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Validated All-in-One™ qPCR Primer for MYC(NM_002467.5) Search again
Product ID:
HQP088534
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
MRTL, MYCC, bHLHe39, c-Myc
Gene Description:
MYC proto-oncogene, bHLH transcription factor
Target Gene Accession:
NM_002467.5(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 multifunctional, nuclear phosphoprotein that plays a role in cell cycle progression, apoptosis and cellular transformation. It functions as a transcription factor that regulates transcription of specific target genes. Mutations, overexpression, rearrangement and translocation of this gene have been associated with a variety of hematopoietic tumors, leukemias and lymphomas, including Burkitt lymphoma. There is evidence to show that alternative translation initiations from an upstream, in-frame non-AUG (CUG) and a downstream AUG start site result in the production of two isoforms with distinct N-termini. The synthesis of non-AUG initiated protein is suppressed in Burkitt's lymphomas, suggesting its importance in the normal function of this gene. [provided by RefSeq].
Gene References into function
- Alternative translation initiation from an upstream, in-frame non-AUG (CUG) and a downstream AUG start site results in the production of two isoforms with distinct N-termini.
- Review: EBV regulates c-MYC, apoptosis, and tumorigenicity in Burkitt's lymphoma
- We have located a region in the c-myc promoter that is required for the complete activation by the immunoglobulin heavy chain gene enhancer
- In Situ studies demonstrate enhanced mRNA expression of the proto-oncogene c-myc in stenotic venous bypass grafts.
- c-Myc physically interacts with Smad2 and Smad3 involved in TGF-beta signaling.c-Myc promotes cell growth and cancer development partly by inhibiting the growth inhibitory functions of Smads
- Uteroglobin promoter-targeted c-MYC expression in transgenic mice cause hyperplasia of Clara cells and malignant transformation of T-lymphoblasts and tubular epithelial cells
- initiates illegitimate recombination of ribonucleotide reductase 2 gene
- Acute hyperglycaemia induces an up-regulation of seven major genes, four of which were not previously reported in the literature. Northern blot analyses, performed on these 4 genes, confirm macroarrays results for alphav, beta4, c-myc, and MUC18.
- Activation of c-MYC and c-MYB proto-oncogenes is associated with decreased apoptosis in tumor colon progression.
- amplification in acute nonlymphocytic leukemia
- Repression of alpha-fetoprotein gene expression under hypoxic conditions in human hepatoma cells: characterization of a negative hypoxia response element that mediates opposite effects of hypoxia inducible factor-1 and c-Myc.
- Retinoic acid-induced cell cycle arrest of human myeloid cell lines is associated with sequential down-regulation of c-Myc and cyclin E.
- Scatter factor/hepatocyte growth factor stimulation of glioblastoma cell cycle progression through G(1) is c-Myc dependent and independent of p27 suppression, Cdk2 activation, or E2F1-dependent transcription.
- complex with Nmi and BRCA1 inhibits c-Myc-induced human telomerase reverse transcriptase gene promoter activity in breast cancer
- c-myc-induced apoptosis in polycystic kidney disease is independent of FasL/Fas interaction.
- The N-myc and c-myc downstream pathways include the chromosome 17q genes nm23-H1 and nm23-H2
- estrogen and Myc negatively regulate EphA2 expression in mammary epithelial cells
- A novel form of the RelA nuclear factor kappaB subunit is induced by and forms a complex with this proto-oncogene protein
- overexpressed in acute myeloid leukemia while translocations associated with this gene are absent
- The proto-oncogene c-myc in hematopoietic development and leukemogenesis
- c-Myc can induce DNA damage, increase reactive oxygen species, and mitigate p53 function
- Overexpression of c-myc mRNA was found in an Achilles tendon clear cell sarcoma and may have a role in its malignant progression.
- TRRAP binding and the recruitment of histone H3 and H4 acetyltransferase activities are required for the transactivation of a silent TERT gene in exponentially growing human fibroblasts by c-Myc or N-Myc protein.
- Effects of fluid shear stress on expression of proto-oncogenes c-fos and c-myc in cultured human umbilical vein endothelial cells.
- the in vitro effects of iron on the proliferation of a primary, human synovial fibroblast cell line and the involvement of c-myc in this process as a model for c-myc proto-oncogene expression in hemophilic synovitis
- role of c-Myc increasing susceptibility to tumor necrosis factor mediated apoptosis
- Myc activates transcription by stimulating elongation and that P-TEFb is a key mediator of this process
- dysregulated beta-catenin may cause a transcriptional upregulation of the c-myc gene; the c-Myc protein expression appears to be further regulated by posttranscriptional mechanism(s) during neoplastic progression in colorectal adenocarcinomas
- C-Myc may be a downstream target of anaplastic lymphoma kinase (ALK)signaling and its expression a defining characteristic of ALK-positive anaplastic large cell lymphomas
- c-myc induces programmed cell death in a process requiring glutathione in human tumor cells
- Amplifications of c-myc and CCND1 are associated with detrusor-muscle-invasive transitional cell carcinoma
- results reveal a novel cytoskeletal function for Myc and indicate the feasibility of quantitative whole-proteome analysis in mammalian cells
- This review describes the role of MYC in tumor progression
- c-myc and c-erbB2 amplification in breast cancer
- Marked intratumoral heterogeneity of this and cyclinD1 but not of c-erbB2 amplification in breast cancer
- Beta-catenin mutations correlate with over expression of C-myc and cyclin D1 Genes in bladder cancer.
- CD19+ cells from transgenic mice with a lamba-humanMYC construct driven by B-cell elements overexpressed both C-MYC and protein kinase A-Cbeta.
- c-Myc promotes cell survival under stressful conditions.
- the mechanism of apoptosis induced by c-myc gene in oral squamous cell
- Reduction in the c-myc protein was correlated with neck metastasis in nasopharyngeal carcinoma.
- c-myc translation is regulated by hnRNP C via internal ribosomal entry site binding
- c-Myc binds to TFIIIB, a pol III-specific general transcription factor, and directly activates pol III transcription
- examination of functionality of basic domains compared with Mad
- repression of differentiation-induced p21 expression through Miz-1 may be an important mechanism by which Myc blocks differentiation
- Expression of c-Myc in primary central nervous system diffuse large B-cell lymphoma may be a prognostic marker for poor overall survival.
