Use your antibodies-online credentials, if available.
Il n’y a pas de produits dans votre liste de comparaison.
Votre panier est vide.
Afficher tous les synonymes
Sélectionnez vos espèces d'intérêt
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 (Montrer CYBA Protéines)) and activation of the ROS (Montrer ROS1 Protéines)/p53 (Montrer TP53 Protéines)/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 (Montrer NR2E3 Protéines) 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 (Montrer FOXM1 Protéines) 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 (Montrer SRPX Protéines))) required for transcriptional regulation of the B-myb (MybL2 gene) promoter.
B-Myb repressor function is regulated by cyclin A phosph (Montrer CCNA2 Protéines)orylation and sequences within the C-terminal domain.
B-Myb has a role in regulation of c-Myc (Montrer MYC Protéines) expression by cytosolic phospholipase A2 (Montrer PLA2G4A Protéines)
results suggest that B-Myb-A3B (Montrer SGCB Protéines) contributes to DNA damage and could be targeted by inhibiting EGF receptor (Montrer EGFR Protéines).
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 (Montrer IGFBP3 Protéines) in NSCLC cells.
MYBL2 is a key downstream factor of Akt (Montrer AKT1 Protéines)/FoxM1 (Montrer FOXM1 Protéines) 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 (Montrer SOCS3 Protéines), VAPA (Montrer VAPA Protéines), and COL5A2 (Montrer COL5A2 Protéines), are speculated to have roles in the pathogenesis of acute myocardial infarction; 2 transcription factors FOXO3 (Montrer FOXO3 Protéines) and MYBL2, and 2 miRNAs hsa (Montrer CD24 Protéines)-miR (Montrer MLXIP Protéines)-21-5p and hsa (Montrer CD24 Protéines)-miR (Montrer MLXIP Protéines)-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 (Montrer EPAS1 Protéines) stabilized VHL (Montrer VHL Protéines) 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 (Montrer EPAS1 Protéines) knockdown, suggesting that stabilization of B-Myb by HIF-2alpha (Montrer EPAS1 Protéines) may play a role in specific gene expressions.
The MuvB multiprotein complex, together with B-MYB and FOXM1 (Montrer FOXM1 Protéines) (MMB-FOXM1 (Montrer FOXM1 Protéines)) 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 (Montrer VHL Protéines) 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 (Montrer VHL Protéines) plays a critical role in von Hippel-Lindau disease.
B-Myb (MYBL2)repressor function is regulated by cyclin A (Montrer CCNA2 Protéines) phosphorylation and sequences within the C-terminal domain.
B-Myb represses SMC (Montrer DYM Protéines) elastin (Montrer ELN Protéines) gene expression and cyclin A (Montrer CCNA2 Protéines) plays a role in the developmental regulation of elastin (Montrer ELN Protéines) 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