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Validated All-in-One™ qPCR Primer for MYBL2(NM_002466.3) Search again
Powered by BiozBy default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Summary
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. [provided by RefSeq].
Gene References into function
- B-Myb transactivates the IGFBP-5 promoter
- ZPR9 plays an important role in modulation of the transactivation by B-MYB and cellular growth of neuroblastoma cells
- B-Myb repressor function is regulated by cyclin A phosphorylation and sequences within the C-terminal domain.
- it is evident that B-Myb protein may promote cell proliferation by a non-transcriptional mechanism that involves release of active cyclin/cyclin dependent kinase 2 from cyclin-dependent inhibitor 1C p57(KIP2)
- MRGX can repress or activate the B-myb promoter depending on the cell type studied, suggesting that there may be tissue-specific functions of this protein
- B-Myb has a role in regulation of c-Myc expression by cytosolic phospholipase A2
- Human B-Myb reduces neointima formation after vascular injury in transgenic mice.
- regulated by temperature to activate genes required for cell survival.
- overexpressed during the S phase of the cell cycle compared with the G0/1 phase
- Chromosomal fragmentation and other aberrations, including shorter, thicker chromatids, end-to-end fusion, and loss of a chromatid, suggest that reduced B-Myb activity is also associated with structural chromosomal instability.
- 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
- human LIN-9, together with B-MYB, has a critical role in the activation of genes that are essential for progression into mitosis
- 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.
- The expression of stable, hypophosphorylated B-MYB in neuroblastoma may promote cell survival and induce aggressive tumour growth.
- Some B-MYB alleles might be associated with a reduced risk of developing neoplastic disease.
- MYBL2 gene expression was significantly higher in colorectal cancer patients than in healthy volunteers.
- Insight into the influence of B-Myb in human breast cancer, which is of potential clinical importance for determining disease risk and for guiding treatment.