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loss-of-function mutation (crb) in bmyb causes defects in mitotic progression and spindle formation and genome instability in embryos, and cancer susceptibility in adult crb heterozygotes
Downregulation of B-myb induced senescence by upregulation of p22(phox (show CYBA ELISA Kits)) and activation of the ROS (show ROS1 ELISA Kits)/p53 (show TP53 ELISA Kits)/p21 pathway
B-myb is an essential regulator of hematopoietic stem cell and myeloid progenitor cell development.
MYBL2 haploinsufficiency increases susceptibility to age-related haematopoietic neoplasia.
Results coupled with functional studies demonstrate that B-MYB not only controls and accelerates cell cycle progression in ESCs (show NR2E3 ELISA Kits) it contributes to fate decisions and maintenance of pluripotent stem cell identity.
Our data suggest that B-Myb is required as a pioneer factor to enable FoxM1 (show FOXM1 ELISA Kits) binding to G2/M gene promoters and explains how these transcription factors may collaborate to induce mitosis.
Mybl2 upregulation induces fast growth and progression of premalignant and malignant liver, through cell cycle deregulation and activation of genes and pathways related to tumor progression.
The transcription factor B-Myb is maintained in an inhibited state in target cells through its interaction with the nuclear corepressors N-CoR and SMRT.
Results describe the characterization of a corepressor site (downstream repression site (DRS (show SRPX ELISA Kits))) required for transcriptional regulation of the B-myb (MybL2 gene) promoter.
B-Myb repressor function is regulated by cyclin A phosph (show CCNA2 ELISA Kits)orylation and sequences within the C-terminal domain.
B-Myb has a role in regulation of c-Myc (show MYC ELISA Kits) expression by cytosolic phospholipase A2 (show PLA2G4A ELISA Kits)
A total of 41 differentially expressed genes, such as SOCS3 (show SOCS3 ELISA Kits), VAPA (show VAPA ELISA Kits), and COL5A2 (show COL5A2 ELISA Kits), are speculated to have roles in the pathogenesis of acute myocardial infarction; 2 transcription factors FOXO3 (show FOXO3 ELISA Kits) and MYBL2, and 2 miRNAs hsa (show CD24 ELISA Kits)-miR (show MLXIP ELISA Kits)-21-5p and hsa (show CD24 ELISA Kits)-miR (show MLXIP ELISA Kits)-30c-5p may be involved in the regulation of the expression of these differentially expressed genes.
Results suggested that the oncogenic transcription factor HIF-2alpha (show EPAS1 ELISA Kits) stabilized VHL (show VHL ELISA Kits) disease suppressor B-Myb, which is also a transcription factor, by physical interaction. Some B-Myb-dependent gene expression was similarly affected by B-Myb or HIF-2alpha (show EPAS1 ELISA Kits) knockdown, suggesting that stabilization of B-Myb by HIF-2alpha (show EPAS1 ELISA Kits) may play a role in specific gene expressions.
The MuvB multiprotein complex, together with B-MYB and FOXM1 (show FOXM1 ELISA Kits) (MMB-FOXM1 (show FOXM1 ELISA Kits)) regulate the expression of mitotic kinesins in breast cancer cells.
MYBL2 overexpression promotes Gallbladder Cancer cell proliferation through the regulation of the cell cycle at the S and G2/M phase transitions. Thus, MYBL2 could serve as a potential prognostic and therapeutic biomarker in Gallbladder Cancer patients.
Study identified B-Myb as a substrate of the pVHL (show VHL ELISA Kits) ubiquitin ligase complex, which targets it for degradation via the ubiquitin-proteasome pathway. It also, provide evidence that the regulation of B-Myb by pVHL (show VHL ELISA Kits) plays a critical role in von Hippel-Lindau disease.
Data indicate that gene expression alterations in endometrial carcinoma samples with high ATAD2 (show ATAD2 ELISA Kits) expression showed upregulation of several cancer-related genes including B-MYB gene.
We found that B-Myb upregulated expression of the key epithelial-to-mesenchymal transition regulator snail (show SNAI1 ELISA Kits) and that it mediated epithelial-to-mesenchymal transition activation and cell invasion by B-Myb.
conclude that downregulation of MYBL2 activity below levels predicted by classical haploinsufficiency underlies the clonal expansion of hematopoietic progenitors in a large fraction of human myeloid malignancies
Suggest B-myb had critical roles in both cell cycle progression and tumorigenesis in breast cancer.
B-Myb plays a role in suppression of keratinocyte differentiation and maintenance of the undifferentiated proliferative phenotype by modulating the expression levels of cell cycle regulatory proteins, expressed in the S and G2/M phases of the cell cycle
B-Myb (MYBL2)repressor function is regulated by cyclin A (show CCNA2 ELISA Kits) phosphorylation and sequences within the C-terminal domain.
B-Myb represses SMC (show DYM ELISA Kits) elastin (show ELN ELISA Kits) gene expression and cyclin A (show CCNA2 ELISA Kits) plays a role in the developmental regulation of elastin (show ELN ELISA Kits) gene expression in the aorta
The protein encoded by this gene, a member of the MYB family of transcription factor genes, is a nuclear protein involved in cell cycle progression. The encoded protein is phosphorylated by cyclin A/cyclin-dependent kinase 2 during the S-phase of the cell cycle and possesses both activator and repressor activities. It has been shown to activate the cell division cycle 2, cyclin D1, and insulin-like growth factor-binding protein 5 genes. Transcript variants may exist for this gene, but their full-length natures have not been determined.
v-myb myeloblastosis viral oncogene homolog (avian)-like 2
, myb-related protein B
, v-myb myeloblastosis viral oncogene homolog-like 2
, myb-like protein 2
, myb-related protein 1
, myeloblastosis oncogene-like 2