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found no significant differences in the genetic distribution and allelic frequency of MYB and SOX-6 gene polymorphisms
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.
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.
C-Myb expression in the laryngeal squamous cell carcinoma.YB-1 regulates miR-155 expression via c-Myb in the laryngeal squamous cell carcinoma.
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.
Both cases harbored the MYB-NFIB 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-150 expression is decreased. c-Myb was negatively correlated with miR-150.
genome-wide association analyses identified a new genome-wide significant locus on the HBS1L-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-associated gene rearrangement is a frequent genetic event in vulvar adenoid cystic carcinomas. Chromosome translocations involving NFIB 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 fusion oncogene in mammary tissue resulted in hyperplastic glands that developed into adenocarcinoma.
A trend toward superior PFS was noted with the MYB/NFIB rearrangement, although this was not statistically significant. NGS revealed three tumors with 4q12 amplification, producing increased copies of axitinib-targeted genes PDGFR/KDR/KIT.
Rearrangement of MYB did not affect OS.
Exosomes isolated from cultured AML or the plasma from mice bearing AML xenografts exhibited enrichment of miR-150 and miR-155. HSPCs cocultured with either of these exosomes exhibited impaired clonogenicity, through the miR-150- and miR-155-mediated suppression of the translation of transcripts encoding c-MYB
identification of SNPs within the IQCJ, NXPH1, PHF17 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.
deficiency alters the expression of a crucial subset of TAL1- and NOTCH1-regulated genes, including the MYB and MYC oncogenes, respectively.
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.
MYB acts on MAPK signaling by directly regulating transcription of the gene encoding the negative modulator SPRY2.
This study provides evidence that c-Myb might serve as a new target for the prevention of aminoglycoside-induced hair cells loss.
these results identify a key role for miR-150 in memory CD8 T cells through a c-Myb-controlled enhanced survival circuit.
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.
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.
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.
Data suggest that the upregulations of Myb and Peg3 are likely the key anti-cancer events of EGCG in vivo.
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.
These results Myb as a critical component of the gene regulatory network controlling effector Treg cell differentiation and function.
Production of dendritic-like cells and resident monocytes was not affected by the c-MybE308G mutation.
Myb expands the ISC pool within which CRC is initiated while co-operating with TSG loss
c-Myb regulates proliferation/differentiation of adventitial Sca1+ vascular smooth muscle progenitor cells by transcriptional activation of myocardin.
the key role of the transcription factor c-Myb in regulating the T-bet-mediated anti-viral program, is reported.
p38 and NOX1 are essential for the protective effect of c-Myb and that NOX1 acts upstream of p38 activation.
These findings reveal that miR-150 acts as a pivotal regulator of pressure overload-induced cardiac fibrosis by regulating c-Myb.
MYB and C/EBPalpha activities are inter-dependent in controlling Flt3 expression to influence lineage commitment of multipotential progenitors.
Myb regulates Cyclin E1 expression in normal gastrointestinal tract epithelial cells and is required during intestinal tumorigenesis
Identify regulatory link between Nkx2-1, miR-200c, and the transcription factors Nfib and Myb, adding new players to the regulatory mechanisms driven by Nkx2-1 in lung epithelial cells that may have implications in lung development and tumorigenesis.
Myb has a role in K14+ epithelial cells in the preservation of mouse adult skin integrity and function in a process involving TGFbeta and collagen type I
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.
cMyb plays a hitherto unidentified role in dictating physiologic HSPC migration by modulating Sdf1a signaling.
show that knockdown of miR-126 results in increased c-Myb levels and promotes erythropoiesis at the expense of thrombopoiesis in vivo
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.
expression of CD41 and cmyb marks nascent HSCs in the zebrafish AGM, and provide the means to further dissect HSC generation and
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.
c-myb protein (140 AA)
, proto-oncogene c-Myb
, transcriptional activator Myb
, gag-myb protein
, myb proto-oncogene protein
, myeloblastosis proto-oncogene product
, tumor-specific myb protein
, myeloblastosis oncogene
, Avian myeloblastosis viral (v-myb) oncogene homolog
, v-myb myeloblastosis viral oncogene homolog (avian)
, transcriptional activator Myb-like
, DNA-binding transcriptional regulator
, c-myb proto-oncogene
, transcription factor cmyb
, v-myb myeloblastosis viral oncogene homolog
, v-myb avian myeloblastosis viral oncogene homolog