HCSGD entry for ID1
1. General information
| Official gene symbol | ID1 |
|---|---|
| Entrez ID | 3397 |
| Gene full name | inhibitor of DNA binding 1, dominant negative helix-loop-helix protein |
| Other gene symbols | ID bHLHb24 |
| Links to Entrez Gene | Links to Entrez Gene |
2. Neighbors in the network
3. Gene ontology annotation
GO ID | GO term | Evidence | Category |
|---|---|---|---|
| GO:0000122 | Negative regulation of transcription from RNA polymerase II promoter | IEA | biological_process |
| GO:0001525 | Angiogenesis | TAS | biological_process |
| GO:0001886 | Endothelial cell morphogenesis | IEA | biological_process |
| 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:0005737 | Cytoplasm | IEA | cellular_component |
| GO:0006351 | Transcription, DNA-templated | IEA | biological_process |
| GO:0007179 | Transforming growth factor beta receptor signaling pathway | TAS | biological_process |
| GO:0007507 | Heart development | IEA | biological_process |
| GO:0010621 | Negative regulation of transcription by transcription factor localization | TAS | biological_process |
| GO:0030509 | BMP signaling pathway | IEA | biological_process |
| GO:0031648 | Protein destabilization | IEA | biological_process |
| GO:0032963 | Collagen metabolic process | IEA | biological_process |
| GO:0043066 | Negative regulation of apoptotic process | IEA | biological_process |
| GO:0043392 | Negative regulation of DNA binding | IEA | biological_process |
| GO:0043408 | Regulation of MAPK cascade | IEA | biological_process |
| GO:0043433 | Negative regulation of sequence-specific DNA binding transcription factor activity | IDA | biological_process |
| GO:0043534 | Blood vessel endothelial cell migration | TAS | biological_process |
| GO:0045668 | Negative regulation of osteoblast differentiation | IEA | biological_process |
| GO:0045765 | Regulation of angiogenesis | IEA | biological_process |
| GO:0045892 | Negative regulation of transcription, DNA-templated | IDA | biological_process |
| GO:0046677 | Response to antibiotic | IEA | biological_process |
| GO:0046983 | Protein dimerization activity | IEA | molecular_function |
| GO:0048514 | Blood vessel morphogenesis | TAS | biological_process |
| GO:0060425 | Lung morphogenesis | IEA | biological_process |
| GO:0060426 | Lung vasculature development | IEA | biological_process |
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4. Expression levels in datasets
- Meta-analysis result
| p-value up | p-value down | FDR up | FDR down |
|---|---|---|---|
| 0.2184861175 | 0.0005033091 | 0.8991716698 | 0.0412697819 |
- 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 | -0.6594725696 |
| GSE13712_SHEAR | Down | -0.1879457994 |
| GSE13712_STATIC | Up | 0.7541610960 |
| GSE19018 | Down | -1.3673805830 |
| GSE19899_A1 | Down | -2.2177680739 |
| GSE19899_A2 | Down | -1.3565096600 |
| PubMed_21979375_A1 | Up | 0.6794811837 |
| PubMed_21979375_A2 | Down | -3.0665944426 |
| GSE35957 | Down | -0.7639276741 |
| GSE36640 | Up | 0.6815722968 |
| GSE54402 | Up | 0.6801119874 |
| GSE9593 | Down | -3.7095829568 |
| GSE43922 | Down | -0.3994466334 |
| GSE24585 | Up | 0.6724151332 |
| GSE37065 | Up | 0.1705887025 |
| GSE28863_A1 | Up | 0.1650203052 |
| GSE28863_A2 | Down | -3.3002876631 |
| GSE28863_A3 | Down | -0.2614732339 |
| GSE28863_A4 | Up | 0.0244793061 |
| GSE48662 | Down | -0.0946209227 |
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-100-5p | MIMAT0000098 | MIRT003418 | Microarray//qRT-PCR | Functional MTI (Weak) | 19396866 |
| hsa-miR-520h | MIMAT0002867 | MIRT004739 | Microarray//qRT-PCR | Functional MTI (Weak) | 19435428 |
| hsa-miR-124-3p | MIMAT0000422 | MIRT022546 | Microarray | Functional MTI (Weak) | 18668037 |
| hsa-miR-215-5p | MIMAT0000272 | MIRT024947 | Microarray | Functional MTI (Weak) | 19074876 |
| hsa-miR-192-5p | MIMAT0000222 | MIRT026397 | Microarray | Functional MTI (Weak) | 19074876 |
| hsa-miR-26b-5p | MIMAT0000083 | MIRT029333 | Microarray | Functional MTI (Weak) | 19088304 |
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- mirRecord
MicroRNA name | mirBase ID | Target site number | MiRNA mature ID | Test method inter | MiRNA regulation site | Reporter target site | Pubmed ID |
|---|---|---|---|---|---|---|---|
| hsa-miR-125b-5p | MIMAT0000423 | NA | hsa-miR-125b | 18056640 |
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6. Text-mining results about the gene
Gene occurances in abstracts of cellular senescence-associated articles: 21 abstracts the gene occurs.
