that p73-dependent induction of 14-3-3sigma plays an important role in the regulation of chemo-sensitivity of breast cancers bearing p53 mutation.
- Collectively, our results suggest that a loss of the cisplatin sensitivity is at least in part due to a lack of cisplatin-induced p53 phosphorylation, and p73 might cooperate with MDM2 to be involved in this process.
- The rapid shift from a shorter p53 protein form (delta) toward the full-length protein (alpha) underscores the complexity of p53 protein modulation in patients undergoing chemotherapy.
- COX-2 and p53 may have roles in microsatellite instability in colorectal cancer
- REIVEW: posttranslational phosphorylation status of mutant p53 and novel biological functions of phosphorylation in carcinogenesis
- MDM2-single nucleotide polymerase 309 favours tumour selection of non-dominant negative P53 mutations in colorectal cancer, which also show an earlier age of tumour onset.
- None of the p53 mutations were stabilized by ZBP-89 except for the A161T p53 mutation, which exhibited constitutive transcriptional activity.
- The p53-46F mutant with enchanced ability to induce p53-dependent apoptosis was reported.
- The results indicate that overexpressed ER-beta may induce LoVo cell apoptosis and anti-proliferation by increasing p53 signaling in a ligand-dependent manner, and without hTNF-alpha involvement.
- The Bcl-2 protein expression has a close correlation with p27 and p53 protein expressions and the proliferation activity determined by MIB-1 counts in invasive ductal carcinoma of the breast.
- MAGE-A2 targets p53 transactivation function through histone deacetylase recruitment
- p53 accumulation is believed to be an early event in neoplastic progression of the tongue
- HER-2/neu and p53 may have a role in chemoresistance in patients with non-small cell lung cancer
- genomic instability is an early event that occurs at precancerous stages prior to changes in tumor suppressor genes (p53 and adenomatosis polyposis coli) in Barrett's esophagus-associated tumorigenesis in patients
- Significant association was found between Aurora-A amplification and TP53 mutations in non-BRCA2 mutation carrier tumours.
- PCNA, L2DTL and the DDB1-CUL4A complex play critical and differential roles in regulating the protein stability of p53 and MDM2/HDM2 in unstressed and stressed cells.
- identification of polymorphisms in lung carcinoma of never smokers
- p53 is functional in the absence of p14(ARF) in malignant pleural mesothelioma
- whereas exogenous p73 exhibits similar transcriptional activity to p53 in H1299 cells, the endogenous p73 that accumulates upon DNA damage in HCT116 cells is unable to compensate for p53 function
- p53 binding to the central domain of Mdm2 is regulated by phosphorylation
- Tumour protein p53 plays a role in facilitating histone H2AX phosphorylation, an important step in the mobilization of the DNA repair machinery at the site of DNA double-strand breaks.
- p53 plays a role in regulation of cullin 7 activity
- p53 expression is not an independent prognostic predictor of progression-free survival or overall survival in ovarian cancer.
- p53 mutations and deletions correlated with extreme sensitivity (IC50 < 1 nM) to Trabectedin
- The unfolded protein response pathway triggers p53 accumulation and activation, which directly contributes to p53-dependent cell cycle arrest.
- suggest a novel role for DEK in cellular survival, involving the destabilization of p53 in a manner which is likely to contribute to human carcinogenesis
- These results suggest that DFNA5 plays a role in the p53-regulated cellular response to genotoxic stress probably by cooperating with p53.
- Wip1 overexpression abrogates the homeostatic balance maintained through the p38-p53-Wip1 pathway, and contributes to malignant progression by inactivating wild-type p53 and p38 MAPK as well as decreasing p16 protein levels in human breast tissues.
- Hdmx is an important determinant of the outcome of P53 activation
- Epigenetic alteration of XAF1 is frequent in human urogenital cancers and may contribute to the malignant progression of tumors by rendering tumor cells a survival advantage partially through the attenuated p53 response.
- germ-line p53 mutations and sex had significant effects on cancer risk in patients with Li-Fraumeni syndrome
- p53 mutations in plasma DNA from healthy individuals suggest that p53 mutations in plasma DNA may be a marker of carcinogen exposure from tobacco smoke.
- our data suggest that wt p53 enhances the ability of HCMV to replicate and produce high concentrations of infectious virions in permissive cells.
- Our results provide evidence of how poliovirus counteracts p53 antiviral activity by regulating PML and NBs, thus leading to p53 degradation.
- Acetylation promotes p53 tetramerization, which, in turn, is required for the PTEN-p53 interaction and subsequent maintenance of high p53 acetylation.
- The transformation of melanocytes to melanoma cells is characterised by abnormal proliferation due to cell cycle alterations. This occurs through alterations in the retinoblastoma (Rb) and p53 tumour suppressor pathways.
- results show that p53 transcriptionally activates the alpha(II) collagen prolyl-4-hydroxylase [alpha(II)PH] gene, resulting in the extracellular release of antiangiogenic fragments of collagen type 4 and 18
- We conclude that hypoxia triggers a p53-dependent gene expression pattern distinct from that induced by other stress agents and that Fas/CD95 is a critical regulator of p53-dependent apoptosis upon hypoxia.
- Caspase 7 promoter was found to have p53-binding sites and prohibitin activated this promoter through p53.
- presence of a codon 72 of p53 germline variant genotype increased the risk for HHV6 infection more than five times after kidney transplant
- In this study, the p53 protein immunoreactivity was not a marker of malignant transformation of chronic actinic cheilitis to squamous cell carcinoma.
- Results show that suppression of phosphatidylcholine-specific phospholipase C (PC-PLC) inhibits apoptosis and p53 expression induced by apoptosis in young cells, but not in senescent cells, and depressed intracellular ROS levels in both cell types.
- these findings identify the first instance of a ubiquitin ligase that causes stabilization of p53 while inactivating its transcriptional activities.
- hHR23B thus plays a critical role in the activation and function of p53 after specific genotoxic exposures.
- Wnt signaling activation significantly decreased the viability of retinoblastoma cell lines by inducing cell cycle arrest, which was associated with upregulated p53
- The alterations of the p53 gene evaluated by DNA sequence analysis is relatively accurate. Expression of P53 protein could not act as an independent index to estimate the prognosis of cholangiocarcinoma.
- Data suggest that the TP53 and CHEK2 mutations can substitute each other in at least 25% (21/84) of prostate cancers and that DNA damage-signaling pathway plays an important role in prostate cancer tumorigenesis.
- Antisense ODN to p53 impairs secretion of VEGF in the undifferentiated thyroid cancer cell line FTC-133.
- Biopsy specimens of 53 squamous dysplastic and 13 keratotic/hyperplastic lesions of upper digestive tract were immunocychemically stained.
- p53 preferentially occupied the promoters of growth arrest genes p21 and GADD45 in senescent normal human diploid fibroblasts.
- The p53-positive tumors had more lymph node metastasis, and p53-positive had the worst prognosis with gastric cancer.
- In the complex crystal structure of p53 tumor suppressor bound to large T-antigen (LTag) oncoprotein, p53 inhibits LTag helicase function through direct complex formation.
- The results obtained demonstrated that, at least in vitro, the p53 family members tested (TAp63alpha, TAp73alpha, DeltaNp63alpha, but not DeltaNp73alpha) were able to drive transcription from the PKCdelta promoter.
- Mutant p53 binds NF-Y target promoters and, upon DNA damage, recruits p300, leading to histone acetylation
- p53 directly regulatescarboxylesterase 2expression in a colonic cancer cell line.
- iASPP binds to and regulates the activity of p53 Pro72 variant more efficiently than that of p53 Arg72
- p53 appears to regulate EphA2 expression and clinical outcome in ovarian cancer.
- mutations or modifications that affect p53 oligomerization interfere with DNA binding and also with its intracellular distribution; an intact microtubule network is important in the trafficking of crucial cellular proteins
- distinct single nucleotide changes in the BRCT domain of BRCA1 affect binding of this protein to the tumor suppressor p53
- data suggest that the sensitization to radiation results from NBS1-siRNA-mediated suppression of DNA repair and/ or X-ray-induced cell survival signaling pathways through NFKB and XIAP.
- study showed the joint effects on the risk of carotid atherosclerosis between the genetic polymorphisms of GSTP1 and p53, and arsenic exposure
- These experiments describe the identification of novel p53 target genes and the subsequent discovery of distinctly different expression phenomena for p53 target genes under different stress scenarios.
- The functional consequences of the identified PIDD/nucleolin interaction remain to be elucidated, but may be related to a recently discovered new role for PIDD in the activation of NF-kappaB upon genotoxic stress.
- harbouring alternative translation initiation sites, the p53 mRNA gives rise to different levels of the p53 isoforms which help to orchestrate the cell biological outcome of p53 activation
- p53 activation and the transcriptional induction of its target gene PUMA play an important role in the sensitivity of cancer cells to apoptosis induced by proteasome inhibition
- incidence of somatic mutagenesis of p53 oncosuppressor protein in malignant tumors of the stomach and genetic polymorphism of p53
- The cooperative effects of phenotypes determined by mdm-2, p53, and bcl-2 expression may predict survival in patients with muscle-invasive TCC of the bladder
- KRAS and p53 gene mutations, which are rarely simultaneous and are associated with specific DI aneuploid values, do not represent a synergistic evolutionary pathway but may influence mechanisms of chromosomal instability
- Interval between the onset of rheumatoid arthritis and lymphoproliferative disorders development was significantly longer in patiets with p53 gene mutations and had more advanced diseases and an unfavorable prognosis
- p52 can regulate p53 function and influence p53-regulated decision-making following DNA damage and oncogene activation.
- high frequency of somatic TP53 gene mutations implicates TP53 as a predominant factor for breast carcinogenesis in moderate risk ethnic Kashmiri population
- Tumor cells having disruptions in BRCA1/2 network genes and TP53 together are more sensitive to cisplatin than cells with either disruption alone.
- Misfolded species, which can aggregate in vitro and may be degraded in the cell, leads to p53 inactivation.
- By downregulating Cdc25A expression, p53 may impair transition from G(1) to S phase independently of p21(WAF1/CIP1)
- Alkyl resorcinol exerts its cytotoxic effect in both hepatocellular cell lines through apoptotic cell death. For Hep3B, cells with mutated p53 and Fas, apoptosis would proceed by p53- or Fas-independent pathways.
- Phosphorylation of specific serine and/or threonine residues reduces the affinity of the S100B-p53 interaction.
- p53 and pRB can be sumoylated by SUMO-2/3 in vivo, and such modification of p53 and pRB may play roles in premature senescence and stress response
- p53 family proteins are potent therapeutic agents for human papilomavirus-associated uterine cervical cancers.
- results suggest that the development of endometrial carcinoma is probably mediated through a multi-step carcinogenesis pathway and mutation of TP53 does not necessarily result from the presence of microsatellite instability in BAT26.
- transcriptional activation of the IGF-IR gene by Cav-1 requires an intact p53 signaling pathway
- Klotho normally regulates cellular senescence by repressing the p53/cyclin-dependent kinase inhibitor 1A pathway
- ANXA7 and p53 can distinctly regulate LOX transcription that is potentially relevant to the arachidonic acid -mediated cell growth control in tumor suppression.
- Results show that the p53beta isoform is the only p53 species to be endogenously expressed in the neuroblastoma (NB)cell line SK-N-AS, suggesting that the C-terminus truncated p53 isoforms may play an important role in NB tumor development.
- Data show that the acrolein-DNA binding pattern is similar to the p53 mutational pattern in human lung cancer, and suggest that it contributes to lung carcinogenesis through DNA damage and inhibition of DNA repair.
- Although p53 is a main regulator of apoptosis in mammalian cells, the Tfpt induced apoptosis appears p53-independent.
- Using a combination of 2-dimensional gel electrophoresis and isotope-coded affinity tagging proteomic techniques, study found a total of 111 secreted proteins, 39 of which showed enhanced and 21 inhibited secretion in response to p53 expression.
- Our findings show that p53 is a transcriptional regulator of ECK in mediating apoptosis.The discovery of the novel p53-binding motif in the promoter may lead to the identification of a new class of p53 target genes.
- RNPC1a is required to maintain the stability of p21 transcript induced by p53.
- Stimulation of macrophage inhibitory cytokine 1-dependent S phase arrest in normal gut epithelial cells might help to revitalize the clinical use of N-phosphonacetyl-l-aspartate, which has been limited by gut toxicity
- Thus, our present results strongly suggest that AICD triggers apoptosis through the p53-dependent mechanisms.
- ZNF415 isoforms in COS-7 cells inhibits the transcriptional activities of AP-1 and p53, suggesting that the ZNF415 protein may be involved in AP-1- and p53-mediated transcriptional activity.
- the reduction of KAP1 levels promotes p53-dependent p21 induction and inhibits cell proliferation in actinomycin D-treated cells.
- Risk of cancer is markedly increased in heavy smokers (>20 pack-years) with squamous-cell carcinoma carrying an amino acid substitution.
- analysis of mechanism of formation of the principal MDM2 isoforms, differential effects of p53 on the production of these isoforms, and differential abilities of human MDM2 isoforms as regulators of the MDM2/TSG101 and p53/MDM2 feedback control loops
- Activation of PI3K signaling by mutations in PTEN or PIK3CA can lead to activation of p53-mediated growth suppression.
- p53 mutation was observed in 87% of esophageal squamous cell carcinoma, in 80% of esophageal dysplasia, in 0% of normal mucosa.
- The p53 pathway is inactivated in most bladder ccancers, but do not independently predict prognosis.
- Expression of p53 expression was weak or not detected in dental follicles with reduced and stratified squamous epithelium
- p53 mutation spectrum shows that the UV component of sunlight is the major risk factor and modulated DNA repair by immunosuppressive drug treatment may be significant in the skin carcinogenesis of renal transplantation patients.
- A new G-to-A transition at position +1 at the invariant G at the exon 8 donor splice site leads to numerous aberrant splicing-products.
- In transfected cells and KSHV-infected B lymphoma cells, KSHV-encoded latency-associated nuclear antigen (LANA) expression stimulates degradation of tumor suppressors von Hippel-Lindau and p53.
- p53 mutants can bind DNA and adopt a wild-type conformation in vitro, but are transcriptionally inactive in vivo, points to the involvement of cellular factors required for transactivation.
- The Pro/Pro genotype of the p53 codon 72 polymorphism carries a higher risk for gastric cancer in general and is also associated with a much higher risk for early gastric cancer than advanced gastric cancer.
- Negative control by p53 on Nrf2 transactivation appears to be aimed to prevent the generation of a strong anti-oxidant intracellular environment that could hinder the induction of apoptosis.
- Our findings suggest a role for MMP-9 in soft tissue sarcoma (STS) progression and expand the role of p53 in molecular control of STS growth and metastasis.
- p53 mutation and human papilloma virus mediated p53 inactivation possibly constitute two independent pathways of head and neck squamous cell carcinoma tumourigenesis
- data provide evidence that the p53 pathway is inactivated in retinoblastoma and that this cancer does not originate from intrinsically death-resistant cells as previously thought
- The T-helper cell activity of wild-type p53(25-35) peptide is likely to benefit p53-targeted immune responses and should be considered as a component of p53-based immunotherapy in the future.
- Survivin fused to a nuclear localization signal augmented basal expression levels of p53 and Bax and enhanced sensitivity for intrinsic apoptosis
- mapped binding sites of p53 in the genome of HCT116 cells, along with those of acetylated H3, acetylated H4, and methylated H3-K4
- a detailed atomic model for the DNA-p53 tetramer complex delineating the roles of DNA-p53, p53 dimer-dimer interactions, and DNA sequence in specific p53 binding-induced DNA conformational changes
- The expression of p53, Bcl-2 and Bax was altered in lung cancer tissue compared to histologically normal bronchial epithelium.
- Although pterygium has limited local invasion and ainability to metastasize, concomitant presence of altered p53 in 8-OHdG-immunoreactive cells could provide evidence of apparent genetic instability, which is in contrast to its benign clinical course.
- data do not indicate a strong link between variation in TP53 and osteosarcoma risk, although they provide preliminary evidence of an increased risk of osteosarcoma associated with variants at IVS2+38 and Pro72Arg
- These results demonstrate that IGF1R is downregulated by P53, and that siRNA targeting of IGF1R increases liver cancer cells sensitivity to adriamycin and promotes apoptosis.
- FBXO11 promotes the Neddylation (NEDD8) of p53 and inhibits its transcriptional activity
- Inhibition of KSP induces apoptosis independently of p53 and that p53 is dispensable for spindle checkpoint function. Thus, KSP inhibitors should be active in p53-deficient tumors.
- p53 effects on the IGF (insulin-like growth factor) axis are more complex than previously appreciated, and overall transform the axis from IGF-mediated mitogenesis to growth inhibition and apoptosis.
- Bcl-2 inhibition might therefore improve the efficacy of existing acute myeloid leukemia therapies by inactivating this suppression of wild-type p53 activity
- Using pancreatic juice to detect mutations of p53 can help distinguish patients with pancreatic cancer from those without evidence of pancreatic neoplasia.
- CK2-site phosphorylation of p53 is induced in DeltaNp63 expressing basal stem cells in UVB irradiated human skin
- PCNA is not significally increased in proliferative endometrial carcinoma.
- a positive association between p53 reactivity and higher grade pancreatic tumors.
- p53 mutation is not an important mechanism for beta-catenin activation in primary cutaneous T-cell lymphoma; p53 codon 72 polymorphism may influence negative feedback control involving beta-catenin and p53.
- Chromatin immunoprecipitation analyses show that LKB1 is recruited directly to the p21/WAF1 promoter, as well as to other p53 activated promoters, in a p53-dependent fashion.
- E4F1 is a key posttranslational regulator of p53, which modulates its effector functions involved in alternative cell fates: growth arrest or apoptosis.
- MDMX is an important regulator of p53 response to ribosomal stress and RNA-targeting chemotherapy agents.
- analysis of the human p53 tetramerization domain
- TP53 codon 72 polymorphism might be implicated in breast carcinogenesis, with the Arg/Arg genotype being associated with an increased susceptibility for this malignancy.
- Cancer-associated missense mutations targeting MDM2's central zinc finger disrupt the interaction of MDM2 with L5 and L11.
- Hec50co is a TP53-null cell line possessing one TP53 42bp deletion mutation allele and the other lost allele.
- p53-dependent staurosporine-induced caspase-3 activation is affected by the C-terminal products of cellular prion protein processing, C1 and C2
- suggest a mechanism for elevated CXCR4 expression and metastasis of breast cancers with p53 mutations or isoform expression
- Human p53 and various human-mouse chimeric proteins are generally less effective in inhibiting growth of mouse cells compared to mouse p53, due partly to codon 72 polymorphism-specific effects of human p53.
