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Myb knockdown in Setbp1 (show SETBP1 Proteins) and Setbp1 (show SETBP1 Proteins) missense mutations-induced AML (show RUNX1 Proteins) cells also efficiently induced their differentiation in culture and significantly prolonged the survival of their secondary recipient mice.
These findings reveal miR (show MLXIP Proteins)-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.
The analysis points to a critical role for Hoxa9 (show HOXA9 Proteins) and PU.1 in distal regulation of c-myb expression in murine myeloid cells during iL-6 (show IL6 Proteins)-induced cell differentiation.
Data suggest that the upregulations of Myb and Peg3 are likely the key anti-cancer events of EGCG in vivo.
deficiency alters the expression of a crucial subset of TAL1 (show TAL1 Proteins)- and NOTCH1 (show NOTCH1 Proteins)-regulated genes, including the MYB and MYC (show MYC Proteins) oncogenes, respectively.
MYB acts on MAPK (show MAPK1 Proteins) signaling by directly regulating transcription of the gene encoding the negative modulator SPRY2 (show SPRY2 Proteins).
This work provides important mechanistic insight into how spatiotemporal expression of the Rag genes is tightly controlled during B lymphocyte (show AKAP17A Proteins) development to prevent mistimed dsDNA breaks and their deleterious consequences.
These results Myb as a critical component of the gene regulatory network controlling effector Treg cell differentiation and function.
Myb expands the ISC pool within which CRC is initiated while co-operating with TSG (show TWSG1 Proteins) loss
c-Myb regulates proliferation/differentiation of adventitial Sca1+ vascular smooth muscle progenitor cells by transcriptional activation of myocardin.
NFIB (show NFIB Proteins)-associated gene rearrangement is a frequent genetic event in vulvar adenoid cystic carcinomas. Chromosome translocations involving NFIB (show NFIB Proteins) but with an intact MYB indicate the presence of novel oncogenic mechanisms for the development of adenoid cystic carcinomas of the vulva.
Expression of the MYB-NFIB (show NFIB Proteins) fusion oncogene (show RAB1A Proteins) in mammary tissue resulted in hyperplastic glands that developed into adenocarcinoma.
A trend toward superior PFS was noted with the MYB/NFIB (show NFIB Proteins) rearrangement, although this was not statistically significant. NGS revealed three tumors with 4q12 amplification, producing increased copies of axitinib-targeted genes PDGFR (show PDGFRB Proteins)/KDR (show KDR Proteins)/KIT.
Rearrangement of MYB did not affect OS.
Exosomes isolated from cultured AML (show RUNX1 Proteins) or the plasma from mice bearing AML (show RUNX1 Proteins) xenografts exhibited enrichment of miR (show MLXIP Proteins)-150 and miR (show MLXIP Proteins)-155. HSPCs cocultured with either of these exosomes exhibited impaired clonogenicity, through the miR (show MLXIP Proteins)-150- and miR (show MLXIP Proteins)-155-mediated suppression of the translation of transcripts encoding c-MYB
identification of SNPs within the IQCJ, NXPH1 (show NXPH1 Proteins), PHF17 (show PHF17 Proteins) and MYB genes partly explaining the large interindividual variability observed in plasma triglyceride levels in response to an n-3 fatty acid supplementation
The data indicate that MAZ (show MAZ Proteins) is essential to bypass MYB promoter repression by RB family members and to induce MYB expression.
A mutant of c-Myb, D152V, specifically affects c-Myb's ability to regulate genes involved in differentiation, causing failure in c-Myb's ability to block differentiation.
This gene encodes a transcription factor that is a member of the MYB family of transcription factor genes. The protein contains three domains, an N-terminal DNA-binding domain, a central transcriptional activation domain and a C-terminal domain involved in transcriptional repression. This protein plays an essential role in the regulation of hematopoiesis and may play a role in tumorigenesis. Alternative splicing results in multiple transcript variants.
, Avian myeloblastosis viral (v-myb) oncogene homolog
, v-myb myeloblastosis viral oncogene homolog (avian)
, transcriptional activator Myb-like
, gag-myb protein
, myb proto-oncogene protein
, myeloblastosis proto-oncogene product
, proto-oncogene c-Myb
, transcriptional activator Myb
, tumor-specific myb protein
, c-myb protein (140 AA)
, DNA-binding transcriptional regulator
, c-myb proto-oncogene