PubMed ID of the article | Sentenece the gene occurs |
|---|---|
| 27067789 | The prognosis of patients was evaluated according to Endoglin and ID1 expression |
| 27067789 | Endoglin and ID1 expression was evaluated by Western blot |
| 26941359 | In addition, CD146 suppression in hUCB-MSCs caused downregulation of other cellular senescence regulators, including Bmi-1, Id1, and Twist1 |
| 26873092 | We found that circ-Foxo3 was mainly distributed in the cytoplasm, where it interacted with the anti-senescent protein ID-1 and the transcription factor E2F1, as well as the anti-stress proteins FAK and HIF1alpha |
| 26873092 | CONCLUSION: We conclude that ID-1, E2F1, FAK, and HIF1alpha interact with circ-Foxo3 and are retained in the cytoplasm and could no longer exert their anti-senescent and anti-stress roles, resulting in increased cellular senescence |
| 25311168 | In addition, increased expression of CDKN2A and its transcriptional activators ETS1 and ARHGAP18 (SENEX) along with decreased expression of CDKN2A inhibitor ID1 were detected in FECD samples |
| 24950189 | Notch1 positively regulated the expression of inhibitor of DNA binding 1 (Id1) and MAP kinase phosphatase 1 (MKP1), while MKP1 further up-regulated Id1 expression by inhibiting p38MAPK-induced protein degradation |
| 24950189 | Over-expression of Id1 down-regulated p16 expression, thereby inhibiting premature senescence of Notch1-deleted endothelial cells |
| 24122992 | UNLABELLED: Inhibitor of differentiation proteins (Id1, 2, 3 and 4) are dominant negative regulators of basic helix loop helix transcription factors and play dominant roles in cancer cells, spanning several molecular pathways including senescence, invasion, metastasis, proliferation and apoptosis |
| 24122992 | In contrast to high Id1, Id2 and Id3 expression, the expression of Id4 is epigenetically silenced in prostate cancer |
| 21933340 | Smurf2-mediated ubiquitination and degradation of Id1 regulates p16 expression during senescence |
| 21933340 | Here, we report for the first time the identification of Smurf2 as the E3 ligase that ubiquitinates Id1 and Id3 |
| 21933340 | Smurf2-mediated ubiquitination and consequent degradation of Id1 or Id3 plays an important role in the regulation of Id expression in senescent cells |
| 21933340 | Furthermore, we found that Id1 is the mediator through which Smurf2 regulates p16 expression, providing a mechanistic link between Smurf2 and p16 expression during senescence |
| 21099353 | Senescence is driven by the activation of PKCalpha, which induces p16(Ink4a)/Rb through a MEK-dependent downregulation of Id1, and PKCdelta, which downregulates Lats1/Warts, a mitotic exit network kinase required for cytokinesis |
| 18378907 | Id1 cooperates with oncogenic Ras to induce metastatic mammary carcinoma by subversion of the cellular senescence response |
| 18378907 | Id1 has been implicated in the control of senescence in vitro, and elevated expression of Id1 is found in a number of solid cancers, so we tested whether overexpression of Id1 regulates senescence in vivo |
| 18378907 | Although overexpression of Id1 in the mammary epithelium was not sufficient for tumorigenesis, mice with expression of both Id1 and activated Ras developed metastatic cancer |
| 18378907 | These tumors expressed high levels of p19(Arf), p53, and p21(Waf1), demonstrating that Id1 acts to make cells refractory to p21(Waf1)-dependent cell cycle arrest |
| 18378907 | Inactivation of the conditional Id1 allele in established tumors led to widespread senescence within 10 days, tumor growth arrest, and tumor regression in 40% of mice |
| 18378907 | Mice in which Id1 expression was inactivated also exhibited greatly reduced pulmonary metastatic load |
