HCSGD entry for SUV39H1
1. General information
| Official gene symbol | SUV39H1 |
|---|---|
| Entrez ID | 6839 |
| Gene full name | suppressor of variegation 3-9 homolog 1 (Drosophila) |
| Other gene symbols | KMT1A MG44 SUV39H |
| Links to Entrez Gene | Links to Entrez Gene |
2. Neighbors in the network
3. Gene ontology annotation
GO ID | GO term | Evidence | Category |
|---|---|---|---|
| GO:0000183 | Chromatin silencing at rDNA | IDA | biological_process |
| GO:0000775 | Chromosome, centromeric region | IEA | cellular_component |
| GO:0000792 | Heterochromatin | IDA | cellular_component |
| GO:0000794 | Condensed nuclear chromosome | TAS | cellular_component |
| GO:0003682 | Chromatin binding | TAS | molecular_function |
| GO:0005515 | Protein binding | IPI | molecular_function |
| GO:0005634 | Nucleus | IDA IEA | cellular_component |
| GO:0005652 | Nuclear lamina | IEA | cellular_component |
| GO:0005654 | Nucleoplasm | IEA | cellular_component |
| GO:0005677 | Chromatin silencing complex | IDA | cellular_component |
| GO:0005694 | Chromosome | IEA | cellular_component |
| GO:0006325 | Chromatin organization | TAS | biological_process |
| GO:0006351 | Transcription, DNA-templated | IEA | biological_process |
| GO:0006364 | RRNA processing | IEA | biological_process |
| GO:0007049 | Cell cycle | IEA | biological_process |
| GO:0008270 | Zinc ion binding | IEA | molecular_function |
| GO:0008757 | S-adenosylmethionine-dependent methyltransferase activity | IDA | molecular_function |
| GO:0016032 | Viral process | IEA | biological_process |
| GO:0018022 | Peptidyl-lysine methylation | IDA | biological_process |
| GO:0018024 | Histone-lysine N-methyltransferase activity | IDA IEA | molecular_function |
| GO:0030154 | Cell differentiation | IEA | biological_process |
| GO:0033553 | RDNA heterochromatin | IDA | cellular_component |
| GO:0042054 | Histone methyltransferase activity | IDA | molecular_function |
| GO:0046974 | Histone methyltransferase activity (H3-K9 specific) | IDA | molecular_function |
| GO:0047485 | Protein N-terminus binding | IPI | molecular_function |
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4. Expression levels in datasets
- Meta-analysis result
| p-value up | p-value down | FDR up | FDR down |
|---|---|---|---|
| 0.2205005623 | 0.0598893811 | 0.9019175229 | 0.4605166228 |
- 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 | 0.1540507872 |
| GSE13712_SHEAR | Up | 0.4799146026 |
| GSE13712_STATIC | Up | 0.0283545990 |
| GSE19018 | Up | 0.0575911472 |
| GSE19899_A1 | Up | 0.0215193620 |
| GSE19899_A2 | Down | -0.5961153217 |
| PubMed_21979375_A1 | Up | 0.9112981423 |
| PubMed_21979375_A2 | Up | 0.8617499625 |
| GSE35957 | Down | -0.8241018455 |
| GSE36640 | Down | -2.5953579960 |
| GSE54402 | Up | 0.4289916398 |
| GSE9593 | Down | -0.9137673161 |
| GSE43922 | Up | 0.0489784271 |
| GSE24585 | Down | -0.4029861672 |
| GSE37065 | Down | -0.3574218579 |
| GSE28863_A1 | Down | -0.1673481275 |
| GSE28863_A2 | Up | 0.5913014490 |
| GSE28863_A3 | Down | -0.1734905124 |
| GSE28863_A4 | Up | 0.0306759851 |
| GSE48662 | Down | -0.3903937162 |
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-98-5p | MIMAT0000096 | MIRT027407 | Microarray | Functional MTI (Weak) | 19088304 |
| hsa-miR-615-3p | MIMAT0003283 | MIRT040438 | CLASH | Functional MTI (Weak) | 23622248 |
| hsa-miR-331-3p | MIMAT0000760 | MIRT043442 | 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: 13 abstracts the gene occurs.