- results show that Ser727/Tyr701-phosphorylated Stat1 plays a key role as a prerequisite for the ATRA-induced down-regulation of c-Myc; cyclins A, B, D2, D3, and E; and simultaneous up-regulation of p27Kip1, associated with arrest in the G0/G1 phase
- results indicate that Nijmegen breakage syndrome 1 gene (NBS1) is a direct transcriptional target of c-Myc and links the function of c-Myc to the regulation of DNA double-strand break repair pathway
- c-myc binds to the hTERT promoter and is involved in the pathway for regulation of cellular immortalization through BRCA1
- A detailed structure-function analysis of the Myc N-terminal domain in deletion & point mutants studied their ability to induce cell cycle progression, apoptosis & transformation as well as repress & activate endogenous target genes.
- Up-regulation of c-Myc protein could disturb the signaling pathway of ceramide & sphingosine, endogenous modulators mediating apoptosis. c-Myc protein is a mediator of cytoprotective effect of PKC pathway in HL-60 cells.
- Myc down-regulation might directly mediate the growth-inhibitory properties of 3'-5' RNA exonuclease
- inverse correlation between TMEFF2 and c-Myc expression
- findings suggest that Myc-mediated functions can be negatively regulated by KRAB box containing zinc finger protein (Krim-1)
- MYC recruits the TIP60 histone acetyltransferase complex to chromatin
- c-myc gene is regulated by nitric oxide via inactivating NF-kappa B complex
- c-Myc together with its heterodimeric partner, Max, occupy >15% of gene promoters tested in Burkitt lymphoma cells. Overexpressed c-Myc plays a role in global transcriptional regulation in some cancer cells and functions in malignant transformation.
- the PI3K/p70 S6K/c-Myc cascade plays an important role in neutrophilic proliferation in HL-60 cells.
- Induction of hTERT by Myc/E6 was independent of Myc phosphorylation at Thr-58/Ser-62 within the transactivation domain. E6 associates with Myc complexes & activates a Myc-responsive gene, hTERT.
- Inhibition of this oncoprotein limits the growth of human melanoma cells by inducing cellular crisis
- expression of MYC oncogene is reduced at the mRNA level and MYC protein has an increased half-life in Adenovirus infected Hela cells resulting in constant steady state levels.
- results demonstrate that MYC directly stimulates transcription of the Werner syndrome gene,WRN; propose that WRN up-regulation by MYC may promote MYC-driven tumorigenesis by preventing cellular senescence
- hematopoietic growth factors induce cell cycle progression via internal ribosome entry site-mediated translation of c-myc though the PI3K pathway in human factor-dependent leukemic cells
- overexpression of MYC disrupts the repair of double-strand DNA breaks, resulting in a several-magnitude increase in chromosomal breaks and translocations
- the mutated version of the c-myc IRES that is prevalent in patients with multiple myeloma bound hnRNPK more efficiently in vitro and was stimulated by hnRNPK to a greater extent in vivo.
- p53 and c-Myc expression may have a role in regulation of telomerase activity in ovarian tumours
- c-Myc regulates cell growth and proliferation by the coordinated induction of cdk activity and rRNA processing
- contribution of JNK to the regulation of c-Myc protein stability under normal growth conditions
- identified an evolutionarily conserved boundary at which the c-myc transcription unit is separated from the flanking condensed chromatin enriched in lysine 9-methylated histone H3
- PLZF expression maintains a cell in a quiescent state by repressing c-myc expression and preventing cell cycle progression.
- we review Myc-induced pathways that contribute to the apoptotic response.
- These data also suggest that location of intragenic PTEN mutations and their coexistence with the CMYC amplification may play a crucial part in the development of various subtypes of endometrial carcinoma.
- Data suggest that cyclin dependent kinase 4 is involved in the development of tobacco-mediated oral carcinogenesis, and that c-myc expression is absent in normal and high in later stages of oral cancer development.
- c-myc may have a role in the development of Burkitt's lymphoma, through an RNA-mediated gene silencing pathway
- c-Myc may control the activity of multiple signal pathways involved in cellular transformation by induction of HSP90A
- Aurora-A induces telomerase activity and hTERT by up-regulation of c-Myc
- MYC has a role in tumor progression in BRCA1-associated breast cancers
- c-Myc expression is regulated by cytosolic phospholipase A2 in a process that involves B-myb
- c-Myc does not play a major role in gene regulation of the catalytic subunit of telomerase (hTERT) in human hepatocellular carcinoma.
- c-Myc can support self-renewal of HSCs as a downstream mediator of Notch and HOXB4.
- Myc is an integral part of a novel HIF-1alpha pathway, which regulates a distinct group of Myc target genes in response to hypoxia.
- Levels of both c-myc and beta-catenin increased in Cyr61 stably transfected H520 cells.
- Gene amplification of c-myc may play key role in regulating expression of its mRNA and protein in high-grade breast cancers
- c-Myc can specifically recognize the HIV-1 initiator element surrounding the start site of transcription and linker scanning mutagenesis experiments confirmed a loss of c-Myc-mediated repression in the absence of this region
- High nuclear expression of c-myc is correlated with locally advanced colorectal cancer
- C-Myc over-expression was significantly associated with high sVEGF and normal sFlt-1 level in DLBCL patients, suggesting a complex interrelationship between c-Myc oncogene expression and angiogenic regulators
- expression of c-Myc protein is increased not only in uterine cervix cancer but also in the premalignant lesions
- Translocations involving the MYC locus were detected in six cases of B-cell lymphoma, five of them derived from a MYC/IGH juxtaposition and one from a translocation involving a non-IG gene partner.
- c-myc transactivates rat and human adrenomedullin genes and accelerates the degradation rate of adrenomedullin mRNA.
- c-myc mRNA was detected in 18 of 59 cases, and was associated with shorter patient survival times on both univariate and multivariate analyses. The presence of c-myc mRNA was also significantly associated with tumor anaplasia.
- cMyc is a target of ARF tumor suppressor
- Myc binds well to conserved canonical E boxes, but not nonconserved E boxes. Results show Myc is an important regulator of glycolytic genes, suggesting that MYC plays a role in a switch to glycolytic metabolism during cell proliferation or tumorigenesis.
- c-myc oncogene has not shown to be a prognostic factor for laryngeal squamous cell carcinoma of the supraglottic larynx.
