HCSGD entry for MMP1
1. General information
| Official gene symbol | MMP1 |
|---|---|
| Entrez ID | 4312 |
| Gene full name | matrix metallopeptidase 1 (interstitial collagenase) |
| Other gene symbols | CLG CLGN |
| Links to Entrez Gene | Links to Entrez Gene |
2. Neighbors in the network
3. Gene ontology annotation
GO ID | GO term | Evidence | Category |
|---|---|---|---|
| GO:0004222 | Metalloendopeptidase activity | IDA | molecular_function |
| GO:0005509 | Calcium ion binding | IEA | molecular_function |
| GO:0005576 | Extracellular region | TAS | cellular_component |
| GO:0005578 | Proteinaceous extracellular matrix | IEA | cellular_component |
| GO:0006508 | Proteolysis | IEA | biological_process |
| GO:0007596 | Blood coagulation | TAS | biological_process |
| GO:0008270 | Zinc ion binding | IEA | molecular_function |
| GO:0016032 | Viral process | IEA | biological_process |
| GO:0022617 | Extracellular matrix disassembly | TAS | biological_process |
| GO:0030198 | Extracellular matrix organization | TAS | biological_process |
| GO:0030574 | Collagen catabolic process | TAS | biological_process |
| GO:0044267 | Cellular protein metabolic process | TAS | biological_process |
| GO:0050900 | Leukocyte migration | TAS | biological_process |
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4. Expression levels in datasets
- Meta-analysis result
| p-value up | p-value down | FDR up | FDR down |
|---|---|---|---|
| 0.0000093993 | 0.7566897990 | 0.0115777778 | 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 | 6.2706997313 |
| GSE13712_SHEAR | Up | 3.0186406037 |
| GSE13712_STATIC | Up | 4.2378115088 |
| GSE19018 | Up | 2.6495591928 |
| GSE19899_A1 | Up | 1.0745311314 |
| GSE19899_A2 | Up | 2.0301454898 |
| PubMed_21979375_A1 | Up | 1.8630396145 |
| PubMed_21979375_A2 | Up | 0.6960073893 |
| GSE35957 | Up | 2.2297750103 |
| GSE36640 | Down | -0.3330362803 |
| GSE54402 | Up | 1.4311559848 |
| GSE9593 | Up | 0.0343524500 |
| GSE43922 | Up | 0.8070117385 |
| GSE24585 | Down | -0.0356401905 |
| GSE37065 | Up | 1.1568510858 |
| GSE28863_A1 | Down | -0.9848063935 |
| GSE28863_A2 | Up | 3.0327555227 |
| GSE28863_A3 | Down | -0.6756507453 |
| GSE28863_A4 | Up | 0.3095366120 |
| GSE48662 | Down | -0.3305247514 |
5. Regulation relationships with compounds/drugs/microRNAs
- Compounds
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- Drugs
Name | Drug | Accession number |
|---|---|---|
| Marimastat | DB00786 | APRD00559 |
| N-HYDROXY-2(R)-[[(4-METHOXYPHENYL)SULFONYL](3-PICOLYL)AMINO]-3-METHYLBUTANAMIDE HYDROCHLORIDE | DB07556 | - |
| N-[3-(N'-HYDROXYCARBOXAMIDO)-2-(2-METHYLPROPYL)-PROPANOYL]-O-TYROSINE-N-METHYLAMIDE | DB07926 | - |
| METHYLAMINO-PHENYLALANYL-LEUCYL-HYDROXAMIC ACID | DB08403 | - |
| [[1-[N-HYDROXY-ACETAMIDYL]-3-METHYL-BUTYL]-CARBONYL-LEUCINYL]-ALANINE ETHYL ESTER | DB08482 | - |
| N-HYDROXY-2-[4-(4-PHENOXY-BENZENESULFONYL)-TETRAHYDRO-PYRAN-4-YL]-ACETAMIDE | DB08491 | - |
- MicroRNAs
- mirTarBase
MiRNA_name | mirBase ID | miRTarBase ID | Experiment | Support type | References (Pubmed ID) |
|---|---|---|---|---|---|
| hsa-miR-222-3p | MIMAT0000279 | MIRT000136 | Flow//Luciferase reporter assay//Microarray//qRT-PCR//Western blot | Functional MTI | 19487542 |
| hsa-miR-145-5p | MIMAT0000437 | MIRT021518 | Reporter assay;Microarray | Functional MTI | 21351259 |
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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-222-3p | MIMAT0000279 | 1 | hsa-miR-222 | {Western blot} | {overexpression by miRNA mimics tranfection} | 19487542 |
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6. Text-mining results about the gene
Gene occurances in abstracts of cellular senescence-associated articles: 23 abstracts the gene occurs.