| 18378907 | These data demonstrate that established tumors remain sensitive to senescence and that Id1 may be a valuable target for therapy |
| 18240291 | Id1 delays senescence of primary human melanocytes |
| 18240291 | We have also demonstrated that Id1 expression is upregulated in early stage primary human melanomas and may be an important marker for early malignancy |
| 18240291 | In order to further define the role of Id1 in human melanoma development, we have evaluated the function of Id1 in primary human melanocytes |
| 18240291 | Here we show that constitutive expression of Id1 in primary human melanocytes leads to delayed cellular senescence and decreased expression of the familial melanoma gene, p16/INK4a |
| 18240291 | Although melanocytes constitutively expressing Id1 are shown to possess extended lifespans, this is not associated with an appreciable change in cell growth or telomere length |
| 18240291 | We conclude that Id1 delays cellular senescence in primary human melanocytes through inhibition of p16/INK4a expression and suggest that Id1 may contribute to the malignant conversion of primary human melanocytes through extension of cellular lifespan |
| 17026941 | The binding of these proteins to INK4a promoter can be inhibited by proteins Id-1 or -4 after heterodimer formation |
| 16686600 | Id-1 modulates senescence and TGF-beta1 sensitivity in prostate epithelial cells |
| 16686600 | BACKGROUND INFORMATION: Loss of sensitivity to TGF-beta1 (transforming growth factor beta1)-induced growth arrest is an important step towards malignant transformation in human epithelial cells, and Id-1 (inhibitor of differentiation or DNA binding-1) has been associated with cell proliferation and cell-cycle progression |
| 16686600 | RESULTS: Using an immortalized prostate epithelial cell line, NPTX cells, we suppressed Id-1 expression through antisense strategy |
| 16686600 | We found that inhibition of Id-1 expression suppressed cell proliferation and at the same time induced cellular senescence and G2/M cell-cycle arrest |
| 16686600 | CONCLUSION: Our results indicate that endogenous Id-1 levels might be a crucial factor in the development of resistance to TGF-beta1-induced growth suppression in human prostate epithelial cells |
| 15659210 | Senescence was accompanied by a decline in transcript levels of the polycomb gene Bmi-1, Ets1 and Ets2 transcription factors, and Id1, Id2 and Id3 helix-loop-helix proteins, suggesting roles for these genes in maintenance of cardiomyocyte proliferative capacity |
| 15138269 | Regulation of cellular senescence and p16(INK4a) expression by Id1 and E47 proteins in human diploid fibroblast |
| 15138269 | Id1, a member of Id family of helix-loop-helix transcriptional regulatory proteins, is implicated in cellular senescence by repressing p16(INK4a) expression, but the mechanisms and cellular effects in human diploid fibroblasts remain unknown |
| 15138269 | Here we analyzed the patterns of p16(INK4a) and Id1 expression during the lifespan of 2BS cells and presented the inverse correlation between these two proteins |
| 15138269 | Immunoprecipitation assays demonstrated the presence of endogenous interaction of Id1 and E47 proteins that was strong in young 2BS cells and weakened during replicative senescence and, thereby, influenced the transcription activation of p16(INK4a) by E47 |
| 15138269 | Silencing Id1 expression in young cells by RNA interference induced an increased p16(INK4a) level and premature cellular senescence, whereas silencing E47 expression inhibited the expression of p16(INK4a) and delayed the onset of senescent phenotype |
| 15138269 | The present study demonstrated not only the capacity of Id1 to regulate p16(INK4a) gene expression by E47, but also the phenotypic consequence of the regulation on cellular senescence, moreover, raised the possibility of Id1-specific gene silencing for human cancer therapy |
