Browse our anti-C-MYC (MYC) Antibodies

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

1. 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

2. hUTP14a interacts with c-Myc and protects c-Myc from ubiquitination and degradation in a USP36-dependent way.

3. MYC is a key regulator of autophagic memory in pathogenic T cells in human arthritis.

4. SUMO and MYC mediate opposite effects upon global transcription by controlling the level of CDK9 sumoylation.

5. evidence supports a role for Pygo2 as an essential component of MYC oncogenic activity required for mitosis.

6. study reveals a novel role for TSC1 in securing homeostasis between MYC and mTORC1 that is required for cell survival and tumor maintenance in Burkitt's lymphoma. The study identifies TSC1/2 inhibition and/or mTORC1 hyperactivation as a novel therapeutic strategy for MYC-driven cancers.

7. MYC promotes human iPSC generation primarily by facilitating the escape of an OCT3/4, SOX2, and KLF4 (OSK)-induced proliferation blockade in early reprogramming cells. It does this by repressing retinoblastoma protein (RB) rather than enhancing OSK binding, suppressing fibroblast-specific genes, or inducing metabolic changes.

8. Temporal dynamics of Wnt-dependent transcriptome reveal an oncogenic Wnt/MYC/ribosome axis.

9. inhibition of PLK1 triggered degradation of MYC and of the antiapoptotic protein MCL-1, and PLK1 inhibitors showed synergy with BCL-2 antagonists in blocking DHL cell growth, survival, and tumorigenicity, supporting clinical targeting of PLK1 in DHL.

10. MYC amplification in patient-derived glioblastoma stem-like cells (GSCs) generates sensitivity to PARPi via Myc-mediated transcriptional repression of CDK18.

11. these data establish the synthetic lethal interaction of the IRE1/XBP1 pathway with MYC hyperactivation and provide a potential therapy for MYC-driven human breast cancers.

12. Identify a high incidence of MYC rearrangements in Primary cutaneous diffuse large B-cell lymphoma, leg type compared to nodal diffuse large B-cell lymphoma.

13. Results show that c-Myc protein expression and transcriptional activity are upregulated by R1 which interacts with its NH2-terminal domain enhancing protein stability.

14. A total of 688 common DEGs were identified between survivors and non-survivors of sepsis, and 96 genes were involved in survival networks. The crucial genes Signal transducer and activator of transcription 5A (STAT5A), CCAAT/enhancer-binding protein beta (CEBPB), Myc proto-oncogene protein (MYC), and REL-associated protein (RELA) were identified and showed increased expression in sepsis survivors.

15. These data demonstrated that AXL promotes epirubicin resistance through transcriptional upregulation of c-MYC in esophageal adenocarcinoma cells.

16. Study identified ADREG5 as a MYC target gene able to discriminate between Burkitt lymphoma and diffuse large cell lymphoma (DLBCL) irrespectively of the presence of MYC breaks in DLBCL.

17. Authors observed that c-MYC regulates lncRNAs that have important roles on proliferation, cell cycle and etc. Further studies will give us a light to identify molecular mechanisms related to MYC-lncRNA regulatory pathways in breast cancer.

18. The processed SNHG15 is overexpressed in CRC tumors and its expression is highly correlated with poor survival of patients. Interestingly, SNHG15 is more highly expressed in tumors with high levels of MYC expression, while MYC protein binds to two E-box motifs on SNHG15 sequence, indicating that SNHG15 transcription is directly regulated by the oncogene MYC.

19. cMyc decreases pyruvate levels by promoting thyroid hormone-binding protein (PKM2) and lactate dehydrogenase A (LDHA) levels, consequently decreasing inhibition to histone deacetylase 3 (HDAC3) and protecting cancer cells from apoptosis.

20. The present study demonstrated that PRMT5 epigenetically silenced the expression of the tumor suppressor FBW7, leading to increased cMyc levels and the subsequent enhancement of the proliferation of and aerobic glycolysis in pancreatic cancer cells

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. Mouse medulloblastoma driven by CRISPR activation of cellular Myc.

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

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

4. 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.

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

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

7. 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.

8. 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.

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

10. 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.

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

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

13. 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.

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

15. 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.

16. 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.

17. High myc is associated with tumourigenic transformation.

18. 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.

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

20. amino acid-controlled cMyc has an essential role in NK cell metabolism and function

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.