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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 Proteins)) and activation of the ROS (show ROS1 Proteins)/p53 (show TP53 Proteins)/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 Proteins) 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 Proteins) 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 Proteins))) required for transcriptional regulation of the B-myb (MybL2 gene) promoter.
B-Myb repressor function is regulated by cyclin A phosph (show CCNA2 Proteins)orylation and sequences within the C-terminal domain.
B-Myb has a role in regulation of c-Myc (show MYC Proteins) expression by cytosolic phospholipase A2 (show PLA2G4A Proteins)
MYBL2 is a key downstream factor of Akt (show AKT1 Proteins)/FoxM1 (show FOXM1 Proteins) signaling to promote progression of human glioma, and could be a new candidate gene for molecular targeting therapy and biomarker for radiotherapy of glioma.
These results suggested that overexpression of MYBL2 might serve as a novel prognostic biomarker in pancreatic ductal adenocarcinoma patients
A total of 41 differentially expressed genes, such as SOCS3 (show SOCS3 Proteins), VAPA (show VAPA Proteins), and COL5A2 (show COL5A2 Proteins), are speculated to have roles in the pathogenesis of acute myocardial infarction; 2 transcription factors FOXO3 (show FOXO3 Proteins) and MYBL2, and 2 miRNAs hsa (show CD24 Proteins)-miR (show MLXIP Proteins)-21-5p and hsa (show CD24 Proteins)-miR (show MLXIP Proteins)-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 Proteins) stabilized VHL (show VHL Proteins) 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 Proteins) knockdown, suggesting that stabilization of B-Myb by HIF-2alpha (show EPAS1 Proteins) may play a role in specific gene expressions.
The MuvB multiprotein complex, together with B-MYB and FOXM1 (show FOXM1 Proteins) (MMB-FOXM1 (show FOXM1 Proteins)) 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 Proteins) 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 Proteins) plays a critical role in von Hippel-Lindau disease.
Data indicate that gene expression alterations in endometrial carcinoma samples with high ATAD2 (show ATAD2 Proteins) 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 Proteins) 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
B-Myb (MYBL2)repressor function is regulated by cyclin A (show CCNA2 Proteins) phosphorylation and sequences within the C-terminal domain.
B-Myb represses SMC (show DYM Proteins) elastin (show ELN Proteins) gene expression and cyclin A (show CCNA2 Proteins) plays a role in the developmental regulation of elastin (show ELN Proteins) 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