- p53 to NF-kappaB signaling has a role in chemotherapy responsiveness of neuroblastoma
- BCCIP in maintaining the transactivation activity of wild type p53; down-regulation of BCCIP as a novel mechanism to impair the p53 function in cells harboring wild type p53
- 20% of sarcoma tumors showed p53 rearrangement by PCR/SSCP and Southern blot. Allelic deletion of p53 was detected in 78% of sarcoma and 55% of Rb tumors.
- p53 mediates the suppression of TR3 on MDM2 at both transcriptional and post-transcriptional level and suggest TR3 as a potential target to develop new anticancer agents that restrict MDM2-induced tumor progression.
- In an analysis of breast cancer-specific survival up to 5 years, high Ki-67, high p53, and negative ER as well as aneuploidy of the tumour were significant prognostic factors.
- The p53 level was higher than in normal larynxes, whereas laryngeal cancer presented the lowest levels.
- Endogenous p53 protein binds to the promoter region of the RGC32 gene, implying p53-dependent transcriptional activity.
- Moreover, these M6P/IGF2R 3'UTR mutations and the TP53 mutations detected previously were mutually exclusive in most of the tumors, suggesting two independent pathways to HCC development.
- The differential ability of p53 and p73 to inhibit glucocorticoid receptor transcription activity is due, in part, to differences in their N-terminal and C-terminal sequences.
- Our results imply that HERV-I LTR, while under negative control by its LTR cis-elements and by wild type p53, may become active upon p53 mutation
- study found associations of risk haplotypes and protective haplotypes in p53 for glioblastoma and in ATM for meningioma; study provides new data that could add to our understanding of brain tumour susceptibility
- Using different antibodies recognizing different epitopes of p53 protein, abundant p53 expression was observed both in nuclear and in cytoplasmic compartments of first-trimester cytotrophoblastic cells.
- While the DNA replication checkpoint is unlikely to regulate the assembly of a p21 promoter initiation complex, it signals to one or more factors involved in the process of transcriptional elongation.
- analysis of nonconserved residues that enforced p53 core domain binding with BRCA1-BRCT in a way similar to p53-53BP1 binding
- the endoplasmic reticulum-resident ubiquitin ligase 'Synoviolin' destroys p53
- 1,25 dihydroxyvitamin D3 photoprotection is associated with an increase in p53 and a decrease in nitric oxide products
- Ser46 phosphorylation activates p53-dependent apoptosis induced by DNA damage and cellular senescence induced by oncogenic stress.
- Smad7 plays a crucial role upstream of ATM and p53 to protect the genome from insults evoked by extracellular stress.
- These data suggest TIS11D as a candidate p53 target gene that may be part of the network of genes responsible for p53-dependent apoptosis.
- Study demonstrates that the p53-mediated induction of RhoE in response to DNA damage favors cell survival partly through inhibition of ROCK I-mediated apoptosis.
- p53 Arg homozygosity and high risk-papillomavirus 18 E6 positive simultaneously can predict the fate of cervical lesions
- Cellular p53 antagonists must be inhibited for sustained p53 activity if E6 siRNA therapy is attempted and if no combined genotoxic therapy is applied in breast cancer.
- This is the first report showing loss of heterozygosity at the intron 1 region of p53 gene in human brain tumors.
- Notch signaling downregulated p53-dependent apoptosis induced by ultraviolet irradiation.
- Results describe four novel single nucleotide polymorphisms within the promoter region of the p53 gene and their associations with uterine leiomyoma.
- p53 and Ki-67 were expressed with increasing frequency, and bcl-2, p21, and mdm-2 with decreasing frequency in thyroid carcinoma progression. p27 and cyclin D1 were expressed in <15% of cases, with a trend toward decreasing expression.
- Tip60-dependent acetylation of p53 at K120 modulates the decision between cell-cycle arrest and apoptosis, and it reveals that the DNA-binding core domain is an important target for p53 regulation by posttranslational modifications.
- We describe a previously unknown posttranslational modification of the DNA-binding domain of p53. This modification, acetylation of lysine 120 (K120), occurs rapidly after DNA damage and is catalyzed by the MYST family acetyltransferases hMOF and TIP60.
- There are different immunohistochemical expression patterns of p16INK4A and p53 between intraductal papillary-mucinous neoplasm and pancreatic intraepithelial neoplasm
- Considering the p53 protein overexpression in a relatively high percentage of patients, it seems that p53 mutation plays an important role in development of colorectal carcinoma.
- By comparing the expression of p53, cyclin D1, p16, hTERT, and TSP-1 in spontaneously regressing keratoacanthoma and squamous cell carcinoma, the changes in the expression of these proteins to specific stages of skin carcinogenesis, is defined.
- somatic alterations in p53 and EGFR have roles in progression of primary lung cancer
- Genotoxic responses to ultraviolet radiation, like increase in the phosphorylation of histone H2AX, induction of p53 protein and binding of this protein to its DNA consensus sequence, were all decreased on the restrictive substrate.
- study reveals that the TP53 Arg allele, active smoking and human papillomavirus infection infection are the important risk factors in lung cancer development in the north part of Iran, Mazandaran province
- BPDE-like DNA adducts are indeed detected in pterygium samples, and they are only minor contributors to the abnormal p53 gene.
- individual variations in radiosensitivity and in the level of induction of TP53 (and consequently CDKN1A) are congruent, irrespective of the genetic background of the nontransformed fibroblasts
- the gene encoding Ku86 (XRCC5) is an essential gene in human somatic cells, and its absence cannot be suppressed by the loss of p53 function
- These data demonstrate the importance of Noxa induction in determining the apoptotic response to fenretinide and emphasise the role of Noxa in p53-independent apoptosis.
- type of TP53 mutation, especially missense mutation, is a strong prognostic indicator for disease-free survival and disease-specific survival in node-negative breast cancer, particularly in combination with ERBB2 amplification
- study indicated only p53 & RNASEL genotypes had significant influence on age of onset of Lynch syndrome in an additive mode of inheritance & that effects of both variants are purely additive supporting the notion that p53 & RNaseL pathways do not interac
- We showed that renal cell carcinoma with rhabdoid features is a very aggressive neoplasm with a poor prognosis. We observed an overexpression of p53 in the rhabdoid component that may be implicated in the tumor dedifferentiation.
- Overexpression of p53 is associated with pancreatic cancer
- Our data demonstrate that the effects of 9-HSA on U2OS correlate with posttranslational modifications of p53.
- The basal-like subtype was associated with p53 overexpression.
- findings show that RTK/Ras/MAPK (mitogen-activated protein kinase) activity induces p53 N-terminal phosphorylation, enabling the interaction of p53 with the TGF-beta-activated Smads; this mechanism promotes TGF-beta cytostasis in human cells
- no specific pattern for p53 mutations was observed in HCV genotype 4-associated hepatocellular carcinoma and no significant relation between p53 mutations, HCV-NS3 expressions or any HCV sub-genotype-4 sequence in Egyptian patients
- 5-FU treatment triggers a ribosomal stress response so that ribosomal proteins L5, L11, and L23 are released from ribosome to activate p53 by ablating the MDM2-p53 feedback circuit
- Patients with pathologically N0 disease and p53 gene mutation must be carefully monitored for local recurrence or distant metastasis.
- Data suggest that cytoplasmic mutant p53 increases Bcl-2 expression in estrogen receptor-positive breast cancer cells.
- TP53 mutational status seems to be an important prognostic factor in patients undergoing surgical resection of colorectal cancer with hepatic metastases.
- p53 binds to and positively regulates BLIMP1.
- Review of ongoing work on biological functions of p53 tumor suppressor in different cell types and under various physiological conditions will help to unravel the complexity of molecular circuits that orchestrate the biological response to p53 activation
- Cytoplasmic monoubiquitylated p53, generated by Mdm2-type ligases, is subject to a binary switch from inactivation via subsequent polyubiquitylation and degradation in unstressed cells, to activation via mitochondrial trafficking.
- Galectin-1 was found to be negatively regulated by transfection with TP53 in a glioblastoma cell line.
- Autoantibodies against the p53 proteins (p53 Abs) can be detected in the serum, ascites, saliva and pleural effusions of various malignant patients with tuberculosis pleurisy
- human Ada3 has an essential role in p53 acetylation
- Renal cell carcinoma frequently has p53 mutations, so therapy restoring p53 may markedly improve the response rate of immunochemical therapy combining IFN-alpha and 5-FU.
- our present findings suggest that p53 plays an important role in the DNA-damage response in certain neuroblastoma cells and it seems to be important to search for p53 mutations outside DNA-binding domain.
- Most non-small cell lung cancers (NSCLCs) have mutations of p53.[Review]
- Mutation in codon 72 of TP53 gene was not associated with breast cancer in Iranian patients.
- modified LDL results in an increased transfer of mitochondria-derived superoxide anion to p53, which stimulates a conformational change in Bax favoring its translocation to the mitochondria with resultant apoptosis of progenitor cells
- a genetic instability of the 17p13 region, occurring early in adrenocortical cancer development, involves various genes located in this region, including TP53
- Cytoplasmic relocalization of HIPK2 induced by HMGA1 overexpression is a mechanism of inactivation of p53 apoptotic function.
- The evolutionary perspective in this review indicates that p53 evolved so as to play a subtle but very important role during development, and suggests that p53 was primarily selected for its developmental role and not as a tumor suppressor gene.
- result combined with our two previous analyses indicates that the p53 Y220C mutation was expressed in 6/50 HLA-A2+ squamous cell carcinomas of the head and neck tumors tested
- CPH domain interaction surface of p53 resides in the tetramerization domain and is formed by residues contributed by at least two subunits
- An association between polymorphisms in GSTP1 and ABCB1 and risk of acquiring intratumoral TP53 mutations suggests the existence of putative predisposing genotype backgrounds.
- Both kinetics and free energy landscape analyses indicate that bound MDM2 unfolds in the order of p53 unbinding, tertiary unfolding, and finally secondary structure unfolding.
- The Pro/Pro genotype of the TP53 codon72 polymorphism increases oral cancer risk in non-smokers and worsens their prognosis.
- Results suggest that p53 negatively regulates tumor vessel formation and cell growth via the SEMA3F-NRP2 pathway.
- p53 induces monocytic differentiation and the G2-phase cell cycle arrest, but not apoptosis of BM2 monoblasts, implying independence of the p53-driven apoototic and differentiation/proliferation pathways.
- These data suggest that p53 suppresses cancer progression to malignancy by modulating the quality of Ras signaling.
- No siatistically significant value in assocation with survival or event-free survival in head and neck squamous cell carcinoma.
- Mutant p53 may contribute to its 'gain of function' effects which accelerate the oncogenesis and promotion of lung adenocarcinoma.
- S7 binds to MDM2, in vitro and in vivo, and the interaction between MDM2 and S7 leads to modulation of MDM2-p53 binding by forming a ternary complex among MDM2, p53 and S7.
- CDA1 induces p53- and MEK/ERK1/2 MAPK-dependent expression of p21 by acting through the p53 responsive element in the p21 promoter and this contributes to its antiproliferative activity
- MAML1 has a coactivator function for p53, independent of its function as a coactivator of Notch signaling pathway
- Eight of the nine samples showed a loss of 17pter-->p13, the locus of tumor suppressor TP53 preceding the amplified area 17p12-->p11.2.
- a family with Li-Fraumeni syndrome in which initially a novel germline TP53 intron 5 splice site mutation was found
- results indicate that both BstUI and MspI p53 polymormphisms might play the role in the breast cancer development especially in women younger than 50 years
- Overexpression of S100A4 in rheumatoid arthritis synovial tissue can influence p53 function and modulate the expression of several genes that are potentially implicated in the disease process.
- Critical role of subcellular localization in the dominant-negative action of p53.
- MORC3 (microrchidia3)-ATPase activated p53 and induced cellular senescence in normal fibroblasts but not p53-/- fibroblasts
- p53, rather than its homologues p63 and p73, may contribute to control of the first metaphase/anaphase transition of mammalian meiosis by downregulation of Cks2 expression
- not only the activation of p21 promoter but also the recruitment to p21 promoter by c-Abl is dependent on the interaction between c-Abl and p53 protein.
- BOX-V motif of p53 has evolved the capacity to bind to enzymes that mediate either p53 phosphorylation or ubiquitination
- These findings indicate that DYRK2 regulates p53 to induce apoptosis in response to DNA damage.
- These findings establish HIPK2 as an MDM2 target and support a model in which, upon nonsevere DNA damage, p53 represses its own phosphorylation at Ser46 due to HIPK2 degradation.
- Study provides biochemical and genetic evidence demonstrating that UV induction of pro-opiomelanocortin /alpha-melanocyte-stimulating hormone in skin is directly controlled by p53.
- findings suggest that mutations of p53 and hMSH2 genes may be deeply involved in not only the progression of hepatocellular carcinoma but also the recurrence development of hepatocellular carcinoma
- Adenovirus E4orf6-mediated p53 degradation requires Cul5.
- Data demonstrate a novel link between p53 and Notch1 in keratinocyte differentiation upon genotoxic stress and suggest a novel tumor suppressor mechanism of p53 in the development of HPV-induced tumors.
- if p53 staining is strongly positive survival is significantly worse than in tumors scored as negative or weak positive
- The researchers found that p53 (-) status was a solid predictor for FR in pre-radiation biopsy specimens.
- the binding of nuclear p53 to the specific sites within the PUMA promoter is essential for its ability to induce apoptosis and is likely to be required for its tumor suppressive capacity
- expression of hTERT reduces the number of foci and the level of active p53, thereby decreasing sensitivity to growth factor depletion
- The mutant p53 protein was unable to activate apaf1, which caused a reduced expression of apaf1 in chronic myelogenous leukemia patients.
- Cancer-associated mutant p53 can augment the induction of nuclear factor kappaB (NFkappaB) transcriptional activity in response to the cytokine tumor necrosis factor alpha (TNFalpha).
- Nutlin-3a shows antitumor activity in vivo in a mouse xenograft model, exploiting new options for exploiting reactivation of p53 as treatment for virally-induced lymphoma.
- Radiation-induced somatic mutations were observed in TP53 indicating an early role of TP53 in the radio-sarcomagenesis indicating gene activation in sarcoma.
- results argue that Mdm2 is needed for full inhibition of Cdk2 activity by p21, thereby positively contributing to p53-dependent cell cycle arrest
- this study reveals protein targets of p53 and highlights the role of transcription-independent effects for the p53-induced biological response
- Our finding that two different p53 haplotypes are associated with colorectal adenoma and cancer, respectively, suggests that each of these haplotypes may independently impact on p53 function within different genetic pathways of colorectal carcinogenesis.
- xeroderma pigmentosum group C protein polymorphism might affect p53 alteration and the molecular pathway defined by the p53 alteration in the development of muscle-invasive bladder cancer
- This study strengthens the rationale for targeting p53 deubiquitylation by drugs like Nutlin as a promising new strategy in Neuroblastoma therapy.
- Taurolidine induces apoptosis and necrosis, activates p53 and sensitizes cells to cisplatin, whereas PVP-I inhibits cell growth via necrosis.
- findings point to the calpain pathway as a key player to maintain steady state levels of p53 in resting cells without affecting its activity.
- p53 modulates DNA DSB repair by, in part, inducing hnRNP G
- The delay in traversing S phase was reduced by the presence of p53 in HCT 116 cells exposed to cytotoxic drugs.
- The Arg72Pro polymorphism of p53 alters the transcription of p53 target genes and modifies the apoptotic potential of cells but there are inconclusive results with respect to breast cancer risk
- results suggest that some cells from head and neck cancer may contain the oncogenic mutation of the p53 gene, and the oncogenic p53 protein prevents cancer cells from undergoing apoptosis after DNA damage
- Comparative genomic hybridization and immunohistochemical assessment of EGFR, PTEN, p53, and MIB-1 expression in 13 oligodendrogliomas, one oligoastrocytoma and 23 high-grade astrocytomas is reported.
- results indicate an important role of p53 in esophageal squamous cell carcinoma (ESCC) also in low-incidence regions; in combination with the p53 Arg72 variant HPV infection could contribute to risk of ESCC in these cases
- p53 upregulates restin transcription through an indirect mechanism rather than by direct interaction with the cis-activating element of the restin promoter.
- Collectively, the present findings provide the first evidence of p53 regulation of STC1 expression in human cancer cells.
- Data show that wild-type p53 was abnormally accumulated in the cytoplasm of the human hepatoblastoma-derived Huh6 cells, and suggest that the abnormal cytoplasmic localization of p53 might contribute at least in part to the development of hepatoblastoma.
- identified FLJ11259/DRAM as a p53-inducible member of a novel family of transmembrane proteins. FLJ11259/DRAM may be an important modulator of p53 responses in diverse tumor types.
- Lack of evidence that p53 Arg72pro influences lung cancer prognosis: an analysis of survival in 619 female patients.
- The central domain of the p53 protein targeted by 80% of p53 mutations is associated with the DNA-binding activity of the p53 protein;it is the binding site for proteins that play a key role in p53 regulation such as ASPP proteins or BclxL.
- We summarize here current knowledge on the respective roles of p53 mutagenesis and biological selection of mutations with specific functional characteristic in shaping the patterns and phenotypes of mutations observed in human cancers.
- both viruses and chemicals are implicated in the etiology of TP53 mutations during the molecular pathogenesis of hepatocellular carcinoma .
- The ability to associate with DNA appears to be crucial for the master role of mutant p53 proteins in coordinating oncogenic transcriptional responses.
- Target response element sequences (REs) that provide for p53 regulation of target genes, chromatin, accessory proteins and transcription machinery, are discussed
- This review describes the present knowledge about the transcriptional activities of mutant p53 and the mechanisms that might underlie its target gene specificity.
- We will focus mainly on the transcriptional activity of mutant p53 proteins.
- We focus here on a proposed mechanism by which a subset of tumor-derived p53 mutants physically interact with p53 family members, p63 and p73, and negatively regulate their proapoptotic function.
- The structure of p53 and how it responds to mutation is discussed.
- There was no association between p53 genotype and basal levels of DNA damage, oxidative DNA damage sensitivity, or DNA repair capacity. R72 dominantly increased the in vitro sensitivity of cells to UVB-induced apoptosis.
- p53 can form a complex with dephosphorylated Bad thereby converting it to a pro-apoptotic player.
- data indicate that the p53 codon 72 proline allele is less permissive for the growth of cancer cells in a hypoxic environment
- Non-small cell lung cancer cells with nonfunctional TP53 might be sensitized against radiation by genistein or estradiol.
- LSD1 has a pro-oncogenic function by modulating pro-survival gene expression and p53 transcriptional activity
- high and low P-glycoprotein, glutathione S-transferase pi expression, excision repair cross-complementing 1 alterations, and tumor suppressor p53 mutation were candidates for future clinical trials of chemosensitivity tests in lung cancer patients.
