Aperçu des produits pour MYB Protéines (MYB)

Human V-Myb Myeloblastosis Viral Oncogene Homolog (Avian) (MYB) interaction partners

1. Breast adenoid cystic carcinomas probably constitute a convergent phenotype, whereby activation of MYB and MYBL1 and their downstream targets can be driven by the MYB-NFIB fusion gene, MYBL1 rearrangements, MYB amplification, or other yet to be identified mechanisms.

2. Data observe that increasing and decreasing the helical stability of c-Myb over a broad range has a small effect on the binding affinity to KIX domain of CREB binding protein. To reduce the binding affinity by more than 1 kcal/mol, it was necessary to introduce glycine or proline in the middle of the c-Myb helix.

3. In the present study, MYB or MYBL1 locus rearrangement was detected in nearly all adenoid cystic carcinoma cases, and therefore it would be a good diagnostic marker for adenoid cystic carcinoma.

4. Collectively, our data showed that ZFAS1 contributed to the development of AML by sequestering miR-150 from Myb or Sp1, elucidating the central roles of ZFAS1/miR-150/Myb and ZFAS1/miR-150/Sp1 pathways in the tumorigenesis of AML and deepening our understanding on the etiology of leukemia.

5. The presence of the MYB fusion in intermediate-grade and hybrid carcinomas that at least partially exhibit an epithelial-myoepithelial carcinoma phenotype may in fact point to an adenoid cystic carcinoma.

6. The c-Myb gene encodes a transcription factor that regulates cell proliferation, differentiation, and apoptosis through protein-protein interaction and transcriptional regulation of signaling pathways. The protein is frequently overexpressed in human leukemias, breast cancers, and solid tumors suggesting that it is a bona fide oncogene. c-MYB is often overexpressed by chromosomal translocation in human tumors. [review]

7. Low c-myb expression promotes breast cancer lung metastasis.

8. High c-myb expression is associated with In-Stent Restenosis in Peripheral Artery Disease.

9. Data provide evidences supporting the role of Sema5A in melanoma progression and the involvement of Bcl-2, miR-204 and c-Myb in regulating its expression.

10. The data demonstrate that c-Myb plays a critical role in the activation of NK cells and therefore is a therapeutic target for cancer and viral diseases.

11. found no significant differences in the genetic distribution and allelic frequency of MYB and SOX-6 gene polymorphisms

12. Salivary gland ACC cases expressing the MYB-NFIB chimeric gene showed significantly higher blood vessels density compared to non-expressing cases, and suggested that higher VEGF production capability in the former cases may be the cause. The findings also suggested that MYB-NFIB chimeric gene expression may be related to the onset age of ACC.

13. These results indicated that low expression of Mda-7/IL-24 along with high expression of C-myb are predictors for poor prognosis of Burkitt lymphoma patients; this outcome suggests that Mda-7/IL-24 and C-myb might be potential targets for clinical treatment of Burkitt lymphoma.

14. C-Myb expression in the laryngeal squamous cell carcinoma.YB-1 regulates miR-155 expression via c-Myb in the laryngeal squamous cell carcinoma.

15. Data indicate a pioneer factor model in which c-Myb binds to regions of closed chromatin and then recruits histone acetyltransferases. By binding to histones, c-Myb facilitates histone acetylation, acting as a cofactor for p300 at c-Myb binding sites. The resulting H3K27ac leads to chromatin opening and detachment of c-Myb from the acetylated chromatin.

16. Both cases harbored the MYB-NFIB gene fusion as demonstrated by FISH and RNA-sequencing

17. Expression of c-Myb, a regulatory factor of B lymphocytes, is increased in B lymphocytes of AIHA/Evans patients, while miR-150 expression is decreased. c-Myb was negatively correlated with miR-150.

