HCSGD entry for HDAC9
1. General information
| Official gene symbol | HDAC9 |
|---|---|
| Entrez ID | 9734 |
| Gene full name | histone deacetylase 9 |
| Other gene symbols | HD7 HD7b HD9 HDAC HDAC7 HDAC7B HDAC9B HDAC9FL HDRP MITR |
| Links to Entrez Gene | Links to Entrez Gene |
2. Neighbors in the network
3. Gene ontology annotation
GO ID | GO term | Evidence | Category |
|---|---|---|---|
| GO:0000118 | Histone deacetylase complex | TAS | cellular_component |
| GO:0000122 | Negative regulation of transcription from RNA polymerase II promoter | IDA IEA | biological_process |
| GO:0003714 | Transcription corepressor activity | IEA ISS | molecular_function |
| GO:0004407 | Histone deacetylase activity | IDA | molecular_function |
| GO:0005080 | Protein kinase C binding | IPI | molecular_function |
| GO:0005515 | Protein binding | IPI | molecular_function |
| GO:0005634 | Nucleus | IDA | cellular_component |
| GO:0005654 | Nucleoplasm | TAS | cellular_component |
| GO:0005667 | Transcription factor complex | IDA | cellular_component |
| GO:0005737 | Cytoplasm | IDA TAS | cellular_component |
| GO:0006351 | Transcription, DNA-templated | IEA | biological_process |
| GO:0006954 | Inflammatory response | TAS | biological_process |
| GO:0007219 | Notch signaling pathway | TAS | biological_process |
| GO:0007507 | Heart development | IEA ISS | biological_process |
| GO:0008134 | Transcription factor binding | IDA IPI | molecular_function |
| GO:0016575 | Histone deacetylation | IDA | biological_process |
| GO:0030183 | B cell differentiation | TAS | biological_process |
| GO:0032041 | NAD-dependent histone deacetylase activity (H3-K14 specific) | IEA | molecular_function |
| GO:0032869 | Cellular response to insulin stimulus | IDA | biological_process |
| GO:0033558 | Protein deacetylase activity | IDA | molecular_function |
| GO:0034983 | Peptidyl-lysine deacetylation | IDA | biological_process |
| GO:0035097 | Histone methyltransferase complex | IEA ISS | cellular_component |
| GO:0042113 | B cell activation | TAS | biological_process |
| GO:0042826 | Histone deacetylase binding | IDA IPI | molecular_function |
| GO:0045892 | Negative regulation of transcription, DNA-templated | IDA | biological_process |
| GO:0046872 | Metal ion binding | IEA | molecular_function |
| GO:0046969 | NAD-dependent histone deacetylase activity (H3-K9 specific) | IEA | molecular_function |
| GO:0046970 | NAD-dependent histone deacetylase activity (H4-K16 specific) | IEA | molecular_function |
| GO:0048742 | Regulation of skeletal muscle fiber development | IEA ISS | biological_process |
| GO:0051153 | Regulation of striated muscle cell differentiation | ISS | biological_process |
| GO:0070491 | Repressing transcription factor binding | IDA IEA IPI ISS | molecular_function |
| GO:0070932 | Histone H3 deacetylation | IDA | biological_process |
| GO:0070933 | Histone H4 deacetylation | IDA | biological_process |
| GO:0090050 | Positive regulation of cell migration involved in sprouting angiogenesis | IMP | biological_process |
| GO:0097372 | NAD-dependent histone deacetylase activity (H3-K18 specific) | IEA | molecular_function |
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4. Expression levels in datasets
- Meta-analysis result
| p-value up | p-value down | FDR up | FDR down |
|---|---|---|---|
| 0.0027847916 | 0.9787866608 | 0.1417765957 | 1.0000000000 |
- 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 | 0.5781584302 |
| GSE13712_SHEAR | Up | 0.6335974783 |
| GSE13712_STATIC | Up | 0.6875149800 |
| GSE19018 | Up | 0.5309105584 |
| GSE19899_A1 | Up | 0.2337075024 |
| GSE19899_A2 | Up | 1.5803157131 |
| PubMed_21979375_A1 | Up | 1.1900320489 |
| PubMed_21979375_A2 | Up | 1.3020707606 |
| GSE35957 | Up | 1.0220733301 |
| GSE36640 | Up | 0.8225065425 |
| GSE54402 | Up | 0.4133651491 |
| GSE9593 | Up | 0.4922259427 |
| GSE43922 | Up | 0.0525774476 |
| GSE24585 | Up | 0.0731241110 |
| GSE37065 | Up | 0.3194381960 |
| GSE28863_A1 | Down | -0.7787621859 |
| GSE28863_A2 | Up | 0.0413427972 |
| GSE28863_A3 | Down | -0.3005112947 |
| GSE28863_A4 | Down | -0.0854980545 |
| GSE48662 | Down | -0.0388629490 |
5. Regulation relationships with compounds/drugs/microRNAs
- Compounds
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- Drugs
Name | Drug | Accession number |
|---|---|---|
| Panobinostat | DB06603 | - |
- MicroRNAs
- mirTarBase
No target information from mirTarBase
- mirTarBase
- mirRecord
No target information from mirRecord
- mirRecord
6. Text-mining results about the gene
Gene occurances in abstracts of cellular senescence-associated articles: 30 abstracts the gene occurs.