- p53 codon 72 polymorphism in Italian women have a minor role in determining genetic susceptibility to endometriosis
- p53 gain-of-function mutants promote tumorigenesis by a novel mechanism involving active disruption of critical DNA damage-response pathways.
- we have identified PROX1 as a novel target gene that is hypermethylated and transcriptionally silenced in primary and metastatic breast cancer.
- p53 plays an essential role in the autophagic pathway downstream of the DNA mismatch repair system.
- Bivariate analysis of p53/BAX proteins possibly may provide further prognostic evidence in colon cancer.
- The negative role played by the WTH3 gene in MDR development is through its proapoptotic potential that is regulated by multiple mechanisms at the transcription level, and one of these mechanisms is linked to the p53 gene.
- R248W may predispose to composite tumors and to neuroblastoma in individuals with Li-Fraumeni syndrome.
- common polymorphisms in the ATM, BRCA1, BRCA2, CHEK2 and TP53 cancer susceptibility genes are not shown to increase breast cancer risk
- high incidence of p53 exon 4 mutations were found in soft tissue sarcoma
- Our results suggest that phosphorylation of CBP by IKKalpha regulates the CBP-mediated crosstalk between NF-kappaB and p53 and thus may be a critical factor in the promotion of cell proliferation and tumor growth.
- p53 expression in gastric cancer was associated with poorer survival and was an independent predictor of tumor behavior and patient response to therapy.
- No correlation between Pidd expression and the p53 mutation status of oral squamous cell carcinoma, suggesting that Pidd expression may be regulated by p53-independent mechanisms.
- A complex between tetrameric p53 and p300 in which four domains of p300 wrap around the four transactivation domains of p53.
- Mutations of p53 were associated with lymph node metastases and III/IV stage of tumors that are signs of unfavorable prognosis in colorectal cancer.
- Common variation in the TP53 gene could modify the risk of invasive breast cancer.
- nuclear IKK-alpha-mediated accumulation of p73alpha is one of the novel molecular mechanisms to induce apoptotic cell death in response to CDDP, which may be particularly important in killing tumor cells with p53 mutation
- p14ARF signals through hAda3 to stimulate p53 acetylation and the induction of cell senescence
- CARF may exert a vital control on p53-HDM2-p21(WAF1) pathway that is central to the cell cycle control, senescence, and DNA damage response of human cells
- stress-induced premature senescence (SIPS) from hydrogen peroxide is associated with a transient increase in DNA-binding activity of p53 and an increased expression of p21(WAF-1) in human hTERT fibroblasts
- H pylori-associated chronic gastritis expressed the mutant-type p53, which was significantly associated with more severe atrophic and metaplastic changes.
- Te strong nuclear expression of p53 in these and other pediatric GBMs could indicate that p53 dysregulation is important to tumorigenesis.
- in addition to growth arrest and induced differentiation, OSM also sensitizes normal and transformed osteoblasts to apoptosis by a mechanism implicating (i) activation and nuclear translocation of STAT5 and p53 and (ii) an increased Bax/Bcl-2 ratio
- variant TP53 Arg72 allele was associated with a decrease in radiosensitivity, presumably due to suboptimal function leading to less stringent control of cell division
- P53 mediated regulation of metallothionein transcription in breast cancer cells is reported.
- Expression of c-erbB-2 and p53 has no prognostic value in patients with early-stage breast cancer in which axillary lymph node metastasis is absent.
- Aberrant entry into the mitotic phase is due to downregulation of p53 caused by direct physical interaction with PBK.
- A new signaling pathway, DHA-PPAR-gamma-p53, in mediating the apoptotic effect of DHA in Reh cells.
- The evaluation of a large number of actinic keratosis specimens have found a low gene mutation rate in low-graded AK lesions. p53 mutations rather than p16(INK4a) and/or Ha-ras mutations may be an early event in the development of AK to cutaneous SCC.
- impact of TP53 mutations and codon 72 genotype on survival of ovarian cancer patients
- Bub1 compromise triggers p53-dependent senescence, which limits the production of aneuploid and potentially cancerous cells.
- The present study showed elevated expression of topo-I, Ki-67, and mutant p53 in patients with uterine carcinosarcoma suggesting sensitivity to topo-I-targeted drug treatment.
- The downregulation of p53 expression in type II Hec50co cells is linked to gefitinib resistance.
- These results demonstrate that, in the cells investigated, the level of NS is regulated by p14(ARF) and the control of the G1/S transition by NS operates in a p53-dependent manner.
- mutations were found mainly in more advanced stages of urinary bladder cancer & at the CIS stage (carcinoma in situ); it cannot be excluded that the observed polymorphism at codon 213 may be a predisposing factor for urinary bladder carcinoma development
- Pathways of signaling by S100A4, by its interaction with and sequestration of p53, and by Notch also seem differentially operational in the induction of apoptosis
- transcription factors p53, NF-kappaB, and AP-1 may be important determinants of the heterogeneous pattern of gene expression, whereas STAT3 and EGR1 may broadly enhance gene expression in head and neck squamous cell carcinomas
- initially p53-negative tumors and initially p63-positive tumors that retain this labeling pattern may follow less aggressive biological courses and present better prognoses
- theaflavins induce apoptosis in human prostate cancer cells through induction of p53, down-regulation of NF-kappa B and mitogen-activated protein kinases pathways
- ubiquitination-mediated repression of p53 by Mdm2 acts at least, in part, through inhibiting the sequence-specific DNA binding activity
- Positive staining of p53 was significantly correlated with increased stage, lymph node metastases, and a nonendometrioid histology in endometrial carcinoma.
- no association between the distribution of p53 polymorphism and susceptibility to HPV-associated cervical cancer in the Western Cape Province, South Africa populations was observed
- TP53 mutation status and gene-expression based groups are important survival markers of breast cancer.
- tissue-specific epigenetic regulatory mechanisms might be involved in p53 instability in breast cancer.
- G alpha(12/13) regulate basal p53 levels via mdm4, which constitutes a cell signaling pathway distinct from p53 phosphorylations elicited by genotoxic stress.
- A microtubule-facilitated nuclear import pathway for p53 is described.
- Nutlin-3 could protect both endogenous and exogenous p53 from MDM2-mediated inactivation
- Rad51 has a role in chemoresistance in human soft tissue sarcoma cells along with p53 and activator protein 2 transcriptional regulation
- The ability of mutant p53 to prevent arrest induced by replicational stress per se is primarily dependent on preventing p21CIP1 up-regulation.
- p53 has a role in skin pigmentation as well as in skin neoplasms
- alteration and/or a modulation of the p53-p21 pathway in response to UV could be determinant for human papillomavirus 16-infected keratinocyte survival and HPV-associated carcinogenic process
- p53 genetic alterations found in gastric stump carcinomas & intestinal-type primary gastric carcinomas could originate from a similar pathway; no association found between p53 gene status & P-gp expression
- direct interaction between HAUSP and p53 is not absolutely required for it to antagonize efficiently Mdm2-mediated ubiquitination of p53
- Over expression of H179Y-mutant p53 promoted G1 to S phase transition with enlarged cell size and increased cyclin A1 and Cdk4 expression in HELF cells.
- These results suggest that the Val allele of CYP1A1 Ile462Val polymorphism and the Pro allele of TP53 Arg72Pro polymorphism contribute to an increased risk of gallbladder cancer among Japanese women and men, respectively.
- transcription mediated by p53 is impaired by mutations of the HIPK2 gene in acute myeloid leukemia and myelodysplastic
- Review. Induction of transfected murine ARF led to a rapid increase in ARF expression in human cells, resulting in p53 stabilization. The p19ARF/oncogene stress pathway induces the acetylation of p53 at lysine 120 in the DNA-binding domain.
- NFBD1 plays an important role in the decision of cell survival and death after DNA damage through the regulation of p53
- Tumor suppressor p53 Arg72Pro polymorphism leads to increased longevity, but not to decreased risk of cancer.
- immunoreactivity of p53, MDM2, WAF1, and BCL-2 were measured in soft tissue sarcomas cases consisting of 54 low-grade, 40 intermediate-grade, and 58 high-grade sarcomas
- The Pro/Pro genotype of TP53 codon 72 appears to be an independent prognostic marker in breast cancer patients.
- hypoxia may decrease tumor cell radiosensitivity through the suppression of p53 activity in some tumor cell lines
- in addition to regulating the expression of hundreds of protein-coding genes, p53 also modulates the levels of microRNAs
- Global miRNA expression analyses identified a cohort of miRNAs that exhibit p53-dependent upregulation following DNA damage.
- TP53 is not a major contributor to BRCA1 and BRCA2 mutation-negative breast and/or ovarian cancer families of French Canadian descent
- The threshold level of p53 for the initiation of apoptosis and the time sequence in the course of apoptotic events were determined in X-irradiated MOLT-4 cells.
- Hypoxia/reoxygenation exposure induced p53 expression.
- SNP309 of HDM2 is a frequent event in bladder cancer, related to earlier onset of superficial disease and TP53 mutation status
- nutlin-3A stabilized p53 by preventing MDM2-mediated p53 degradation in and Reed-Sternberg (HRS) cells of Hodgkin's lymphoma (HL)
- the p53 codon 72 polymorphism may be associated with gastric cancer among Asians, and that difference in genotype distribution may be associated with the location, stage, and histological differentiation of gastric cancer (Review)
- These observations demonstrate a novel regulatory role for p53 as a uPAR mRNA binding protein that down-regulates uPAR expression, destabilizes uPAR mRNA, and thereby contributes to the viability of human airway epithelial or lung carcinoma cells.
- BAG-1 negativity in association with p53 and c-erbB2 positivity identified a subgroup of tongue cancer patients with an aggressive phenotype
- P53 expression in H1299 cells reduced the sub-G1 fraction. p53 enhanced the repair of UV-induced DNA damage. Human p53, unlike CHO-K1 p53, may play active roles in both UV-induced apoptosis & repair.
- Regulation of miRNA expression into the transcriptional network regulated by p53.
- KRAS G34A mutation was relatively common to all classes of specimen, whereas TP53 gene C742T and G818C mutations were significantly more frequent in lichen sclerosus than normal genital skin.
- shielding of reactive cysteines contributes to a negative regulation for human p53 and imply that such an inactivation of the transcription factor may represent an acute defensive response with significant consequences for oncogenesis.
- a new role for YY1 as both an inducer of p53 instability in smooth muscle cells, and an indirect repressor of p21WAF1/Cip1 transcription, p21WAF1/Cip1-cdk4-cyclin D1 assembly and intimal thickening.
- p53 intron 7 ApaI polymorphism may be associated with human NSCLC.
- the presence of p53 mutations in the surgical margins of squamous cell carcinoma of the head and neck may not increase the risk of local-regional recurrence, but probably increases the risk of developing distant metastases or second primary tumors
- P53 immunohistochemical profile may be useful in detecting colorectal adenomas with a malignant potential.
- A sensitive immunodetection method was developed for pseudo-mutant conformation of TP53 in cells using immune complexes with protein A conjugates.
- MMS-induced micronuclei were eliminated under mild hyperthermia via TP53 metabolism in lymphocytes.
- In C33-A cells, arsenic treatment leads to a transient increase in p53 followed by a drastic reduction in its nuclear levels and an increase in cell proliferation.
- Telomere length in peripheral blood cells of germline TP53 mutation carriers is shorter than that of normal individuals of corresponding age
- In response to TNF, Zfra is upregulated and modulates TNF-mediated cell death via interacting with TRADD, FADD and RIP (death-inducing signaling complex) at the receptor level, and downstream effectors NF-kappaB, p53, WOX1, and JNK1.
- phosphorylation of Pirh2 may act as a fine-tuning to maintain the balance of p53-Pirh2 autoregulatory feedback loop, which facilitates the tight regulation of p53 stability and tumor suppression
- MEG3 non-coding RNA may function as a tumor suppressor, whose action is mediated by both p53-dependent and p53-independent pathways
- data suggest that this tumor suppressor gene plays a critical role in the multistep carcinogenesis process for esophageal squamous cell cancer
- two p53 haplotypes harboring the intron 3 polymorphic (+16bp) allele are associated with a higher risk of breast cancer in the Turkish population
- study of EGFR, HER2, TP53& KRAS mutations of p14arf expression of non-small cell lung cancers in relation to smoking
- study reveals there are differences in the frequencies & types of K-ras & p53 mutations found in pancreatic adenocarcinomas of patients in high-pollution & low-pollution regions in Egypt & suggests that environmental factors may explain these differences
- Therefore, using p53-p-Ser15 as a general marker of radiation sensitivity has confounding factors which may impair proper radiosensitivity prediction.
- Photodynamic therapy resistant HT29 cell variants are differentially sensitized to UVA compared with UVC due, in part at least, through the altered expression levels of BNip3, Hsp27 and mutant p53.
- Positivity for p53 was strong and diffuse in 5 uterine tumors and in 3 ovarian tumors. p53 expression in 6 of the uterine specimens and 7 of the ovarian specimens was present in fewer tumor cells, of weak intensity, or both.
- p53 mutation was observed in 4 of 13 specimens of endometriosis coexisting with ovarian clear cell carcinoma, whereas no mutations were detected in solitary endometriosis or endometriosis coexisting with ovarian endometrioid carcinoma.
- The phosphorylation of p53 was associated with its transcriptional activity and stability modulated by LMP1
- Ser(46) phosphorylation of p53 is not required for adriamycin-induced apoptosis.
- In a proteomic screen for p53 interactors the cullin protein Cul7 efficiently associates with p53.
- study found that lymphomas harboring p53 missense mutation with/without nonsense mutation had a highly significantly larger nuclear gross area than lymphomas with silent p53 mutation or lacking mutation
- Nutlin-3 abrogates both pre-osteoclastic proliferation and differentiation through a p53-dependent pathway
- The combined immunohistochemical and genetic data of carcinoma ex pleomorphic adenoma and intraductal carcinoma showed genetic or morphological evidence of dysfunctional p53, indicating that this is an early event in malignant transformation.
- These data provide evidence that there is a novel signaling pathway from Dishevelled to p53.
- The association of p53 codon 72 and CDKN1A codon 31 polymorphisms with oral cancer risk in a Taiwanese population were investigated.
- We observed that the Pro72/Pro72 genotype of p53 is much less represented in children with nonsyndromic mental retardation than in controls and suggest that subjects carrying the Pro allele are protected from this disease.
- New gain of function of the common p53 cancer mutants in inducing genetic instability.
- p53 NLS-selective nuclear import pathway and that both soluble and insoluble proteins are involved in its function.
- These findings support a novel p53 --> CDIP --> TNF-alpha apoptotic pathway that directs apoptosis after exposure of cells to genotoxic stress.
- Coxsackievirus B3 (CVB3) infection markedly reduced ATF3 expression at mRNA and protein levels in parallel with p53 degradation, and preservation of p53 expression rescued CVB3 infection-induced ATF3 downregulation.
- a crucial role of p53 in determining p27 upmodulation following HER2 activation
- analysis of the transactivation function of p53 alleles in cancer
- Distribution of a single nucleotide polymorphism in the TP53 codon 72 (Arg/Pro) was studied in Southeast Asia and Oceania where information about this polymorphism was lacking.
- Mutations in exons 5-9 of the p53 gene were screened for using the non-isotopic RNase cleavage assay (NIRCA) and confirmed by direct sequencing, followed by immunohistochemical analysis for p53 protein
- p53 like other binding partners of cdc25C, regulates entry into mitosis by binding to cdc25C
- RNA interference experiments demonstrate that CDK8 functions as a coactivator within the p53 transcriptional program.
- interphase Fish on samples from 30 MCL patients revealed p53 deletions in 13 cases
- RbAp48-mediated transformation of HPV16 is probably because of the regulation by RbAp48 of tumor suppressors retinoblastoma and p53, apoptosis-related enzymes caspase-3 and caspase-8, E6, E7, cyclin D1 (CCND1), and c-MYC.
- transcription-based stress response involving replication protein A, ATR, and p53 has evolved as a DNA damage-sensing mechanism to safeguard cells against DNA damage-induced mutagenesis
- the MDM2 and MDMX complex has a role in abundance and activity of p53
- analysis of the p53-Mdm2 feedback loop using protein lysate microarrays
- In lung cancer patients, p53 accumulation could be due to a decrease in full-length MDM2 isoform together with an increase of the 57-kDa MDM2 isoform that was unable to stimulate p53 degradation.
- Electron microscopy on the conformationally mobile, unbound p53 selected a minor compact conformation
- cigarette smoking may influence breast cancer risk through interaction with p53.
- HIPK2-induced p53Ser46 phosphorylation activates the KILLER/DR5-mediated caspase-8 extrinsic apoptotic pathway.
- p53 mediates interstitial cystitis APF-induced growth inhibition of human urothelial cells.
- Results show that p14ARF regulates E2F-1 ubiquitination and degradation via a p53-dependent mechanism.
- Results suggest that the roles of p53 and nucleotide excision repair in the recovery from UV-induced replication are separable and DDB2-independent.
- Data suggest that p53 regulates cellular responses to environmental carcinogen benzo[a]pyrene-7,8-diol-9,10-epoxide in human lung cancer cells.
- Bloom symdrome-independent role for p53 in etoposide-induced, topoisomerase II-mediated DNA damage in human cells.
- In the Italian population there is no association between codon 72-p53 gene polymorphism and the occurrence of rheumatoid arthritis.
- Changes in the intrinsic thermodynamic stability of p53 reduce the level of folded and hence functional p53 substantially in E. coli.
- Fluorouracil may show translational regulation and control p53 expression in a colon cancer cell line.
- TP53BP1 variants may have protective effects on head and neck cancer risk.
- These findings suggest novel Cdk1/cyclin A phosphorylation sites, which appear to be associated with p53-independent cell death following etoposide treatment.
- metformin treatment forces a metabolic conversion that p53(-/-) cells are unable to execute
- P53 Arg72Pro and MDM2 T309G polymorphisms contribute to the risk of developing stomach cancer.
- damage-activated switch in Hdm2 ubiquitin ligase preference from P53 to itself and Hdmx is central to P53 activation
- N33, STK11 (19p13) and TP53 might play a role in the development of metastasis in larynx and pharynx squamous cell carcinomas.
- correlation between p53 gene deletion and mammary gland carcinoma
- Results suggest that the cross talk between lysine methylation and acetylation is critical for p53 activation in response to DNA damage and that Set7/9 may play an important role in tumor suppression.
- The expression of p53 was significantly higher in esophogeal squamous cell neoplasm than in non-tumorous tissue.
- Deletion or mutational inactivation of the p53 gene represents an important step in the tumorigenicity of pancreatic cancer.
- PEDF induces human umbilical vein endothelial cells apoptosis through the sequential induction of PPARgamma and p53 overexpression.
