Browse our C-MYC Proteins (MYC)

Human V-Myc Myelocytomatosis Viral Oncogene Homolog (Avian) (MYC) interaction partners

1. High C-MYC expression is associated with non-small cell lung cancer.

2. C-MYC overexpression may contribute to PCa progression by activating SOX4. Findings highlight an important role of C-MYC/SOX4 in PCa progression in a subset of PCa patients.

3. Summary the coamplification of PVT1 and MYC in cancer, the positive feedback mechanism, and the latest promoter competition mechanism of PVT1 and MYC, as well as how PVT1 participates in the downstream signaling pathway of c-Myc by regulating key molecules.[review]

4. These results suggest that ROS generation and c-MYC suppression play important roles in tetrandrine-induced autophagy and differentiation, and the results from in vivo experiments were consistent with those from in vitro studies.

5. inhibition of PIM1 attenuates prostate tumor growth and migration by stabilizing c-Myc.

6. Long non-coding RNA LINC00310 promoted cell proliferation by regulating c-Myc expression in vitro.

7. MYC induced the expression of the tryptophan transporters SLC7A5 and SLC1A5 and the enzyme arylformamidase (AFMID), involved in the conversion of tryptophan into kynurenine.

8. These data individuate Che-1 as a possible novel target in the treatment of B-cell precursor acute lymphoblastic leukemia able to affect c-Myc-driven tumorigenicity.

9. PIM1-mediated phosphorylation of c-Myc activates the expression of the transcription factors to synergistically promote epithelial-mesenchymal transition.

10. we demonstrated that MYC recruited DNMT3A to the miR-200b promoter, resulting in proximal CpG island hypermethylation and subsequent miR-200b repression. MiR-200b directly inhibited DNMT3A expression and formed a feedback loop in Triple-negative breast cancer (TNBC) cells

11. TP53 mutations define a subset of ALK-translocated non-small cell lung carcinoma tumours with recurrent MYC amplication that harbour chromosomal instability, leading to the co-occurrence of pathogenic aberrations.

12. STAT3 activation and MYC expression were critical for the proliferation and survival of Aggressive NK-cell Leukemia cells.

13. Myc is functionally important target gene of METTL3 in bladder cancer.AFF4 directly regulates MYC gene expression.

14. Identify SETDB1 as a prominent oncogene in breast cancer. The c-MYC-BMI1 axis is essential for SETDB1-mediated breast tumourigenesis.

15. Data how that transcription factor myc (MYC) directly occupied the -11.7 kb and -0.35 kb regulatory regions in the microRNA 150 (MIR150) gene.

16. study uncover that the RING domain of XIAP supports c-Myc protein stability, providing insight into the molecular mechanism and role of c-Myc overexpression in cancer progression.

17. VWA2 might be a constituent of a larger oncogenic transcriptional program regulated by c-Myc.

18. results reveal a previously unappreciated mechanism in which the YY1/c-Myc/miR-141 axis plays a critical role in nasopharyngeal carcinoma (NPC) progression and may provide some potential and valuable targets for the diagnosis and treatment of NPC.

19. Using mass spectrometry of both MYC and Pol II complexes, we show here that MYC controls the assembly of Pol II with a small set of transcription elongation factors that includes SPT5, a subunit of the elongation factor DSIF. MYC directly binds SPT5, recruits SPT5 to promoters, and enables the CDK7-dependent transfer of SPT5 onto Pol II

20. G variant of rs6983267 single nucleotide polymorphism (SNP) in CCAT2 gene and MYC enhancer region functions as an independent risk factor for cervical squamous cell carcinoma (SCC). MYC transcript levels are increased in cancerous and normal tissue in carriers of GG polymorphism compared with carriers of TT polymorphism

Cow (Bovine) V-Myc Myelocytomatosis Viral Oncogene Homolog (Avian) (MYC) interaction partners

1. Ouabain-induced proliferation might be attributed, at least in part, to decrease of intracellular free calcium and increase of c-myc mRNA expression, and that may be directly or indirectly involved in regulation of blood pressure.