| 15064751 | Epstein-Barr virus latent membrane protein 1 (LMP1) upregulates Id1 expression in nasopharyngeal epithelial cells |
| 15064751 | In this study, we report a novel function of LMP1 to induce Id1 expression in nasopharyngeal epithelial cells (NP69) and human embryonal kidney cells (HEK293) |
| 15064751 | The Id1 is a basic helix-loop-helix (bHLH) protein and a negative transcriptional regulator of p16(INK4a) |
| 15064751 | With the combination of both specific chemical inhibitors and genetic inhibitors of cell signaling, we showed that induction of Id1 by LMP1 was dependent on its NF-kappaB activation domain at the carboxy-terminal region, CTAR1 and CTAR2 |
| 15064751 | Induction of Id1 by LMP1 may facilitate clonal expansion of premalignant nasopharyngeal epithelial cells infected with EBV and may promote their malignant transformation |
| 14580871 | Similar to cellular senescence, TGF-beta stimulation resulted in an increase of SA-beta galactosidase (SA-beta-gal) activity, flattened and enlarged cell morphology, and down-regulation of the inhibitor of differentiation Id-1 |
| 12177246 | Although previous studies have demonstrated the expression of Id-1 in endothelium, the regulation of Id-1 has not been studied in these cells |
| 12177246 | In this report, a retroviral vector was used to overexpress Id-1 in human endothelial cells |
| 12177246 | The cells, however, were not immortalized and did eventually undergo senescence despite elevated Id-1 levels |
| 12177246 | These results demonstrate the importance of Id-1 in endothelial cell proliferation and indicate that Id-1 represses p16 expression, resulting in delayed senescence |
| 11427735 | Id1 regulation of cellular senescence through transcriptional repression of p16/Ink4a |
| 11427735 | Although much recent data has implicated Id1 in playing a critical role in modulating cellular senescence, no direct genetic evidence has been reported to substantiate such work |
| 11427735 | Our data provide, to our knowledge, the first genetic evidence for a role for Id1 as an inhibitor of cellular senescence and suggest that Id1 functions to delay cellular senescence through repression of p16/Ink4a |
| 11234019 | The induction of p16INK4a by Ets2, which is abundant in young human diploid fibroblasts, is potentiated by signalling through the Ras-Raf-MEK kinase cascade and inhibited by a direct interaction with the helix-loop-helix protein Id1 (ref |
| 11234019 | In senescent cells, where the Ets2 levels and MEK signalling decline, the marked increase in p16INK4a expression is consistent with the reciprocal reduction of Id1 and accumulation of Ets1 |
| 8934878 | The helix-loop-helix protein Id-1 and a retinoblastoma protein binding mutant of SV40 T antigen synergize to reactivate DNA synthesis in senescent human fibroblasts |
| 8934878 | These included c-fos, c-jun, Id-1, Id-2, E2F-1, and cdc2 |
| 8934878 | Only the helix-loop-helix (HLH) protein, Id-1, restored the ability of T[K1] to reactivate DNA synthesis in senescent cells |
| 8934878 | This activity of Id-1 was not shared by Id-2, a related protein, and depended on an intact HLH domain |
| 8934878 | It did not appear that Id-1 interacted directly with pRb or p107 |
| 8934878 | Constitutive Id-1 expression failed to rescue proliferating cells from growth inhibition by pRb, p107, or p130, and failed to interact with pRb in the yeast two hybrid system |
| 8294468 | Id-1H and Id-2H seem to be human homologues of mouse Id-1 and Id-2, respectively, and have potential to encode 154 and 135 amino acid proteins |
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