- c-MYC activated transcription from the upstream binding factor promoter
- A prolactin signalling cascade in W53 cells involves Src kinases that mediate stimulation of c-Myc expression.
- There is no obvious correlation between breakpoint locations within the immunoglobulin H locus and the amount of MYC mRNA.
- polyamine-induced nuclear c-Myc interacts with Max, binds to the specific DNA sequence, and plays an important role in stimulation of normal intestinal epithelial cell proliferation.
- p53-independent checkpoint to prevent c-Myc-mediated tumorigenesis
- Inhibition of c-Myc (and c-Raf-1) significantly reduced the growth and invasiveness of rheumatoid arthritis synovial fibroblasts in the SCID mouse model.
- There was a significant positive correlation between the levels of c-myc mRNA expression and the occurrence of apoptosis in 59 hepatocellular carcinomas.
- novel iron-dependent cell cycle regulatory mechanism involving modulation of translocated c-myc gene expression
- c-myc downregulation and release from the endogenous p21WAF1/CIP1 promoter contributes to transcriptional activation of the p21WAF1/CIP1 in HeLa cells
- Myc is essential for the regulation of a large number of growth-related genes in B cells, and cannot be replaced by other serum-induced factors.
- CREB binding protein is essential for keeping c-myc in a repressed state in G(1) and thereby preventing inappropriate entry of cells into S phase.
- c-Myc antagonized the induction of p21Cip1 mediated by oncogenic H-, K-, and N-Ras and by constitutively activated Raf and ERK2
- chromosomal c-myc replicator activity can be altered by transcription factors that induce transcription
- Myc stimulates VEGF production by a rapamycin- and LY294002-sensitive pathway.
- LMP1 activates telomerase via c-myc
- c-myc expression is regulated by TFIIH using an expanded proximal promoter
- the increased affinity for the duplex state due to mutation in the nuclease hypersensitive element could play a functional role in the aberrant regulation of c-myc
- c-myc and mad1 can regulate the hTERT transcript in a different manner in hTERT positive cells, but not in normal cells
- the entire N and C-terminal regions of c-Myc transactivation domain act in concert to achieve high specificity and affinity to two structurally and functionally orthogonal target proteins
- Tyrosine residues become phosphorylated following receptor engagement and, as such, form two Grb2 binding sites, which have been proposed to be differentially coupled to Myc-dependent survival.
- This paper reports the first solution structure of a G-quadruplex found to form in the promoter region of an oncogene (c-MYC).
- frequency and chromosomal features of this der(8)t(8;14;18) in a series of acute leukaemias and malignant lymphomas
- c-Myc coordinates the activity of all three nuclear RNA polymerases, and thereby plays a key role in regulating ribosome biogenesis and cell growth
- stimulation of rRNA synthesis by c-Myc is a key pathway driving cell growth and tumorigenesis
- Stimulation of islet expression by 30 mmol/l glucose results from activation of a distinct, probably oxidative-stress-dependent signalling pathway.
- c-Myc has a pivotal function in the development of breast cancer; data show that decreasing the c-Myc protein level in MCF-7 cells by RNAi could significantly inhibit tumor growth both in vitro and in vivo
- c-MYC amplification is an early event in breast cancer progression, while ZNF217 and Her2/neu amplification may play a role in the later stage of tumor development
- expression of ESRA, bcl-2 and c-myc gene expression in fibroadenomas and adjacent normal breast is related to nodule size, hormonal and reproductive features
- observed, subsequent to knocking down CRD-BP/IMP1, decreased c-myc expression, increased IGF-II mRNA levels, and reduced cell proliferation rates
- p16(INK4A) reconstitution in p16(INK4A)-deficient T-ALL cells induced cell cycle arrest in the presence of cyclin E and c-Myc expression, uncoupled growth from cell cycle progression and caused a sequential process of growth, differentiation and apoptosi
- elevated levels of Myc counteract p53 activity in human tumor cells.This mechanism could contribute to explain the c-Myc deregulation frequently found in cancer
- chromatin remodeling at the c-myc gene involves the local exchange of histone H2A.Z
- the c-MYC gene is sufficient to induce carcinogenesis for prostate cancer
- c-Myc activates expression of a cluster of six miRNAs on human chromosome 13
- results are consistent with the possibility that IL-5 inhibits apoptosis in JYTF-1 cells via the upregulation of c-myc expression
- The presence of activated beta-catenin and c-myc in the epidermis of chronic wounds may serve as a molecular marker of impaired healing
- conclude that alterations of the CMYC gene, including copy number gains and amplifications, are linked to genetically unstable bladder cancers that are characterized by a high histologic grade and/or invasive growth
- A pivotal role for Myc in regulating mitochondrial biogenesis was shown.
- tumor-specific isoforms of Bin1 are precluded from interaction with c-Myc through an intramolecular polyproline-SH3 domain interaction. Furthermore, c-Myc/Bin1 interaction can be inhibited by phosphorylation of c-Myc at Ser62.
- c-Myc overexpression showed an upregulation of beta4 promoter activity
- Kinetic analysis of the interconversion between the duplex and the quadruplex forms of the human c-myc promoter.
- mutant MYC proteins, by selectively disabling a p53-independent pathway, enable tumour cells to evade p53 action during lymphomagenesis
- p53 represses c-myc transcription through a mechanism that involves histone deacetylation
- 17-beta-estradiol promotes survival signals in breast cancer cells through mammalian target of rapamycin-dependent increase in Myc expression
- MYC family genes might affect oncogenesis through distinct sets of targets, in particular implicating the importance of transcriptional repression
- p300 can acetylate DNA-bound Myc:Max complexes and that acetylated Myc:Max heterodimers efficiently interact with Miz-1
- The MYC protein phosphorylation and turnover are thus linked to cell cycle exit in primary mouse CGNP cultures and the developing cerebellum.
- replicative senescence-specific factors may block c-Myc inhibition of Miz-1 activation of hMad4 expression, and the continual presence of hMad4 protein may transcriptionally repress selected c-Myc target genes
- Increased wild-type MYC expression occurs frequently in human cancers, except in Burkitt's lymphoma.
- c-MYC binds to the genomic MTA1 locus and recruits transcriptional coactivators, which is essential for the transformation potential of c-MYC.
