HCSGD entry for SMARCB1
1. General information
| Official gene symbol | SMARCB1 |
|---|---|
| Entrez ID | 6598 |
| Gene full name | SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily b, member 1 |
| Other gene symbols | BAF47 INI1 MRD15 RDT RTPS1 SNF5 SNF5L1 Sfh1p Snr1 hSNFS |
| Links to Entrez Gene | Links to Entrez Gene |
2. Neighbors in the network
3. Gene ontology annotation
GO ID | GO term | Evidence | Category |
|---|---|---|---|
| GO:0000228 | Nuclear chromosome | IEA | cellular_component |
| GO:0001741 | XY body | IEA | cellular_component |
| GO:0001835 | Blastocyst hatching | IEA | biological_process |
| GO:0002039 | P53 binding | IPI | molecular_function |
| GO:0003713 | Transcription coactivator activity | IMP NAS | molecular_function |
| GO:0005515 | Protein binding | IPI | molecular_function |
| GO:0005634 | Nucleus | IDA | cellular_component |
| GO:0005654 | Nucleoplasm | TAS | cellular_component |
| GO:0005730 | Nucleolus | IDA | cellular_component |
| GO:0006281 | DNA repair | IBA | biological_process |
| GO:0006337 | Nucleosome disassembly | IDA | biological_process |
| GO:0006338 | Chromatin remodeling | IDA IEA | biological_process |
| GO:0006351 | Transcription, DNA-templated | IEA | biological_process |
| GO:0006357 | Regulation of transcription from RNA polymerase II promoter | NAS | biological_process |
| GO:0007399 | Nervous system development | IEA | biological_process |
| GO:0008285 | Negative regulation of cell proliferation | IBA | biological_process |
| GO:0015074 | DNA integration | TAS | biological_process |
| GO:0016514 | SWI/SNF complex | IDA | cellular_component |
| GO:0030154 | Cell differentiation | IBA | biological_process |
| GO:0030957 | Tat protein binding | IPI | molecular_function |
| GO:0039692 | Single stranded viral RNA replication via double stranded DNA intermediate | IDA | biological_process |
| GO:0043044 | ATP-dependent chromatin remodeling | IBA | biological_process |
| GO:0043923 | Positive regulation by host of viral transcription | IMP | biological_process |
| GO:0044772 | Mitotic cell cycle phase transition | IBA | biological_process |
| GO:0045944 | Positive regulation of transcription from RNA polymerase II promoter | IDA | biological_process |
| GO:0051091 | Positive regulation of sequence-specific DNA binding transcription factor activity | IDA | biological_process |
| GO:0071564 | NpBAF complex | ISS | cellular_component |
| GO:0071565 | NBAF complex | ISS | cellular_component |
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4. Expression levels in datasets
- Meta-analysis result
| p-value up | p-value down | FDR up | FDR down |
|---|---|---|---|
| 0.9766829110 | 0.0152873333 | 0.9999902473 | 0.2429828002 |
- 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 | Up | 0.0095081050 |
| GSE13712_SHEAR | Down | -0.2207258315 |
| GSE13712_STATIC | Down | -0.5963580194 |
| GSE19018 | Up | 0.0498698208 |
| GSE19899_A1 | Down | -0.2380325026 |
| GSE19899_A2 | Down | -1.7870638560 |
| PubMed_21979375_A1 | Down | -1.5629904575 |
| PubMed_21979375_A2 | Down | -0.6546055408 |
| GSE35957 | Down | -0.0887994167 |
| GSE36640 | Down | -1.5386812053 |
| GSE54402 | Down | -0.2755471763 |
| GSE9593 | Down | -0.0350148639 |
| GSE43922 | Down | -0.1763882674 |
| GSE24585 | Up | 0.0641826898 |
| GSE37065 | Down | -0.2540246089 |
| GSE28863_A1 | Up | 0.2236006222 |
| GSE28863_A2 | Down | -0.1353140591 |
| GSE28863_A3 | Down | -0.0692417704 |
| GSE28863_A4 | Down | -0.0762275326 |
| GSE48662 | Up | 0.1764496925 |
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-192-5p | MIMAT0000222 | MIRT004861 | Luciferase reporter assay//qRT-PCR//Reporter assay;Microarray;Other | Functional MTI | 19074876 |
| hsa-miR-1 | MIMAT0000416 | MIRT023864 | Proteomics | Functional MTI (Weak) | 18668040 |
| hsa-miR-215-5p | MIMAT0000272 | MIRT024448 | Microarray | Functional MTI (Weak) | 19074876 |
| hsa-let-7b-5p | MIMAT0000063 | MIRT051937 | CLASH | Functional 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: 3 abstracts the gene occurs.
