HCSGD entry for TIMP1
1. General information
| Official gene symbol | TIMP1 |
|---|---|
| Entrez ID | 7076 |
| Gene full name | TIMP metallopeptidase inhibitor 1 |
| Other gene symbols | CLGI EPA EPO HCI TIMP |
| Links to Entrez Gene | Links to Entrez Gene |
2. Neighbors in the network
3. Gene ontology annotation
GO ID | GO term | Evidence | Category |
|---|---|---|---|
| GO:0001775 | Cell activation | IEA | biological_process |
| GO:0002020 | Protease binding | IEA | molecular_function |
| GO:0002576 | Platelet degranulation | TAS | biological_process |
| GO:0005515 | Protein binding | IPI | molecular_function |
| GO:0005576 | Extracellular region | IEA NAS TAS | cellular_component |
| GO:0005604 | Basement membrane | IEA | cellular_component |
| GO:0007568 | Aging | IEA | biological_process |
| GO:0007596 | Blood coagulation | TAS | biological_process |
| GO:0008191 | Metalloendopeptidase inhibitor activity | IDA IEA | molecular_function |
| GO:0008284 | Positive regulation of cell proliferation | TAS | biological_process |
| GO:0010951 | Negative regulation of endopeptidase activity | IDA | biological_process |
| GO:0022617 | Extracellular matrix disassembly | TAS | biological_process |
| GO:0030168 | Platelet activation | TAS | biological_process |
| GO:0030198 | Extracellular matrix organization | TAS | biological_process |
| GO:0031093 | Platelet alpha granule lumen | TAS | cellular_component |
| GO:0034097 | Response to cytokine | IEA | biological_process |
| GO:0042060 | Wound healing | IEA | biological_process |
| GO:0043066 | Negative regulation of apoptotic process | IEA | biological_process |
| GO:0043249 | Erythrocyte maturation | IEA | biological_process |
| GO:0043434 | Response to peptide hormone | IEA | biological_process |
| GO:0046872 | Metal ion binding | IEA | molecular_function |
| GO:0051045 | Negative regulation of membrane protein ectodomain proteolysis | IDA | biological_process |
| GO:0052548 | Regulation of endopeptidase activity | IDA | biological_process |
| GO:1901164 | Negative regulation of trophoblast cell migration | IMP | biological_process |
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4. Expression levels in datasets
- Meta-analysis result
| p-value up | p-value down | FDR up | FDR down |
|---|---|---|---|
| 0.0130126097 | 0.9861929334 | 0.2841881426 | 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 | 0.4265557076 |
| GSE13712_SHEAR | Up | 0.1730778063 |
| GSE13712_STATIC | Up | 0.2748975056 |
| GSE19018 | Down | -0.0585655970 |
| GSE19899_A1 | Up | 0.3132605073 |
| GSE19899_A2 | Up | 0.3868243754 |
| PubMed_21979375_A1 | Up | 1.6811505166 |
| PubMed_21979375_A2 | Up | 0.0452866889 |
| GSE35957 | Up | 0.0372383903 |
| GSE36640 | Up | 0.9178571604 |
| GSE54402 | Up | 0.5743832027 |
| GSE9593 | Up | 0.1973033402 |
| GSE43922 | Up | 0.2329521358 |
| GSE24585 | Down | -0.0969428414 |
| GSE37065 | Up | 0.0332732643 |
| GSE28863_A1 | Down | -0.0545022977 |
| GSE28863_A2 | Down | -0.1549142773 |
| GSE28863_A3 | Up | 0.5172273604 |
| GSE28863_A4 | Down | -0.0281728853 |
| GSE48662 | Up | 0.7307897009 |
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-519a-3p | MIMAT0002869 | MIRT006638 | Luciferase reporter assay//qRT-PCR//Western blot | Functional MTI | 22262409 |
| hsa-miR-26b-5p | MIMAT0000083 | MIRT028755 | Microarray | Functional MTI (Weak) | 19088304 |
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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 |
|---|---|
| 24475901 | Photodynamic therapy inhibits the formation of hypertrophic scars in rabbit ears by regulating metalloproteinases and tissue inhibitor of metalloproteinase-1 |
| 24475901 | In addition, mRNA levels of matrix metalloproteinase (MMP)-2, MMP-3, MMP-9 and tissue inhibitor of metalloproteinase (TIMP)-1, and concentration of beta-galactose were all measured to confirm cell senescence |
| 24475901 | RESULTS: Our data indicate that PDT can accelerate fibroblast ageing by increasing the ratio of MMPs to TIMP, in addition to promoting degradation of collagen and extracellular matrix, thereby inhibiting HS formation |
| 22385081 | In contrast, the tissue inhibitors of metalloproteinases, TIMP-1 and TIMP-2, were increased in 10/11 OSMF fibroblast cultures relative to normal and non-diseased paan user controls |
| 22385081 | TIMP levels correlated with replicative lifespan of the cultures but not with the presence of senescent cells, as senescent cell depletion in OSMF fibroblast cultures did not result in a reduction in either TIMP-1 or TIMP-2 |
| 22385081 | However, the introduction of unrepairable DDBs into normal oral fibroblasts by ionizing radiation increased TIMP-1 and TIMP-2 secretion by two-fold and seven-fold, respectively, within 5 days, replicating early senescence and the elevation seen in OSMF cultures |
| 20362703 | Here, we demonstrate that FGFR3 signaling is also capable of inducing premature senescence in chondrocytes, manifested as reversible, ERK-dependent growth arrest accompanied by alteration of cellular shape, loss of the extracellular matrix, upregulation of senescence markers (alpha-GLUCOSIDASE, FIBRONECTIN, CAVEOLIN 1, LAMIN A, SM22alpha and TIMP 1), and induction of senescence-associated beta-GALACTOSIDASE activity |