- transcription activity is repressed by various MM-1 isoforms
- expression of cyclin D1 and c-Myc in epithelial ovarian cancer reaffirms the notion that they are crucial components in the pathway of tumorigenesis
- data demonstrate that the sphingosine-recycling pathway for the generation of endogenous long-chain ceramide in response to exogenous C6-cer is regulated by ROS, and plays an important biological role in controlling c-Myc function
- Myc induces nuclear encoded mitochondrial gene expression and mitochondrial biogenesis, thereby directly linking Myc's transcriptional properties to mitochondrial ROS production, promotion of genomic oxidative damage, and genomic instability.
- These results identify glycogen synthase kinase 3beta and FBW7 as potential cancer therapeutic targets and MYC as a critical substrate in the GSK3beta survival-signaling pathway.
- c-Myc isoforms differentially regulate cell growth and apoptosis in a species-specific manner
- Site-specific ubiquitination regulates the switch between an activating and a repressive state of the Myc protein, and they suggest a strategy to interfere with Myc function in vivo.
- dual roles for p300-CBP-associated factor in Myc regulation: as a Myc coactivator that stabilizes Myc and as an inducer of Myc instability via direct Myc acetylation
- decreased internal ribosome entry site (IRES)-dependent Myc mRNA translation accounts for the phenotypic changes induced by inhibition of the BCR/ABL-ERK-dependent HNRPK translation-regulatory function.
- C-myc expression shows a positive association with increasing grade of breast carcinoma.
- 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.
- up-regulation of mitochondrial CLIC4, together with a reduction in Bcl-2 and Bcl-xL, sensitizes Myc-expressing cells to the proapoptotic action of Bax.
- Down-regulation of MYC is not necessary to abolish malignant phenotypes by induction of terminal monocyte-macrophage differentiation in leukaemic cells carrying t(9;11)(p22;q23).
- Miz-1 is essential for Myc-mediated apoptosis
- interferon-gamma, which induces HLA-DR antigens on the cell surface, also suppresses c-myc expression in situ, and is a possible non-immunological mechanism involved in the better long-term survival of colorectal cancer patients
- Data show that hepatitis B virus X protein blocks the ubiquitination of c-myc through a direct interaction with the F box region of Skp2 and destabilization of the SCF(Skp2) complex.
- dominant-negative forms of c-Myc block transformation by activated Notch1, E6 and E7, suggesting that c-Myc is required for HPV16-mediated transformation
- study shows that p14ARF directly associates with Myc and relocates Myc from the nucleoplasm to the nucleolus, in addition, p14ARF down regulates Myc activated transcription
- overexpression of c-myc protects melanoma cells from IFN-beta-mediated growth inhibition
- PEG10 is a direct target of c-MYC; findings link cancer genetics and epigenetics by showing that a classic proto-oncogene, MYC, acts directly upstream of a proliferation-positive imprinted gene, PEG10
- c-myc seems to play a causal role in inducing anaplasia in medulloblastoma; it is proposed that c-myc dysregulation is involved in the progression of these malignant embryonal neoplasms
- 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
- Modifications in iron metabolism, resulting from the strong basal expression of c-Myc, and amplified by iron addition, could lead to a disruption in homeostasis and consequently to growth arrest in Burkitt's lymphoma.
- abnormal expression of REST/NRSF and MYC in undifferentiated neural stem/progenitor cells causes cerebellum-specific tumors. Furthermore, these results suggest that such a mechanism plays a role in the formation of human medulloblastoma.
- Positive C-MYC staining is detected mainly in the cytoplasm of esophageal cancer cells.
- These findings provide a molecular basis for increased TFRC1 expression in human tumors, illuminate the role of TFRC1 in the c-Myc target gene network
- p16(INK4a) expression was regulated by the Polycomb group repressor Bmi-1, which is shown as a direct transcriptional target of c-Myc.
- Doubling the hMYC level by breeding homozygous transgenic animals switched the phenotype from primarily monocytic tumors to exclusively T-cell tumors. Results imply that MYC level affects the spontaneous acquisition of synergistic oncogenic mutations.
- In both Richter's transformation and prolymphocytic transformation, high-levels of AID mRNA expression and high-frequency mutations of c-MYC genes were detected.
- there is an alternative mechanism for the hypoxic induction of VEGF in colon cancer that does not depend upon HIF-1alpha but instead requires the activation of PI3K/Rho/ROCK and c-Myc
- Results showed that certain regulation involved in c-myc, c-fos, and c-jun was present in the apoptosis, and the c-Myc dependent-on and Jun N-terminal kinase (JNK) pathway also play roles.
- Bcl2, in addition to its survival function, may also suppress DNA repair in a novel mechanism involving c-Myc and APE1, which may lead to an accumulation of DNA damage in living cells, genetic instability, and tumorigenesis
- Taken together, these findings suggest that Bax and caspase activation, together with PKCdelta signaling are involved in c-Myc-dependent etoposide-induced apoptosis.
- Myc and E2F1 engage the ATM signaling pathway to activate p53 and induce apoptosis [review]
- These data suggest that an increase in c-Myc phosphorylation in response to prolonged ERK phosphorylation negatively auto-regulates c-Myc gene expression, leading to the suppression of its target gene expression and cell cycle block.
- Results describe the roles of the FarUpStream Element (FUSE), FUSE Binding Protein (FBP), FBP Interacting Repressor (FIR), and TFIIH in the regulation of c-myc expression.
- APL-like case lacking t(15;17) and the retinoic acid receptor alpha (RARA) breakpoint and also has the deletion MYC of 8q24 associated with the occurrence of MYC amplification on double-minute chromosomes (dmin).
- Results show that the CT-element is not especially susceptible to the formation of breakpoints leading to chromosomal translocations in Burkitt's lymphoma.
- MYC activation, triggered by the insertion of human papillomavirus DNA sequences, can be an important genetic event in cervical oncogenesis.
- 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
- p21Cip1 is one of the direct mediators of induced c-Myc following increased polyamines and that p21Cip1 repression by c-Myc is implicated in stimulation of normal intestinal epithelial cell proliferation
- This study provides the first evidence for regulation of global chromatin structure by an oncoprotein and may explain the broad effects of Myc on cell behavior and tumorigenesis.
- TGFbeta suppresses TERT by Smad3 interactions with c-Myc and the hTERT gene
- c-Myc is only required for pre-TCR-induced proliferation but is dispensable for developmental progression from the DN to the DP stage
- Having an S allele in the L-myc gene may increase the risk of renal failure.