- There is strong evidence that low grade dysplasia is a neoplastic lesion and that p53 point mutation is deeply involved in esophageal carcinogenesis.
- The results suggest that p53 expression in gonads of human male fetuses significantly increases in the 20th week.
- variant codon 72 p53 genotypes and the absence of the glutathione S transferase 1 (GSTM1) detoxification pathway, act in multiple myeloma disease progression
- The data suggest the miRNA34s might be key effectors of p53 tumor-suppressor function, and their inactivation might contribute to certain cancers.
- TERT association with TP53 mutations indicates that TERT activity is downregulated by functional p53 protein in breast tumors.
- The Pro allele in the codon 72 of TP53 was observed in 5/9 glioma tumors.
- TP53 mutations had low diagnostic accuracy for pancreatic neoplasms.
- Downregulation of caveolin-1 expression affects bleomycin-induced cell cycle arrest and subsequent cellular senescence that is driven by p53 and p21.
- Overexpression of stathmin is an early protumorigenic event in human hepatocarcinogenesis, and its up-regulation can be mediated by gain-of-function mutations in p53.
- KLF6 and p53 mutations are involved in the development of nonpolypoid colorectal carcinoma, whereas K-ras and B-raf mutations are not
- study investigated the correlation of p53 abnormalities in 15 patients with pulmonary large cell carcinomas; 5/15 expressed p53 and none had mutant p53 sequences; there was a negative survival correlation with positive p53 immunostaining (P = 0.05)
- CHIP might be a direct chaperone of wild type p53 that helps p53 in maintaining wild type conformation under physiological condition as well as help resurrect p53 mutant phenotype into a folded native state under stress condition.
- p53 mutation is associated with intraductal papillary mucinous neoplasms of the pancreas
- abrogation of p53 function in post-selection human mammary epithelial cells inactivates cell cycle checkpoints
- pGSK-3beta-ser-9 may confer the cisplatin resistance of ovarian carcinomas through the stabilization of p53 expression
- these preliminary data suggest that polymorphism at codon 72 of the p53 gene influences the clinical course of ulcerative colitis, with continuous disease associated with p53 Pro homozygosity
- our data support the view that patients with P53 overexpression are significantly associated with an unfavorable outcome, whereas
- Study shows that p53 over expression in Crohn's Disease is associated with dysplasia that may progress to a higher grade of neoplasia over time.
- Alterations in TGF-betaRII, BAX, IGFIIR, caspase-5, hMSH3 and hMSH6 genes of microsatellite instability are rare in urinary bladder carcinoma and they are not associated with microsatellite instability or the presence of p53 mutations.
- HPV18 E6 oncoprotein contributes to tumor angiogenesis by inducing VEGF transcription from the promoter in a p53-independent manner.
- results suggest that gene-smoking and gene-gene interactions may impact the prevalence of p53 mutations in breast tumors
- The up-regulation of PTEN inhibited Akt and MDM2, which enhanced the level of p53, thereby inducing G(2)/M arrest and apoptosis.
- Study of conformational mutant p53 as a new putative marker to discriminate Alzheimer disease(AD) from non-AD patients.
- patients with chronic lymphocytic leukemia (CLL) we have identified a novel p53 splicing variant, lacking the whole coding sequence of exon 6.
- accumulation of VRK1 in tumours with mutant p53 could result in stimulation of other signalling pathways
- Isoleucine 31-type p53 may be partly involved in familial gastric cancer because of its low transcriptional activity and low cell proliferation suppressing activity.
- by disrupting the DNA binding activity of E2F1, BTG3 participates in the regulation of E2F1 target gene expression. Therefore, our studies have revealed a previously unidentified pathway through which the activity of E2F1 may be guarded by activated p53.
- frequency of TP53 mutations using purified tumor DNA from ovarian serous carcinomas was 80.3%, which is much higher than reported. We found that TP53 is not directly involved in development of drug resistance in high-grade ovarian serous carcinomas.
- The apoptogenic activity of BM-ANF1 was mediated through p53 tumor-suppressor gene expression followed by the expression of p21(Cip1) and p27(Kip1)linking it with cell cycle arrest at G1 phase in cancer cells.
- TAp73 is a stress-response gene and a downstream effector in the p53 pathway
- Risk for head and neck squamous cell carcinoma may be assocated with single-nucleotide polymorphism in the promoter region.
- the p53 protein encoded by the 770delT allele is as abundant as the wild-type protein, as removal of the C-terminal p53 domain leads to a stabilized mutant protein, whose abundance is markedly increased when NMD is inhibited.
- no mutation of p53 and RB2/p130 genes was identified in any of the blood samples from Malaysian nasopharyngeal carcinoma; there was an identical G-->4 C nucleotide change at codon 280 of p53 gene in all the NPC cell lines
- Aberrations of the p53, Rb and p27 pathways are associated with aggressive clinical behavior in DLBCL.
- An animo acid substituition is a risk factor for breast cancer.
- HCMV uses a shift from p53 to HDM2 ubiquitination and destabilization to obtain protracted high levels of p53, while promoting cell cycle traverse
- Bcl-x(L) interacts with the DNA binding site of p53, but Bak does not interact with this site
- Results unravel a novel mechanism by which ERalpha opposes p53-mediated apoptosis in breast cancer cells.
- levels of c-myc expression were up-regulated and those of p53 expression were down-regulated by HCV F protein.
- Study reports that p18(Hamlet) can also mediate the cell cycle arrest induced in response to gamma-irradiation, by participating in the p53-dependent upregulation of the cell cycle inhibitor p21(Cip1) (CDKN1A).
- bcl-2 and p53 expression in neuroblastoma is related to DNA fragmentation
- Azurin binds to the flexible L(1) and s(7)-s(8) loops of the p53 DBD and stabilizes them through protein-protein tight packing interactions.
- p53 mutation was exhibited in pulmonary sclerosing haemangioma. The mutation rate in polygonal cells was higher than that in surface cuboidal cells
- Report genetic alterations of TP53 in Korean colorectal cancer patients.
- This study identifies SET8 as a p53-modifying enzyme, monomethylating p53 at lysine 382(p53K382me1) and identifying (p53K382me1) as a regulatory posttranslational modification of p53.
- Results identify cross talk between the p53 and nonsense-mediated mRNA decay pathways that regulates the expression levels of H-ras splice variants.
- Patients with primary colorectal cancer with low TSP-1 expression, with or without detection of mp53 gene product, are more likely to harbor lymph node metastasis than patients with higher expression.
- p53 expression may have a role in the carcinogenesis of squamous cell cervical carcinoma whereas Bcl-2 expression has no role. Ki-67 expression can not be used in determining the aggressiveness of CIN lesions
- It is recorded that borealin is a cell cycle regulator, down-regulated in response to p53/Rb-signaling, and up-regulated in many types of cancerous tissues.
- The results indicate protective associations of p53 Arg72Pro heterozygous variant with postmenopausal and MDM-2 SNP309G along with p53 Arg72Pro heterozygous variant with premenopausal breast cancer risk.
- Data show that knockdown of either p53,but not p16(INK4a) or Rb, allows cells to bypass premature senescence that is induced by BS69 knockdown.
- Activation of AKT, possibly through the PI3K-AKT pathway, is an important component of ASCC tumorigenesis that contributes to MDM2 and TP53 accumulation in the nucleus.
- Some mutant forms can be reactivated by amifostine, mostly in the DNA-binding domain.
- Alterations in p53 were more commonly observed in localized GISTs at higher risk of relapse, and suggesting that they are significant as an independent, poor prognostic factor.
- During fludarabine treatment of Raji and MEC1 cells, proteolytic derivatives of p53 with MW of ~47 and ~40 kDa appeared. There were 8 phosphorylated forms. These could play crucial roles in apoptosis induction.
- These data implicate a role for p73 in squamous cell carcinoma of the oesophagus and suggest a complex interaction between p53, p73 and HPV in the aetiology of the disease.
- p53 is a direct transcriptional target gene of hPitx1. This observation is concordant with the recent identification of hPitx1 as a tumor suppressor gene.
- Data suggest that cylindrospermopsin induces stress responses that result in the activation of the p53 transcription factor.
- modulation of p53Pro72Pro-mediated susceptibility to cervical cancer by immunogenetic factors could possibly be mediated through cross talk between HPV16/18-induced immune evasion and cell transformation
- PC4 interacts with the DNA binding and C-terminal domains of p53 through its DNA binding domain, which is essential for the stimulation of p53 DNA binding.
- Wild-type and mutant p53 are shown to differentially regulate MMP-13 expression in malignant peripheral nerve sheath tumors.
- The targeted degradation of p53 by E6 may contribute to the invasive phenotype exhibited by cervical cells that contain high-risk HPV types.
- insulin-like growth factor binding protein-5 plays a role in the regulation of cellular senescence via a p53-dependent pathway and in aging-associated vascular diseases
- the histone lysine-specific demethylase LSD1 interacts with p53 to repress p53-mediated transcriptional activation and to inhibit the role of p53 in promoting apoptosis
- TP53 levels were not helpful in identifying patients who would benefit from neoadjuvant treatment of rectal cancer.
- Paclitaxel has potential for use as a radiosensitizer in the treatment of patients with prostate cancer with either wild-type or mutant p53 genetic status.
- p53 and Ki-67, but not bcl-2, cyclin D1 or HER-2 may have roles in the process of tumor genesis in non-small cell lung carcinoma
- ATP binding function of MDM2 can mediate its chaperone function toward the p53 tumor suppressor
- p53 codon-249 mutations are associated with X-ray repair cross complementing protein 1 polymorphism Arg399Gln among the Guangxi population of China.
- p53 mutations at CpG dinucleotides provide further evidence for a molecular link between chronic inflammation and esophageal malignancy.
- findings suggest no association between oligodendroglial tumors and the SNP in codon 72 of TP53; also no correlation was found among the TP53 codon 72 polymorphism and prognosis, p53 expression, and chromosomes 1p and 19q status
- provide new insight into a potential role of p53 as a component involved in the dynamic regulation of the major pathway of cytotoxic T-lymphocyte-mediated cell death and may have therapeutic implications
- human papillomavirus 18 E6 protein sensitizes HeLa cells to Herpes simplex virus-dependent apoptosis through hTERT and p53.
- Though not formally excluded, these results do not support models in which p53 binds specific RNA partners in vivo.
- Mutant p53 attenuates TGF-beta1 signaling. This was exhibited by a reduction in SMAD2/3 phosphorylation and an inhibition of both the formation of SMAD2/SMAD4 complexes and the translocation of SMAD4 to the cell nucleus.
- Signaling of DNA damage is not sufficient to induce p53 response: (re)activation of wt p53 protein strongly depends on cellular context.
- CSN5 is a pivotal regulator for both p53 and MDM2
- TP53 DNA-binding mutations were the most significant predictor of poor OS; TRAILreceptor-2 (DR5) was the most differentially underexpressed gene in the TP53 mutated cases
- Tumors that contained wild-type p53 were significantly more likely to express WT1, and presence of WT1 in glioma support that WT1 expression is important in glioma biology.
- In light of current treatment regimens for AIDS-related primary effusion lymphoma, this review discusses the benefits of using reactivation of the p53 pathway as a novel principle for the treatment of this virally induced highly aggressive malignancy.
- Required for the elimination of cells with aberrant CD43 expression.
- the ectopic expression of IKKalpha into cells silenced for USP11 restores p53 expression, demonstrating that USP11 functions as an upstream regulator of an IKKalpha-p53 signaling pathway.
- There is no association between radon exposure and p53 expression, indicating that maybe the effect of radon is not mediated through p53 alterations.
- Cells expressing mutant forms of E6 that are unable to bind p300/CBP or bind p53 failed to block acetylation of p53 at lysine 382 and were sensitive to growth arrest by interferon.
- molecular dynamics simulations of wild-type p53 and the R337His mutant at several different pH and salt conditions
- AG490 enhances UCN-01-induced cytotoxicity in p53 defective cell lines by suppression of BAD phosphorylation and induction of BAX and PARP cleavage
- A strong correlation was found between the expression of p53 and p130, which was apparent in Stages 1 and 3, but not in Stage 2. These results suggest a novel p53/p130 axis in bladder tumors.
- Data suggest that Pin1 is required for efficient loading of p53 on target promoters upon stress, and that after phosphorylation of p53 triggered by cytotoxic stimuli, Pin1 mediates p53's dissociation from iASPP, promoting cell death.
- We report the histological and genetic study of two glioblastomas, one case arising de novo and the other case arising 3 years after a previously diagnosed anaplastic astrocytoma, with concurrent EGFR amplification and TP-53 mutation
- Mutant and wild-type p53 proteins are ubiquitinated and degraded through overlapping but distinct pathways.
- rerview of NF-kappaB gene signatures and p53 mutations in head and neck squamous cell carcinoma [review]
- NF-kappaB promotes expression of a novel NF-kappaB-related gene signature and cell survival in HNSCC that weakly express TP53, a subset previously associated with inactivated wild-type TP53, greater resistance to chemoradiotherapy, and worse prognosis
- In breast cancer, bone morphogenetic protein 7 (BMP7) is a novel target gene regulated by the p53 family and mediates the cell survival function of the basal physiologically relevant level of p53.
- this large collaborative study did not find an association of MDM2 SNP309 and TP53 R72P, separately or in interaction, with breast cancer
- ZNF307 might suppress p53-p21 pathway through activating MDM2 and EP300 expression and inducing p53 degradation
- p53 is predominantly nuclear and functional in neuroblastoma regardless of differentiation status.
- MAGED2, a novel protein, is a p53-dissociator.
- p53 Arg/Arg genotype does not seem to represent a risk marker for the development of cervical lesions in the majority of the European countries analysed.
- These data suggest that P1 promoter is the main driving force for transcribing the bcl-2 gene and P1 activity is modulated by M and P2 in a p53-dependent and -independent manner.
- study to identify the common factors governing the DNA-binding loss of p53c upon substitution of Arg 273 to His or Cys,which are abundant in human tumour
- This is an overview/review of studies of the p53-protooncogene protein MDM2 module and associated pathways from a systems biology perspective.
- Loss of TP53-DNA interaction induced by p.C135R point mutation in lung cancer
- compromise of either p53 or Rb pathways during melanocyte transformation leads to up-regulation of survivin expression in melanoma
- study describes the presence of different p53 gene mutations in astrocytic gliomas in direct correlation to histologic characteristics of dissected tumor areas
- by NF-kappaB activation, Tax elevates the level of the cellular p53 in human T-cells
- among p53 Arg/Arg carriers, HPV infection, smoking, and drinking might further increase the risk of esophageal squamous cell carcinoma development
- results of the present study have indicated that p53 mutations occur at the ileovesical anastomosis in patients who have undergone clam ileocystoplasty
- lymphocytes showed repeatedly an extensive proportion of TP53 mutated cells, harboring various TP53 mutations, mostly single-point, in individual cells. The mutation targeting exhibited characteristic traits of the somatic hypermutation process
- No significant difference in the distribution of p53 codon 72 genotypes was observed between endometriosis patients and controls.
- Here we report a significant trend toward lower frequency of TP53 mutations with increasing number of Pro72 alleles (P = 0.02). Overall, Pro72 allele carriers had significantly lower frequency of TP53 mutations compared with Arg72 homozygotes (P = 0.02).
- p53 function is not sufficient to suppress glucose uptake in cells and tumors that could theoretically support aerobic glycolysis.
- p53 is an indispensable component of cellular signaling system which is regulated by caveolin-1 expression, involving Akt activation and increase in cyclin D1, thereby promoting proliferation of breast cancer cells.
- Discuss how tissue specificity, polymorphisms of genes associated with the p53 pathway, other genetic alterations, or p53 mutant heterogeneity can have a profound impact on the spectrum of p53 mutations (review).
- Wip1 acts as a gatekeeper in the Mdm2-p53 regulatory loop by stabilizing Mdm2 and promoting Mdm2-mediated proteolysis of p53.
- Loss of heterozygosity (LOH) of the hDMP1 gene was detectable in approximately 35% of human lung carcinomas, which was found in mutually exclusive fashion with LOH of INK4a/ARF or that of P53. DMP1 is a pivotal tumor suppressor for human lung cancers.
- p53 activity is differentially regulated by Brm- and Brg1-containing SWI/SNF chromatin remodeling complexes
- These findings provide evidence that activation of TP53 gene transcription by PKCdelta triggers TP53-dependent apoptosis in response to DNA damage.
- crystal structure of N-terminal domain of Mdmx bound to 15-residue p53 peptide was determined; structure reveals that although principle features of Mdm2-p53 interaction are preserved, the Mdmx hydrophobic cleft on which the p53 peptide binds is altered
- Embryos have varying sensitivity to the stresses of production and culture in vitro, and this resulted in variable expressivity of TRP53.
- Immunohistochemistry localized elevated p53 to a mainly nuclear distribution in neurons and glia in sections from temporal lobe epilepsy hippocampus
- K-cyclin/Cdk9 interaction greatly enhanced the kinase activity of Cdk9 toward p53.
- p53 plays a role in regulation of replication timing of the human genome through the control of cell-cycle checkpoints.
- Upregulation of MDR1 by DeltaNp73alpha is mediated by interaction with p53 at the MDR1 promoter.
- Monomeric but not trimeric clathrin heavy chain regulates p53-mediated transcription.
- Individuals with the Pro/Pro genotype have an increased risk of developing nasopharyngeal carcinoma in Tunisia.
- reveal a direct regulatory connection between p53-responsive stress signaling and Hbo1-dependent chromatin pathways
- This review discusses implications of recent studies of the capacity of p53 to control the expression of specific microRNAs which may subsequently become involved in cancer and other critical biological processes.
- The ultimate activation status of p53 target genes can be defined at steps downstream of p53 binding to chromatin and p53iated recruitment of histoneifiying activities.
- The results presented in this report emphasized flow cytometry as an important tool for the fast evaluation of p53 protein expression levels as bioindicator of individual exposure to acute ionizing radiation.
- Suggest beta-catenin deregulation is involved in sporadic hepatoblastoma and also suggests that mismatch repair defects and p53 mutations contribute to this rare liver cancer.
- Active regulator of SIRT1 (AROS) is the first direct SIRT1 regulator to be identified that modulates p53-mediated growth regulation.
- We conclude that the free radical scavenger edaravone suppresses X-ray-induced apoptosis in MOLT-4 cells by inhibiting p53.
- show an important link between ATM activity and the tumor-suppressive function of B56gamma-protein phosphatase 2A
- High frequency of BRCA1/2 and p53 somatic inactivation in sporadic ovarian cancer.
- Findings may indicate p53 codon 72 polymorphism as a risk factor for HNSCC.
- These data suggest a more complex role for TRIM22 during T lymphocyte activation than merely as an antiproliferative factor.