PubMed ID of the article | Sentenece the gene occurs |
|---|---|
| 25737447 | Specifically, we show that sodium butyrate (NaB) and panobinostat (LBH589), two broad-spectrum HDAC inhibitors up-regulate hsa-miR-31 (miR-31) |
| 25672483 | Additionally, ING2 recruits histone methyltransferase (HMT) activity for gene repression, which is independent of the HDAC class I or II pathway |
| 25070040 | Inhibition of HDAC increases the senescence induced by natural polyphenols in glioma cells |
| 25070040 | These polyphenols modulate the activity of several proteins involved in cell growth and death in cancer cells, including histone deacetylases (HDAC), but the role of HDAC in senescence induced by Rsv and Quer is unclear |
| 25070040 | The HDAC inhibitor sodium butyrate (NaB) potentiated the pro-senescent effect of Rsv and Quer in human and rat glioma cell lines but not in normal rat astrocytes |
| 25070040 | Altogether, these data support a positive role of HDAC inhibition on the senescence induced by these polyphenols, and therefore co-treatment of HDAC inhibitors and polyphenols emerges as a potential alternative for gliomas |
| 24721210 | HDAC inhibitors induce apoptosis but not cellular senescence in Gadd45alpha-deficient E1A+Ras cells |
| 24721210 | HDAC inhibitors (HDIs) induce irreversible cell cycle arrest and senescence in E1A+Ras expressing cells |
| 24304587 | Epigenetic modulation by HDAC inhibition is a potentially valuable approach for hepatocellular carcinoma treatment |
| 24304587 | In present study, we evaluated the anticancer effects of sodium valproate (SVP), a known HDAC inhibitor, in human hepatocarcinoma cells |
| 23841748 | For instance, valproic acid (VPA), a histone deacetylase (HDAC) inhibitor, has been shown to promote self-renewal/expansion of hematopoietic stem cells and facilitate the generation of induced pluripotent stem cells (iPSCs) |
| 25961265 | HDAC inhibitors repress cancer growth and are used in various clinical trials |
| 25961265 | We found that the HDAC inhibitors NaBu and valproic acid (VPA) induce cellular senescence in tumor cells |
| 25961265 | Interestingly, also an inhibitor of SIRT1, a class HDAC III, induces cellular senescence |
| 25961265 | These results indicate an epigenetic regulation and an association of HDAC inhibition and ROS production with cellular senescence |
| 25961265 | The data underline that tumor cells can be driven towards cellular senescence by HDAC inhibitors, which may further arise as a potent possibility for tumor suppression |
| 21598691 | The capacity of HDAC inhibitor sodium butyrate to induce senescence in cells derived from rat embryonic fibroblasts transformed by E1A+E1B19 kDa oncogenes has been studied |
| 21420382 | Herein, we report that the growth and division of tumor cells were significantly repressed by overexpression of histone deacetylase (HDAC) 1 with the Tet-off induced system or transient transfection |
| 21383005 | Depletion of EZH2 synergistically activates p21/CDKN1A expression in combination with the HDAC inhibitor trichostatin A |
| 21228624 | These changes in chromatin ultrastructure also correlated with increased histone H4 acetylation, and treatment with the HDAC inhibitor TSA failed to further increase PML NB number |
| 20935470 | HDAC inhibitors (HDACI) induce senescence and/or apoptosis in many types of tumor cells |
| 20692358 | HDAC inhibitor-induced activation of NF-kappaB prevents apoptotic response of E1A+Ras-transformed cells to proapoptotic stimuli |
| 20692358 | HDAC inhibitors (HDACIs) are capable of suppressing the cell growth of tumour cells due to the induction of apoptosis and/or cell cycle arrest |
| 20692358 | In this report, we addressed the issue by analysing effects produced in E1A+Ras-transformed MEF cells by HDAC inhibitors sodium butyrate (NaB), Trichostatin A (TSA) and some others |
