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The analysis points to a critical role for Hoxa9 (zeige HOXA9 ELISA Kits) and PU.1 in distal regulation of c-myb expression in murine myeloid cells during iL-6 (zeige IL6 ELISA Kits)-induced cell differentiation.
Data suggest that the upregulations of Myb and Peg3 (zeige PEG3 ELISA Kits) are likely the key anti-cancer events of EGCG in vivo.
deficiency alters the expression of a crucial subset of TAL1 (zeige TAL1 ELISA Kits)- and NOTCH1 (zeige NOTCH1 ELISA Kits)-regulated genes, including the MYB and MYC (zeige MYC ELISA Kits) oncogenes, respectively.
MYB acts on MAPK (zeige MAPK1 ELISA Kits) signaling by directly regulating transcription of the gene encoding the negative modulator SPRY2 (zeige SPRY2 ELISA Kits).
This work provides important mechanistic insight into how spatiotemporal expression of the Rag genes is tightly controlled during B lymphocyte (zeige AKAP17A ELISA Kits) 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 (zeige SCRIB ELISA Kits) is initiated while co-operating with TSG (zeige TWSG1 ELISA Kits) loss
c-Myb regulates proliferation/differentiation of adventitial Sca1 (zeige ATXN1 ELISA Kits)+ vascular smooth muscle progenitor cells by transcriptional activation of myocardin (zeige MYOCD ELISA Kits).
the key role of the transcription factor c-Myb in regulating the T-bet-mediated anti-viral program, is reported.
p38 (zeige CRK ELISA Kits) and NOX1 (zeige NOX1 ELISA Kits) are essential for the protective effect of c-Myb and that NOX1 (zeige NOX1 ELISA Kits) acts upstream of p38 (zeige CRK ELISA Kits) activation.
Expression of the MYB-NFIB (zeige NFIB ELISA Kits) fusion oncogene (zeige RAB1A ELISA Kits) in mammary tissue resulted in hyperplastic glands that developed into adenocarcinoma.
A trend toward superior PFS was noted with the MYB/NFIB (zeige NFIB ELISA Kits) rearrangement, although this was not statistically significant. NGS revealed three tumors with 4q12 amplification, producing increased copies of axitinib-targeted genes PDGFR (zeige PDGFRB ELISA Kits)/KDR (zeige KDR ELISA Kits)/KIT.
Rearrangement of MYB did not affect OS.
Exosomes isolated from cultured AML (zeige RUNX1 ELISA Kits) or the plasma from mice bearing AML (zeige RUNX1 ELISA Kits) xenografts exhibited enrichment of miR (zeige MLXIP ELISA Kits)-150 and miR (zeige MLXIP ELISA Kits)-155. HSPCs cocultured with either of these exosomes exhibited impaired clonogenicity, through the miR (zeige MLXIP ELISA Kits)-150- and miR (zeige MLXIP ELISA Kits)-155-mediated suppression of the translation of transcripts encoding c-MYB
identification of SNPs within the IQCJ, NXPH1 (zeige NXPH1 ELISA Kits), PHF17 (zeige PHF17 ELISA Kits) 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 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.
l genetic alterations were limited to two fusion genes, EWSR1 (zeige EWSR1 ELISA Kits)-PATZ1 and SLMAP (zeige SLMAP ELISA Kits)-NTRK2 (zeige NTRK2 ELISA Kits), both in gangliogliomas. Alterations in BRAF (zeige BRAF ELISA Kits), FGFR1 (zeige FGFR1 ELISA Kits), or MYB account for most pathogenic alterations in low-grade neuroepithelial tumors
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