18. genome-wide association analyses identified a new genome-wide significant locus on the HBS1L-MYB intergenic region for platelet-to-lymphocyte ratio

19. identified a high frequency of MYB rearrangements that promoted the MYB transcriptional activity in BPDCN. MYB split FISH analysis can constitute a valuable diagnostic tool for detecting MYB rearrangements

20. Studied association of BCL11A single nucleotide polymorphisms(snps) and HBS1L-MYB Intergenic snps with Hereditary Persistence of Fetal Hemoglobin (HPFH) in a cohort of sickle cell patients.

Mouse (Murine) V-Myb Myeloblastosis Viral Oncogene Homolog (Avian) (MYB) interaction partners

1. Findings identify myb proto-oncogene protein (c-Myb) as a pivotal regulator of CD8(+) T cell stemness and suggest its therapeutic potential.

2. Low c-myb expression promotes breast cancer lung metastasis.

3. This study provides evidence that c-Myb might serve as a new target for the prevention of aminoglycoside-induced hair cells loss.

4. these results identify a key role for miR-150 in memory CD8 T cells through a c-Myb-controlled enhanced survival circuit.

5. Myb knockdown in Setbp1 and Setbp1 missense mutations-induced AML cells also efficiently induced their differentiation in culture and significantly prolonged the survival of their secondary recipient mice.

6. These findings reveal miR-301b as a new controller of inflammatory response by repressing c-Myb function to inhibit the anti-inflammatory response to bacterial infection, representing a novel mechanism for balancing inflammation.

7. The analysis points to a critical role for Hoxa9 and PU.1 in distal regulation of c-myb expression in murine myeloid cells during iL-6-induced cell differentiation.

8. Data suggest that the upregulations of Myb and Peg3 are likely the key anti-cancer events of EGCG in vivo.

9. deficiency alters the expression of a crucial subset of TAL1- and NOTCH1-regulated genes, including the MYB and MYC oncogenes, respectively.

10. MYB acts on MAPK signaling by directly regulating transcription of the gene encoding the negative modulator SPRY2.

11. This work provides important mechanistic insight into how spatiotemporal expression of the Rag genes is tightly controlled during B lymphocyte development to prevent mistimed dsDNA breaks and their deleterious consequences.

12. These results Myb as a critical component of the gene regulatory network controlling effector Treg cell differentiation and function.

13. Production of dendritic-like cells and resident monocytes was not affected by the c-MybE308G mutation.

14. Myb expands the ISC pool within which CRC is initiated while co-operating with TSG loss

15. c-Myb regulates proliferation/differentiation of adventitial Sca1+ vascular smooth muscle progenitor cells by transcriptional activation of myocardin.

16. the key role of the transcription factor c-Myb in regulating the T-bet-mediated anti-viral program, is reported.

17. p38 and NOX1 are essential for the protective effect of c-Myb and that NOX1 acts upstream of p38 activation.

18. These findings reveal that miR-150 acts as a pivotal regulator of pressure overload-induced cardiac fibrosis by regulating c-Myb.

19. MYB and C/EBPalpha activities are inter-dependent in controlling Flt3 expression to influence lineage commitment of multipotential progenitors.

20. Myb regulates Cyclin E1 expression in normal gastrointestinal tract epithelial cells and is required during intestinal tumorigenesis

Zebrafish V-Myb Myeloblastosis Viral Oncogene Homolog (Avian) (MYB) interaction partners

1. studies show that merestinib effectively blocks eIF4E phosphorylation in AML cells and suppresses primitive leukemic progenitors from AML patients in vitro and in an AML xenograft model in vivo.

2. cMyb plays a hitherto unidentified role in dictating physiologic HSPC migration by modulating Sdf1a signaling.

3. show that knockdown of miR-126 results in increased c-Myb levels and promotes erythropoiesis at the expense of thrombopoiesis in vivo

4. Results suggest that the key role of c-myb in definitive hematopoiesis is similar to that in mammals and must have become established early in vertebrate evolution.

5. expression of CD41 and cmyb marks nascent HSCs in the zebrafish AGM, and provide the means to further dissect HSC generation and