| 20652617 | Here, we observed that the cellular senescence of human umbilical cord blood-derived multipotent stem cells (hUCB-MSCs) caused by inhibition of histone deacetylase (HDAC) activity leads to down-regulation of high mobility group A2 (HMGA2) and, on the contrary, to up-regulation of p16(INK)(4)(A), p21(CIP)(1)(/WAF)(1) and p27(KIP)(1) |
| 20049504 | Similarly, HDAC inhibitors induced cellular senescence through downregulation of PcGs and upregulation of JMJD3 |
| 20049504 | Regulation of PcGs was associated with HDAC inhibitor-induced hypophosphorylation of RB, which causes RB to bind to and decrease the transcriptional activity of E2F |
| 20049504 | These results suggest that HDAC activity might be important for MSC self-renewal by balancing PcGs and JMJD3 expression, which govern cellular senescence by p16(INK4A) regulation |
| 19689470 | OBJECTIVES: Histone deacetylase (HDAC) is an important therapeutic target in cancer |
| 19689470 | Two of the main anticancer mechanisms of HDAC inhibitors are induction of terminal differentiation and inhibition of cell proliferation |
| 19689470 | To investigate the role of HDAC in maintenance of self-renewal and cell proliferation, we treated mesenchymal stem cells (MSCs) that originated from adipose tissue or umbilical cord blood with valproic acid (VPA) and sodium butyrate (NaBu) |
| 19689470 | The expression level of p16(INK4A), a cdk inhibitor that is closely related to cellular senescence, was not changed by HDAC inhibitor treatment |
| 19689470 | We performed controlled differentiation into bone, fat, cartilage and nervous tissue to elucidate the role of HDAC in the pluripotency of MSC to differentiate into functional tissues |
| 19689470 | In contrast, osteogenic differentiation was elevated by HDAC inhibitor treatment |
| 19689470 | CONCLUSION: HDAC activity is essential for maintaining the self-renewal and pluripotency of MSCs |
| 19583777 | We also show that histone deacetylase (HDAC) 3 and HDAC4 inhibited p16(INK4a) promoter activity in a dose-dependent manner |
| 19442115 | The ING proteins function as tethering molecules that physically link the HDAC and HAT enzymatic complexes to chromatin |
| 19122829 | In this study, the effects of histone deacetylase (HDAC) inhibitors on the activation, proliferation, migration and senescence of corneal stromal cells were evaluated |
| 19122829 | The responses of corneal stromal cells to HDAC inhibitors were characterized by cDNA microarray, real time PCR, immunocytochemistry and western blot analysis |
| 19122829 | The effects of HDAC inhibitors on corneal fibroblast proliferation, cell cycle distribution, migration and senescence were also assessed in vitro |
| 19122829 | RESULTS: Fetal bovine serum and TGFbeta1 activated the transdifferentiation of corneal stromal cells into fibroblasts and myofibroblasts, indicated by cell spreading, renewed assembly of actin filaments and enhanced expression of extracellular matrix components, all of which were suppressed by the addition of HDAC inhibitors |
| 19122829 | HDAC inhibitors inhibited the proliferation of corneal fibroblasts by decreasing the proportion in the S-phase and increasing the proportion in the G0/G1 and G2/M cell cycle checkpoints |
| 19122829 | HDAC inhibitors showed a dose-dependent inhibitory effects on the migration of corneal fibroblasts |
| 19122829 | In addition, HDAC inhibitors induced the senescence of corneal myofibroblasts as shown by enhanced staining of beta-galactosidase and upregulated expression of p16(ink4a) |
| 19122829 | CONCLUSIONS: HDAC inhibitors may affect corneal stromal cells by inhibiting myofibroblastic differentiation, cell proliferation, migration and by inducing cell senescence |