- defects in the p53 regulatory cascade do not appear operational in this leukemia
- The combination of p53 and p21 expressions in biopsy findings can thus predict the histological effectiveness of hyperthermochemoradiotherapy.
- The functional interplay between EGFR overexpression, hTERT activation, and p53 mutation in esophageal epithelial cells with activation of stromal fibroblasts induces tumor development, invasion, and differentiation.
- Analysis of neuroblastoma cell lines indicated that in contrast to previous reports, wild-type p53 was fully functional in all neuroblastoma lines tested; inactivation of p53 in neuroblastoma cells resulted in establishment of a MDR phenotype.
- Superior outcome of t(8;21) acute myeloid leukemia patients is partly due to an activated p53 pathway, and that loss of the p53 response pathway is associated with disease progression.
- the potential use of R-Roscovitine as a bitargeted anticancer drug that functions by simultaneously causing p53 activation and NF-kappaB suppression.
- These results indicate that mutations and consequent dysfunction of P53 gene may result in chronic inflammation and hyperplasia in RA (Rheumatoid Arthritis) patients.
- Results show that p53 seemed to have a significant role in cellular glucose metabolism and G2/M checkpoint, according to beta-irradiation, and could cause a different therapeutic response of (18)F-FDG uptake in cancer cells.
- Single nucleotide polymorphisms within p53 are associated with chronic lymphocytic leukemia.
- loss of IFI16 activates p53 checkpoint through NBS1-DNA-PKcs pathway
- TP53 mutations are frequent events in bladder cancer progression and gelsolin relates to TP53 status, tumor staging and clinical outcome.
- Detailed mapping of chromosome 17p deletions reveals HIC1 as a novel tumor suppressor gene candidate telomeric to TP53 in diffuse large B-cell lymphoma
- p53 and p73 repress a number of growth-related genes and that in many instances this repression may be through the induction of p21.
- Combination of PTEN/p53/PCNA represent an independent prognostic factor for tumor recurrence and disease-specific survival in hepatocellular carcinoma after surgery.
- Human head and neck squamous cell carcinoma cells transfected with mutant TP53 injected subcutaneously into hind legs of nude mice show reduced sensitivity due to repair of radiation-induced damage.
- study showed higher frequency of p53 mutations in esophageal adenocarcinoma (EAC)than previously reported, but only as a late event in carcinogenesis; 72R allelic polymorphism was of potential significance in the development of Barrett esophagus &/or EAC
- Genome-scale chromosomal copy number alteration profiles and mutational statuses of p53 and beta-catenin in 87 hepatocellular carcinoma tumors were clarified.
- Mutation of the IP6-binding sites impair oligomerization, reduce interaction with Mdm2, and inhibit p53-dependent antiproliferative effects of beta-arr2
- p53 homolog, p63, may participate in governing global repair instead of p53 in keratinocytes
- although p53 mutation is relatively rare, the type and distribution of mutations in low-grade B-cell malignancy patients does not differ significantly from other forms of cancer
- Compar. proteome anal.to RNA expr. array showed modest correl. of RNA and protein level = relevance of post-trans. regul. in lymphomagenesis. Data bank search identified 13 out of 17 referenced proteins (76%) as members of a TP53-dependent network.
- The acetylation of two lysine residues in p53 promotes recruitment of the TFIID subunit TAF1 to the p21 promoter through its bromodomains.
- reveal a novel p53 apoptotic pathway in which it initiates apoptosis by transcriptionally repressing ARC
- ability of p53 to down-modulate osteoprotegerin production by endothelial cells may be an additional important mechanism
- The role of p53 in DNA damage-mediated cytotoxicity overrides its ability to regulate nucleotide excision repair in human fibroblasts
- ChIP and expression studies for individual genes indicate that human endogenous retrovirus p53 sites are likely part of the p53 transcriptional program and direct regulation of p53 target genes
- HPV16/18 E6 is expressed in HPV DNA-positive lung tumors and is involved in p53 inactivation to contributing to HPV-mediated lung tumorigenesis
- These results suggested that Annexin A2 may play roles in p53 induced apoptosis and it is also involved in regulation of cell proliferation.
- Serum p53 antibodies are expressed in the early stages of colorectal cancer
- dThdPase, but not mutant p53, plays an important role in tumor angiogenesis in ductal adenocarcinoma of the pancreas
- Protein expression neither of p16(INK4a) nor of p53 correlated with high-risk human papillomavirus status
- Extent of mutation predicts response to antineoplastic agents.
- homeodomain interacting protein kinase 4 phosphorylates p53 at serine 9 is important for p53 mediated transcriptional repression.
- DEC1 is induced by the p53 family and DNA damage in a p53-dependent manner. p53 family proteins bind to, and activate, the promoter of the DEC1 gene.
- p53 dissociation from some promoters is due to DNA-mediated charge transport through the base-pair stack. Photo-oxidative dissociation, despite being triggered from distance, is sequence-selective. Disulfide bonds are formed.
- Can physically interact with the transcription elongation complex and influence transcription elongation.
- p53 mutations are present in a subset of pituitary carcinomas and are usually associated with a high percentage of tumor cells overexpressing the p53 protein.
- The increase of cell membranous phosphatidylcholines containing unsaturated fatty acid residues induces phosphorylation of p53 through activation of ATR.
- ATM or TP53 deletion is associated with high expression level of CD38 and TP53 deletion as a possible prognostic factor in Chinese patients with chronic lymphocytic leukemia
- levels of p53/p21waf1 mRNA in blood lymphocytes collected before chemotherapy may predict the chemoresponses of lung cancer patients.
- Furthermore, results indicate that induction of apoptosis in HCT-116 p53(wt) cells after ibuprofen treatment is in part dependent on a signalling pathway including the neutrophin receptor p75(NTR), p53 and Bax.
- mutant p53 loses its ability to suppress DNMT1 expression, and thus enhances methylation levels of the p16 ( ink4A ) promoter and subsequently down-regulates p16(ink4A )protein.
- p53 mutation is associated with non-small cell lung carcinoma
- Activation of p53 mediated pathways in the glia of HIV-associated dementia patients may contribute to neuroinflammatory processes that promote neurodegeneration by inhibiting glial proliferation and/or promoting glial cell dysfunction.
- Alterations in the expression of p53, survivn, and bcl-2 take place in a concerted fashion, implying that many of these cases may share common abnormalities.
- Based on these results, we conclude that HO activity is involved in the regulation of p53 expression in a ROS-independent mechanism.
- p63 exhibits several transcriptional and stress-response properties similar to those of p53
- TP53 Arg72Pro polymorphism, but not p73 G4C14>A4TA4 and p21 Ser31Arg, contribute to risk of cutaneous melanoma
- The increased apoptosis of peripheral blood lymphocytes from adult-onset Still's disease patients may be associated with the effect of IL-18 through up-regulation of FasL and p53 transcripts.
- In alternative lengthening of telomere cells, TRF2 inactivation/silencing triggers cellular senescence and substantial loss of telomeric DNA upon stable TRF2 knockdown.
- Histone deacetylase inhibitors may overcome neuroblastoma drug resistance by restoring p53 tumour-repressor function via its hyper-acetylation and nuclear migration.
- Splicing fidelity is p53 dependent.
- CP-31398 induced mitochondrial translocation of p53, leading to changes in mitochondrial membrane permeability pore transition (MPT) and consequent cytochrome c release in these cells.
- Examine interaction between TP53 and the C-terminal fragment of p53 (M protein).
- data indicate that in early and advanced gastric tumors, p53 and bcl-2 protein accumulation is more intense in gastric mucosa adjacent to advanced tumors and p53 immunoreactivity peaks in advanced carcinomas
- The culture of cells in the Cl(-)-replaced medium significantly increased expressions of p21 mRNA and protein without any effects on p53.
- In this first assessment of the role of TP53 Arg72Pro polymorphism in a large series of Portuguese glioma tumors, no association was observed with glioma susceptibility or overall survival, except for patients submitted to adjuvant therapy.
- Abrogation of G2 checkpoint by Geldanamycin may play a central role in sensitizing p53-negative tumor cells to DNA-damaging and decatenation-inhibiting agents.
- The codon72 and IVS7+72C>T polymorphisms of the p53 gene are unlikely to contribute to the pathogenesis of idiopathic male infertility with spermatogenetic failure.
- Report p53 expression in abberant crypt foci and colorectal neoplasms.
- There is heterogeneity in the requirement for transactivation subdomains 1 and 2 of p53 without any subdomain-specific contribution to p53-induced gene expression.
- In etoposide-treated LNCaP cells, p53 bound the AR promoter, which contains a potential p53 DNA-binding consensus sequence. loss of p53 function in prostate cancer cells contributes to increased expression of AR.
- nuclear apoptosis repressor with caspase recruitment domain (ARC)is induced in cancer cells and negatively regulates p53
- DNA damage combined with hypoxia modulated both the intensity of the p53 response and the composition of downstream target genes.
- suggests the unique role of Chk1 in preventing abrogation of the G2 checkpoint in p53+/+ cells
- Distinct rare missense mutations of the TP53 gene were detected in Capi1 (codon 312) and Capi3 (codon 181); the codon 181 mutation is consistent with a previously reported similar finding in a small series of CUP specimens.
- Inactivation of p53 may be associated with the appearance of central consolidation within pure ground-glass opacity (GGO) on HRCT which reflects invasive features and may be useful as a molecular marker.
- HHV-6B induces p53 Ser392 phosphorylation by an atypical pathway independent of casein kinase 2 protein and p38 kinases.
- Hsp27 may play a general role in regulation of cellular senescence by modulating the p53 pathway.
- p53 status should be taken into account when deciding which therapeutic drug to use in glioblastoma multiforme.
- this study failed to demonstrate correlation between maspin loss and p53 expression in malignant melanoma using both individual slides and tissue microarray of carcinomas.
- Maspin expression is inversely correlated with mutant p53 expression in gastric cancer, which suggests that maspin expression is regulated by the p53 pathway.
- The proliferative activity and p53 overexpression increased with the dedifferentiation of tranitional cell bladder carcinoma.
- Stroma-specific loss of heterozygosity or allelic imbalance is associated with somatic TP53 mutations and regional lymph-node metastases in sporadic breast cancer but not in hereditary breast cancer.
- Disruptive TP53 mutations in tumor DNA are associated with reduced survival after surgical treatment of squamous-cell carcinoma of the head and neck.
- expression of p53 and Ki-67 antigen is helpful to predict tumor recurrence and prognosis in skull base chordomas.
- P53 overexpression and changes in phenotypic expression could contribute to the malignant transformation of colorectal precursor lesions.
- linear relationship and prognostic role of the p53/p21/PCNA pathway in gastrointestinal stromal tumors. Abnormalities of the p53/p21WAF1 pathway lead to increased proliferating states, thereby triggering the progression of GISTs.
- Overexpression of p53 was associated with poor survival in gallbladder carcinomas.
- Id-1 regulates Bcl-2 and Bax expression through p53 and NF-kappaB in MCF-7 breast cancer cells
- The p53 codon 72 and 16-bp duplication polymorphisms were not associated with the increased risk of gastric cancer and did not seem to contribute to gastric cancer susceptibility among Koreans.
- p53 regulated transcripts including Puma/BBC in tetraploid but not diploid tumor cells is modulated by Chk1 inhibition
- the Hes6-CBP complex in PML-NB may influence the proliferation of cells via p53-dependent and -independent pathways.
- interplay between TFIIEalpha and the tumor suppressor protein p53 in regulating transcriptional activation that may be modulated by the phosphorylation status of p53
- the presence of both HPV infection and TP53 mutations may define a particular group of tumors with a more aggressive phenotype in advanced oral squamous cell carcinoma
- circulating anti-p53 antibodies (anti-p53Ab) in sera of cancer patients may have a role in disease progression
- an important role for the DNA damage response mediated by ATR-Chk2 in p53 activation and renal cell apoptosis during cisplatin nephrotoxicity.
- Genetic alterations of the p53 tumor suppressor gene were seen in a mixed serous carcinoma of the endometrium.
- the germinal center phenotype, P53 accumulation, and t(14;18) were independent factors for simian virus 40 association (P=0.029, 0.006, and 0.014, respectively) in diffuse large B-cell lymphomas
- germ line and somatic alterations of the p53 pathway influence the incidence and survival of ovarian carcinoma
- NUMB enters in a tricomplex with p53 and the E3 ubiquitin ligase HDM2 (also known as MDM2), thereby preventing ubiquitination and degradation of p53
- a network involving signal coactivation of NF-kappaB and STAT3, differentially modified by p53 inactivation or mutation, promotes altered BAX/BCL-XL expression and cell survival in HNSCC.
- Stimulation of KLF6 expression by IGF-I in a p53-dependent manner may constitute a novel mechanism of action of IGF-I, with implications in normal cell cycle progression and cancer biology.
- A high proportion of familial microsatellite instability cases and a lower incidence of TP53 mutations were found in Saudi colorectal carcinoma.
- p53 mutations and microsatellite instability differ in patients with gallbladder carcinoma between two distinct high-incidence areas
- p53 Arg72Pro heterozygous genotype was overall an independent prognostic factor...of lung cancer
- The expression of iNOS induces oxidative stress in nasopharyngeal carcinoma. p53 mutation was associated with iNOS overexpression. This suggests that the p53 gene is not the direct target of DNA damage by 8-OHdG accumulation.
- the role of triptolide as a sensitizer to TRAIL-induced apoptosis in part by independent modulation of XIAP expression and p53 signaling.
- The proper combination of IFNalpha and conventional chemotherapeutic agents may be a rational strategy for the treatment of human osteosarcoma with functional p53.
- E6-AP not only enhances the degradation of p53 but also regulates the neuronal cell growth.
- An important role for autophagy in tumor suppression via full-length ARF in both p53-dependent and p53-independent manners, depending on cellular context.
- High p53 expression level with low MDM2 and p14 ARF levels may be the characteristic features of low differentiated endometrial carcinoma
- Describe a novel p53 rescue compound that induces p53-dependent growth arrest and sensitises glioma cells to Apo2L/TRAIL-induced apoptosis.
- in a Portuguese population, the p53 R72P polymorphism is not associated with an increased susceptibility to squamous intraepithelial lesions or cervical cancer development
- Transcription regulation assays with MCL-1 promoter deletion mutants showed that most of the p53 inhibitory effect was mediated by the -41 to +16 bp promoter binding sites only for TATA-binding protein and other basal transcription factors.
- a combined expression of survivin and p53 was associated with an increased risk of tumor local progression.
- results suggested that beta1,4GalT II might serve as a target gene of p53 transcription factor during adriamycin-induced HeLa cell apoptosis, which elucidated a new mechanism of p53-mediated cell apoptosis
- identified the binding site of the p53 and FAK interaction and demonstrated that mutating this site and targeting the site with peptides affects p53 functioning and viability in the cells.
- PUMA exerts a negative feedback on p53 and p21, leading to p21-dependent growth suppressive and survival changes.
- IGF-1R-dependent UVB-induced premature senescence required the phosphorylation of p53 serine 46.
- p14ARF hypermethylation is common but INK4a-ARF locus or p53 mutations are rare in Merkel cell carcinoma.
- significantly higher levels of HCV RNA replication and viral protein expression in Huh7 cells when their p53 expressions were knocked down; p53 found to directly interact with IRF9
- Aberrations could be considered markers responsible for the development of odontogenic lesions.
- although HPV16 (human papiloma virus 16) and mutated p53 may coexist in a subset of squamous cell carcinomas of the head and neck, HPV16 and disruptive p53 mutations seem to be nonoverlapping events
- the p53 gene does not appear to play a major role in pheochromocytoma tumorigenesis.
- functional interaction of NEDL1 with p53 might contribute to the induction of apoptosis in cancerous cells bearing wild-type p53.
- TP53 mutations reduce the prostate cancer (PCa)-free survival time in patients with needle biopsy of the prostate and primary benign diagnosis; Exon 6 mutations enhance the risk of being affected by PCa 32-fold
- Tacrolimus ointment neither blocks ultraviolet B nor affects expression of thymine dimers and p53 in human skin.
- In the group of patients < or =53 yrs and with TP53(-) tumors platinum-based therapy is possibly equally efficient.
- Findings suggest TP53 PIN3 Ins16bp polymorphism as a real risk modifier in breast cancer disease, either in sporadic and familial breast cancer. Furthermore, both TP53 polymorphisms are associated with higher incidence of lymph node metastases.
- Our results indicate that nicotinamide treatment attenuates p21WAF1 expression through Sp1 downregulation, and suggest a possible involvement of nicotinamide metabolism in cellular gene expression.
- These studies suggest that PARC-interacting peptides are promising candidates for the enhancement of p53-dependent apoptosis in tumors with wt cytoplasmic p53.
- These results indicate that in thyroid cancer cells, TAp73alpha is able to increase p53 protein level and function by interfering with Mdm2-mediated p53 degradation.
- SS18-SSX1 can negatively regulate p53 tumor-suppressive function by increasing the stability of its negative regulator HDM2.
- This review emphasizes various mechanisms activated by p53 signalling that can confer protection to cells with damaged DNA in the context of p53's pro-apoptotic and pro-survival activities.
- p53-mediated apoptosis occurs by a PIDD- and caspase 2-dependent mechanism, and p53's full transcriptional regulatory functions may be required only for events that are downstream of cytochrome c release
- Results describe the interrelationship between H pylori and Epstein-Barr virus infection in gastric carcinogenesis, focusing on p53 mutation and c-Myc, Bcl-2 and Bax expression.
- results support the notion that acetaldehyde plays a role in TP53 mutations in esophageal cancers
- that Skp2 controls p300-p53 signaling pathways in cancer cells, making Skp2 a potential molecular target for cancer therapy.
- following DNA damage, PML facilitates Thr18 phosphorylation by recruiting p53 and CK1 into PML nuclear bodies, thereby protecting p53 from inhibition by Mdm2, leading to p53 activation.
- These findings indicate that R337H may be a low penetrance mutant which predisposes to multiple cancers
- Therefore, our results suggest that the interaction between Sirt2 and 14-3-3 beta/gamma is a novel mechanism for the negative regulation of p53 beside the well-characterized Mdm2-mediated repression.
- The distinction between various populations may be because of differences in racial composition and/or exposure to distinct environmental factors that have a different impact on systemic lupus erythematosus incidence along with the Argp53Pro genotype.
- optimal binding of STAGA to p53 involves interactions of STAGA subunits TAF9, GCN5, and ADA2b, respectively
- Current study showed p53 was associated with induction of apoptosis and cell proliferation in early stage gastric cancers, but not in the subserosa of advanced gastric cancer.
- Ki-67- and p53-immunostained cells were mainly located in the suprabasal layers. p63-positive cells were found throughout the lining cystic epithelium.
