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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) and activation of the ROS/p53/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 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 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)) required for transcriptional regulation of the B-myb (MybL2 gene) promoter.
B-Myb repressor function is regulated by cyclin A phosphorylation and sequences within the C-terminal domain.
B-Myb has a role in regulation of c-Myc expression by cytosolic phospholipase A2
B-Myb represses SMC elastin gene expression and cyclin A plays a role in the developmental regulation of elastin gene expression in the aorta
Mip/LIN-9 is required for the expression of B-Myb, and both proteins collaborate in the control of the cell cycle progression via the regulation of S phase and cyclin A, cyclin B, and CDK1
The repressor complex that Mip/LIN-9 forms with p107 takes functional precedence over the transcriptional activation linked to the Mip/LIN-9 and B-Myb interaction.
proliferation-inhibiting A(2B)AR is itself an inducible receptor regulated by B-Myb.
Lin-9 and B-Myb were both required for transcription of G(2)/M genes such as Cyclin B1 and Survivin.
Given that high expression of B-Myb correlates with global loss of repression of DREAM target genes in breast and ovarian cancer, our findings offer mechanistic insights for aggressiveness of cancers with MYBL2 amplification, and establish the rationale for targeting B-Myb to restore cell cycle control.
High MYBL2 expression is associated with Breast Cancer Cell Proliferation.
results suggest that B-Myb-A3B contributes to DNA damage and could be targeted by inhibiting EGF receptor.
The structure and biochemical analysis provide an understanding of how oncogenic B-Myb is recruited to regulate genes required for cell-cycle progression, and the MMB interface presents a potential therapeutic target to inhibit cancer cell proliferation.
B-Myb is an independent prognostic marker and serves as a potential target in the diagnosis and/or treatment of NSCLC, and that B-Myb functions as a tumor-promoting gene by targeting IGFBP3 in NSCLC cells.
MYBL2 is a key downstream factor of Akt/FoxM1 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, VAPA, and COL5A2, are speculated to have roles in the pathogenesis of acute myocardial infarction; 2 transcription factors FOXO3 and MYBL2, and 2 miRNAs hsa-miR-21-5p and hsa-miR-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 stabilized VHL 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 knockdown, suggesting that stabilization of B-Myb by HIF-2alpha may play a role in specific gene expressions.
The MuvB multiprotein complex, together with B-MYB and FOXM1 (MMB-FOXM1) 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 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 plays a critical role in von Hippel-Lindau disease.
Data indicate that gene expression alterations in endometrial carcinoma samples with high ATAD2 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 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 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
Results show that E7 interacts with the B-Myb, FoxM1 and LIN9 components of this activator complex, leading to cooperative transcriptional activation of mitotic genes in primary cells and E7 recruitment to the corresponding promoters.
MYBL2 expression analysis could be useful to define subgroups of patients with poor prognosis.
MALAT1-depleted cells display reduced expression of B-MYB (Mybl2), an oncogenic transcription factor involved in G2/M progression, due to altered binding of splicing factors on B-MYB pre-mRNA and aberrant alternative splicing
Low MYBL2 expression is associated with haematopoietic neoplasia.
B-Myb (MYBL2)repressor function is regulated by cyclin A phosphorylation and sequences within the C-terminal domain.
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