PubMed ID of the article | Sentenece the gene occurs |
|---|---|
| 26899446 | Subsequent cell cycle analysis was performed and expression level of COL1A1, elastin and MMP-1 were evaluated |
| 26899446 | Additionally, transfection of miR-34b-5p mimics induced cell cycle arrest in HDFs, decreased the expression of both COL1A1 and elastin and increased MMP-1 expression |
| 26899446 | MiR-34 in HDFs modulated the cell function and expression of MMP-1, COL1A1 and elastin |
| 26337541 | H2O2-senescent cells were found to possess a catabolic phenotype, mainly characterised by the up-regulation of extracellular matrix-degrading enzymes (MMP-1, -2, -9 and ADAMTS-5) and the down-regulation of their inhibitors (TIMPs), as well as of several proteoglycans, including aggrecan, the major component of the nucleus pulposus |
| 25819580 | Real-time PCR analysis showed that matrix metalloproteinase 1 (MMP-1) and MMP-13 mRNA were significantly increased by SIRT6 inhibition |
| 25101957 | PUVA-treated fibroblasts grown in the presence of Octa are partially but significantly rescued from the features of the cellular senescence-like phenotype, such as cytoplasmic enlargement, the expression of senescence-associated-beta-galactosidase, matrix-metalloproteinase-1, and cell cycle proteins |
| 24685639 | N-terminal 5-mer peptide analog P165 of amyloid precursor protein inhibits UVA-induced MMP-1 expression by suppressing the MAPK pathway in human dermal fibroblasts |
| 24685639 | Our previous study showed that P165, the N-terminal 5-mer peptide analog of amyloid precursor protein, exerts a protective effect on ultraviolet A (UVA)-induced loss of collagen type I in human dermal fibroblasts (HDFs) by inhibiting the generation of intracellular reactive oxygen species and MMP-1 |
| 24685639 | In this study, we focused on specific signal transduction pathways to elucidate the possible photoprotective mechanisms of P165 in controlling MMP-1 inhibition |
| 24685639 | These findings suggest that P165 exerts photoprotective activity in UVA-treated HDFs by regulating MMP-1 generation |
| 23504375 | Skin equivalents generated with late passage fibroblasts had a thinner dermis, which could partly be explained by increased matrix metalloproteinase-1 secretion |
| 23278893 | We found that PUVA-treated HDFs grown in the presence of AzA maintained their morphology and reduced MMP-1 release and SA-beta-galactosidase-positive cells |
| 23030720 | The mRNA levels of MMP-1, MMP-3 and type I (alpha1) collagen were determined by quantitative real-time PCR |
| 23030720 | Moreover, 10-HDA suppressed the UVA-induced expression of MMP-1 and MMP-3 at both the transcriptional and protein levels |
| 23030720 | CONCLUSION: The data obtained in this study provide evidence that 10-HDA could prevent UVA-induced damage and inhibit MMP-1 and MMP-3 expressions |
| 22566095 | During aging, collagen production is reduced and collagen fragmentation is increased, which is initiated by matrix metalloproteinase-1 (MMP-1) |
| 22566095 | Replicative senescent dermal fibroblasts also expressed significantly reduced levels of type I procollagen and increased levels of MMP-1 |
| 22500976 | AIR promoted MMP-3 and inhibited MMP-1 appearance to some extent, but did not affect expression of other major MMPs |
| 22454193 | RESULTS: Chondrocytes stimulated by IL-1beta showed increased MMP-1, MMP-3, and MMP-13 levels, whereas the expression of COL2A1 and ACAN decreased |
| 22454193 | However, in cells co-treated with IL-1beta and Rg3, the levels of MMP-1 and MMP-13 were lower than in cells treated with IL-1beta alone, and COL2A1 and ACAN expression levels recovered from the low values seen when cultured only in the presence of IL-1beta |
| 22358238 | The expression levels of ELN, COL1A1, MMP1, CCND1, RB1, and IL6 genes were determined using the quantitative real-time polymerase chain reaction |
| 22358238 | CCND1, RB1, MMP1, and IL6 were upregulated in senescent fibroblasts |
| 22350144 | The results showed that expression of skin aging related genes encoding MMP1, 2, and 3 was inhibited by reduced transcription factor expression of p-p38 and c-fos by A |
| 21341274 | Depletion of OSMF fibroblasts of senescent cells showed that these cells accounted for 25-83 times more MMP-1 and -2 than their pre-senescent counterparts |
| 19407340 | Enhanced endothelial cell senescence by lithium-induced matrix metalloproteinase-1 expression |
| 19407340 | Herein, we show that lithium induces a rapid and pronounced up-regulation of the matrix metalloproteinase (MMP)-1, an inflammation and senescent cell marker, at the mRNA and protein levels, whereas the induction of two other senescent cell markers is either weak (interleukin-8) or delayed (plasminogen activator inhibitor-1) |
