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Validated All-in-One™ qPCR Primer for RB1(NM_000321.2) Search again
Product ID:
HQP016131
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
OSRC, PPP1R130, RB, p105-Rb, p110-RB1, pRb, pp110
Gene Description:
RB transcriptional corepressor 1
Target Gene Accession:
NM_000321.2(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.
Validated result:
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| A | B |
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Each All-in-One™ qPCR Primer is experimentally validated to yield a single dissociation curve peak and to generate a single amplification of the correct size for the targeted gene. A cDNA Pool, containing reverse transcript products of 8 different human tissue total RNA(Liver, Testis,Muscle,Thyroid,Brain,Spleen,Stomach,Small Intestine)),was used as the qPCR validation template. qPCR was performed using 0.2 µM primer with 2XAll-in-One™ qPCR Mix (Catalog#: QP001,QP002,QP004,QP005). Reactions were incubated for 10min. at 95°C, followed by 40 cycles of 95°C for 10 sec.; 60°C, 20 sec. and 72°C, 15sec. using Bio-Rad iQ5™ Instrument. At the end of the last cycle, temperature was increased from 72 to 95°C to produce a melting curve. Panel A: Validated Result for Amplification Curve; Panel B: Validated Result for Melting Curve. |
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Summary
The protein encoded by this gene is a negative regulator of the cell cycle and was the first tumor suppressor gene found.
Gene References into function
- E2F target genes display elevated levels in Rb-/- MEFs. Absence of functional Rb is sufficient for S-phase entry under growth-limiting conditions, indicating that the E2F complexes containing Rb protein may be rate limiting for the G1/S transition.
- Rb interacts with the AP-2 transcription factor and activates the E-cadherin gene expression
- Rb is a coactivator of AP-2 in epithelial cells
- K616E in exon 19 (c.1846A>G), an AA insertion in exon 7 (c.684-685insAA), R500G in exon 16 (c.1498A>G), and an A insertion in exon 23 (c.2391-2392insA).
- novel mutations found in Polish patients with familial and/or bilateral retinoblastoma
- Suppression of tumorigenicity of rat liver tumor cells by human chromosome 13: evidence against the involvement of pRb and BRCA2
- Tumor suppression by a severely truncated species of retinoblastoma protein
- Allelic deletions of Rb in urine from bladder cancer patients
- Activation of caspase-3 and cleavage of Rb are associated with p16-mediated apoptosis in human non-small cell lung cancer cells.
- Results show that Tax directly interacts with CDK4. The Tax/CDK complex represents an active holoenzyme which capably phosphorylates the Rb protein in vitro and is resistant to repression by the inhibitor p21(CIP).
- A parent-of-origin effect in two families with retinoblastoma is associated with a distinct splice mutation in the RB1 gene.
- Three regions of the pRB pocket domain affects its inactivation by human papillomavirus E7 proteins in Hela cells
- Human telomerase accelerates growth of lens epithelial cells through regulation of the genes mediating RB/E2F pathway
- Oxidized low density lipoprotein induces the cyclin-dependent kinase inhibitor p21(waf1) and the tumor suppressor Rb.
- Lack of functional pRb results in attenuated recovery of mRNA synthesis and increased apoptosis following UV radiation in human breast cancer cells.
- The cyclin D1 high and cyclin E high subgroups of breast cancer: separate pathways in tumorogenesis based on pattern of genetic aberrations and inactivation of the pRb node.
- The alpha-MSH-induced differentiation of COLO 853 human melanoma cells is associated with decreased pRB phosphorylation and accumulation of cells in the G(1) phase.
- pRB expression and function are normal in 63 of 66 NHL cases, including 12 of 13 lymphomas with loss of one RB1 allele.There was no association between pRB expression/RB1 copy number and apoptotic fraction.
- Expression of RB C pocket fragments in HSF induces delayed cell cycle progression and sensitizes to apoptosis upon cellular stresses.
- The spectrum and frequencies of RB1 structural defects were studied in tumors and peripheral blood lymphocytes of patients with various forms of retinoblastoma
- Localization and phosphorylation kinetics of this protein correlate with the cellular phenotype of cultured breast adenocarcinoma cells.
- Low-penetrance retinoblastoma due to exons 24 and 25 deletions in the Rb1 gene
- Review. Rb suppresses tumor formation through its multiple biological activities. A theme throughout its multiple cellular functions is its central role in controlling activities that involve chromatin remodeling. Rb may control global genome fluidity.