- that the recruitment of YB1, PURalpha, and H1.2 to the p53 target gene Bax is required for repression of p53-induced transcription.
- p53 codon 72 variant genotypes modify the risk of human papiloma virus 16-associated SCCOP and may be markers of genetic susceptibility to HPV16-associated squamous cell carcinoma of the mouth and pharynx.
- p53 codon 72 and intron 3 polymorphisms are associated with non-small cell lung cancer
- The DNA binding domains of p73 exhibited enhanced thermodynamic stability relative to the p53 DBD, and the p73 surface is less complementary for DNA binding, which may account for the differences in affinity and specificity for p53 REs.
- MDM2 SNP309, alone or in combination with TP53 R72P, was not associated with oligodendroglial tumors.
- AEN is an important downstream mediator of p53 in apoptosis induction in cancer.
- p53 has a role in preventing centrosome amplification, ERalpha phenotypic heterogeneity and metastasis in breast cancer
- The data support that the frequencies and patterns of somatic mutation of the p53 genes in colorectal cancer are variable among populations.
- p53 is required for the efficient removal of cross links in human cells; cytotoxic cross links persist in p53-deficient cells.
- p53 positivity was significantly associated with higher risk of disease-specific and recurrence-free mortality in HPV-HR head and neck neoplasms.
- The demonstration that p53 binds directly to the PIK3CA promoter and inhibits its activity identifies a novel mechanism whereby these two mediators regulate cellular functions.
- The p53 target sequences possessing the inverted repeat symmetry were shown to form a cruciform structure in sufficiently negative supercoiled DNA.
- p53 mutation spectra and differences with histology in lung cancers.
- differences in cellular responses to stress between the TP53 codon 72 genotypes contribute to the differences in cancer incidence and longevity observed earlier for these genotypes
- polymorphism at codon 72 modulates the risk of lung cancer in Brazilian patients with African ethnical background
- Defective p53 signaling in p53 wild-type tumors attenuates p21waf1 induction and cyclin B repression rendering them sensitive to Chk1 inhibitors that abrogate DNA damage-induced S and G2 arrest.
- the functions of p53 play substantial roles in many other pathologies as well as in the aging process [review]
- The p53 Pro72 homozygous non-small cell lung cancer patients often presented high-grade tumours and had significantly poorer survival rates than patients with R72 homozygotes or heterozygotes.
- Together our results show that hDDA3 is a p53- and DNA-damage down-regulated target that exhibits oncogenic characteristics.
- Point mutation at exon 5 of the p53 gene was present in colonic and stomach neoplasms, they could be considered to be of the same origin originated from a common epithelial stem cells.
- CARF exerts a vital control on the p53-HDM2-p21WAF1 pathway that is frequently altered in cancer cells.
- Investigation of the mechanism underlying p53 reactivation in hepatitis B virus X-protein-expressing cells.
- The morphology and cell cycle proteins immunoexpression of the novel probable preinvasive lesion - bronchiolar columnar cell dysplasia (BCCD), is decribed.
- A novel cis-element in the 5' coding region of p53 mRNA and its interaction with heterogeneous nuclear ribonucleoprotein (hnRNP)C1/C2, is described.
- Flotillin 2 is a direct transcriptional target of the p53 family member genes in human cancer cells.
- enhanced phosphorylation of p38 and p53 (ser15) in ZS cells was normalized after suppression of Gadd45 by siRNA
- Deletion of the 9p21 locus inhibits p53 protein; studies of the ARF-MDM2-P53 pathway link survival and chemoresistance in patients with abnormalities in 17p and 9p
- findings provide a molecular rationale for the role of human Spot 14 protein in the p53-dependent transcriptional activation of specific genes via diverse pathways in cells
- A novel isochroman derivative inhibited apoptosis in vascular endothelial cells through depressing the levels of integrin beta4 and TP53.
- the ability to promote Lys(63)-mediated polyubiquitination of COMMD1 is a novel property of ARF independent of p53
- Hibiscus syriacus extract exhibits a cytotoxic effect on lung cancer cells by activation p53 and AIF.
- p53beta and Delta40p53 are expressed in melanoma and this may have important implications for understanding resistance of melanoma to DNA-damaging chemotherapy.
- study examined the presence of mutations in TP53 at codon 249 (Ser-249, considered as a hallmark of mutagenesis by aflatoxin) and in CTNNB1 in circulating free DNA of patients with hepatocellular carcinoma or chronic liver disease from Alexandria, Egypt
- P53 mutations are associated with higher levels of Intratumoral T cells.
- The prevalence of MDM2 gene amplifications and single nucleotide polymorphism 309 in 284 colorectal tumors in relation to TP53 mutational status and genomic instability, is analyzed.
- Both germ line and somatic alterations of the TP53 pathway influence incidence and survival of ovarian carcinoma.
- analysis of solar light-induced p53 mutagenesis in SKH-1 mouse skin
- ERK and JNK MAPK/Elk-1/Egr-1 signal cascade is required for p53-independent transcriptional activation of p21(Waf1/Cip1) in response to curcumin in U-87MG human glioblastoma cells
- PKC epsilon mediates TRAIL resistance by Akt-mediated phosphorylation of Hdm2 resulting in suppression of p53 expression and downregulation of Bid in breast cancer cells
- There is no any association of polymorphous marker C(-594)CC of TP53 gene with DPN in Russian patients with type 1 diabetes mellitus living in Moscow.
- Identification of anomalous, detectable conformational state of p53 from sporadic Alzheimer's disease (AD) patients allows differentiation of fibroblasts from those of age-matched non-AD subjects and suggests a role for conformationally altered p53 in AD
- mutations in different exons of p53 are related to different phenotypes
- quercetin stabilized p53 at both the mRNA and protein levels to reactivate p53-dependent cell cycle arrest and apoptosis in HepG2 cells
- p53 status and efficacy of primary anthracycines/alkylating agent-based regimen according to breast cancer molecular classes are reported.
- tumor cell incubation with pioglitazone results in increased levels of p53 and p27 and decreased levels of cyclin D1
- These findings suggest that inhibition of the class I PI3K signaling pathway is a potential strategy for managing gastric cancers.
- Results correlate P53 status and mutation site/type with nuclear protein accumulation, clinicopathologic variables and data on K-ras mutations and high-level microsatellite instability.
- Non-smoking and non-drinking patients with squamous cell carcinoma have the same risk for developing multiple tumors as their smoking and drinking counterparts without an increased expression of p53.
- investigation of the involvement of the CDKN2A, CDKN2B and p53 genes in actinic keratosis (AK) and in the progression of AK to squamous cell carcinoma
- Rb antagonizes gankyrin to inhibit MDM2-mediate p53 ubiquitination in cancer cells and suggest that the status of both p53 and Rb is important for efficacy of cancer chemotherapy.
- p53 is of limited value only, being largely overshadowed by the prognostic capability of FIGO stage and extent of residual disease.
- Changes in p53 expression seen in urothelial and sinonasal inverted papillomas suggest they may share common evolution.
- p16(INK4a), p21(WAF1/CIP1), p27(KIP1), and p53 are expressed in human corneal endothelial cells despite donor ages.
- the expression manner of PTEN, beta-catenin, and p53 immunocytochemistry was observed in the normal endometrium (proliferative, secretory, and atrophic, and endometrial glandular and stromal breakdown
- the expression manner of PTEN, beta-catenin, and p53 immunocytochemistry was observed in the normal endometrium (proliferative, secretory, and atrophic, and endometrial glandular and stromal breakdown[beta-catenin]
- [Review] Besides its ability to promote apoptosis through transcription dependent mechanisms, p53 may also be able to activate apoptosis independent of transcriptional regulation.
- Polymorphism Arg72Pro in tumor suppressor gene TP53 increases the risk of lung cancer, especially for small cell lung cancer and heavy smokers.
- An analysis of the clinical and biologic significance of TP53 loss and the identification of potential novel transcriptional targets of TP53 in multiple myeloma.
- PTEN acquires unexpected properties by enhancing gain-of-function mutant p53 (mut-p53) protein levels. PTEN restoration to cells harboring mut-p53 leads to induction of G(1)-S cell cycle progression and cell proliferation and to inhibition of cell death.
- Tubal p53 signature merits serious consideration as an important early event in serous carcinogenesis in BRCA+ women.
- nuclear extracts immunodepleted of p53 or nuclear extracts of p53-null cells were unable to excise UVC-induced DNA adducts, and introduction of p53 by transfection restored the excision activity
- p53 family may play a role in the epithelial cell response to H pylori infection.
- The association oxaliplatin/TRAIL should be restricted to patients harbouring a non-functional p53 protein.
- p53 and p16(INK4A) are promising candidates for the pulmonary molecular screening of heavy smokers healthy individuals.
- conclude that the effect of p53 codon 72 genotype on breast cancer survival is dependent on p53 gene status, the P/P variant is strongly associated with poor prognosis among patients with a wild-type p53 tumor
- confirmed 27 TP53 mutations in 68 primary breast cancers analyzed by high-resolution melting curve scanning and direct sequencing. Using scanning and automatic calling, there was high specificity (>95%) across all DNA preparation methods
- mutated over wild-type P53 mRNA exists in glioblastoma cells with heterozygous mutations of this gene.
- High zinc status in normal bronchial epithelial cells upregulates p53 expression which in turn elevates p21, inducing G2/M blockage.
- The specific binding of the C-terminal acidic domain (AC-D) of the human TFIIEalpha subunit to the pleckstrin homology domain (PH-D) of the human TFIIH p62 subunit is demonstrated.
- stabilization of MDMX by Akt may be an alternative mechanism by which Akt up-regulates MDM2 protein levels and exerts its oncogenic effects on p53 in tumor cells
- p53 codon 72 polymorphism appears to be an independent prognostic factor in gastric cancer patients treated with 5-FU-based adjuvant chemotherapy.
- Notch-1 upregulates EGFR expression and also demonstrate Notch-1 regulation of p53 in gliomas.
- Smo mutants augment p53 binding to the E3 ubiquitin-protein ligase Mdm2 and promote p53 ubiquitination.
- polymorphisms and haplotypes in the TP53 gene, including Arg72Pro, were not significantly associated with lung cancer in a Korean population
- cytosolic p53 may participate in the regulation of clathrin-mediated endocytosis to control the correct signaling from EGFR
- Results could not indicate significance of P53 mutations for evaluation of residual clone malignancy.
- Alterations in the p53 gene may be indicative of poorer prognosis and greater recurrence in patients with urothelial bladder tumor.
- Body mass index is not associated with a higher TP53 mutation frequency in bladder tumors
- Skin cells grown in culture showed a notable decrease in the UVB fingerprint mutation on the p53 tumor suppressor gene in fibroblasts during proliferation.
- Mutation of p53 gene is probably one of the most important factors to initiate the endometrial serous carcinogenesis.
- p53 overexpression strongly downregulates the transcriptional efficiency driven by an H ferritin promoter construct containing only the NF-Y recognition sequence.
- a high level of p53 downregulates the beta-catenin expression, but this effect is attenuated by non-functional AXIN2 or betaTrCP in lung cancer.
- Conclude that the Ki-67 and p53 labeling indices are useful additional tools in discriminating atypical from benign or anaplastic meningiomas.
- Elevated p53 expression is associated with dysregulation of the ubiquitin-proteasome system in dilated cardiomyopathy.
- B7-H4 was expressed more often in pancreatic ductal carcinoma than was p53.
- Microsatellite alterations, and p53 tumor mutations are associated with non-small cell lung cancer patients
- Neither germline variants in p53 nor MDM2 SNP309 play an underlying role in the development of very early onset CRC
- CARPs together with MDM2 enhance p53 degradation, thereby inhibiting p53-mediated cell death.
- Increased TP53 expression was associated with invasive adenocarcinoma of the prostate
- A correlation of p53 expression with AI and PI was found in pilocytic astrocytoma but not in glioblastoma.
- results support Killin as a missing link between p53 activation and S phase checkpoint control designed to eliminate replicating precancerous cells, should they escape G(1) blockade mediated by p21.
- Intrinsic radiosensitivity of 39 human tumor cell lines segregate into distinct genotype-dependent radiosensitivity groups that associate with mutATM, wtTP53, mutTP53, and an unidentified factor in some glioblastoma cells.
- in endometrial carcinoma p53 overexpression was directly associated with unfavorable clinicopathologic factors: advanced stage, histologic subtype, advanced patient age and nodal metastasis
- observations confirm a new role for p53 as a uPA mRNA binding protein that down-regulates uPA mRNA stability and decreases cellular uPA expression
- p53 single-nucleotide polymorphism is associated with the early development of hepatocellular carcinoma in Korean patients with chronic HBV infection.
- determined the average ensemble structure of the intrinsically disordered N-terminal transactivation domain in both the full-length tetrameric p53 protein and in its complex with a specific DNA response element
- the functional regulation of p53 by triptolide was mediated by an intranuclear association of p53 with glycogen synthase kinase-3beta (GSK3beta), which was inactivated by protein kinase C (PKC).
- Fbw7 regulates the activity of endoreduplication mediators and the p53 pathway to prevent drug-induced polyploidy.
- acute loss of p53 in normal HKc induces EGFR expression by a mechanism that involves YY1 and Sp1 and does not require p53 binding to the EGFR promoter
- TP53 Pro47Ser and Arg72Pro SNPs are not associated with risk and prognosis of human gliomas
- TP53 Pro47Ser and Arg72Pro SNPs are not involved either in susceptibility to developing gliomas or in patient survival
- The R allele of the TP53 R72P polymorphism may contribute to the etiology of liver metastases, particularly among those with positive P53 expression tumors. Both TP53 C-8343G and C-1863T may be not associated with colorectal liver metastases risk.
- the functional role of the intrinsic activation of p53 during Mk differentiation is to control polyploidization and the transition to endomitosis by impeding cell cycling and promoting apoptosis.
- study showed that p53 expression is directly correlated with undifferentiated endometrial carcinoma, lymph-node involvement and risk of death
- disruption of the spindle-assembly checkpoint does not directly influence p53 activation, but the shortening of the mitotic arrest allows cyclin E-CDK2 to be activated before the accumulation of p21(CIP1/WAF1).
- UNC5H4 amplifies p53-dependent apoptotic response.
- These findings indicate that p53 is a transcriptional regulator of DUSP1 in stress responses.
- New triterpenoid from Panax ginseng exhibits cytotoxicity through p53 and the caspase signaling pathway in the HepG2 cell line.
- structural analysis of the tumor suppressor p53 [review]
- Lentiviral delivery of small hairpin RNA targeting Tthymidylate kinase in combination with a low dose of doxorubicin as a new approach to kill colon cancer cells regardless of p53 status.
- p53/47 controls the folding, the oligomerisation and the post-translational modification of p53 complexes and that it diversifies p53 properties in a cell stress-dependent fashion.
- KAI-1 and p53 show inverse expression in uterine and endometrial carcinomas and sarcomas. The reduced KAI-1 expression may be the result of dysregulated p53 function and could be a step in endometrial carcinogenesis.
- Downregulation of caspase 2 levels by p53 may help to determine cell fate by preventing cell death when unnecessary.
- Thus, elevated levels of CCN3 protein regulated by p53 might influence cell adhesion.
- Data show that germ cell single base substitution mutation frequencies are very similar to somatic tissue TP53 mutation frequencies.
- Trichostatin A causes p53 to switch oxidative-damaged colorectal cancer cells from cell cycle arrest into apoptosis.
- in epithelial cells, some of the functions of p53 leading to cell-cycle arrest and apoptosis are restrained by HHV-6B infection, whereas other cellular defences, causing inhibition of virus transcription, are partially retained.
- p53 codon 72 SNP ws not associated with susceptibility to or age at onset of OSCC or OSF. p53 codon 72 SNP Arg/Arg polymorphism was associated with progression of OSCC, OS and DSF in irradiated patients.
- inflammatory levels of NO inhibit epithelial cell migration, because of suppression of ERK1/2 signaling, and activation of HIF-1alpha and p53, with potential consequences for epithelial repair and remodeling during airway inflammation
- Results suggest that the parthenolide-induced apoptosis of A549 cells is due to the direct suppression of NF-kappaB activity in a p53- and hsp72-independent manner based on NF-kappaB signaling.
- data suggest that UVB-induced, stress-induced premature senescence in skin fibroblasts plays an important role in p53-related apoptosis resistance and tumor suppression activity
- Results suggest that genetic analysis of TP53 can select patients at high risk of bladder tumour progression that should be followed closely and may benefit from early radical surgical procedures.
- K-ras and p53 genes are altered in Tamoxifen-associated endometrial carcinoma
- These results suggest that a p53-dependent cell cycle checkpoint monitors changes of cellular NS levels via the impediment of MDM2 function.
- an interactive effect was detected such that MDM2 TT TP53 Arg/Arg double homozygotes, and individuals carrying both a MDM2 G allele and a TP53 Pro allele, were at increased risk of t-AML
- DLBCL in pre-menopausal women of central European Caucasian ethnicity was not associated with SNP309 G. Neither SNP309 nor SNP72 seem to be correlated with age of onset, diagnosis, or survival of diffuse large B-cell non-Hodgin lymphoma patients.
- p53 is activated by stimulation of mismatch repair in response to the misincorporation of deoxynucleotides into newly synthesized DNA, long before the lack of pyrimidine nucleoside triphosphates causes the rate of DNA synthesis to slow appreciably.
- TGF-beta(1) production in carcinoma cells was associated with doxorubicine-mediated p53 expression in MCF-7 cells or high basal level of p53 in T47D cells.
- oxidative modification of p53 could be involved in the neuronal loss observed in neurodegenerative conditions
- p53-mediated mir34a, mir34b, and mir34c up-regulation and ING2 down-regulation may be involved in the senescence pathway.
- Overexpression of p53 is associated with several different clinicopathological features of ovarian carcinoma including parameters of stage, tumor grade and prognosis.
- might be markers of depth of invasion or lymph node involvement in patients with gastric cancers
- Data show that the elimination of the salt bridge and the inversion of the flexibility of L1 and L3 are directly or indirectly responsible for deactivating the tumor suppressor p53.
- p53-Driven apoptosis limits centrosome amplification and genomic instability downstream of NPM1 phosphorylation
- autophagy is regulated by cytoplasmic p53
- p53 promotes theaflavin-induced apoptosis in a transcription-dependent manner through mitochondrial death cascade.
- Combined increased p53 and reduced membranous beta-catenin protein expression indicated a very poor prognosis in patients with esophageal squamous cell carcinoma.
- The role of p53 in the sustained phosphorylation of c-Jun-N-terminal kinase mediating melanoma apoptosis induced by 2-acetyl furanonaphthaquinone is reported.
- Induced the transition from cardiac hypertrophy to heart failure through the suppression of hypoxia inducible factor-1(HIF-1), which regulates angiogenesis in the hypertrophied heart and promotes apoptosis.