Rabbit V-Myc Myelocytomatosis Viral Oncogene Homolog (Avian) (MYC) interaction partners

1. report the isolation of complete coding regions of rabbit SOX2, KLF4, C-MYC and NANOG, which encode transcription factors that play crucial regulatory roles during early mammalian embryonic development

Mouse (Murine) V-Myc Myelocytomatosis Viral Oncogene Homolog (Avian) (MYC) interaction partners

1. cardiomyocytes compete according to their combined Myc and Mycn levels and that cell competition eliminates flawed cardiomyocytes, suggesting its relevance as a quality control mechanism in cardiac development.

2. Mouse medulloblastoma driven by CRISPR activation of cellular Myc.

3. the c-Myc/miR17-92/PTEN axis tunes PI3K activity to control the expression of RAGs in proB cells.

4. MYC proteins orchestrate a rewiring of somatic cell metabolism early in cell reprogramming.

5. These results suggest that MYC hijacks a major epigenetic pathway - H3K4 methylation - to facilitate its molecular activity in target binding and to coordinate its oncogenic program for efficient tumorigenesis, meanwhile creating "epigenetic vulnerability." DPY30 and the H3K4 methylation pathway are thus potential epigenetic targets for treating certain MYC-driven cancers.

6. A1 contributes to the survival of malignant Emicro-Myc-driven B lymphoid cells.

7. these results provide genetic evidence of YAP/TAZ as oncogenic initiators and drivers for gastric tumors with MYC as the key downstream mediator.

8. deleting Mettl3 from myeloid cells using Lysm-cre did not impact myeloid cell number or function. RNA sequencing revealed 2,073 genes with significant m(6)A modifications in HSCs. Myc was identified as a direct target of m(6)A in HSCs. Mettl3-deficient HSCs failed to upregulate MYC expression following stimulation to differentiate and enforced expression of Myc rescued differentiation defects of Mettl3-deficient HSCs.

9. data reveal a regulatory circuit involving Egr2-Id3-E2A, which normally restricts the population size of gammadelta NKT cells by adjusting Egr2 dosage and c-Myc expression.

10. c-Myc regulates both sebocyte proliferation and differentiation in sebaceous glands.

11. We also describe that B lymphocytes lacking Myc, Max, or both show upregulation of signaling pathways associated with the B-cell receptor. These data suggest that c-Myc/Max heterodimers are not essential for the initiation of a subset of important biological processes in B lymphocytes, but are required for fine-tuning the initial response after activation.

12. Reprogramming factors (Oct4, Sox2, Klf4, c-myc) induce proliferation and inhibit apoptosis of melanoma cells by changing the expression of particular genes.

13. These findings suggest Myc-nick as a novel proresolving mediator that has a fundamental function in maintaining homeostasis under inflammatory conditions

14. We propose Myc as a candidate susceptibility gene, regulated by the gene desert locus, and a potential role for Fam84b in modifying breast cancer development.

15. observed that Myc and ChREBP cooperatively up-regulated virtually all ribosomal protein genes

16. Across cell types Dppa4 shows a preference for binding to regions with active chromatin signatures, and can influence chromatin modifications at target genes. Data provide novel insights into Dppa4 function in both pluripotent and oncogenic contexts.

17. Sustained exposure of cells to TGF-beta resulted in recovery from proliferative arrest in association with amplification of the Myc proto-oncogene, with MYC inhibiting TRIM26 induction by TGF-beta.

18. High myc is associated with tumourigenic transformation.

19. Our results show that reprogramming is enhanced in MEFs deficient in BAK and BAX, but only when MYC is part of the reprogramming cocktail. Thus, the propensity for Myc overexpression to elicit apoptosis creates a significant roadblock to reprogramming under OKSM conditions.

20. These findings established a link between GCN5 and the FGF signaling pathway and highlighted specific GCN5-MYC partnerships in gene regulation during early differentiation.

Zebrafish V-Myc Myelocytomatosis Viral Oncogene Homolog (Avian) (MYC) interaction partners

1. Cxcl12 and Myc facilitate glycolysis to promote fast migratory responses during development and repair during kidney injury and development

2. Methylparabens exposure increased malformations, LPO, apoptosis, ccnd1 and myca expressions, and decreased GST activities and NO levels compared with the control group.