- Gene aberrations at chromosome 13 are involved in the progression of laryngeal squamous cell carcinoma; results provided further evidence for the putative role of the RB1 gene alterations in the metastatic process
- Data show that the retinoblastoma protein specifically activates transcription of the survival gene bcl-2 in epithelial cells but not in NIH 3T3 mesenchymal cells.
- Aberrant methylation inactivating RB1 was detected in 14 (27%) tumors.Complex testing for RB1 mutations, loss of heterozygosity, and functional inactivation of the two genes revealed a molecular defect in at least one allele in 51 (98%) tumors.
- Activation of cyclin D1-Cdk4 and Cdk4-directed phosphorylation in diabetic mesangial hypertrophy
- novel mutations in Mexican patients with retinoblastoma: SSCP sequence showed new non-described mutations that produced a frameshift on the open reading frame
- REVIEW: The retinoblastoma tumour suppressor in development and cancer
- pRB has a role in eye cancer [review]
- data suggest that hypophosphorylated Rb is anchored in the nucleus by the interaction of pocket C with LAP2alpha-lamin A/C complexes
- 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.
- inactivation of both p16(INK4a) and pRb is associated with immortalization of human cells including fibroblasts and epithelial cells and telomerase-positive cells and ALT-positive cells
- 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.
- Rb and its inactive phospho-isoform exhibit distinct expression patterns in Parkinson disease neurons most commonly associated with the disease, as well as in neurons elsewhere in the brain that also contribute to disease progression or symptoms.
- Expression of p57kip2, Rb protein and PCNA and their relationships with clinicopathology in human pancreatic cancer.
- RB1 CpG island hypermethylation is a common epigenetic event that is associated with the development of malignant nervous system tumours.
- first preimplantation genetic diagnosis of hereditary retinoblastoma using microsatellite markers of this protein
- p55gamma binds to Rb and modification of this association can lead to cell cycle arrest
- retinoblastoma protein has cyclin D1-inducing activity that is abolished by adenovirus E1A and that involves multiple pocket sequences that are independently involved in cyclin D1 activation
- report shows hypophosphorylation of the retinoblastoma family proteins induced by H2O2 was because of the activity of protein phosphatase 2A and pRb dephosphorylation may induce an intra-S-phase response that leads to a reduced rate of DNA synthesis
- We found that E2F1 was present at most of the CpG islands bound by pRb, independent of the phase of the cell cycle, our data suggest that the majority of DNA-bound pRb is recruited to E2F target promoters during both G(0)/G(1) and S phases.
- Senescence-associated heterochromatic foci formation coincides with the recruitment of heterochromatin proteins and the retinoblastoma (Rb) tumor suppressor to E2F-responsive promoters and is associated with the stable repression of E2F target genes.
- EBV LMP1 blocks p16INK4-RB pathway by promoting nuclear export of E2F-4 and E2F-5.
- These results indicate that PAI-2 may enhance Rb's tumor suppressor activity and suggest a potential therapeutic role for PAI-2 against HPV-transformed lesions.
- C/EBPepsilon interacts with Rb and E2F1 during granulocytic differentiation
- p21WAF1/CIP1, pRB, Bax and NF-kappaB have roles in induction of growth arrest and apoptosis by resveratrol in tumor cell lines
- The survival data on 129 glioblasstoma patients were correlated with the results of a detailed analysis of this gene.
- RB1CC1 induces the expression of RB1, especially of underphosphorylated forms, then suppresses cell cycle progression in human neoplastic cells
- cell lines lacking an active RB gene are more resistant than cell lines with an active RB gene
- kinetic framework of RB tumor suppressor action in transcriptional repression and cell cycle regulation
- Rb and ASC-2 have roles in androgen receptor transactivation
- Androgens repress Bcl-2 expression via activation of RB in prostate cancer cells.
- results establish that tumor necrosis factor alpha targets insulin-like growth factor-I induced E2F-transcription facor 1 synthesis, leading to inhibition of accumulation in cyclin A and hyperphosphorylation of RB protein
- Rb is present in rat and human islets, and overexpression of cyclin D(1)/cdk-4 led to strikingly enhanced Rb phosphorylation.
- Fortythree novel mutations found in RB1, the mutational spectrum displayed a surprising amount of splice mutations and large deletions.
- Calcitrio may signal cell differentiation of HL 60 cells which in turn regulates expresson of RB protein.