PubMed ID of the article | Sentenece the gene occurs |
|---|---|
| 18332116 | We found previously that, in MRT cells, hSNF5 is required for p16(INK4a) induction, mitotic checkpoint activation, and cellular senescence |
| 18332116 | Gene activation by hSNF5 is strictly dependent on the SWI/SNF motor subunit BRG1 |
| 16288006 | Loss of the hSNF5 gene concomitantly inactivates p21CIP/WAF1 and p16INK4a activity associated with replicative senescence in A204 rhabdoid tumor cells |
| 16288006 | In MRT cell lines, reexpression of hSNF5 induces G1 cell cycle arrest, elevated p16INK4a, and activated replicative senescence markers, such as beta-galactosidase (beta-Gal) and plasminogen activator inhibitor-1 |
| 16288006 | To compare the replicative senescence caused by hSNF5 in A204 cells to normal cellular senescence, we examined the activation of both p16INK4a and p21CIP/WAF1 |
| 16288006 | Analogous to normal cellular senescence, both p16INK4a and p21CIP/WAF1 were up-regulated following hSNF5 restoration |
| 16288006 | Furthermore, we found that hSNF5 bound the p16INK4a and p21CIP/WAF1 promoters, suggesting that it directly regulates transcription of these genes |
| 16288006 | Using p16INK4a RNA interference, we showed its requirement for the replicative senescence caused by hSNF5 but not the growth arrest |
| 16288006 | Instead, p21CIP/WAF1 remained activated by hSNF5 in the absence of high p16INK4a expression, apparently causing the growth arrest in A204 |
| 16288006 | Interestingly, we also found that, in the absence of p16INK4a, reexpression of hSNF5 also increased protein levels of a second cyclin-dependent kinase (CDK) inhibitor, p18INK4c |
| 16288006 | However, our data show that lack of hSNF5 does not abrogate cellular responsiveness to DNA damage or growth-inhibitory factors |
| 16288006 | In summary, our studies suggest that hSNF5 loss may influence the regulation of multiple CDK inhibitors involved in replicative senescence |
| 14604992 | P16INK4a is required for hSNF5 chromatin remodeler-induced cellular senescence in malignant rhabdoid tumor cells |
| 14604992 | The hSNF5 chromatin-remodeling factor is a tumor suppressor that is inactivated in malignant rhabdoid tumors (MRTs) |
| 14604992 | A number of studies have shown that hSNF5 re-expression blocks MRT cell proliferation |
| 14604992 | However, the pathway through which hSNF5 acts remains unknown |
| 14604992 | To address this question, we generated MRT-derived cell lines in which restoration of hSNF5 expression leads to an accumulation in G(0)/G(1), induces cellular senescence and increased apoptosis |
| 14604992 | Following hSNF5 expression, we observed transcriptional activation of the tumor suppressor p16(INK4a) but not of p14(ARF), repression of several cyclins and CD44, a cell surface glycoprotein implicated in metastasis |
| 14604992 | Chromatin immunoprecipitations indicated that hSNF5 activates p16(INK4a) transcription and CD44 down-regulation by mediating recruitment of the SWI/SNF complex |
| 14604992 | Thus, hSNF5 acts as a dualistic co-regulator that, depending on the promoter context, can either mediate activation or repression |
| 14604992 | 1) Overexpression of p16(INK4a) mimics the effect of hSNF5 induction and leads to cellular senescence |
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