3. Apoptosis was also observed with myca expression; introduction of homozygous tp53(-/-) mutation into the myca transgenic fish reduced apoptosis and accelerated tumor progression.

4. MYC down-regulation induces mitochondrial apoptosis in T lymphoblasts.

Xenopus laevis V-Myc Myelocytomatosis Viral Oncogene Homolog (Avian) (MYC) interaction partners

1. These findings not only reveal a novel role of Mad1 in regulating developmental cell death but also suggest that a balance of Mad and Myc controls cell fate determination during adult organ development.

2. Thyroid hormone activates protein arginine methyltransferase 1 expression by directly inducing c-Myc transcription during Xenopus intestinal stem cell development.(

3. c-Myc has a direct role in the control of DNA replication

4. Findings support a model in which Myc, Twist and Slug/Snail2 function in a regulatory circuit within lateral plate mesoderm that directs normal vessel formation in both the vascular and lymphatic systems.

Fruit Fly (Drosophila melanogaster) V-Myc Myelocytomatosis Viral Oncogene Homolog (Avian) (MYC) interaction partners

1. findings reveal an evolutionarily conserved functional link between Myc, the Tip60 complex, and the molecular network controlling cell polarity and asymmetric cell division.

2. An ankyrin-binding motif regulates nuclear levels of L1-type neuroglian and expression of the oncogene Myc in Drosophila neurons.

3. tissue specific downregulation of dMyc (Drosophila homolog of human c-myc proto-oncogene) alleviates h-tau mediated cellular and functional deficits by restricting the formation of NFTs in neuronal tissues.

4. Expression of Drosophila Myc (dMyc) suppresses, whereas loss of dMyc enhances, ectopically activated JNK signaling-induced cell death. dMyc impedes physiologically activated JNK pathway-mediated cell death. Loss of dMyc triggers JNK pathway activation and JNK-dependent cell death.

5. tissue-specific downregulation of the Drosophila homolog of human c-myc proto-oncogene (dMyc) suppresses tau-mediated morphological and functional deficits by reducing abnormal tau hyperphosphorylation and restoring the heterochromatin loss.

6. dMyc has an essential role in preventing JNK-mediated retinal glial activation

7. the key target of the Psi/MED network in controlling developmentally regulated tissue growth is the transcription factor MYC.

8. Myc dosage plays crucial role in determining sex-specific size in Drosophila larvae and adult tissue. Double dose of Myc in females serves at least twice in development to promote sexual size dimorphism.

9. BicC down regulates Myc in the Malpighian tubule.

10. activation of the TOR-Myc axis in midgut stem and progenitor cells influences a variety of traits in Drosophila

11. Drosophila adult muscle precursors display homing behavior to muscle niche and the niche-driven Insulin-Notch-dMyc cascade plays a key role in setting the activated state of adult muscle precursors.

12. a functional link between Myc, a renowned oncogene, and the essential nucleotide biosynthetic enzyme CTPsyn.

13. MYC and S6K cooperate through coordinate activation of the essential Pol I transcription initiation factor TIF-1A.

14. The data demonstrate that dMYC repression and dMYC-dependent overgrowth in the Hfp hypomorph is further impaired in the C-terminal Hay/XPB mutant background.

15. Myc acts as a master regulator of small nucleolar ribonucleoprotein biogenesis.

16. In this review, we focus on studies of MYC in the fruitfly with particular emphasis on metabolism and cell competition, highlighting the contributions of this model system in the last decade to our understanding of MYC's complex biological nature

17. Review discussing competitive interactions that are regulated by cell-to-cell differences in MYC activity and their role in tumor formation.

18. Myc may act as a pro-aging factor, possibly through its ability to greatly increase genome instability

19. a basal level of dMyc expression is required for Intestinal stem cell maintenance, proliferation and lineage differentiation during normal tissue homeostasis.

20. These novel results give additional support for finding future approaches to specifically inhibit the growth of cancer cells addicted to oncogenic Myc.