- Rb negatively regulates p38 activation, leading to decreased MMP-1 secretion in rheumatoid arthritis synovial fibroblasts.
- pRb and p107 do not constitute the last control point for extracellular factors during G(1)-phase progression, and they functionally separate the requirements for serum and cell anchorage in terms of involved cell cycle components.
- role of Rb family memebers in stability of repressor complexes at promoters
- The overall expression of PCNA in all stages of development was higher than pRb1 expression.
- The mechanisms for pRb tumor suppression in the epithelia of two distinct tissues, mammary gland and brain, are indistinguishable. (review)
- Results suggest that acetylation regulates the differentiation-specific function(s) of retinoblastoma tumor-suppressor protein.
- Rb regulates apoptotic genes differently in human and in mouse cells
- A non-cdk8-associated cellular pool of cyclin C combines with cdk3 to stimulate pRb phosphorylation at S807/811 during the G0/G1 transition, and this phosphorylation is required for cells to exit G0 efficiently.
- Data show that Oct-1 occupies the endogenous HLA-DRA promoter when the HLA-DRA promoter is inactive in retinoblastoma protein-defective cells.
- Rb is absent or phosphorylated in most anaplastic large cell lymphoma cell lines and tumors and absence of Rb expression is associated with better clinical outcome in patients with ALCL.
- A novel Cdk4 docking motif has been defined within a stretch of 19 amino acids from the C-terminal domain of the Rb protein that are essential for Cdk4 binding.
- In mice, Rb/p107 loss has cell-specific effects in retina: evidence for a naturally death resistant cancer cell-of-origin
- RB can repress U6 snRNA gene transcription at critical steps subsequent to RNA polymerase III recruitment
- Rb acts as a link between apoptotic and proliferative pathways by interacting with distinct kinases and occupying different promoters
- Hereditary retinoblastoma is an autosomal dominant disorder caused by mutations in the RB1 gene [Review]
- Generation of Rb pathway lesions in normal and transformed cells produces aberrant Mad2 expression and mitotic defects leading to aneuploidy, such that elevated Mad2 contributes directly to these defects
- Immortalization of MRC5hTERT cells was associated with repression of the cyclin-dependent kinase inhibitor p16INK4a and up-regulation of pRB.
- 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
- RB/E2F signaling pathway activation is required for the modulation of hepatitis C virus core protein-induced cell growth in liver and non-liver cells
- Results demonstrate that p16ink4A-mimicking peptides can induce apoptosis in vitro and inhibit tumor growth in vivo in p16-defective, retinoblastoma protein-expressing human melanoma cells.
- p21(WAF1), acting through the phosphorylation of pRb, regulates whether 2BS cells cease to proliferate and become senescent but resistant to apoptosis, or whether they accelerate proliferation while becoming more susceptible to apoptotic stimuli
- dynamic equilibrium between CDKs and PP2A modulates phosphorylation of pRB
- Constitutional RB1 germ-line mutations were studied in a series of Argentine families.
- the central acidic domain of MDM2 is critical in inhibition of retinoblastoma-mediated suppression of E2F and cell growth
- Raf-1 links mitogenic signaling to Retinoblastoma Protein and that disruption of this interaction could aid in controlling proliferative disorders
- Aberrant expression of pRb and p16, alone and in combination, heralds poor prognosis in patients with CRC.
- Evaluation of phosphorylated retinoblastoma protein in melanocytic tumors could become a helpful adjunct in clinicopathological routine.
- p16-Rb pathway plays important role in tumor progression and prognosis in vertical growth phase melanomas
- phosphorylation promoted by HPV16 E6 protein
- These results suggest that Mdm2 regulates function of retinoblastoma gene product (pRB) via ubiquitin-dependent degradation of pRB.
- a model whereby Tax targets Rb to the proteasome by acting as a molecular bridge bringing Rb into contact with the proteasome for degradation
- the derepression of Rb-E2F-regulated genes leads to apoptosis through inactivation of focal adhesion kinase and activation of caspase-8
- Rb, p21Cip1, and PCNA have roles in cAMP-mediated inhibition of DNA replication and S phase progression
- BMP-2 inhibits DHT-induced growth of LNCaP cells through a decrease in E2F protein expression and suppression of E2F activity by hypophosphorylation of Rb
- Mutation of p16 and Rb genes might be correlated with progression of gallbladder carcinoma
- Rb and p53 have roles in progression of primary non-small cell lung carcinoma
- a functional interaction between pRB and HIF-1alpha is confirmed by showing that HIF-1alpha reverses the transcription repressor function of pRB.