- proteins implicated in replication initiation are selectively and differentially bound across the c-myc replicator, dependent on discrete structural elements in DNA or chromatin
- Ras and c-Myc play important roles in the up-regulation of nucleophosmin/B23 during proliferation of cells associated with a high degree of malignancy, thus outlining a signaling cascade involving these factors in the cancer cells.
- Together, these results demonstrate that ectopic activation of NFATc1 and the Ca2+/calcineurin signaling pathway is an important mechanism of oncogenic c-myc activation in pancreatic cancer.
- Ketogenesis is an undesirable metabolic characteristic of the proliferating cell, which is down-regulated through c-Myc-mediated repression of the key metabolic gene HMGCS2.
- Functional promoter analyses revealed that both the Myc-binding site cluster and the C/EBPalpha-binding site are essential for strong transcriptional activation, and that Myc and C/EBPalpha synergistically activate the WS5 promoter
- c-myc and VEGFA may be involved in the regulation of angiogenesis in esophageal adenocarcinoma
- provide a mechanism for elevated Myc expression in hormone-dependent and hormone-independent breast cancer
- Epstein-Barr virus (EBV) acts as an antiapoptotic in Burkitt lymphoma (BL) by selecting among three transcriptional programs, all of which, unlike the full virus growth-transforming program, remain compatible with high c-myc expression.
- Several genes in the MYCN amplicon, including the DEAD box polypeptide 1 (DDX1) gene, and neuroblastoma-amplified gene (NAG gene), have been found to be frequently co-amplified with MYCN in NB.
- Nuclear arrangement of c-myc genes and transcripts was conserved during cell differentiation and, therefore, independent of the level of differentiation-specific c-myc gene expression.
- NDRG2 expression is repressed by Myc via Miz-1-dependent interaction with the NDRG2 core promoter
- Fluorescent protocol can successfully be applied to diagnostic needle biopsies to identify relative 8q gain in prostate carcinomas and that patients with a MYC/CEP18 ratio > or = 1.5 present a significantly higher risk of dying from the disease.
- repression of BCL2 transcription is the single essential consequence of targeting the MIZ-1 pathway during apoptosis induction, which explains a copperative interaction between c-MYC and BCL2
- Max as a novel co-activator of C/EBPalpha functions, thereby suggesting a possible link between C/EBPalpha and Myc-Max-Mad network.
- Results provide a snapshot of genome-wide, unbiased characterization of direct Myc binding targets in a model of human B lymphoid tumor using ChIP coupled with pair-end ditag sequencing analysis (ChIP-PET).
- identify c-MYC as an essential mediator of NOTCH1 signaling and integrate NOTCH1 activation with oncogenic signaling pathways upstream of c-MYC
- FOXM1c transactivates the human c-myc P1 and P2 promoters synergistically with Sp1, a transcription factor known to bind and transactivate these two promoters
- The c-Myc oncogene expression was very low in normal and cancer tissues but highly increased in papillomatosis.
- E-cadherin repression is necessary for c-Myc-induced cell transformation.
- establish PML-mediated destabilization of Myc and the derepression of cell cycle inhibitor genes as an important regulatory mechanism that allows cell differentiation
- Our data suggest that Mel-18 regulates Bmi-1 expression during senescence via down-regulation of c-Myc.
- MYC amplification is not associated with "basal-like" phenotype and proved to be an independent prognostic factor for breast cancer patients treated with anthracycline-based chemotherapy.
- c-MYC functions are cellular-context-dependent and selectively regulated genes are responsible for its differential properties.
- indicate a role for c-myc in the transcriptional regulation of survivin in breast cancer
- Genes with both c-Myc-and sp1-binding sites have a distinct expression signature when compared to genes with either site alone.
- c-Myc-dependent priming of the mitochondrial pathway is critical for the capacity of TRAIL-induced caspase-8 signals to activate effector caspases and for the establishment of lethal caspase feedback amplification loop in human cells.
- oncogenic deregulation of c-MYC prevents repair of replication-stress induced DNA lesions in G(2)-phase; suggests c-MYC-mediated persistence of DNA lesions during mitosis leads to chromosomal missegregation & underlies c-MYC-induced chromosome instabilit
- The KSHV latency-associated nuclear antigen is responsible for c-myc deregulation by inihibiting glycogen synthase kinase-3beta-mediated phosphorylation of c-Myc threonine 58.
- The effect of gamma-secretase inhibitor on the mTOR pathway was rescued by expression of c-Myc, a direct transcriptional target of Notch, implicating c-Myc as an intermediary between Notch and mTOR
- Subcellular localization of c-Myc and P-c-Myc is not crucial in determining the mode of cell death in prostate carcinoma cell lines.
- Notch1 mediates T cell and epithelial cell transformation at least in part by sustaining c-Myc levels.
- propose that the non-incidental coamplification of Myc and either ERBB2 or EGFR occurred through translocation and subsequent rearrangement
- observations raise the possibility that unscheduled replication origin activation at inserted HPV-18 viral DNA sequences triggers DNA amplification in this cancer cell line and the subsequent overexpression of the MYC oncogene
- VPA downregulated c-Myc expression at transcriptional levels.
- These results provide evidence of direct regulation of Mxi1 by FOXO3a and imply an additional mechanism through which the PI3-kinase/Akt/FOXO pathway can modulate Myc function.
- inhibition of beta-catenin and in effect c-myc expression through activation of PPARgamma may help prostate cancer cells to restore several characteristics of normal prostate cells phenotype
- This study demonstrates that the two consensus Lef/Tcf binding elements (TBE)reported in neoplastic cells are dispensable for c-Myc regulation in normal keratinocytes, which instead use a novel TBE sequence variant.
- repression of c-myc modulates HIF-1 inhibition of mitochondrial biogenesis and cellular respiration
- DKK1 and SFRP1 inhibit the transformed phenotype of breast cancer cell lines, and DKK1 inhibits tumor formation.
- Competitive binding of AUF1 and TIAR to MYC mRNA controls its translation.
- Data indicate that PVT-1 expression is restricted to a low number of normal tissues compared to c-Myc mRNA, whereas the gene is highly expressed in many transformed cell types including neuroblastoma cells that do not express c-Myc.
- Differential repression of c-myc and cdc2 gene expression by ERF and PE-1/METS.