PubMed ID of the article | Sentenece the gene occurs |
|---|---|
| 26160351 | Although WRN plays a role in DNA repair, WRN exerted its effects on aging via maintaining heterochromatin, evidenced by reduced levels of interacting chromatin regulators heterochromatin protein 1alpha (HP1alpha), suppressor of variegation 3-9 homolog 1 (SUV39H1), and lamina-associated polypeptide 2beta (LAP2beta) as well as modified histone H3K9me3 |
| 26160351 | Reducing expression of chromatin modeling co-factors SUV39H1 or HP1alpha in wild-type MSCs recapitulates the phenotype of WRN deficiency, resulting in reduced H3K9me3 levels and increased senescence without induction of markers of DNA damage, suggesting that chromatin disorganization and not DNA damage is responsible for the pathology of WS during aging in animals |
| 25931448 | We show that WRN associates with heterochromatin proteins SUV39H1 and HP1alpha and nuclear lamina-heterochromatin anchoring protein LAP2beta |
| 25931448 | Targeted knock-in of catalytically inactive SUV39H1 in wild-type MSCs recapitulates accelerated cellular senescence, resembling WRN-deficient MSCs |
| 25484892 | SUV39H1 downregulation induces deheterochromatinization of satellite regions and senescence after exposure to ionizing radiation |
| 25484892 | Furthermore, we propose a role of the downregulation of SUV39H1 expression, a histone methyltransferase that specifically trimethylates H3K9, and the corresponding reduction in H3K9me3 levels in the establishment of IR-induced senescence |
| 25359189 | We show that TERRA associates with SUV39H1 H3K9 histone methyltransferase, which promotes accumulation of H3K9me3 at damaged telomeres and end-to-end fusions |
| 25063769 | This indicates that SUV39H1 plays a role in limiting genomic instability in dividing cells and suggests that SUV39H1 downregulation may contribute to the establishment of senescence by increasing genomic instability |
| 25063769 | Thus, based on our findings and the results from previous reports, we propose a model in which SUV39H1 downregulation promotes the establishment of cellular senescence |
| 23945590 | Here we use the Emicro-myc transgenic mouse lymphoma model in which TIS depends on the H3K9 histone methyltransferase Suv39h1 to show the mechanism and therapeutic exploitation of senescence-related metabolic reprogramming in vitro and in vivo |
| 22991213 | Histone lysine methyltransferase, suppressor of variegation 3-9 homolog 1, promotes hepatocellular carcinoma progression and is negatively regulated by microRNA-125b |
| 22991213 | Suppressor of variegation 3-9 homolog 1 (SUV39H1), the prototype of histone methyltransferase, is the major enzyme responsible for histone H3 lysine 9 trimethylation, which, essentially, is involved in heterochromatin formation, chromosome segregation, and mitotic progression |
| 22991213 | However, the implication of SUV39H1 in hepatocarcinogenesis remains elusive |
| 22991213 | In this study, we found that SUV39H1 was frequently up-regulated in human HCCs and was significantly associated with increased Ki67 expression (P < 0 |
| 22991213 | SUV39H1 overexpression remarkably enhanced HCC cell clonogenicity, whereas knockdown of SUV39H1 substantially suppressed HCC cell proliferation and induced cell senescence |
| 22991213 | In addition, ectopic expression of SUV39H1 increased the migratory ability of HCC cells, whereas a reduced migration rate was observed in SUV39H1 knockdown cells |
| 22991213 | We also identified microRNA-125b (miR-125b) as a post-transcriptional regulator of SUV39H1 |
| 22991213 | Ectopic expression of miR-125b inhibited SUV39H1 3'-untranslated-region-coupled luciferase activity and suppressed endogenous SUV39H1 expression at both messenger RNA and protein levels |
| 22991213 | The tumor-suppressive miR-125b served as a negative regulator of SUV39H1 |
| 20818171 | Other gene products like p53, SUV39H1 or TGFbeta promoted senescence, which together with apoptosis contributed to tumor suppression |
| 20227040 | Accordingly, neutralization of TGF-beta action, like genetic inactivation of the senescence-related histone methyltransferase Suv39h1, significantly accelerates Myc-driven tumor development via cancellation of cellular senescence |
| 20069564 | This nuclear arrangement was influenced by deficiency of the histone methyltransferase SUV39h, LMNA deficiency, and the histone deacetylase inhibitor Trichostatin A (TSA) |
| 20069564 | This association was increased by SUV39h deficiency and decreased by LMNA deficiency |
| 20069564 | These differences could be explained by differing levels of the telomerase subunit, TERT, in SUV39h- and LMNA-deficient fibroblasts |
| 20069564 | Taken together, our data show that SUV39h and A-type lamins likely play a key role in telomere maintenance and telomere nuclear architecture |
| 19345325 | Furthermore, Rb heterozygous mice additionally lacking any of Ink4a, Arf, or Suv39h1 generated C cell adenocarcinomas, suggesting that cellular senescence antagonizes Rb-deficient carcinogenesis |
| 16705168 | The ablation of prohibitin prevented the recruitment of HPIgamma, but not Suv39H, to the promoters upon senescence |
| 16079837 | Recently, Rb-mediated silencing of growth-promoting genes by heterochromatin formation associated with methylation of histone H3 lysine 9 (H3K9me) was identified as a critical feature of cellular senescence, which may depend on the histone methyltransferase Suv39h1 |
| 16079837 | Here we show that Emicro-N-Ras transgenic mice harbouring targeted heterozygous lesions at the Suv39h1, or the p53 locus for comparison, succumb to invasive T-cell lymphomas that lack expression of Suv39h1 or p53, respectively |
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