- an alternatively translated form of pRb is expressed during normal myelopoiesis and in tumour-associated macrophages
- experiments suggest that both catalytic and non-catalytic functions of cyclin D1 can collaborate to inactivate pRb-mediated cell cycle exit
- Rb interacts with the NeuroD1/Beta2 transcription factor and activates the POMC gene
- Rb is a coactivator of NeuroD1/Beta2 on the POMC promoter
- Suppression of pRb may be characteristic for papillary thyroid carcinomas with a tendency to early metastasizing.
- Mitf-mediated activation of p21Cip1 expression and consequent hypophosphorylation of Rb1 will contribute to cell cycle exit and activation of the differentiation programme
- Data showed that disabling of the Rb pathway was frequent event in oral carcinoma.
- an early event in neuronal cell death is p25/Cdk5-mediated retinoblastoma phosphorylation
- Dehydroepiandrosterone diminished the levels of phosphorylated retinoblastoma protein.
- Knockdown of the gene in colorectal carcinoma cells caused resistance to antitumor agents.
- Rb acts as a coactivator of HNF-4 and is recruited to the alpha1-AntiTrypsin promoter during the enterocyte differentiation of Caco2 cells
- Rb enhances the POMC promoter activation by the CRH hormone in mouse AtT-20 corticotroph cells
- Rb interacts with and acts as a potentiator of the p160 transcriptional coactivator SRC-2/GRIP1/TIF-2
- Rb interacts with the nuclear receptors : NGFI-B/Nur77, HNF4, SF-1, and ER and enhances their activity during hormone responsivness and cell differentiation
- Rb potentiates the activity of the SRC-2/GRIP1/TIF-2, SRC-1 and SRC-3 coactivators on the nuclear receptors: NGFI-B/Nur77, Nur1, NOR-1, HNF-4, SF-1 and ER.
- the RB1 gene is conserved in human and primates
- RB gene might be down-regulated at the transcriptional level in human testicular seminoma cells.
- Smad7 acts to functionally inactivate RB and de-repress E2F without blocking the activation of TbetaRI and the nuclear translocation of Smad2/3, allowing TGF-beta1 to exert effects in a cancer cell that is resistant to TGF-beta1-mediated growth inhibitio
- p130/p107/p105Rb has a role in transcriptional repression in DNA-damage-induced cell-cycle exit at G2
- nuclear import conferred by the RB nuclear localization sequence has distinct properties, in part due to the affinity of its interaction with IMPalpha
- The Aberrant expression of Rb 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).
- RB1 gene has a major role in the development of human vestibular schwannomas, increased levels of RB1 mRNA, total pRb and the phosphorylated form of it suggests that RB1 gene in these tumors may have anti-apoptotic function
- Germline RB1 mutations in 77 out of 85 bilateral RB patients (91%), 7 out of 10 familial unilateral (70%), and 6 out of 85 unilateral patients with no family history of RB (7%), were identified.
- developmental expression of RB, p130 and p107 in mouse and human retina
- Deregulation of both pRb and p53 pathways is associated with malignant transformation in oral tumorigenesis
- Modulates the subcellular localization of BAG-1 in colorectal tumor cell susrvival.
- Gross deletions and insertions in the RB1 gene are associated with retinoblastoma.
- data suggest that loss of Rb creates strong selective pressure, via DSB accumulation, for inactivating p53 mutations and that E2F1 contributes to the genetic instability associated with transformation and tumorigenesis
- data show that E2F1 has potential binding activity to the retinoblastoma control element and a different transcriptional regulation pathway which cooperates with the retinoblastoma tumor suppressor protein
- results show that phosphorylation site-mutated RB exerts disparate effects on apoptotic response to different stimuli, and that cell cycle arrest does not always associate with resistance to apoptosis
- pRB degradation involved in gastric tumor cell apoptosis is p53-independent
- Methylation in the p16 promoter region is biologically significant, being associated with phosphorylation of pRb and cell growth in human hepatocellular carcinoma cells
- RB expression may be a useful biomarker for assessing the risk of developing esophageal cancer.
- DGKzeta may act in vivo as a downstream effector of pRB to regulate nuclear levels of diacylglycerol and phosphatidic acid
- Sars virus 7a protein expression was correlated with phosphorylation of retinoblastoma (Rb) protein at ser795 and ser809/811 and prevention of cell cycle progression at the G0/G1 phase.
