Aperçu des produits pour C-MYC Protéines (MYC)

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

1. Results show that MYC expression and its targets in breast cancer is regulated by EPIC1.

2. ATT selectively destabilizes c-Myc in human cancer cells.

3. Case Reports: B lymphoblastic leukemia/lymphoma with Burkitt-like morphology and IGH/MYC rearrangement in which MYC translocation may be acquired at an immature stage of differentiation.

4. Translocations involving the 8q24 MYC locus more frequently manifest as t(6;8)(p21;q24), and, given its association with specific clinicopathological features suggesting even more aggressive behaviour, t(6;8)(p21;q24) indicate a genetically defined subgroup within blastic plasmacytoid dendritic cell neoplasm

5. In esophageal squamous cell carcinoma (ESCC) tissues, c-Myc expression was inversely correlated with NS1-binding protein (NS1-BP) levels, and was associated with a shorter disease-specific survival (DSS).

6. these findings identify c-Myc not only as being responsible for miRNA repression in Leishmania-infected macrophages but also as a novel and essential virulence factor by proxy that promotes Leishmania survival.

7. We demonstrate that VCP regulates many nuclear and chromatin-associated proteins and promotes the degradation and activity of the transcription factor c-Myc.

8. Whereas the frequency of MYC amplification was similar to adenocarcinoma (10.5% versus 4%, P = .2), the frequency of PTGER4 amplification was higher than adenocarcinoma (10.5% versus 0.3%, P = .01)

9. c-Myc expression is regulated by nitric oxide in the epidermal stem cells.FOXG1 induces transcriptional activity of the c-Myc gene promoter.

10. Genomewide ChIP-seq experiments suggest that Che-1 acts as a downstream effector of c-Myc. These results identify the pivotal role of Che-1 in the control of B-cell precursor acute lymphoblastic leukemia (BCP-ALL) proliferation and present the protein as a possible therapeutic target in children with relapsed BCP-ALL

11. Study demonstrated that the expression of EP4 receptors was up-regulated by c-Myc by binding to Sp-1 under low cellular density conditions but was down-regulated under high cellular density conditions via the increase in the expression levels of HIF-1alpha protein, which may pull out c-Myc and Sp-1 from DNA-binding.

12. Using isothermal calorimetry, the study found that Myc phosphorylation destabilizes this ternary protein-DNA complex by decreasing Myc's affinity for Max by 2 orders of magnitude, suggesting a major effect of phosphorylation on this complex.

13. Results showed that c-Myc mRNA expression levels of gastric cancer (GC) were higher in DDX6 up-regulated-GC clinical samples. Also, DDX6 associated with c-Myc mRNA. Moreover, enforced overexpression of DDX6 promoted both mRNA and protein expression of c-Myc in GC cells. On the other hand, the gene silencing of DDX6 induced growth suppression through down-regulation of c-Myc in GC cells.

14. BCL6 translocation was detected in 15 (12%) cases. Translocation involving MYC and BCL2 was identified in 3 cases (3.8%) and 1 case (1.3%) respectively. One double hit lymphoma was discovered with both MYC/BCL2 translocation (1.3%).

15. a phosphorylation mutant form of Mxi1 (Mxi1-S160A), which cannot be degraded by S6K1 and beta-Trcp, is much more stable and efficient in suppressing the transcriptional activity of Myc and radioresistance in lung cancer cells.

16. High protein expression of the glutamine-proline enzymes were all associated with high MYC protein in Luminal B tumours only (P<0.001).

17. Inhibiting phosphorylation of GSK3 substrates c-Myc on T58 and beta-catenin on S33/S37/T41 and their subsequent upregulation contribute to the antitumor activity of GSK3 inhibition.

18. EGF activated Myc and Myc overexpression inhibited miR-26b by recruitment of HDAC3, which in turn induced the expression of EZH2 and promoted the progression of epithelial-mesenchymal transition in human lens epithelial cells

19. High MYC expression is associated with diffuse large B-cell lymphoma.

20. the findings of this study demonstrate that hsamiR24 suppresses metastasis in nasopharyngeal carcinoma by regulating the cMyc/EMT axis, suggesting that hsamiR24 may be used as a prognostic factor and as a novel target for the prevention of nasopharyngeal carcinoma metastasis.

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. High myc is associated with tumourigenic transformation.

2. 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.

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

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

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

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

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

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

9. 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.

10. MYC binding is enriched at neuroendocrine genes in tumor cells and loss of MYC reduces ductal-neuroendocrine lineage heterogeneity, while deregulated MYC expression in KRAS mutants increases this phenotype.

11. Although either BCR or CD40 ligation induced c-Myc in naive B cells, both signals were required to highly induce c-Myc, a critical mediator of GC B cell survival and cell cycle reentry.

12. Myc is a component that links neuromesodermal progenitors maintenance and pre-somitic mesoderm maturation during the body axis elongation stages of mouse embryogenesis.

13. Myc potentiates the Wnt/beta-catenin signalling pathway, which cooperates with the transcriptional regulatory network in sustaining embryonic stem cell self-renewal.

14. Although mnt heterozygosity clearly slowed lymphomagenesis in vavP-MYC10 and Emu-myc mice, the change(s) in cellular properties responsible for this effect remain to be identified.

15. clusters of enhancers, such as BENC in the myc gene, form highly combinatorial systems that allow precise control of gene expression across normal cellular hierarchies and which also can be hijacked in malignancies

16. Conditional deletion of Myc in hyaloid vascular endothelial cells suppressed both proliferation and cell death.

17. c-Myc repression during development is crucial for the maturation of preacinar cells, and c-Myc overexpression can contribute to pancreatic carcinogenesis through the induction of a dedifferentiated state.

18. MYC negatively regulated the expression of genes involved in mitochondrial biogenesis and maintenance but positively regulated genes involved in DNA and histone methylation. Knockdown of MYC in colorectal cancer cells reset the altered metabolism and suppressed cell growth.

19. High myc expression is associated with Intestinal Tumorigenesis.

20. results shed light on how overexpressed MYC alters the various phases of the RNAPII cycle and the resulting transcriptional response.

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. 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.

2. 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.

3. 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.

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

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

6. 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.

7. BicC down regulates Myc in the Malpighian tubule.

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

9. 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.

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

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

12. 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.

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

14. 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

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

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

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

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

19. this study shows that puf genetically and physically interacts with dMyc and the ubiquitin ligase archipelago (ago) to modulate a dMyc-dependent cell growth phenotype, and that varying Puf levels in both the eye and wing phenocopies the effects of altered dMyc abundance.

20. Drosophila Myc controls cell competition during larval wing development. (Review)