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anti-Rat (Rattus) MYBL2 Antibodies:
anti-Mouse (Murine) MYBL2 Antibodies:
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Rat (Rattus) Polyclonal MYBL2 Primary Antibody for ELISA, WB - ABIN251665
Shepard, Amatruda, Stern, Subramanian, Finkelstein, Ziai, Finley, Pfaff, Hersey, Zhou, Barut, Freedman, Lee, Spitsbergen, Neuberg, Weber, Golub, Glickman, Kutok, Aster, Zon: A zebrafish bmyb mutation causes genome instability and increased cancer susceptibility. in Proceedings of the National Academy of Sciences of the United States of America 2005
Cow (Bovine) Polyclonal MYBL2 Primary Antibody for IHC, WB - ABIN2792568
Tashiro, Sumi, Uozumi, Shimizu, Nakamura: B-Myb-dependent regulation of c-Myc expression by cytosolic phospholipase A2. in The Journal of biological chemistry 2004
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 Antibodies)) and activation of the ROS (show ROS1 Antibodies)/p53 (show TP53 Antibodies)/p21 (show D4S234E Antibodies) 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 Antibodies) 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 Antibodies) 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 Antibodies))) required for transcriptional regulation of the B-myb (MybL2 gene) promoter.
B-Myb repressor function is regulated by cyclin A phosph (show CCNA2 Antibodies)orylation and sequences within the C-terminal domain.
B-Myb has a role in regulation of c-Myc (show MYC Antibodies) expression by cytosolic phospholipase A2 (show PLA2G4A Antibodies)
Results suggested that the oncogenic transcription factor HIF-2alpha (show EPAS1 Antibodies) stabilized VHL (show VHL Antibodies) 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 Antibodies) knockdown, suggesting that stabilization of B-Myb by HIF-2alpha (show EPAS1 Antibodies) may play a role in specific gene expressions.
The MuvB multiprotein complex, together with B-MYB and FOXM1 (show FOXM1 Antibodies) (MMB-FOXM1 (show FOXM1 Antibodies)) 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 Antibodies) 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 Antibodies) plays a critical role in von Hippel-Lindau disease.
Data indicate that gene expression alterations in endometrial carcinoma samples with high ATAD2 (show ATAD2 Antibodies) 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 Antibodies) 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
Results show that E7 interacts with the B-Myb, FoxM1 (show FOXM1 Antibodies) and LIN9 (show LIN9 Antibodies) components of this activator complex, leading to cooperative transcriptional activation of mitotic genes in primary cells and E7 recruitment to the corresponding promoters.
B-Myb (MYBL2)repressor function is regulated by cyclin A (show CCNA2 Antibodies) phosphorylation and sequences within the C-terminal domain.
B-Myb represses SMC (show DYM Antibodies) elastin (show ELN Antibodies) gene expression and cyclin A (show CCNA2 Antibodies) plays a role in the developmental regulation of elastin (show ELN Antibodies) 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