- Review. RB1 is a marker of retinoblastoma. It maps to 13q14.2 & encodes a 110-kDa nuclear phosphoprotein, cell-cycle-regulated phosphorylation of which plays a major role in cell proliferation control. Most point mutations are in exons 3, 8, 18 & 20.
- Down-regulation of the retinoblastoma tumor suppressor by the hepatitis C virus NS5B RNA-dependent RNA polymerase.
- These findings suggest that overexpression of Mdm2 can perturb a RB pathway regardless of the p53 gene status, promoting carcinogenesis.
- EBNA3C forms a stable complex with Rb in cells when the proteasome machinery is inhibited and interacts with Rb in vitro, mapping to a conserved domain at the terminus of EBNA3C
- 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.
- Findings explain the requirement of the Rb C-terminal domain for high-affinity E2F binding and growth suppression, and establish a mechanism for the regulation of Rb-E2F association by phosphorylation.
- Rb binding to HPV 18 E7 is modified by transglutaminase 2 with different polyamines
- RB1 was not implicated, suggesting the participation of another tumor suppressor gene in this region.
- Possible role for the G-quadruplex in control of DNA synthesis at the 5' end of the retinoblastoma susceptibility gene.
- Our data suggests that RB1 may play a role in colorectal tumorigenesis through functional regulation of the transcript and protein rather than through its tumour suppressor role by gene inactivation.
- These findings suggest heterogeneous abnormalities of CCND and RB in cutaneous T-cell lymphomas, in which dysregulated CCND and RB1 may lead to impaired cell cycle control.
- Differences in oncoprotein expression between endometriotic and adenomyotic tissues provide further evidence that the pathogenesis of endometriosis is different from that of adenomyosis.
- determination that Rb is not activated in hTERT immortalization of urothelial cells
- RB1 gene was methylated in seven samples (14%) and each patient had refractory anemias(RA).
- A molecular study of first and second RB1 mutational hits in retinoblastoma patients was performed.
- intracellular distribution of nucleolin in epithelial cells is Rb-dependent, and an altered nucleolin localization in human cancerous tissues results from a loss of Rb
- when nontransformed CV1 epithelial cells and Hs578T breast cancer cells are treated with cytosine arabinoside,Thr-821 of Rb is rapidly dephosphorylated,with dissociation of the PP1 regulatory subunit PNUTS (phosphatase nuclear targeting subunit)from PP1.
- facets of RB protein function in cell cycle control in retinoblastoma (review)
- Membrane depolarization may stimulate cellular proliferation by augmenting the expression of cyclin E leading to increases in Cdk2 activity and RB phosphorylation in a neuroblastoma cell line.
- These findings reveal that phosphorylation of threonine-373 by CDK2-cyclin E represent a potentially crucial event in the inactivation of the pRb protein.
- Relationship between Rb and Ini1 in tumor suppression indicate that Ini1 plays a role in maintaining the morphologic and functional differentiation of corticotrophic cells.
- 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.
- nonphosphorylated p68 inhibited the stimulation of pol-alpha activity by hyperphosphorylated retinoblastoma protein, suggesting that p68 might impede the association of ppRb with p180
- The antiproliferative effects of Lf can likely be attributed to the elevated levels of hypophosphorylated Rb.
- Determination of intraepithelial height of immunohistochemical staining for p16, p53, pRb, and Ki-67 in upper aerodigestive tract lesions with reference to degree of dysplasia
- these studies highlight p38 MAPK, HBP1, and RB as important components for a premature-senescence pathway with possible clinical relevance to breast cancer.
- CDCA4 participates in the regulation of cell proliferation, mainly through the E2F/retinoblastoma protein pathway
- 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
- Results uncover an unexpected role for the p16(INK4a)-Rb pathway and provide a new insight into how senescent cell-cycle arrest is enforced.
- Data suggest that in Ehrlich ascites tumor cells, growth inhibition by 1'-acetoxychavicol acetate involves decreased Rb and p27(kip1) phosphorylation and increased nuclear localization of p27(kip1), dependent on cellular thiol status.
- significant cytoplasmic mislocalization of ordinarily nuclear RB in cells harboring Cdk4 mutations
- Promoter methylation of retinoblastoma Protein is associated with malignant fibrous histiocytomas
- mutation of Rb gene is frequent in gastric carcinoma; expression of altered protein inversely correlates with tumor invasion
- The pRb level was higher than in normal larynxes, whereas laryngeal cancer presented the lowest levels.