| 18691180 | The ING family of tumor suppressor proteins affects cell growth, apoptosis and response to DNA damage by modulating chromatin structure through association with different HAT and HDAC complexes |
| 18691180 | Gene expression appears to be altered by targeting of HDAC complexes to gene promoters since INGla associates with several-fold higher levels of HDAC1 in senescent, compared to replication-competent cells and ING1 is found on the PCNA promoter by chromatin immunoprecipitation analysis |
| 18231726 | Several cellular stresses have been shown to induce a senescence-like growth arrest including shortened telomeres, DNA-damaging stresses, and drastic changes in chromatin structure, for example, through histone deacetylase (HDAC) induction |
| 18193082 | We therefore propose a novel mechanism of class I HDAC regulation by a class III HDAC |
| 17657594 | Cytoplasmic and nuclear fractions of treated cells were tested for HDAC activity at 2 and 12 h both in the presence and absence of TSA, however, there was no significant change in their HDAC activity |
| 17578512 | This senescence response is likely due to chromatin modifications because RB complexes from senescent melanocytes contain increased levels of histone deacetylase (HDAC) activity and tethered HDAC1 |
| 17409421 | Histone deacetylase (HDAC) inhibitors are emerging as promising cancer therapeutics |
| 17409421 | HDAC inhibitors have been found to induce cellular activities that are strikingly similar to p53-mediated responses to genotoxic stress |
| 17409421 | For example, HDAC inhibitors induce cell cycle arrest, apoptosis, and cellular senescence |
| 17409421 | Because at least 11 HDACs are affected by the current HDAC inhibitors, the HDAC critical for tumor cell survival and proliferation remains unknown |
| 17409421 | Thus, for the first time, our data suggest that HDAC inhibitors function through the p53 pathway, at least in part, by activating p53-DNA binding activity |
| 17316622 | Treatment with a histone deacetylase (HDAC) inhibitor has activated the expression of p15(INK4b) in wild-type MEFs but has no effect in MEFs lacking Oct-1, suggesting that Oct-1 represses p15(INK4b) gene expression in an HDAC-dependent manner |
| 16250917 | Here we examine the influence of HDAC inhibitors on the expression of senescent markers in pre- and post-senescent WI-38 cells |
| 16250917 | RESULTS: Pre- and post-senescent WI-38 cells were treated with the HDAC inhibitors butyrate or trichostatin A (TSA) |
| 16250917 | Following HDAC inhibitor treatment, pre-senescent cells increased p21WAF1 and beta-galactosidase expression, assumed a flattened senescence-associated morphology, and maintained a lower level of proteasome activity |
| 16250917 | These alterations also occurred during normal replicative senescence of WI-38 cells, but were not accentuated further by HDAC inhibitors |
| 16167330 | At the molecular level, ING proteins are thought to function as chromatin regulatory molecules, acting as co-factors for distinct histone and factor acetyl-transferase (H/FAT) and deacetylase (HDAC) enzyme complexes |
| 15489886 | Lastly, we have identified two genes, topoisomerase IIalpha and HDAC9, whose expression was specifically altered under several conditions associated with senescence, suggesting that these two molecules may be novel biomarkers for senescent human fibroblasts |
| 15263087 | Here we show the small-molecule-based identification of the assembly and disassembly of E2F-pocket protein-histone deacetylase (HDAC) complex as a key mechanistic basis for the repression and activation of hTERT in normal human cells |
| 15263087 | CGK1026 inhibits the recruitment of HDAC into E2F-pocket protein complexes assembled on the hTERT promoter |
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