- there was a highly significant correlation between breakpoints 5' of MYC cluster 1 and fusions to IGH switch gamma region and breakpoints downstream of MYC cluster 2 and fusions to IGH switch alpha region in spoadic Burkitt's lymphoma
- High expression levels of USP28 are found in colon and breast carcinomas, and stabilization of MYC by USP28 is essential for tumour-cell proliferation.
- c-myc gene expression may be regulated by intranuclear localization of its RNA
- While cMyc-Asp11Ser can be considered a putatively functional polymorphism located in the N-terminal domain, it is not associated with breast cancer risk, tumor characteristics or survival.
- Rac1 activates proliferation of normal fibroblasts through stimulation of c-myc phosphorylation without affecting ERK1/2 activity
- C-myc gene had the same location chromosome 8 in pluripotent and in differentiated human embryonic stem cells
- Amplification of the c-myc proto-oncogene occurs in hepatocellular carcinoma(HCC) and colorectal adenocarcinoma(MCA); its detection may have a useful diagnostic significance in differentiating intrahepatic cholangiocarcinoma(ICC)from MCA or HCC from ICC.
- findings identify a critical function of c-Myc in DNA replication and suggest a novel mechanism for its normal and oncogenic functions
- These results identify L11 as a feedback inhibitor of c-Myc and suggest a novel role for L11 in regulating c-Myc-enhanced ribosomal biogenesis.
- Deficiency in glutamine but not glucose induces MYC-dependent apoptosis in human cells.
- interphase Fish on samples from 30 MCL patients revealed 8 numerical c-myc-aberrations and 6 delp16
- 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.
- atorvastatin, by inhibiting HMGcoA reductase, induces changes in phosphoprotein signaling that in turn prevent MYC-induced lymphomagenesis
- Kaposi's sarcoma-associated herpesvirus latency-associated nuclear antigen stabilizes c-Myc.
- Results establish a new function for PIM1 as a MYC cofactor that phosphorylates the chromatin at MYC-target loci and suggest that nucleosome phosphorylation, at E boxes, contributes to MYC-dependent transcriptional activation and cellular transformation.
- Both MYC amplification and TERT expression appear to be associated with high genomic instability and proliferation.
- Myc, Sp1, and HDAC1 coexist in the same DNA-protein complex at the HIV promoter. Short hairpin RNA inhibition of c-Myc reduces both c-Myc and HDAC1 occupancy, blocks c-Myc repression of Tat activation, and increases LTR expression.
- the tumorigenic growth effects of MYC in TGFalpha-expressing liver progenitor cells are not solely dependent on its apoptotic activity.
- Erf provides a direct link between the RAS/ERK signaling and the transcriptional regulation of c-Myc and suggests that RAS/ERK attenuation actively regulates cell fate
- levels of c-myc expression were up-regulated and those of p53 expression were down-regulated by HCV F protein.
- A truncated form of N-Myc wild type can fully rescue the proliferation defect in myc-null fibroblasts, but rescue is dependent on the highly conserved Myc homology box II.
- blockage of terminal differentiation upon arsenic trioxide treatment may be mediated through c-Myc.
- This review proposes that a positive feedback loop of c-myc and Wnt signaling operates in breast cancer.
- These findings indicate that vIRF-3 can effectively stimulate c-Myc function in primary effusion lymphoma cells and consequently contribute to de-regulation of B-cell growth and differentiation.
- These results suggest that c-Myc may be involved in the regulation of telomere length through its direct binding with TRF1/PIN2.
- Suppression of oncogenic properties of c-Myc by LKB1-controlled epithelial organization.
- Review describes a microRNA cluster induced by oncogenic transcription factor c-myc that is implicated in inhibiting proliferation, as well as inhibiting apoptosis and promoting angiogenesis.
- HIF-1 cooperates with dysregulated c-Myc to promote glycolysis by induction of hexokinase 2 and pyruvate dehydrogenase kinase 1.
- Various nucleotide substitutions in the wild-type sequence from the c-MYC nuclease-sensitive element were ranked for their effects on transcription, the results implicated the triplex structure in the transcription arrest.
- These data indicate that DKC1 is a direct and conserved transcriptional target of c-MYC, and suggest a biologic basis for DKC1 overexpression in neoplasia.
- Usp28 dissociates from Fbw7alpha in response to UV irradiation, providing a mechanism how Fbw7-mediated degradation of Myc is enhanced upon DNA damage.
- ZO-2 down-regulates cyclin D1 transcription by interacting with the c-Myc/E box element and by recruiting histone deacetylase 1
- c-Myc activates DR4 transcription through E-box DNA-response elements located in the DR4 promoter, thereby increasing the expression of cell-surface pro-apoptotic death receptors in TRAIL-resistant cell lines
- Results suggest a general model by which a proliferation factor (c-Myc) and a differentiation factor (HNF4alpha1) may compete for control of genes involved in cell proliferation and differentiation.
- MYC and PVT1 contribute independently to ovarian and breast pathogenesis when overexpressed because of genomic abnormalities
- Myc down-regulation is a mechanism to activate the Rb pathway in STAT5A-induced senescence
- c-Myc oncoprotein deregulation is associated with overall genomic instability and its levels were a measure of progression in premalignant cervical lesion.
- Thus the c-myc P2E behaves as a dual-purpose STAT3 element with anomalous characteristics in HepG2 cells.
- synergistic effect of MYC and BCL6 mutations could explain the survival and clonal selection of a t(3;8) carrying cell in lymphoma progression
- The PKB-dependent mechanism of insulin-stimulated c-Myc expression in HT29 cells was shown to involve the activation of mTOR in c-Myc translation
- Diffuse large B-cell lymphomas (DLBCL) with concurrent t(14;18) and 8q24/c-MYC rearrangement is a subgroup of germinal center-DLBCLwith poor outcome
- BP1 may regulate bcl-2 and c-myc expression
- Expression of Ets-2, SRC-1 and c-Myc individually are all associated with reduced disease-free survival in breast cancer
- cooperative role for c-Met and c-Myc in large-cell anaplastic medulloblastoma formation
- Through the analysis of human and mouse models of B cell lymphoma, study shows here that Myc regulates a much broader set of miRNAs than previously anticipated.
- Functional link between MYC and hTERT seems to be impaired depending on the molecular essential thrombocytthemia subtype.