- The clinical outcome for breast cancer patients is significantly different for different TP53 mutation types.
- p53 was not associated with survival after radiotherapy in high-risk breast cancer, but BCL2 might be.
- Compared to PAI-1 protein levels, Chalkley counts and MIB-1, HER2+ and mutations of TP53 were the strongest independent markers of poor prognosis irrespective of nodal statusin breast cancer.
- Chromosome instability in human hepatocellular carcinoma depends on p53 status and aflatoxin exposure.
- Pim-1 induces the p53 pathway in cultured cells and correlate with increased Mdm2 in mantle cell lymphoma
- The p53 codon 72 polymorphisms are associated with a higher risk of CRC and are associated with more advanced and undifferentiated tumours.
- a novel role for p53 as an mRNA-binding protein that regulates increased PAI-1 expression and stabilization of PAI-1 mRNA in human lung epithelial and carcinoma cells
- the deregulation of both the p53 and the p73 pathways plays an important role in inducing head and neck cancers
- Data suggest that p53 pulses result from repeated initiation by ATM, which is reactivated by persistent DNA damage.
- Inhibition of methylation in hnRNP K attenuated the recruitment of p53 to p21 promoter, and reduced p53 transcriptional activity.
- Different mutant/wild-type p53 combinations cause a spectrum of increased invasive potential in nonmalignant immortalized human mammary epithelial cells
- The data show that immunostaining for p53 and HbF as well as karyotype analysis are useful for the differential diagnosis of myelodysplastic syndrome and aplastic anemia.
- MMR-dependent intrinsic apoptosis is p53-independent, but stimulated by hMLH1/c-Abl/p73alpha/GADD45alpha retrograde signaling
- ATO-induced activation of Chk2/p53 and p38 MAPK/p53 apoptotic pathways can be enhanced by siRNA-mediated suppression of Wip1 expression, further indicating that ATO inhibits Wip1 phosphatase in vivo
- HIPK2 has a critical role in maintaining the transactivation activity of wtp53; low expression of HIPK2 may impair the p53 function in tumors harboring wtp53
- Study identifies p53 acetylation as an indispensable event that destabilizes the p53-Mdm2 interaction and enables the p53-mediated stress response.
- c-Abl and Cdk5 cooperatively regulate maximal activation of p53, resulting in neuronal death in response to oxidative stress by hydrogen peroxide.
- review of kinase-independent interaction of FAK with p53with focus on FAK and p53 signaling, which link signal transduction pathways
- Elevated levels of pro-apoptotic p53 and its oxidative modification by the lipid peroxidation product, HNE, in brain from subjects with amnestic mild cognitive impairment and Alzheimer's disease are reported.
- This study provides the first evidence that p53 is involved in the regulation of EBV lytic cycle initiation.
- Resveratrol displays converse dose-related effects on fluorouracil-evoked colon cancer cell apoptosis: the role of p53 is reported.
- Genetically programmed cell death is related to the p27, cathepsin and survivin pathways in Fuchs' dystrophy and to the p21 and p27 pathways in pseudophakic bullous keratopathy.
- TP53 may have a direct, allele specific, role in 5-FU mediated response.
- identify OKL38 as a novel p53 target gene that is regulated by Peptidylarginine deiminase 4 and plays a role in apoptosis
- MIF physically associates with p53 and negatively regulates p53 function.
- Study shows that mitochondrial p53 is highly efficient in inducing the release of soluble and insoluble apoptogenic factors by severely disrupting outer and inner mitochondrial membrane integrity.
- These results suggest a role of PAD4 in the regulation of p53 target gene expression.
- A signaling cascade for the regulation of p53 in response to ionizing radiation was proposed that involves activation of DNA-PK and Akt/PKB and inactivation of GSK-3 and Mdm2.
- the human glutathione S-transferase P1 gene is a novel transcriptional target of the p53 tumor suppressor gene
- p53Arg homozygosity is associated with the development of sporadic colorectal adenocarcinoma, in the Greek-Caucasian population studied
- A possible correlation between overexpression of p53, proliferating cell nuclear antigen (PCNA), and c-erbB-2, and the clinicopathologic features of laryngeal squamous cell carcinoma, was investigated.
- Results suggest the involvement of the p53 codon 72 polymorphism in the skin tanning response and potential interaction with skin pigmentation on melanoma risk.
- These results represent a definitive argument demonstrating that Li-Fraumeni syndrome results from TP53 haplodeficiency.
- p53 levels were significantly higher in lung parenchyma in subjects with emphysema
- p53 of stromal fibroblasts affects the response of a tumour against chemotherapy by inducting senescence in the fibroblasts which results in the production of growth factors acting onto the cancer cells by paracrine mechanisms.
- homozygous TP53 arginine genotype is not a potential risk factor for development of penile squamous cell carcinoma in subjects of African ethnicity.
- Cyclic pifithrin-alpha sensitizes wild type p53 tumor cells to antimicrotubule agent-induced apoptosis
- The role of p53, followed by Ki-67, as predictive factors
- All of the E6 genes from different HPV types displayed similar abilities to mediate the degradation of both p53 and MAGI-3
- These results establish a link between the p53 tumor suppressor and RNA processing via hnRNPA2/B1 and RNA Helicase A.
- stabilization of p53 mRNA in hepatocellular carcinoma cells is involved in TIP30 control of cellular oxidative stress and apoptosis induction
- BAK oligomerization by p53 utilizes conserved residues of the p53 DNA binding domain
- confirmed a high incidence of TP53 mutations in AML with a complex aberrant karyotype and demonstrated that TP53 mutations are very rare in AML without a complex aberrant karyotype
- Principal component analysis was performed on the atomic contact maps of an experimentally restrained ensemble of the human p53 transcriptional activator domain.
- The existence of a functional binding site for the tumor suppressor p53 near the proximal CCAAT box and the fact that the basal expression of annexin A1 in human colon adenocarcinoma cells is driven by p53 at the transcriptional level, is shown.
- Extra-nuclear p53-dependent apoptosis may constitute a fail-safe mechanism against dominant inhibition.
- p53 mutations are not always associated with malignant transformation in epithelioid angiomyolipoma.
- data clearly show neither association between SNP309 and cancer risk, nor the responsibility of G allele for increased MDM2 or decreased of p53 protein levels in human primary breast tumors.
- interaction of PI3K/Akt/mTOR and p53 pathways after their simultaneous blockade using the dual PI3K/mTOR inhibitor PI-103 and the Mdm2 inhibitor Nutlin-3.
- Data identified TAF3 as an evolutionarily conserved negative regulator of p53 transcription activation function.
- The results show that p53 mutations characterize a small biologically aggressive subgroup of prostate cancers with a high risk of progression after prostatectomy.
- The presence and absence of a dominant negative p53 mutation may thus provide a predictor of early recurrence in oral SCC patients.
- MGMT promoter methylation modulated by p53 status could partially promote p53 mutation occurrence in advanced lung tumors
- L11 cooperates with L5, resulting in a robust inhibition of the E3 activity of MDM2, and a stabilization and activation of p53 approaching that achieved by p14(ARF).
- Expression of p53, in cervical intraepithelial neoplasia and invasive squamous cell carcinoma of the uterine cervix
- Nuclear TP53 accumulation may be relevant in patient's prognosis in neuroblastic tumors.
- was no difference in the expression of EGFR, p185(erbB-2) or Bcl-2, or in nuclear accumulation of p53 in these IDC from pre- vs. post-menopausal women.
- Prognosis of patients with p53-overexpressing ovarian cancer is affected by the MHC class I status of tumour cells and ovarian cancer patients can generate immune responses to the p53 tumour antigen.
- Report relationship of Ki67, TP53, MDM-2 and BCL-2 expressions with WHO 1973 and WHO/ISUP grades, tumor category and overall patient survival in urothelial tumors of the bladder.
- PCAF regulates the balance between cell-cycle arrest and apoptosis in hypoxia by modulating the activity and protein stability of both p53 and HIF-1alpha.
- Oral verrucous carcinoma tumorigenesis may involve the inactivation of p53, which is associated with HPV infection.
- These findings suggest that the histone methyltransferase SETD2 could selectively regulate the transcription of subset genes via cooperation with the transcription factor p53.
- ATM is a key mediator of the MT-hTer-47A dysfunctional telomere response, even in cells lacking wild-type p53.
- A feedforward loop involving c-Myc and eIF4F that serves to link transcription and translation and that could contribute to the effects of c-Myc on cell proliferation and neoplastic growth.
- Expressed in most dysmorphic neurons in focal cortical dysplasia type II.
- Impaired p53 function in tumour stroma might be related to genomic instability and could enable stromal cell survival in the destabilising tumour microenvironment.
- incidence and prognostic impact of TP53 mutations in a cohort of patients with adverse cytogenetics and those with losses on chromosome 17p
- functional inactivity and mutations of p53 differentially affect TS, potentially influencing response to TS inhibitor-based treatment
- These observations suggest that most endopolyploid tumour cells are not reproductively inert and that Aurora-B may contribute to the establishment of resistant tumours post-irradiation.
- Patients with head and neck squamous cell carcinoma having a high portion of tumour cells expressing p53 had a shorter survival than the other groups
- Strong p53 nuclear staining was detected in smokeless tobacco keratosis, squamous cell carcinoma and alveolar ridge keratoses.
- IL-8 and p53 protein expression is regulated through inverse activation of the p38 MAPK and the JNK pathways and the NF-kappaB p65 expression
- p53 expression seems to negatively influence survival in non-smoking non-alcoholic patients with squamous cell laryngeal carcinoma.
- 5-Aza-2'-deoxycytidine restores proapoptotic function of p53 in cancer cells resistant to p53-induced apoptosis.
- Monitoring for sequential change of serum p53-Abs before and after radiotherapy in patients with esophageal carcinoma is uuseful to evaluate the response to the treatment and prognosis of the patients.
- There is a molecular association of the p53 codon 72 arginine allele with tumor aggressiveness and treatment resistance in advanced breast cancer.
- Ubiquitin over-expression promotes the destabilization of the ubiquitin protein ligase E6AP, by a mechanism involving self-ubiquitination, and the stabilization of p53.
- In the absence of p53 function, the resulting derepressed CD44 expression is essential for the growth and tumor-initiating ability of highly tumorigenic mammary epithelial cells.
- p53 over-expression predicted both transformation to diffuse large B-cell lymphoma and poorer overall and cause-specific survival of patients with follicular lymphoma.
- The data showed that hepatocellular carcinoma patients had a significantly higher mean anti-p53 antibody values (p=0.0001), than both liver cirrhosis patients and healthy control groups.
- analysis of 31 bilateral breast cancer (biBC) pairs (12 synchronous & 19 metachronous cases); TP53 sequence alterations were detected in 7 patients; 2 had mutations in both neoplasms & in 5 biBC pairs the TP53 gene was affected in only 1 of the tumors
- Andrographolide inhibits human colorectal cancer Lovo cell growth by G1-S phase arrest and inducing the expression of p53, p21 and p16.
- Damage of exon 5 of p53 gene by arsenic is associated with precarcinomas and carcinomas.
- These results provide a structural explanation for the dominant-negative effect of p53 and its lack of transcriptional activity.
- TP53 methylation was probably not implicated in gastric carcinogenesis
- Phosphorylation of MUC1 by Met modulates interaction with p53 and MMP1 expression.(
- a TP53 mutation in follicular lymphoma may have a role in disease progression
- TAF6delta has a pivotal node in a signaling pathway that controls gene expression programs and apoptosis in the absence of p53
- A significant association was found in Dukes' B stage colorectal cancer patients between the GSTM1 and p53 gene variants and survival.
- induction of p53 and apoptosis are reduced by green tea extract in UVB-irradiated human skin independent of transcriptional controls
- These results indicate that the E1B protein fulfills an early function that correlates efficient entry into the late phase with the localization of E1B and p53 in the nucleus of Ad5-infected normal human cells.
- Although p53 is mutated in trophoblast, it is functionally incompetent towards matrix metalloproteinases in these cells.
- These observations suggest that the relative cytoplasmic abundance of PTB protein, under DNA-damaging conditions, might contribute to regulating the coordinated expression of the p53 isoforms.
- These results indicate that acidic domain of MDM2 provides essential information for acetyltransferase p300 and deacetylase HDAC1 and is indispensable for MDM2 to negatively regulate the acetylation of p53.
- sPDZD2 sensitized mutant p53-positive DU145 cells and wild-type p53-positive MCF-7 cells to apoptosis induction through genotoxic stress imposed by sub-lethal concentration of hydrogen peroxide
- ReportGene expression profiles modulated by the carcinogen aristolochic acid I in human cancer cells and their dependence on TP53.
- No association was detected between the TGFB1, IL10, TP53, and HMOX1 genes and DGF. The G allele of the TNF polymorphism rs3093662 was associated with DGF in an adjusted analysis.
- neither the Ins16bp or Arg72Pro polymorphisms of p53 considered separately, nor any related haplotype, were associated with breast cancer risk in BRCA-mutation negative familial cases.
- Zac1 might be involved in regulating the p21(WAF1/Cip1) gene and protein expression through its protein-protein interaction with p53 and HDAC1 in HeLa cells.
- vascular endothelial growth factor, receptor KDR and p53 protein are expressed in transitional cell carcinoma of the bladder
- This study provides evidence of a positive association between parameters reflective of angiogenesis, and p53 expression in HCCs
- these results imply a regulatory connection between the FA pathway and activation of TP53 for responding to DNA damage
- crystallographic anlaysis of molecules that bind to p53 from a drug screening assay
- P53 has a role in malignancy and epithelioid differentiation in GISTs
- MAP1B light chain can interact with the tumor suppressor p53.
- TP53 gene mutations of lung cancer patients in upper northern Thailand and environmental risk factors are reported.
- A375 cells exposed to selenocystine showed an increase in levels of total p53 and phosphorylated p53
- senescence of primary NHP cells expressing progenitor cell markers CD44, alpha2beta1, p63, hTERT, and CK5/CK18, involves loss of telomerase expression, up-regulation of p16, and activation of p53.
- Its loss of function is critical for the molecular pathogenesis of uterine papillary serous carcinoma.
- CK1 has a role as the Ser20 site kinase for p53 in DNA virus-infected cells
- TP53 mutation is associated with metastatic pulmonary adenocarcinomas.
- p53-independent events regulating expression of protein-coding genes and microRNAs within the network can define the cellular outcome of p53 activation.
- Structure of the human Mdmx protein bound to the p53 tumor suppressor transactivation domain.
- direct interaction of p53 with mitochondrial antiapoptotic proteins including Bcl-2 is the major route for apoptosis induction in CLL cells
- p53 expression in liver tissue was higher in the hepatitis C virus-associated hepatocellular carcinoma (HCC) patients compared to normal controls & correlated well with the HCC grade; p53 is implicated in the poor prognosis of HCV-HCC
- TP53 inactivation may have a role in progression of chronic lymphocytic leukemia
- Proteasome inhibition-mediated premature cell senescence can only be initiated and maintained in the presence of functional p53.
- p53 represses the PDGFRB promoter, facilitating the p53-induced apoptosis, whereas tumor cells with p53 mutation or a high level of DeltaNp73 or Myc could become refractory to the regulation.
- overexpression of p-ATF2, p-STAT3 and possibly p53, but not p63 or p73, may contribute to the tumorigenesis of cutaneous vascular tumors.
- findings suggest that the combined variants of p53 and p73 significantly increase the risk of HPV16-associated oral cancer, especially among never-smokers
- Suppression of inhibitor of differentiation 2, a target of mutant p53, is required for gain-of-function mutations in colonic and pancreatic neoplasms
- data suggests that TP53 mutations are associated with poor outcome in diffuse large B-cell lymphoma of germinal center subtype patients
- Describe TP53 expression in developing pituitary gland.
- Ethnicity determines association of p53Arg72Pro alleles with cervical cancer in China.
- Noncanonical DNA motifs as transactivation targets by wild type and mutant p53 are reported.
- wild type p53 suppressed the S100A6 promoter up to 12-fold in a dose-dependent manner
- the TP53 polymorphism, at the 347 residue, is not associated with any clinicopathological findings of patients with breast cancer.
- These data indicate that elevated Skp2 expression may overcome p53-dependent cell cycle checkpoints in melanoma cells and highlight Skp2 actions that are independent of p27(Kip1) degradation.
- A homozygous p53 R248W gain-of-function mutation as the result of a CGG to TGG transition was identified in one of seven sebaceous gland carcinomas. It has been demonstrated previously that p53 R248W mutants inactivate ATM-directed HRR.
- 15d-PGJ(2) induces vascular endothelial cell apoptosis through the signaling of JNK and p38 MAPK-mediated p53 activation both in vitro and in vivo
- The export of p53 from the nucleus is not sufficient to activate its cytoplasmic apoptotic function which may depend on the ability to deubiquitinate cytoplasmic p53.
- The p53-dependent transcriptional regulation of p21 in response to DNA damage by ultraviolet radiation and ionizing radiation compared.
- Tat contributes to neuronal degeneration through activation of a pathway involving p53 and p73.
- analysis of the coordinated immediate responses by p16INK4A and p53 pathways in UVB-irradiated human skin cells
- TP53 mutations are associated with chemoresistance in breast cancer, defined as progressive disease on therapy for mutations affecting p53 loop domains L2/L3).
- wild-type TP53 in CRC cells favours the progression of tumours expressing markers for hypoxia in their stroma, rather than in the epithelial compartment
- S100A6 is induced by tumor necrosis factor-alpha via an NF-kappaB-dependent mechanism, serving a role in homeostasis to limit tumor necrosis factor-alpha-induced apoptosis by regulating p53 phosphorylation
- Aberrant DNA methylation was not associated with p53 mutations in ovarian carcinoma.
- data link EWS-FLI1 to the NOTCH and p53 pathways and provide a plausible basis both for NOTCH tumor suppressor effects and oncogenesis of cancers that retain wild-type p53
- Results suggest that the Arg/Arg genotype polymorphism of p53 may represent a potential risk factor for the development of lung cancer independent of the human papillomavirus infection.
- Results further strengthen the association between germline TP53 mutations and childhood choroid plexus carcinomas, even when occurring in the absence of familial tumour susceptibility.
- Different from ERbeta, p53 interacts with HDAC1 and CtBP1 and forms an inhibiting transcriptional complex that could compete for binding to Sp1 sites with ERalpha transcriptional complex and inhibit BRCA2 transcription more significantly
- Influence of tetramerization on site-specific post-translational modifications of p53 are reported.
- Data suggest that the R3IM motif of DSS1, in conjunction with the complexes of 19S RP and 20S core particle, regulates proteasome interaction through RPN3/S3 molecule, and utilizes a specific subset of poly-ubiquitinated p53 as a substrate.
