HCSGD entry for MYBL2
1. General information
| Official gene symbol | MYBL2 |
|---|---|
| Entrez ID | 4605 |
| Gene full name | v-myb myeloblastosis viral oncogene homolog (avian)-like 2 |
| Other gene symbols | B-MYB BMYB |
| Links to Entrez Gene | Links to Entrez Gene |
2. Neighbors in the network
3. Gene ontology annotation
GO ID | GO term | Evidence | Category |
|---|---|---|---|
| GO:0000278 | Mitotic cell cycle | TAS | biological_process |
| GO:0003677 | DNA binding | IEA | molecular_function |
| GO:0003682 | Chromatin binding | IEA | molecular_function |
| GO:0003700 | Sequence-specific DNA binding transcription factor activity | IEA | molecular_function |
| GO:0005515 | Protein binding | IPI | molecular_function |
| GO:0005634 | Nucleus | IEA | cellular_component |
| GO:0006351 | Transcription, DNA-templated | IEA | biological_process |
| GO:0007049 | Cell cycle | IEA | biological_process |
| GO:0031523 | Myb complex | IEA | cellular_component |
| GO:0090307 | Spindle assembly involved in mitosis | IEA | biological_process |
Entries Per Page
Displaying Page of
4. Expression levels in datasets
- Meta-analysis result
| p-value up | p-value down | FDR up | FDR down |
|---|---|---|---|
| 0.9881150184 | 0.0013637704 | 0.9999902473 | 0.0715648221 |
- Individual experiment result
( "-" represent NA in the specific microarray platform )
( "-" represent NA in the specific microarray platform )
| Data source | Up or down | Log fold change |
|---|---|---|
| GSE11954 | Down | -0.6128678332 |
| GSE13712_SHEAR | Down | -0.2919252047 |
| GSE13712_STATIC | Down | -0.4671560771 |
| GSE19018 | Up | 0.0926688225 |
| GSE19899_A1 | Down | -0.4102881447 |
| GSE19899_A2 | Down | -1.6761587476 |
| PubMed_21979375_A1 | Down | -0.7306985678 |
| PubMed_21979375_A2 | Down | -1.5046108924 |
| GSE35957 | Down | -0.8629798963 |
| GSE36640 | Down | -1.0753631074 |
| GSE54402 | Down | -0.2523563670 |
| GSE9593 | Down | -1.0194553787 |
| GSE43922 | Down | -1.1638077595 |
| GSE24585 | Up | 0.0568817309 |
| GSE37065 | Down | -0.7532127204 |
| GSE28863_A1 | Down | -0.3164875698 |
| GSE28863_A2 | Up | 0.0747429650 |
| GSE28863_A3 | Up | 0.0075112292 |
| GSE28863_A4 | Up | 0.1381388230 |
| GSE48662 | Down | -0.3737066852 |
5. Regulation relationships with compounds/drugs/microRNAs
- Compounds
Not regulated by compounds
- Drugs
Not regulated by drugs
- MicroRNAs
- mirTarBase
- mirTarBase
MiRNA_name | mirBase ID | miRTarBase ID | Experiment | Support type | References (Pubmed ID) |
|---|---|---|---|---|---|
| hsa-miR-149-3p | MIMAT0004609 | MIRT021213 | Reporter assay;Western blot;qRT-PCR | Functional MTI | 20623644 |
| hsa-miR-423-5p | MIMAT0004748 | MIRT038033 | CLASH | Functional MTI (Weak) | 23622248 |
| hsa-miR-505-3p | MIMAT0002876 | MIRT041019 | CLASH | Functional MTI (Weak) | 23622248 |
| hsa-miR-92a-3p | MIMAT0000092 | MIRT049701 | CLASH | Functional MTI (Weak) | 23622248 |
Entries Per Page
Displaying Page of
- mirRecord
No target information from mirRecord
- 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 |
|---|---|
| 24981831 | Cellular senescence and aging: the role of B-MYB |
| 24981831 | 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 |
| 24981831 | Here, we review the evidence which indicates that loss of B-MYB expression has an important role in causing senescence growth arrest |
| 24981831 | We 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 |
| 24981831 | We 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 |
| 24659628 | With aging, p85alpha, IGF-1 and B-myb muscle levels were lower while the expression of certain cell arrest proteins (p53, p16 and pRB) increased |
| 24659628 | Impaired 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 |
| 24659628 | Thus, 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 |
| 21828240 | B-Myb, cancer, senescence, and microRNAs |
| 21828240 | The transcription factor B-Myb plays a critical role in regulating gene expression and is implicated in controlling carcinogenesis and cellular senescence |
| 21828240 | Transcription of the B-Myb gene is regulated by retinoblastoma proteins acting directly on the B-Myb promoter |
| 21828240 | Recently, we found that microRNAs also control the abundance of B-Myb mRNA during senescence, adding another level of complexity to B-Myb regulation |
| 21828240 | This review focuses on the importance of B-Myb in cancer and senescence, with an emphasis on the regulation of B-Myb expression and activity |
| 21187425 | Expression 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 |
| 21187425 | In 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 |
| 21187425 | These 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 |
| 20734103 | In human embryonic lung fibroblast cells, B-MYB downregulated p16 ( INK4alpha ) expression, whereas knocking down of B-MYB upregulated it |
| 20734103 | Evidence 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 |
| 20734103 | This study provides evidence of the capacity of B-MYB not only to regulate p16 ( INK4alpha ) expression but also the phenotypic consequence on cellular senescence |
| 15923606 | We have shown that MRGX and MRG15 associate with Rb in nucleoprotein complexes and regulate B-myb promoter activity |
| 15610763 | Other 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 |
| 11500496 | MRG15 activates the B-myb promoter through formation of a nuclear complex with the retinoblastoma protein and the novel protein PAM14 |
| 11500496 | Although 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 |
| 11500496 | Significantly we have demonstrated that MRG15 blocks the Rb-induced repression of this promoter, leading to B-myb promoter activation |
| 8853900 | We 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 |
Entries Per Page
Displaying Page of