- Id2 commonly is overexpressed in highly proliferative T-cell lymphomas, and its expression may result from transcriptional activation of myc in these tumors.
- The c-myc translocation is likely crucial to the pathogenesis of the peripheral B-cell lymphoblastic lymphoma.
- Using ectopic expression of Oct4, Sox2, Klf4 and Myc, we have derived iPS cells from fetal, neonatal and adult human primary cells
- variation at putative 8q24 cis-regulator(s) of transcription can significantly alter germline c-MYC expression levels and, thus, contribute to prostate cancer susceptibility by down-regulating the prostate tumor suppressor KLF6 gene.
- These data suggest that TLR3 contributes to the malignant phenotype leading to invasive carcinoma in head and neck squamous cell carcinoma.
- The established renal cell carcinoma consist of two cell populations, one containing four and one containing five copies of the MYC oncogene.
- Downregulation of c-Myc is critical for 2ME2-induced oxidative stress and apoptosis in AML cells.
- expression of the Myc and Pim proto-oncogenes by Jak2V617F was found to be FERM domain dependent.
- bortezomib down-regulation of PRDM1beta preceded decreased IRF4 and c-MYC expression
- 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.
- By misdirecting the activity of Activation-Induced Deaminase (AID) to a conditional MYC transgene, sporadic, AID-dependent MYC activation in germinal center B cells of Vk*MYC mice, is achieved.
- Data demonstrate that c-myc can block myeloid cell differentiation independent of the apoptotic response.
- Epstein-Barr virus EBNA3C residues 130 to 190, previously shown to bind to the SCFSkp2 complex, also can strongly associate with the c-Myc oncoprotein.
- [review]
- MYC alteration is observed in the beginning of gastric carcinogenesis and could be used as a therapeutic target.
- MYC can stimulate epidermal stem cells to differentiate [perspective]
- three cases of FL are described in which both t(14;18) and a C-MYC translocation were identified at presentation, that may identify a particularly aggressive subtype of FL
- Overexpression of Myc stimulated sebocyte differentiation, whereas overexpression of beta-catenin stimulated involucrin and cornifin expression.
- c-Myc inhibited Ras-mediated differentiation by a mechanism that involves the blockade of c-Jun induction in response to Ras signal.
- C-myc RNA signals were positioned in the most internal parts of the cell nuclei preferentially associated with the nucleoli.
- Damaging exercise induced the expression of capZalpha, MCIP1, CARP1, DNAJB2, c-myc, and junD, each of which are likely involved in skeletal muscle growth, remodeling, and stress management.
- ). Nicotinamide and nicotinamide N-oxide drastically decreased c-myc expression, but isonicotinic acid had no effect, suggesting that these compounds differentiate HL-60 to granulocytes through different pathways
- Myc is required to allow the interaction of the E2F1 protein with the E2F gene promoters.
- 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.
- variations in c-myc and p21(WAF1) expression delay apoptosis making PBL resistant to sodium butyrate for several hours
- The (rs13254738) variant of 8q24 has a protective effect for breast cancer.
- Pyk2/ERK 1/2 mediate Sp1- and c-Myc-dependent induction of telomerase activity by epidermal growth factor
- c-MYC plays a role in the early tumorigenesis of astrocytomas.
- Although knockdown of c-Myc or caspase-2 does not affect Bax expression, caspase-2 is important for cytosolic Bax to integrate into the outer mitochondrial membrane, and c-Myc is critical for oligomerization of Bax once integrated into the membrane
- MYC rearrangements are associated with both hyperdiploid and nonhyperdiploid myeloma tumors.
- EBV is not related to the overexpression of Bcl-2 and c-Myc (nuclear) in gastric carcinomas.
- The inhibition of FOXO3a-mediated activation of the p27 gene by the high aberrant expression of c-Myc in many tumor cells likely contributes to their uncontrolled proliferation and invasive phenotype.
- MM-1, a c-Myc interacting protein, interacts with HCV ARFP/F protein, which can result in the enhancement of the c-Myc activity.
- Cdk5 activation in cells that overexpress cyclin G1 leads to c-Myc phosphorylation on Ser-62, which is responsible for cyclin G1-mediated transcriptional activation of cyclin B1.
- These findings establish that Myc, via p400, is an essential downstream target of adenovirus E1A.
- the downregulation of c-Myc mediated by silencing DNA-PKcs
- we found a substantial number of primary diffuse large B-cell lymphomas (DLBCLs) of bone cases with a rearrangement of BCL2 and c -MYC
- hBD-1 expression is mediated by c-Myc and the CLOCK:BMAL1 heterodimer, whereas CRY1 expression represses this complex.
- This study provides a direct link between the growth factor signaling pathways regulated by PI3 kinase/Akt and MAP kinases with Myc-mediated transcription.
- These results suggest a heterogeneous immunophenotype and genotype for c-myc/Ig DLBCL, with CD10(-)/BCL6(+)/MUM1(-) cases the most frequent.
- There was a significant association between an intronic SNP in c-myc and prostate cancer.
- These results indicate that the activated Notch1 receptor and alpha-enolase or MBP-1 cooperate in controlling c-myc expression through binding the YY1 response element of the c-myc promoter to regulate tumorigenesis.
- Continued expression of c-Myc is necessary for maintenance of the growth state in cells expressing FRAT1, implying that c-Myc may be a critical element in oncogenesis induced by FRAT1.
- MYC inactivation induced global permanent changes in gene expression detected by microarray analysis in murine tumor models and human lymphomas.
- C-terminal region of p300 provides corepressor function and facilitates the recruitment of p300 and HDAC3 to the YY1-binding site and represses the c-Myc promoter.
- c-Myc regulates calpain activity through calpastatin; apoptosis induced by calpain inhibition is dependent on c-Myc, and calpastatin knockdown promotes transformation in c-Myc-negative cells
- Study shows that the poly(A) tail enhances 48S complex assembly by the c-myc internal ribosome entry sequences.
- Gains (3-4 copies) of 8q24 (c-myc) were found in the low frequencies in nondysplastic Barrett's esophagus. Frequency increased with stage of dysplasia and reached a high incidence in esophageal adenocarcinoma.
- hnRNP A1 has a role in mediating rapamycin-induced alterations of cyclin D1 and c-myc IRES activity in an Akt-dependent manner and provide the first direct link between Akt and the regulation of IRES activity
- Upregulation of nuclear MYC protein expression is a highly prevalent and early change in prostate cancer; increased nuclear MYC may be a critical oncogenic event driving human prostate cancer initiation and progression.
