HCSGD entry for MYBL2


1. General information

Official gene symbolMYBL2
Entrez ID4605
Gene full namev-myb myeloblastosis viral oncogene homolog (avian)-like 2
Other gene symbolsB-MYB BMYB
Links to Entrez GeneLinks to Entrez Gene

2. Neighbors in the network

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3. Gene ontology annotation

GO ID

GO term

Evidence

Category

GO:0000278Mitotic cell cycleTASbiological_process
GO:0003677DNA bindingIEAmolecular_function
GO:0003682Chromatin bindingIEAmolecular_function
GO:0003700Sequence-specific DNA binding transcription factor activityIEAmolecular_function
GO:0005515Protein bindingIPImolecular_function
GO:0005634NucleusIEAcellular_component
GO:0006351Transcription, DNA-templatedIEAbiological_process
GO:0007049Cell cycleIEAbiological_process
GO:0031523Myb complexIEAcellular_component
GO:0090307Spindle assembly involved in mitosisIEAbiological_process
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4. Expression levels in datasets

  • Meta-analysis result

p-value upp-value downFDR upFDR down
0.98811501840.00136377040.99999024730.0715648221

  • Individual experiment result
    ( "-" represent NA in the specific microarray platform )

Data sourceUp or downLog fold change
GSE11954Down-0.6128678332
GSE13712_SHEARDown-0.2919252047
GSE13712_STATICDown-0.4671560771
GSE19018Up0.0926688225
GSE19899_A1Down-0.4102881447
GSE19899_A2Down-1.6761587476
PubMed_21979375_A1Down-0.7306985678
PubMed_21979375_A2Down-1.5046108924
GSE35957Down-0.8629798963
GSE36640Down-1.0753631074
GSE54402Down-0.2523563670
GSE9593Down-1.0194553787
GSE43922Down-1.1638077595
GSE24585Up0.0568817309
GSE37065Down-0.7532127204
GSE28863_A1Down-0.3164875698
GSE28863_A2Up0.0747429650
GSE28863_A3Up0.0075112292
GSE28863_A4Up0.1381388230
GSE48662Down-0.3737066852

5. Regulation relationships with compounds/drugs/microRNAs

  • Compounds

Not regulated by compounds

  • Drugs

Not regulated by drugs

  • MicroRNAs

  • mirTarBase

MiRNA_name

mirBase ID

miRTarBase ID

Experiment

Support type

References (Pubmed ID)

hsa-miR-149-3pMIMAT0004609MIRT021213Reporter assay;Western blot;qRT-PCRFunctional MTI20623644
hsa-miR-423-5pMIMAT0004748MIRT038033CLASHFunctional MTI (Weak)23622248
hsa-miR-505-3pMIMAT0002876MIRT041019CLASHFunctional MTI (Weak)23622248
hsa-miR-92a-3pMIMAT0000092MIRT049701CLASHFunctional MTI (Weak)23622248
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  • mirRecord
No target information from mirRecord

6. Text-mining results about the gene

Gene occurances in abstracts of cellular senescence-associated articles: 9 abstracts the gene occurs.


PubMed ID of the article

Sentenece the gene occurs

24981831Cellular senescence and aging: the role of B-MYB
24981831MYB-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
24981831Here, we review the evidence which indicates that loss of B-MYB expression has an important role in causing senescence growth arrest
24981831We discuss how B-MYB acts, as the gatekeeper, to coordinate transit through the cell cycle, in conjunction with the multivulval class B (MuvB) complex and FOXM1 transcription factors
24981831We also evaluate the evidence connecting B-MYB to the mTOR nutrient signaling pathway and suggest that inhibition of this pathway leading to an extension of healthspan may involve activation of B-MYB
24659628With aging, p85alpha, IGF-1 and B-myb muscle levels were lower while the expression of certain cell arrest proteins (p53, p16 and pRB) increased
24659628Impaired MPC proliferation resulted from interactions between miR-29 and the 3'-UTR of p85a, IGF-1 and B-myb, suppressing the translation of these mediators of myoblast proliferation
24659628Thus, aging-induced muscle senescence results from activation of miR-29 by Wnt-3a leading to suppressed expression of several signaling proteins (p85alpha, IGF-1 and B-myb) that act coordinately to impair the proliferation of MPCs contributing to muscle atrophy
21828240B-Myb, cancer, senescence, and microRNAs
21828240The transcription factor B-Myb plays a critical role in regulating gene expression and is implicated in controlling carcinogenesis and cellular senescence
21828240Transcription of the B-Myb gene is regulated by retinoblastoma proteins acting directly on the B-Myb promoter
21828240Recently, we found that microRNAs also control the abundance of B-Myb mRNA during senescence, adding another level of complexity to B-Myb regulation
21828240This review focuses on the importance of B-Myb in cancer and senescence, with an emphasis on the regulation of B-Myb expression and activity
21187425Expression of a reporter construct containing the 3'UTR of the B-Myb oncogene is repressed during senescence, and repression is blocked by mutations in conserved miR-29 and miR-30 binding sites in the B-Myb 3'UTR
21187425In proliferating cells, transfection of miR-29 and miR-30 represses a reporter construct containing the wild-type but not the mutant B-Myb 3'UTR, and repression of the mutant 3'UTR is reinstituted by compensatory mutations in miR-29 and miR-30 that restore binding to the mutant sites
21187425These findings demonstrate that miR-29 and miR-30 regulate B-Myb expression by binding to its 3'UTR and suggest that these microRNAs play an important role in Rb-driven cellular senescence
20734103In human embryonic lung fibroblast cells, B-MYB downregulated p16 ( INK4alpha ) expression, whereas knocking down of B-MYB upregulated it
20734103Evidence also showed that overexpression of B-MYB in cells could increase the number of utmost passage and decrease G1 block, whereas knocking down of B-MYB could impair their replicative ability
20734103This study provides evidence of the capacity of B-MYB not only to regulate p16 ( INK4alpha ) expression but also the phenotypic consequence on cellular senescence
15923606We have shown that MRGX and MRG15 associate with Rb in nucleoprotein complexes and regulate B-myb promoter activity
15610763Other genes, such as Cdc28 protein kinase 1 (Cks1b), v-myb myeloblastosis viral oncogene homolog (MybL2), pyruvate kinase, muscle 2 (Pkm2) and Forkhead box M1 (FoxM1), were down-regulated only upon TGF-beta1 treatment but not by cellular senescence
11500496MRG15 activates the B-myb promoter through formation of a nuclear complex with the retinoblastoma protein and the novel protein PAM14
11500496Although the functions of PAM14 have yet to be elucidated, Rb has several well characterized activities, including repression of E2F-activated promoters such as that of B-myb
11500496Significantly we have demonstrated that MRG15 blocks the Rb-induced repression of this promoter, leading to B-myb promoter activation
8853900We show that forced expression of a number of cell cycle-regulatory genes, including erbB-2, v-ras, v-myc, B-myb, ld-1, and E2F-1, alone or in combinations, cannot induce terminally differentiated skeletal muscle cells (myotubes) to synthesize DNA
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