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these results identify a key role for miR (show MLXIP Proteins)-150 in memory CD8 (show CD8A Proteins) T cells through a c-Myb-controlled enhanced survival circuit.
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
Both cases harbored the MYB-NFIB (show NFIB Proteins) gene fusion as demonstrated by FISH and RNA-sequencing
Expression of c-Myb, a regulatory factor of B lymphocytes, is increased in B lymphocytes of AIHA/Evans patients, while miR (show MLXIP Proteins)-150 expression is decreased. c-Myb was negatively correlated with miR (show MLXIP Proteins)-150.
genome-wide association analyses identified a new genome-wide significant locus on the HBS1L (show HBS1L Proteins)-MYB intergenic region for platelet-to-lymphocyte ratio
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
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.
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
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