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V-myb myeloblastosis viral oncogene homolog

B-myb, MYBL2
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, Jul 2008] (from NCBI)
Top mentioned proteins: PCNA, CAN, p53, HAD, E2F1
Papers on B-myb
The p53-p21-DREAM-CDE/CHR pathway regulates G2/M cell cycle genes.
Engeland et al., Leipzig, Germany. In Nucleic Acids Res, Feb 2016
The target gene list was verified by detailed analysis of p53-dependent repression of the cell cycle genes B-MYB (MYBL2), BUB1, CCNA2, CCNB1, CHEK2, MELK, POLD1, RAD18 and RAD54L.
Differential expression of six chicken genes associated with fatness traits in a divergently selected broiler population.
Wang et al., Harbin, China. In Mol Cell Probes, Jan 2016
The six significant SNPs are located in the kinase insert domain receptor (KDR), tumor suppressor candidate 3 (TUSC3), phosphoribosyl pyrophosphate amidotransferase (PPAT), exocyst complex component 1 (EXOC1), v-myb myeloblastosis viral oncogene homolog (avian)-like 2 (MYBL2) and KIAA1211 (undefined) genes.
Indirect p53-dependent transcriptional repression of Survivin, CDC25C, and PLK1 genes requires the cyclin-dependent kinase inhibitor p21/CDKN1A and CDE/CHR promoter sites binding the DREAM complex.
Engeland et al., Leipzig, Germany. In Oncotarget, Jan 2016
Chromatin immunoprecipitation (ChIP) data indicate that promoter binding of B-MYB switches to binding of E2F4 and p130 resulting in a replacement of the MMB (Myb-MuvB) by the DREAM complex.
MYBD employed by HY5 increases anthocyanin accumulation via repression of MYBL2 in Arabidopsis.
Lee et al., Seoul, South Korea. In Plant J, Dec 2015
MYBD expression increased in response to light or cytokinin, and MYBD enhanced anthocyanin biosynthesis via repression of MYBL2, which encodes a transcription factor that has a negative effect on this process.
A Gene Regulatory Program in Human Breast Cancer.
Iida et al., Bar Harbor, United States. In Genetics, Dec 2015
In contrast, group 2 MRs, including FOXM1, EZH2, MYBL2, and ZNF695, display an opposite pattern.
Early Evolution of Vertebrate Mybs: An Integrative Perspective Combining Synteny, Phylogenetic, and Gene Expression Analyses.
Hoffmann et al., São Carlos, Brazil. In Genome Biol Evol, Nov 2015
B-Myb plays an essential role in cell division and cell cycle progression, c-Myb is involved in hematopoiesis, and A-Myb is involved in spermatogenesis and regulating expression of pachytene PIWI interacting RNAs, a class of small RNAs involved in posttranscriptional gene regulation and the maintenance of reproductive tissues.
ATAD2 overexpression links to enrichment of B-MYB-translational signatures and development of aggressive endometrial carcinoma.
Salvesen et al., Bergen, Norway. In Oncotarget, Oct 2015
Gene expression alterations in samples with high ATAD2 expression revealed upregulation of several cancer-related genes (B-MYB, CDCs, E2Fs) and gene sets that previously have been linked to aggressive disease and potential for new targeting therapies.
MYBL2 is an independent prognostic marker that has tumor-promoting functions in colorectal cancer.
Du et al., Shanghai, China. In Am J Cancer Res, 2014
The MYBL2 gene plays an important role in the genesis and progression of tumors; however, few studies to date have defined the role of this gene in colorectal cancer (CRC).
Cellular senescence and aging: the role of B-MYB.
Jat et al., London, United Kingdom. In Aging Cell, 2014
MYB-related protein B (B-MYB/MYBL2), a member of the myeloblastosis family of transcription factors, has recently emerged as a potential candidate for regulating entry into senescence.
B-Myb, cancer, senescence, and microRNAs.
Dimaio et al., New Haven, United States. In Cancer Res, 2011
The transcription factor B-Myb plays a critical role in regulating gene expression and is implicated in controlling carcinogenesis and cellular senescence.
Mybl2 expression is under genetic control and contributes to determine a hepatocellular carcinoma susceptible phenotype.
Pascale et al., Sassari, Italy. In J Hepatol, 2011
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.
miR-34a induces the downregulation of both E2F1 and B-Myb oncogenes in leukemic cells.
Secchiero et al., Trieste, Italy. In Clin Cancer Res, 2011
Owing to the role of B-Myb and E2F1 transcription factors in controlling cell-cycle progression of leukemic cells, the downregulation of these oncogenes by miR-34a suggests the usefulness of therapeutic approaches aimed to modulate the levels of miR-34a.
Activation of v-Myb avian myeloblastosis viral oncogene homolog-like2 (MYBL2)-LIN9 complex contributes to human hepatocarcinogenesis and identifies a subset of hepatocellular carcinoma with mutant p53.
Pascale et al., Sassari, Italy. In Hepatology, 2011
MYBL2 activation is crucial for human HCC progression. In particular, our data indicate that MYBL2-LIN9 complex integrity contributes to survival of DNA damaged p53(-/-) cells.
miR-29 and miR-30 regulate B-Myb expression during cellular senescence.
DiMaio et al., New Haven, United States. In Proc Natl Acad Sci U S A, 2011
miR-29 and miR-30 regulate B-Myb expression by binding to its 3'UTR; these microRNAs play an important role in Rb-driven cellular senescence
Addiction of MYCN amplified tumours to B-MYB underscores a reciprocal regulatory loop.
Sala et al., London, United Kingdom. In Oncotarget, 2010
study concludes that MYCN and B-MYB are engaged in a reciprocal regulatory loop whose pharmacological targeting could be beneficial to patients with the aggressive forms of cancer in which MYCN is amplified
Stem cell pluripotency: a cellular trait that depends on transcription factors, chromatin state and a checkpoint deficient cell cycle.
Boheler, Baltimore, United States. In J Cell Physiol, 2009
Recently, B-MYB (MYBL2) was implicated in the gene regulation of two pluripotency factors and normal cell cycle progression.
Genetic and microenvironmental implications in prostate cancer progression and metastasis.
Alberti, Parma, Italy. In Eur Rev Med Pharmacol Sci, 2008
In metastatic prostate carcinoma some genes, such as MTA1 and MYBL2, are differentially upregulated in comparison to primary site, while IGFBP, DAN1, FAT and RAB5A appear to be downregulated.
B-MYB, a transcription factor implicated in regulating cell cycle, apoptosis and cancer.
Sala, London, United Kingdom. In Eur J Cancer, 2005
B-MYB belongs to the MYB family of transcription factors that include A-MYB and c-MYB.
The latent nuclear antigen of Kaposi sarcoma-associated herpesvirus targets the retinoblastoma-E2F pathway and with the oncogene Hras transforms primary rat cells.
Boshoff et al., London, United Kingdom. In Nat Med, 2000
LNA-1 transactivated an artificial promoter carrying the cell cycle transcription factor E2F DNA-binding sequences and also upregulated the cyclin E (CCNEI) promoter, but not the B-myb (MYBL2) promoter.
Cell cycle regulation of E2F site occupation in vivo.
Müller et al., Marburg an der Lahn, Germany. In Science, 1996
Here, a regulatory B-myb promoter site was shown to bind with high affinity to free E2F and to E2F-pocket protein complexes in an indistinguishable way in vitro.
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