- RB pathway is a critical determinant of tumorigenic proliferation and differential therapeutic response and may represent a critical basis for directing therapy in the treatment of breast cancer.
- Rb induces a proliferative arrest and regulates Brn-2 expression in retinoblastoma cells
- Human papillomavirus E7 repression in cervical carcinoma cells initiates a transcriptional cascade driven by the retinoblastoma family, resulting in senescence.
- aberrant hypermethylation of the key cell cycle regulatory genes occurs at a relatively high frequency in pituitary adenomas, especially in RB1 pathway genes with promoter hypermethylation of the p16(INK4a) gene being the most common deregulation
- Sequence deletion or mutation or gene deletion in retinoblastoma patients in Argentina.
- This study demonstrates that ARF plays a direct role in regulation of Rb and suggests that inactivation of ARF may lead to defects in both p53 and Rb pathways in human cancer development.
- This is the first report of a deep intronic mutation in RB1 and is a proof of concept that some undetected RB1 mutations should be investigated at the cDNA level.
- Presence of LOH at the RB1 gene locus and the increased levels of RB1 RNA and protein and increased percentage of hyperphosphorylated form of pRb are indicative of an overall deregulation of pRb pathway in human brain tumors.
- RB1 may be inactivated in aggressive mantle-cell lymphoma by intragenic deletions.
- TGF-beta1 increased retinoblastoma protein phosphorylation at both Ser807/811 and Ser780 in airway smooth muscle cells
- Radiation-induced somatic mutations are not observeded in radiation-induced sarcoma, although the gene was activated in sarcoma.
- Phosphorylation of pRB at Ser612 by Chk1/2 leads to a complex between pRB and E2F-1 after DNA damage.
- LOH of the retinoblastoma gene in is not shown to have a role in progression of osteosarcoma
- SARS-CoV 3a protein, through limiting the expression of cyclin D3, may inhibit Rb phosphorylation, which in turn leads to a block in the G1 phase of the cell cycle and an inhibition of cell proliferation
- Telomere dysfunction and inactivation of the rb pathway might play a role for pyrothorax-associated lymphoma
- these analyses demonstrate that cyclin A1 exerts antiapoptotic functions by interacting with retinoblastoma and Ku proteins in leukemia cells.
- Abnormal expression of the pRB protein may be implicated in the process of esophageal carcinogenesis.
- In Ishikawa H cells that model type I endometrial cancer in the loss of PTEN and RB1, re-expressing PTEN and RB1 increased the apoptotic and G1 phases and decreased the S and G2-M phases, which further sensitize the cells to gefitinib.
- sufficient Rb levels are important for the cytotoxic and anticlonogenic effects of ErPC3 at levels below the IC(50), but higher concentrations of ErPC3 are less dependent on Rb status
- A microtuble-facilitated nuclear import pathway for RB1 is described.
- Promoter hypermethylation of RB1 was observed.
- Inactivation of retinoblastoma protein is associated with head and neck squamous cell carcinomas
- Down-regulation of Rb Protein is associated with defects in erythroblast islands
- Results identify BNIP3 as a key regulator of hypoxia-induced autophagy and suggest a novel role for the RB tumor suppressor in preventing nonapoptotic cell death by limiting the extent of BNIP3 induction in cells.
- Epstein-Barr virus-encoded latent membrane protein 1inhibited p16(INK4A) expression, promoted phosphorylation of p105 Rb and upregulated E2F1 expression and overexpression of E2F1 alone was sufficient to upregulate telomerase activity.
- the HPV16 E7-associated cullin 2 ubiquitin ligase complex contributes to aberrant degradation of the pRB tumor suppressor in HPV16 E7-expressing cells.
- 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.
- RB depletion dramatically alters the cellular response to therapeutic intervention in prostate cancer cells
- RB reconstitution into RB-deficient NSCLC lines establishes regulation of certain RB/E2F target genes and restores G1 arrest mechanisms
- correlation between RB1 gene deletion and mammary gland carcinoma
- Aberrant methylation of multiple genes (E-cadherin, estrogen receptor, RB1 , p16, p15, p14, and MGMT) is involved in gastric carcinogenesis.
- retinoblastoma protein downregulation is involved in the enhanced cytotoxicity of 4-hydroxytamoxifen plus mifepristone combination therapy versus antiestrogen monotherapy of human breast cancer
- ectopically BRCA2-expressing cells have different intracellular levels of Aurora A, Aurora B, p21, E2F-1, and pRb, suggesting a BRCA2-mediated suppression of polyploidy via stabilization of the checkpoint proteins levels
- Aberrations of the p53, Rb and p27 pathways are associated with aggressive clinical behavior in DLBCL.
