Browse our anti-C-MYC (MYC) Antibodies

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

1. Study shows that DEPTOR, a suppressor of mTOR, is a direct target of Wnt/beta-catenin/c-Myc signaling in colorectal cancer cells. Inhibition of Wnt/beta-catenin or knockdown of c-Myc decreased, while activation of Wnt/beta-catenin or overexpression of c-Myc increased the expression of DEPTOR. c-Myc bound the promoter of DEPTOR and transcriptionally regulated DEPTOR expression.

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

3. This study shows that IG-MYC (+) neoplasms with precursor B-cell phenotype show recurrent NRAS/KRAS mutations, lack of functional B-cell receptor, and IG-MYC translocations due to aberrant VDJ recombination.

4. miR-27a-5p is positively regulated by MYC, and its silencing due to aberrant promoter methylation occurs early in prostate carcinogenesis, concomitantly with loss of MYC regulatory activity.

5. circCDYL functions as a tumor suppressor in bladder cancer by down-regulating the expression of C-MYC

6. the synergistic effect is likely due to two reasons: (i) Plk1 inhibition results in the accumulation of beta-catenin in the nucleus, thus elevation of c-MYC expression, whereas JQ1 treatment directly suppresses c-MYC transcription; (ii) Plk1 and BRD4 dual inhibition acts synergistically in inhibition of AR signaling.

7. We demonstrate that inflammatory bowel disease-associated intestinal adenocarcinomas have a high frequency of c-MYC amplification that is associated with mucinous and signet ring cell differentiation.

8. Study reports that NME2 is an oncogene in osteosarcoma (OS) that is associated with its clinicopathologic features. Downregulation of NME2 could reduce the proliferation of OS cells and arrest the OS cell cycle in the G2/M phase. The deregulation of NME2 enhanced the expression of c-Myc and affected the proliferation of osteosarcoma.

9. MYC is a bona fide oncogene in a clinically significant group of high-risk childhood neuroblastomas.MYC is activated through either focal amplification of distal enhancers or enhancer hijacking mediated by chromosomal translocation.

10. The present results suggest that LSD1 is induced by c-Myc and forms a positive feedback mechanism in transcription reactions by c-Myc.

11. High expression levels of PLK1 and c-Myc were independent prognostic factors for diffuse large B-cell lymphoma.

12. Study using human ATRT cell lines, patient-derived cell culture, ex vivo patient-derived tumor, and orthotopic xenograft models shows that MYC occupies distinct promoter loci in atypical teratoid rhabdoid tumors (ATRT) compared to embryonic stem cells and suggests that SMARCB1 loss alters chromatin occupancy of MYC.

13. Human mesenchymal stem cells were transformed into osteosarcoma-like cells by Rb knockdown and c-Myc overexpression.

14. The association of single nucleotide polymorphisms across the 8q24 chromosome region (positioned at 127180736 and 127183014 near the small es, Cyrillic-MYC gene) with chronic lymphocytic leukemia risk was confirmed.

15. High MYC expression is associated with Choroid Plexus and Ciliary Body Tumors.

16. c-Myc and p53 are potential hepatocellular carcinoma (HCC) diagnostic biomarkers, and convenient combinations of them could improve diagnostic accuracy of HCC.

17. ANRIL acts as onco-lncRNA by regulation of microRNA-24/c-Myc, MEK/ERK and Wnt/beta-catenin pathway in retinoblastoma

18. Expression levels of PAX8AS1:28 and PAX8 were lower in papillary thyroid carcinoma (PTC) tissue and PTC cells than those in healthy tissue and cells. Expression level of MYC was higher in PTC cells than that in normal cells. PAX8AS1:28 silencing reduced the expression level of PAX8 and promoted tumor cell growth, while PAX8AS1:28 overexpression increased the expression level of PAX8 and inhibited tumor cell growth.

19. our findings suggest that the innate role of MYC-mediated cell competition in development is conserved in human cancer, with malignant cells using MYC activity to colonise the organ at the expense of less performant neighbours.

20. REVIEW: MYC and RAF--Key Effectors in Cellular Signaling and Major Drivers in Human Cancer

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

2. 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.

3. 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.

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

5. 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.

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

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

8. 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.

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

10. 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.

11. 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.

12. High myc is associated with tumourigenic transformation.

13. 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.

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

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

16. GATAD2B interacts with C-MYC to enhance KRAS driven tumor growth.

17. Kidney specific MYC activation results in papillary clear cell renal cell carcinoma.

18. c-Myc is essential for tumor initiation, maintenance, and metastasis.

19. Genomic characterization of Emu-Myc mouse lymphomas identifies Bcor as a Myc cooperative tumor-suppressor gene.

20. The data supports an indispensable role for Mule in cardiac homeostasis through the regulation of mitochondrial function via maintenance of Pgc-1alpha and Pink1 expression and persistent negative regulation of c-Myc.

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.