- hTERT gene expression is maintained by a mechanism involving Ets2 interactions with the c-Myc transcription factor and the hTERT gene promoter, a protein-DNA complex critical for hTERT gene expression and breast cancer cell proliferation.
- MYC, LDHB, and CCNB1 may have roles in progression of medulloblastoma
- Elevated c-myc expression in GFs by thrombin was noted after 2 hours of exposure. Moreover, the stimulation of c-myc mRNA expression by thrombin can be attenuated by D-Phe-Pro-ArgCH(2)Cl, a serine-proteinase inhibitor.
- rapamycin limited expression of c-MYC by inhibiting c-Myc mRNA translation
- endothelin-1, via Src/PI-3K signaling, augments c-myc expression leading to enhanced androgen receptor expression in prostate cancer
- Coamplification of HER2 and MYC occurs in a subset of patients with metastatic UCC
- analysis of the induction of nucleotide metabolic genes by c-Myc in multiple system
- a circuit involving c-myc, miR-17-92, and HIF-1 alpha may play a role in cancer cell proliferation under normoxia in a cellular context-dependent manner
- MYC translocations are associated with multiple myeloma
- A novel functional link between C-MYC and dNTP metabolism and identify its role in proliferation of tumor cells.
- one of the major functions of C-MYC overexpression in melanoma progression is to continuous suppress BRAF(V600E)- or NRAS(Q61R)-dependent senescence programs
- MYC stimulates EZH2 expression by repression of its negative regulator miR-26a
- Since expression of c-Myc in antiestrogen-arrested cells can recapitulate many of the effects related to cell cycle progression, the estrogen-regulated genes that are targets of c-Myc are identified using cells inducibly expressing c-Myc in breast cancer
- E2F1 may function as a critical antiapoptotic factor both in human and in rodent liver cancer through its ability to counteract c-Myc-driven apoptosis via activation of PIK3CA/Akt/mTOR and c-Myb/COX-2 pathways
- Translocation is more common in germinal centre-like B (GCB) cell type of adult diffuse large B-cell lymphoma than in non-GCB type, and associated with advanced disease.
- the presence of a MYC gene rearrangement was the strongest statistically independent predictor of OS (relative risk 3.4, P=0.004) and EFS (relative risk 2.5, P=0.015)
- ectopic expression of C/EBPepsilon, as well as C/EBPalpha, can induce the monocytic differentiation of myelomonocytic leukemic cells with MLL-fusion gene through the downregulation of Myc
- show that differential overexpression of Myc transcriptional targets and low expression of genes involved in sympathetic neuronal differentiation predicts relapse and death from disease
- integration of mtDNA into the nuclei of cervical epithelium cells may be involved in the carcinogenesis of cervical epithelium cells and the expression of c-myc might be related to the integration of mtDNA sequence into nuclei of cervical epithelium cell
- c-Myc expression may be useful in predicting tumor recurrence in patients with low-grade meningiomas
- The role of the MYC protooncogene in clear cell renal cell carcinoma.
- MYCN may limit cell adhesion to the extracellular matrix and promote cell migration by downregulating integrin alpha1
- 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.
- c-MYC directly regulates the expression of AP4 via CACGTG motifs in the first intron of the AP4 gene.
- requirement for Myc in the induction of the hTERT promoter by E6 and suggested that occupancy of the promoter by Myc determines the responsiveness of E6 and the downstream induction of telomerase and cell immortalization.
- Data show that activation of Myc inhibited p27-mediated erythroid differentiation without affecting p27-mediated proliferation arrest.
- Results indicate that association of c-Jun, TCF$, and beta-catenin with a downstream enhancer element provides the principal regulation of c-Myc expression.
- In the present review, we focus on the deregulation of the MYC oncogene in gastric adenocarcinoma carcinogenesis, including its association with Helicobacter pylori (H pylori) and clinical applications [review]
- EB1 is controlled by c-Myc, RhoA, and CDC42, which have all been linked to hepatocellular carcinoma (HCC) malignancy.
- The ability of Cdx1 and c-myc to initiate the earliest stages of transdifferentiation of esophageal keratinocytes toward a cell fate characteristic of Barrett's esophagus.
- Myc recruits the Tip60/p400 complex to achieve a coordinated histone acetylation/exchange reaction at activated promoters.
- the domains of GpIbalpha mediating c-Myc-like functions are modular, genetically distinct, and independent of those involved in vWFR signaling.
- c-Myc has a role in regulating proliferation and survival of glioma cancer stem cells
- Expression of the TAF4b gene is induced by MYC through a non-canonical, but not canonical, E-box which contributes to its specific response to MYC.
- These results indicate that c-MYC may promote transformation through the induction of HSP60 expression.
- c-Myc activity is required for growth and maturation of the exocrine pancreas.
- deregulation of c-MYC in lymphoma cells does not overcome the tumor suppressor function of TGF-beta and that repression of E2F-1 transcription is sufficient for the efficient induction of cytostasis.
- a mechanistic link between JNK activity and liver cell proliferation via p21 and c-Myc and suggest JNK1 targeting can be considered as a new therapeutic approach for HCC treatment.
- HIF-alpha effects on c-Myc distinguish two subtypes of sporadic VHL-deficient clear cell renal carcinoma
- analysis of Wnt/beta-catenin and Myc signaling in liver cancer
- c-Myc negatively regulates the expression of BRD7.
- a combinatorial regulatory program in which MYC cobinds to virtually all NOTCH1-bound promoters
- The group of patients with > 5-fold myc amplicon CN showed significantly shorter survival than those with < 5-fold CN (p = 0.045), independent of histological subtype.
- the regulation of c-Myc by Axin1 is impaired in several tested cancer cell lines with known stabilization of c-Myc or loss of Axin1.
- Down-regulation of c-MYC resulted in inhibition of cellular proliferation, clonogenic growth and cell cycle progression.
- Myc down-regulation in astrocytoma cells led to G1 accumulation and an inhibition of cell proliferation characterized by S phase delay
- Mechanisms of WIF1-induced G(1) arrest include (a) SKP2 down-regulation leading to p27/Kip1 accumulation and (b) c-myc down-regulation releasing p21/WAF1 transcription.