- homozygous inactivation of P2RY5 was antecedent to the loss of RB1 during tumor development
- KAP1 contributes to the negative regulation of E2F1 and may serve as a partial backup to prevent E2F1-mediated apoptosis in the absence of pRb
- 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.
- Retinoblastoma deficiency increases chemosensitivity in lung cancer.
- High mobility group protein A1 (HMGA1)disturbs retobblastoma protein-mediated cell arrest, suggesting a negative control of RB by HMGA1.
- Somatic down-regulation of mismatch repair proteins in nodular-trabecular muscle-invasive bladder urothelial carcinomas results in RB1/NF1 microsatellite abnormalities, correlating with higher cellular turnover and longer survival.
- There is more frequent p16 hypermethylation in mantle cell lymphoma and p15 or Rb1 hypermethylation in follicular lymphoma
- Myc down-regulation is a mechanism to activate the Rb pathway in STAT5A-induced senescence
- Human herpesvirus 6A (HHV-6A) and HHV-6B infection was associated with significant reduction of E2F1/Rb complexing, and Rb protein was dephosphorylated early postinfection.
- compromise of either p53 or Rb pathways during melanocyte transformation leads to up-regulation of survivin expression in melanoma
- Ten novel mutations were identified, including four single base substitutions, four small deletions and two small duplications. Predominantly gene-inactivating mutations, i.e. single-base non-sense mutations and splice site mutations.
- mechanisms other than RB1 gene changes may lead to retinoblastoma because not all cases of retinoblastoma show gene alterations
- A novel molecular mechanism for pRb inactivation by a viral oncoprotein.
- Calpain emerges as a central player in E7-mediated degradation of Rb
- underline the importance of Protein phosphatase 2A subunit PR70-Ca(2+) interaction in the signal transduction mechanisms triggered by redox imbalance and leading to pRb dephosphorylation
- The crystal structure of the Rb N-terminal domain (RbN) was determined.
- Study described the use of minigene constructs to study the oncogenic character of intronic RB1 variants detected during mutational screening and show the utility of this approach to ascertain the oncogenic nature of unique RB1 intronic variants.
- These data shed more light on the molecular biology of meningioma cells and suggest that survivin and proteins of the RB pathway could play a determinant role in the development and the treatment of meningiomas.
- RB inactivation, via aberrant nucleocytoplasmic transport, may disrupt normal cell differentiation programs and accelerate the cancer process.
- defines a novel family of cellular factors linked to cell proliferation and pRb/E2F cell cycle pathways in humans, fish, and nematodes
- analyzed RNA from retinoblastoma patients and unaffected carriers with various RB1 gene mutations to determine the patterns of missplicing and associations with phenotypic expression
- In this review, retinoblastoma protein acts along with Skp2 to regulate signal transduction in the cell cycle.
- Loss of both RB1 tumor suppressor gene alleles initiates quiescent RB1(-/-) retinomas with low level genomic instability and high expression of the senescence-associated proteins p16(INK4a) and p130.
- These findings indicate that Epstein-Barr virus C promoter (Cp) is a cell cycle-regulated promoter that is under the control of Rb and the histone demethylase LSD1 in multiple latency types.
- Findings strongly demonstrate that retinoblastoma (RB) and cyclin-dependent kinase 2 (CDK2) on one side and cytokeratin 8 (CK8) and epidermal growth factor receptor 2 (HER2) on the other may affect the clinical course of the disease in 56% of patients.
- The deletion of the RB1 gene plays an important role in the development of acute myelocytic leukemia.
- Our data suggest that p107 and p130, but not pRb, and the repressor E2F, but not activator E2Fs, play a critical role in regulating E2F-responsive gene expression.
- The morphology and cell cycle proteins immunoexpression of the novel probable preinvasive lesion - bronchiolar columnar cell dysplasia (BCCD), is decribed.
- Cdk6 up-regulation in TDP-43-depleted cells is accompanied by an increase in phosphorylation of two of its major targets, the retinoblastoma protein pRb and pRb-related protein pRb2/p130.
- Analysis of the pattern of expression of these biomolecules showed increased p16-positive phenotypes and decreased cyclin D1- and pRB-positive phenotype among the invasive tumors compared to low-grade CIN lesions
- We concluded from these studies that both UL97 kinase activity and the LxCxE retinoblastoma protein (RB) binding motif are required for the phosphorylation and stabilization of RB in infected cells.