| 19407340 | Lithium effect on MMP-1 expression is also specific among other MMPs and not mediated by GSK3beta inhibition |
| 19407340 | However, down-regulation of p53, a target of lithium in EC, dampens both basal and lithium-induced MMP-1 expression, which further links MMP-1 up-regulation with the establishment of cell senescence |
| 19407340 | Although increased MMP-1 levels are usually associated with angiogenesis in enabled proliferative EC, the exogenous addition of activated MMP-1 on lithium- arrested EC increases the number of EC positive for the senescent-associated-beta-galactosidase marker |
| 19407340 | Conversely, down-regulation of MMP-1 expression by small interfering RNAs blunts the lithium-dependent increase in senescent-associated-beta-galactosidase positive cells |
| 19407340 | Altogether our data indicate that lithium-induced MMP-1 may participate in the reinforcement of EC senescence and reveal a novel mechanism for lithium-induced tissue remodeling |
| 19675716 | As devices emitting longer wavelengths are widely used in therapeutic and cosmetic interventions and as the induction of MMP-1 by water-filtered infrared-A (wIRA) had been discussed, it was of interest to assess effects of wIRA on the cellular and molecular level known to be possibly involved in cutaneous degeneration |
| 19675716 | OBJECTIVES: Investigation of the biological implications of widely used water-filtered infrared-A (wIRA) radiators for clinical use on human skin fibroblasts assessed by MMP-1 gene expression (MMP-1 messenger ribonucleic acid (mRNA) expression) |
| 19675716 | Both conventional Reverse Transcriptase Polymerase Chain Reaction (RT-PCR) and quantitative real-time RT-PCR techniques were used to determine the induction of MMP-1 mRNA at two physiologic temperatures for skin fibroblasts (30 degrees C and 37 degrees C) in single exposure regimens (15-60 minutes wIRA(+RL), 340-1360 J/cm(2) wIRA(+RL), 300-1200 J/cm(2) wIRA; 30 minutes UV-A(+BL), 50 J/cm(2) UV-A(+BL)) and in addition at 30 degrees C in a repeated exposure protocol (up to 10 times 15 minutes wIRA(+RL) with 340 J/cm(2) wIRA(+RL), 300 J/cm(2) wIRA at each time) |
| 19675716 | RESULTS: Single exposure of cultured human dermal fibroblasts to UV-A(+BL) radiation yielded a very high increase in MMP-1 mRNA expression (11 +/-1 fold expression for RT-PCR and 76 +/-2 fold expression for real-time RT-PCR both at 30 degrees C, 75 +/-1 fold expression for real-time RT-PCR at 37 degrees C) and a dose-dependent decrease in cell survival |
| 19675716 | In contrast, wIRA(+RL) did not produce cell death and did not induce a systematic increase in MMP-1 mRNA expression (less than twofold expression, within the laboratory range of fluctuation) detectable with the sensitive methods applied |
| 19675716 | Additionally, repeated exposure of human skin fibroblasts to wIRA(+RL) did not induce MMP-1 mRNA expression systematically (less than twofold expression by up to 10 consecutive wIRA(+RL) exposures and analysis with real-time RT-PCR) |
| 19675716 | CONCLUSIONS: wIRA(+RL) even at the investigated disproportionally high irradiances does not induce cell death or a systematic increase of MMP-1 mRNA expression, both of which can be easily induced by UV-A radiation |
| 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 |
| 16280016 | We conclude that chronic UVA irradiation of normal human fibroblasts induces cellular functional changes, leading to accelerated cellular ageing and MMP-1 overexpression |
| 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 |
| 12370286 | Overexpression of APA-1 did not cause cell cycle arrest; but, it induced transcription of the extracellular matrix-remodeling genes MMP1 and PAI2, which are associated with fibroblast senescence |
| 12370286 | MMP1 and PAI2 transcript levels also increased in telomerase-immortalized fibroblasts that had high levels of APA-1, demonstrating that the matrix-remodeling phenotype of senescent fibroblasts was not induced by telomere attrition alone |
| 12370286 | APA-1 was able to transactivate and bind to the MMP1 promoter, suggesting that APA-1 is a transcription factor that regulates expression of matrix-remodeling genes during fibroblast senescence |
| 11900490 | We herein report that PUVA-induced growth arrest, the senescent phenotype with long-term induction of senescence-associated beta-galactosidase, as well as increased expression of matrix metalloprotease-1 are fully reversible at days 100 to 130 post PUVA treatment in four independently tested fibroblast strains |
| 11751876 | The expression of collagenase (matrix metalloproteinase 1) in human fibroblasts increases during aging both in vivo and in vitro |
| 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 |
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