- These results suggest that p53 influences TLR3 expression and function and highlight a role of p53 in innate immune response in epithelial cells.
- STX6 can be induced by DNA damage and Mdm2 inhibitor Nutlin-3 in a p53-dependent manner.
- Ins-72Pro haplotype in p53 with an increased cancer risk in BRCA2 mutation carriers has not been validated
- Transcription from P2 is believed to be controlled by p53 and a single-nucleotide polymorphism (SNP309, T>G) in P2 is reported to be associated with increased risk for, and early development of, malignancies
- Several members of a Malaysian family had a duplication of a GGCGTG motif starting at nucleotide 17579 in exon 10, resulting in an in-frame insertion of two amino acids between residues 334 & 336 in the tetramerization domain of the p53 protein.
- The protein structure prediction of CP2 family in order to elucidate the molecular mechanism of the CP2-directed regulation of gene expression.
- PPARgamma and TP53 genes may be candidates for molecular markers in pediatric MDS, and that these potentially recurrent deletions could contribute to the identification of therapeutic approaches in primary pediatric MDS
- Patients from Kashmir Valley, INdia with TP53 mutant esophageal squamous cell tumor had lower zinc levels than those with no mutation.
- concomitant presence of somatic alteration in mtDNA and the DNA binding domain of the p53 gene facilitates cell survival and tumorigenesis
- Together these results identify ASPP2 as a bona fide DDA3 interacting protein, and suggest that the ASPP2/DDA3 interaction may inhibit ASPP2 in stimulating the apoptotic signaling of p53.
- Proline oxidase, a p53-induced gene, targets COX-2/PGE2 signaling to induce apoptosis and inhibit tumor growth in colorectal cancers
- In this immunohistochemical study, 80% of all vulvar intra-epithelial neoplasia were negative for p53 tumor suppressor protein.
- Alleles of three noncoding TP53 markers were associated with NTD risk.
- there was no association between the p53 antigen G72C polymorhphism and susceptibility or course of disease in patients with Wegeners granulomatosis
- maximum expression of p53-Ser15(P) coincided in time with the peak of Chk2 activation
- results demonstrate that in p53-deficient human gastric cancer cells, restoration of functional miR-34 inhibits cell growth and induces chemosensitization and apoptosis, indicating that miR-34 may restore p53 function
- This review concludes that a selective gain of pro-survival functions of wild-type p53 in cancer cells will confer a survival advantage that counteracts tumor therapy.
- Hsf1 is required for p53 nuclear importation and activation, which implies that heat shock factors play a role in the regulation of p53.
- An unusual p53 mutation detected in Burkitt's lymphoma: 30 bp duplication.
- Immunohistochemistry using antibodies to determine the protein expression of Fas, Fas-L, Bax, Bcl-2, p53 and c-Myc in skin of venous ulcer patients.
- direct interaction between NM23-H1 and macrophage migration inhibitory factor (MIF) is critical for alleviation of MIF-mediated suppression of p53 activity
- p53 phosphorylation and localization status is associated with expression of ADP ribosylation factor like 2.
- the cytoplasmic localization of p53 as the most important feature for p53-mediated autophagy inhibition.
- the detection of a TP53 abnormality in early stage CLL is often associated with progressive disease,however, a subset of these cases with mutated IGHV genes may have stable disease for many years, never requiring therapy
- p53 may induce cell cycle arrest not only by well described mechanisms involving the induction of cyclin-dependent kinase inhibitors but also by the recruitment of pathways that reduce the availability of intracellular iron
- p53 directly affects hPar1 expression and function, thus providing evidence for direct binding between p53 and hPar1 chromatin.
- the kinetic stabilization of microtubules enhances the microtubule-mediated transport of p53 into the nucleus
- analysis of the intramolecular interaction in FOXO3a and its binding with p53
- Low rates of somatic p53 mutations in keratoacanthomas imply a minor role of p53 in the pathogenesis of keratoacanthoma.
- sarcomatous transformation of diffuse-type tenosynovial giant cell tumors involves aberrations of cyclin A, P53, and chromosome arm 15q
- Results describe the location and expression of human papillomavirus 18 E6 and p53 proteins.
- Strap regulation reflects the coordinated interplay between different DNA damage-activated protein kinases, ATM and Chk2 (Checkpoint kinase 2), where phosphorylation by each kinase provides a distinct functional consequence on the activity of Strap.
- PML disruption by EBNA1 requires binding to the cellular ubiquitin specific protease, USP7 or HAUSP, but is independent of p53.
- combined alpha-methylacyl coenzyme A racemase/p53 analysis may represent a helpful tool to confirm dysplasia in inflammatory bowel disease.
- Epistatic analysis that p53 inhibition results in a maximum level of autophagy.
- 53BP1 Tudor domain recognition of p53 dimethylated at lysine 382 in DNA damage signaling
- ANKRD11 has a role as a p53 coactivator and may be involved in a regulatory feedback loop with p53
- Data show that nitric oxide derived from S-nitrosoglutathione activates ASK1 in THP-1 human myeloid macrophages, induces accumulation of HIF-1alpha protein, and induces accumulation of p53 in normal but not HIF-1alpha knockdown THP-1 cells.
- G > A polymorphism at intron 6 of p53 may contribute to the level of DNA damage in occupational exposure to vinyl chloride.
- Data show that hTERT activity or inactivation of p53 can suppress the cell proliferation defects associated with lamin A mutants that are incorrectly processed.
- TP53 mutations in chronic lymphocytic leukemia were significantly associated with del (17p) and complex cytogenetic abnormalities
- knockdown of endogenous MBP-1 is involved in cellular senescence of HFF through p53-p21 pathway.
- Influence of prothymosin alpha and its mutants on activity of the p53 tumor suppressor
- p53 and GLI1 may have a role in tumor cell survival
- 4-HNE is involved in p53-mediated signaling in in vitro cell cultures as well as in vivo that can be regulated by glutathione transferase
- the identification and functional characterization of a novel TP53 germinal mutant allele (Cys275Phe c.824G > T p.C275F) in a large Italian Li-Fraumeni syndrome family
- Myc as an important target for cooperative actions of p53 and Pten in the regulation of normal and malignant stem/progenitor cell differentiation, self-renewal and tumorigenic potential
- TsA markedly down-regulated the expression of cyclin D1 and CDK4, up-regulated the expression of p21WAF1 and p53 and induced cell cycle arrest at the G1 phase in MCF10A-ras cells
- p38 kinase which was activated during p53-induced senescence was not observed in vitamin C-treated EJ cells
- incidence of additional cytogenetic abnormalities, reflecting an increased chromosomal instability, was higher in >or=5%TP53-deleted cases
- TP53 mutations may have a role in progression of breast cancer
- analysis of the expression of fatty acid synthase, Ki-67 and p53 in squamous cell carcinomas of the larynx
- Mdm2 regulates p53 levels also by targeting ribosomal protein L26 for polyubiquitylation and proteasomal degradation.
- Results investigate eight polymorphisms in the region encompassing exon 2 to 4 of TP53 and examine their association with cervical cancer risk.
- three different COX-2 mutations and five different P53 mutations are associated with non-small-cell lung carcinoma
- integrin beta4 is implicated in and associated with p53 in autophagy of lung cancer cells
- p53-dependent downregulation is consistent with an oncogenic function of RHAMM and the recently reported tumor-suppressive function of CD44 transcriptional repression by p53.
- observations provide support for the idea that up-regulation of IFI16 expression by p53 and functional interactions between IFI16 protein and p53 contribute to cellular senescence.
- JS-K inhibits E1 activity and kills transformed cells harboring wild-type p53.
- Results describe the possible involvement of p53 in the osteocyte apoptosis observed in Idiopathic osteonecrosis of the femoral head.
- p53 siRNA enhanced reprogramming efficiency of pluripotent stem cells generation induced from human adult fibroblasts
- Results demonstrate for the first time that the 72R allele of the p53 polymorphism has an increased risk for liver metastases in colorectal cancers positive for p53 overexpression.
- A novel p53-dependent transcriptional mechanism regulates adaptor protein p66shc expression operative in the vascular endothelium and may be important in impairing endothelium-dependent vascular relaxation.
- Germline p53 mutation is associated with adrenocortical carcinoma and subsequent osteosarcoma
- with aging there is an increase of mutant like conformation state of p53 in peripheral blood cells, which is more pronounced in Alzheimer Disease patients
- Inhibition of MT2A expression by siRNA in the HIPK2 knockdown cells restored p53 transcription activity.
- The crystal structures of the p53 core domain incorporating the hot spot mutation R249S, the core domain incorporating R249S and a second-site suppressor mutation H168R and its sequence-specific complex with DNA and of the triple mutant, were determined.
- the new oncogenic p53 target, PRL-1, may contribute to tumor development by the downregulation of p53 by a negative feedback mechanism.
- CARF plays a dual role in regulating p53-mediated senescence and apoptosis, the two major tumor suppressor mechanisms.
- Monocytic leukemia zinc finger (MOZ) interacts with p53 to induce p21 expression and cell-cycle arrest.
- REVIEW. p53 represses RHAMM and CD44 expression
- GBP-2 is regulated by p53 and may have a role in esophageal squamous cell carcinomas
- Doublets in the EGFR and TP53 genes in human lung cancer are elevated about eight- and three-fold, respectively, relative to spontaneous doublets in mouse
- Polygonatum cyrtonema lectin induces apoptosis and autophagy via a mitochondrial-mediated ROS-p38-p53 pathway
- Methylation on arginine residues is an underlying mechanism of control during the p53 response.
- p53 in mitochondria may be a component of an error-repair pathway and serve as guardian of the mitochondrial genome.
- E6 F47R-induced cellular senescence is strongly dependent on p53 signaling pathway.
- TP53 gene expression was significantly higher in colorectal cancer patients than in healthy volunteers.
- KLF6 and TP53 mutations are not frequent events in prostate cancer
- Proton beam induces apoptosis of hypoxic tumor cells by the p53-dependent and p38/JNK MAPK signaling pathways.
- Report differential role of diphenyleneiodonium, a flavoenzyme inhibitor, on p53-dependent and -independent cell cycle progression.
- Pleurotus ostreatus inhibits proliferation of human breast and colon cancer cells through p53-dependent as well as p53-independent pathway.
- Ets-1 binds cooperatively to the EBS palindrome of the hp53 promoter.
- demonstrated no evidence for association of MDM2 SNP 309 or TP53 Arg72Pro allelic variants alone, or in combination, with overall survival (Figure 1A), progression free survival, relapse free survival or time to transformation
- Hdm2 is expressed in pancreatic cancer cells as a result of activated Ras signaling, and regulates cellular proliferation and the expression of target genes by p53-independent mechanisms.
- This study demonstrated that baicalin-induced apoptotic cell death in the breast cancer cells involves the up-regulation of proapoptotic p53 and bax, implying potential crucial roles of bax and p53 in the baicalin-induced apoptosis.
- nucleoplasmic relocation of nucleostemin during nucleolar disassembly safeguards the G2-M transit and survival of continuously dividing cells by MDM2 stabilization and p53 inhibition.
- p53 nucleolar association occurs in lung and bladder carcinomas.
- the presence of the p53 codon 249 mutation from plasma DNA is significantly associated with hepatocellular carcinoma
- expression of miRNAs is downregulated in senescent cells and in breast cancers harboring wild-type p53. These miRNAs are repressed by p53 in an E2F1-mediated manner
- Overexpression of p53 oncoprotein is associated with gastric carcinoma.
- Two conserved CPEs in the p53 3'UTR regulate stability and translation of a reporter mRNA in non-irradiated as well as irradiated cells.
- analysis of p53 gene in prostate adenocarcinoma showed several mutations in high Gleason patients, according to tumor advanced stage; results showed localization of p53 & T antigen (TAg) into cytoplasm, but in TAg-negative tumors, p53 was nuclear
- The authors show that Pirh2-p53 interaction is dependent on the C-terminal zinc binding module of Pirh2, which binds to the tetramerization domain of p53.
- findings of higher DNA concentrations with some p53 mutations in CFDNA from patients with NHL that match the previous reported p53 mutations from tumour DNA may hold promises that CFDNA may serve as a convenient source of tumour-derived DNA
- Results suggest that nonactivated p53 has limited binding activity, whereas upon activation it binds to essentially all its targets. Additional triggers are most likely required to activate the transcriptional program of p53.
- epirubicin-cyclophosphamide treatment induces senescence-like features in TP53 wild-type tumor, while in TP53 mutated tumors, chemotherapy induces mitotic catastrophe and tumor death
- c-Abl and p53 are important for execution of the cell death program initiated in A2E-laden RPE cells exposed to blue light, while JNK might play an anti-apoptotic role
- Completely inhibits Saccharomyces cerevisiae growth under minimal media conditions and down regulates thioredoxin expression.
- HER-2/neu, AR, and p53 are expressed in a subset of histologically and clinically benign pleomorphic adenomas. These markers cannot be used to reliably predict early carcinomatous transformation in pleomorphic adenoma.
- The inactivation of TP53 is similar in familial pancreatic adenocarcinomas as in sporadic pancreatic adenocarcinomas.
- Results suggest that apoptosis inhibitory proteins are highly induced in squamous cell carcinoma/mutated p53 cells after heat treatment when compared to control cells.
- relation with p53 protein expression, p53 gene codon 72 polymorphism and infection with HPV DNA with pterygium
- p53 codon 72 polymorphism (Arg72Pro) frequencies with respect to the susceptibility and the clinical outcome of patients with Soft tissue sarcomas.
- Alterations in both the p53 and p16-Rb pathways are associated with squamous cell carcinoma arising in mature cystic teratoma.
- neither the TP53 Arg72Pro polymorphism nor the MDM2 SNP309 contributes significantly to either susceptibility or disease severity in systemic lupus erythematosus
- Genotoxic stress promotes the p53-dependent up-regulation of the homologous miRNAs miR-192 and miR-215.
- additional inactivation of p53 in malignant primaries and benign recurrences contributes to myoepithelial neoplastic transformation and aggressive tumour growth.
- results support the hypothesis that p53 function is suppressed by aberrant HDM2 activity and suggest the possibility of targeting the p53-HDM2 regulatory axis as a therapeutic strategy in synovial sarcoma
- P53 had neither diagnostic nor prognostic relevancein patients with bladder urothelial tumours
- ING1 variants may modulate p53 activity and subsequently inhibit hepatoma cell growth by at least two possible mechanisms.
- Effect of ROS on angiogenesis in tumors expressing hot-spot p53 mutants was correlated with their ability to increase a content of HIF1 transcriptional factor responsible for up-regulation of VEGF-A mRNAs.
- RYBP decreases MDM2-mediated p53 ubiquitination by interacting with MDM2. RYBP induces cell-cycle arrest and is involved in the p53 response to DNA damage.
- TP53 mutation but no CHEK2*1100DelC variant in familial gliomas.
- p53 mutation is an initiating mutation in the majority of colitis-associated neoplasia, and K-RAS activation is an alternative gatekeeping mutation.
- Spy1 fulfills a novel regulatory role in the intrinsic DNA damage response and maintains the balance between checkpoint activation, apoptosis, repair and cell cycle progression in response to exogenous or intrinsic damage.
- p53-Mdm2 protein-protein and p53 mRNA-Mdm2 interactions affect Mdm2-mediated control of p53 expression using the Phe19Ala p53 mutant.
- The Snail-p53 binding as the new therapeutic target for K-Ras-mutated cancers including pancreatic, lung, and colon cancers.
- data suggest that the Mya arenaria p53 shares some functional similarity with human p53 as well as with other invertebrates, positioning the mollusk at a critical juncture in evolution of this gene family
- This selectivity of flavokawain A for inducing a G(2)-M arrest in p53-defective cells deserves further investigation as a new mechanism for the prevention and treatment of bladder cancer.
- These results highlight the prognostic value of CDK4 amplification and of simultaneous EGFR-p53 alterations in the clinical outcome of patients with primary GBM.
- The aim of the study was to evaluate the correlation between clinical characteristics, histopatologic features and c-erbB-2 as well as p53 expression in cancer tissues.
- CPEB controls senescence and bioenergetics in human cells at least in part by modulating p53 mRNA polyadenylation-induced translation
- Data are the first demonstration that wild-type p53 protein binds to a response element within the EpCAM gene and negatively regulates EpCAM expression, and transcriptional repression of EpCAM contributes to p53 control of breast cancer invasion.
- The authors found that liberation of p53 through chemical antagonism of one of its major ubiquitin ligases, MDM2, using the small-molecule Nutlin-3 led to apoptosis of established LCLs and suppressed EBV-mediated transformation of primary B cells.
- Up-regulation of p53 gene expression is associated with virus-mediated induction of type-I interferons.
- A role for p53 in mediating altered trophoblast cell turnover in response to oxidative stress.
- p53-deficient neuroblastoma cells are largely resistant to nitric oxid (NO) killing and show much reduced maspin and PAI-1 mRNA and protein levels after NO treatment
- TP53 mutation is highly recurrent in basal-like carcinoma independently of BRCA1 status, but not a common feature of BRCA1 luminal tumors.
- p53 Mutations is associated with carcinoma of the esophagus and gastroesophageal junction
- Mdm2-mediated control of p53 synthesis and degradation has evolved in the p53 mRNA sequence and its encoded amino acids.
- Only a small fraction of naturally occurring sequence variations of TP53 cause measurable perturbation of p53 function.
- A TP53 single nucleotide polymorphism is critical for oncogenesis of glioblastoma in young patients.
- Genetic and pharmacologic perturbation of p53 directly influences SULF2 expression in tumor cell lines.
- The combination of the MDM2 SNP309 and the three TP53 polymorphisms appear to be related to a higher grade of endometrial cancer.
- p53 is as a cytotoxic bomb that can be triggered by granzyme K, leading to potentiating killing efficacy.
- Study identifies PHLDA3 as a p53 target gene that encodes a PH domain-only protein and finds that PHLDA3 competes with the PH domain of Akt for binding of membrane lipids, inhibiting Akt translocation to the cellular membrane and activation.
- Tp53 mutant human glioma cells are sensitive to UV-C-induced apoptosis due to impaired cyclobutane pyrimidine dimer removal.
- The p53 codon 72 exon 4 BstUI polymorphism is only weakly associated with the risk of endometrial cancer and prognostic factors in Caucasian women.
- Transcriptome analyses revealed a consistent up-regulation of polo-like kinase 1 (PLK1) as well as other genes controlling the G(2)/M transition in the cells whose TP53 genes were inactivated compared with those with WT TP53 genes.
- SOX4, a new DNA damage sensor, is required for the activation of p53 tumor suppressor in response to DNA damage.
- MDM2 released from p53 by RITA promotes degradation of p21 and the p53 cofactor hnRNP K, required for p21 transcription