- 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.
- Results suggest that Bin1 gene suppression caused by oncogenic E1A via Rb/E2F1 inactivation is an essential step in cell cycle progression promoted by c-Myc, and subsequently, E1A transformation.
- reduced expression of PNUTS leads to activation of Rb-phosphatase and caspase-mediated apoptosis
- The absence of pRB expression renders human breast cancer cells more sensitive to 5-FU and methotrexate and predicts a good clinical outcome for patients treated with adjuvant chemotherapy
- Increased retinoblastoma 1 expression was associated with invasive adenocarcinoma of the prostate
- tumorigenesis of RMS may be associated with retinoma gene alteration
- MRPS18-2 binds to both hypo- and hyperphosphorylated forms of Rb protein specifically. This binding targets the small pocket of pRb, which is a site of interaction with E2F1.
- Human breast cancer-associated fibroblasts show CAV1 down-regulation and RB1 tumor suppressor functional inactivation.
- The current findings demonstrated that loss of Rb and p16/INKa expression and high E2F1 expression indicate impairment of the Rb suppressor pathway
- A rare gliosarcoma with liposarcomatous differentiation showed alteration of pRB in sarcomatous component.
- the Rb/Raf-1 interaction has a role in cell proliferation and angiogenesis
- We screened for RB1 gene sequence alterations in both peripheral blood and tumor specimens from a total of 48 Mexican retinoblastoma patients...mutation analysis was not helpful to distinguish sporadic and hereditary retinoblastoma
- We did not observed any correlation between Rb and other clinocopathological features
- Rb inactivation contributes to tumor progression due to not only loss of cell proliferation control but also conversion to an invasive phenotype.
- SerpinB2 is a cell survival factor that modulates Rb repression of proapoptotic signal transduction
- Low-penetrant RB allele in small-cell cancer shows geldanamycin instability and discordant expression with mutant ras.
- Mutations in RB1 in melanoma by inhibition of nonsense-mediated mRNA decay.
- With tumor suppressor protein p53, RB1 is involved in proteasome inhibition cell senescence.
- These results indicate that PRMT5 overexpression epigenetically alters the transcription of key tumor suppressor genes.
- phosphatases and pRB have important roles in IGF-I/mTOR-mediated cell survival
- Karyotyping and FISH assessment for chromosomal abnormalities in the RB1 gene corrates with survival in B-cell chronic lymphocytic leukemiae.
- MYPT1 may regulate the phosphorylation level of pRb, thereby it may be involved in the control of cell cycle progression and in the mediation of chemoresistance of leukemic cells.
- The patient was found to carry a de novo heterozygous deletion (g.59444 del196) that results in mis-splicing of exon 8 of RB1, producing a non-functional retinoblastoma protein.
- The extreme COOH terminus of the retinoblastoma tumor suppressor protein pRb is required for phosphorylation on Thr-373 and activation of E2F.
- Both siblings in each family described in this report developed unilateral unifocal retinoblastoma as a new germ-line RB1 mutation.
- Functional loss of RB1 is common in basal-like tumours, which may play a key role in dictating their aggressive biology and unique therapeutic responses.
- The p16INK4a/cyclin D1/pRB pathway was altered in gastrointestinal tract endocrine tumors, and the loss of expression of pRB may be helpful in identifying patients at high risk of metastasis in rectal well-differentiated endocrine neoplasms
- by retaining RB1 and amplifying CDK8, colorectal tumour cells select conditions that collectively suppress E2F1 and enhance the activity of beta-catenin
- Proto-oncogene FBI-1 (Pokemon/ZBTB7A) represses transcription of the tumor suppressor Rb gene via binding competition with Sp1 and recruitment of co-repressors.
- Epigenetic inactivation of the RB1 gene as a factor of genomic instability: a possible contribution to etiology of chromosomal mosaicism during human embryo development
- K-RAS point mutations, and anomalies of p16-RB1-cyclin D pathway could occur before LOH on 10q23 (PTEN) and microsatellite instability during tumor progression.
- Immunohistochemical analysis of Rb protein expression in neoplastic cells made it easier to evaluate the mechanisms of cancerogenesis in laryngeal cancer and is closely related to genetic alteration in Rb locus.
- Reduction in Rb1 expression due to methylation is associated with bladder cancer.