| 19085240 | Proliferation, cell viability, mineralization assays, and mRNA levels were assessed for type I and III collagen, platelet-derived growth factor (PDGF)-1, basic fibroblast growth factor (bFGF), metalloproteinase (MMP)-2 and-8, and tissue inhibitor of metalloproteinases (TIMP)-1 and-2 |
| 16834928 | Signal transducers and activators of transcription 3 mediates up-regulation of angiotensin II-induced tissue inhibitor of metalloproteinase-1 expression in cultured human senescent fibroblasts |
| 16834928 | STAT3 antisense oligonucleotides could inhibit both Ang II-induced STAT3-DNA binding activity as well as TIMP-1 expression |
| 16280016 | Extracellular degradation enzyme, matrix metalloproteinase 1 (MMP-1) was overexpressed after repeated UVA irradiation, but tissue inhibitor of metalloproteinase 1 (TIMP-1) expression was hardly changed by chronic UVA irradiation |
| 15610763 | Genes specifically up-regulated by transdifferentiation but not by cellular senescence of PrSCs were metalloproteinase 1 tissue inhibitor (Timp1), transgelin (Tagln), gamma 2 actin (Actg2), plasminogen activator inhibitor 1 (Serpinel), insulin-like growth factor binding protein 3 (Igfbp3), parathyroid hormone-like hormone (Pthlp), Tgfb-1, four and a half LIM domains 2 (Fhl-2), hydrogen peroxide-inducible clone 5 (Hic5) and cartilage oligomeric matrix protein (Comp) |
| 15130753 | Replicative senescent cells showed a decreased ability to induce cell proliferation, probably due to the increased expression of the p53 protein and the decreased expression of the PCNA protein, and also showed increased expression of MMP-1, and decreased expression of tissue inhibitor of metalloproteinase-1 (TIMP-1) and procollagen |
| 12882354 | The expression of collagenases MMP-1, -8 and -13 and tissue inhibitor of metalloproteinases (TIMP)-1 was altered in OA cartilage, but no difference was detected between lesion and distal sites in the same joint (i |
| 9472004 | 8-fold up-regulation of two matrix-degrading enzymes, interstitial collagenase (MMP-1) and stromelysin-1 (MMP-3), over a period of >120 days, while TIMP-1, the major inhibitor of MMP-1 and MMP-3, was only slightly induced |
| 8912720 | Endogenous TGF-beta activity is modified during cellular aging: effects on metalloproteinase and TIMP-1 expression |
| 8912720 | Previously we reported that an early event in the process of replicative senescence was an increase in the synthesis of two connective tissue degrading metalloproteinases, collagenase and stromelysin, and a decrease in the synthesis of the physiological inhibitor of those enzymes, tissue inhibitor of metalloproteinases-1 (TIMP-1) |
| 8912720 | This suggested the hypothesis that the age-specific modulation of collagenase, stromelysin, and TIMP-1 expression is the result of a change in TGF-beta1 activity during replicative senescence |
| 8912720 | In early passage cell cultures, exposure to TGF-beta neutralizing antibody resulted in a significant increase in the expression of collagenase and stromelysin and decreased TIMP-1 expression |
| 8912720 | Quantification of the levels of active TGF-beta, using a growth inhibition assay, indicates that the level of active TGF-beta1 is decreased during replicative senescence, supporting the conclusion that the modulation of collagenase, stromelysin, and TIMP-1 expression results from diminished TGF-beta activity |
| 1322316 | In contrast, the steady-state expression of mRNA for an inhibitor of metalloproteinases, tissue inhibitor of metalloproteinase-1 (TIMP-1), in late-passage cultures was lower than that in young cell cultures (early passage) |
| 1322316 | In normal cell cultures expression of metalloproteinase mRNAs was increased after the culture had completed greater than 90% of the in vitro life span, and the reduction in TIMP-1 mRNA expression occurred after the culture had completed greater than 74% of the in vitro lifespan |
| 1322316 | In Werner syndrome cultures expression of metalloproteinase and TIMP-1 mRNAs was similar to the level of expression observed in late-passage cell cultures |
| 1322316 | Levels of metalloproteinase and TIMP-1 mRNA expression in progeria and Cockayne syndromes were similar to those of early-passage cell cultures |
| 1322316 | Neither cytokine affected the steady-state level of TIMP-1 mRNA |
| 2551704 | We examined the levels of immunoreactive procollagenase and collagenase inhibitor (the tissue inhibitor of metalloproteinases, TIMP) associated with young and senescent fibroblasts cultured in vitro |
| 2551704 | 5%) concentrations of fetal bovine serum respond to increased (10%) serum by increasing levels of procollagenase and TIMP beginning 4 |
| 2551704 | In addition, senescent fibroblasts constitutively express a relatively small amount of TIMP which is not induced upon serum stimulation |
| 2551704 | This altered expression of collagenase and TIMP appears unique to the senescent phenotype and not merely a result of growth inhibition, since young cells growth arrested by density-dependent growth inhibition displayed a temporal pattern of procollagenase and TIMP expression upon serum stimulation similar to that of subconfluent young cultures |
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