EC Number   |
General Information |
Reference |
|---|
   3.4.24.23 | evolution |
matrilysin is a member of the matrix metalloproteinase (MMP) gene family |
733641 |
| 3.4.24.23 | evolution |
the active-site tyrosyl residue, Tyr219, is conserved in all other MMPs |
717745 |
| 3.4.24.23 | evolution |
the enzyme is a member of a zinc-dependent endopeptidases family (MMPs) |
734619 |
| 3.4.24.23 | malfunction |
a nonsynonymous genetic variant D137 of matrix metalloproteinase-7 confers risk of liver cirrhosis, overview |
708642 |
| 3.4.24.23 | malfunction |
epigenetic silencing or knockdown of fibulin-5, a vascular ligand for integrin receptors and a suppressor of lung cancer invasion and metastasis, promotes lung cancer invasion and metastasis by activating MMP-7 expression through the ERK pathway, injection of fibulin-5-deficient and unmodified H-460 cells into nude mice, overview |
707986 |
| 3.4.24.23 | malfunction |
high MMP-7 expression is associated with a worse overall survival of patients with acinic cell carcinoma, while low MMP-7 expression is associated with worse disease-specific survival of patients with acinic cell carcinoma |
707003 |
| 3.4.24.23 | malfunction |
MMP-7 is a proteolytic enzyme that can modify the intestinal microbial replicative niche as well as affect tumorigenesis, and Helicobacter pylori stimulates expression of MMP-7 in gastric epithelial cells in vitro, that may serve to protect the gastric mucosa from pathophysiologic processes which promote carcinogenesis. Enhanced gastritis in Helicobacter pyloriinfected mmp-7-knockout mice is strongly linked to accelerated epithelial cellular turnover. However, more severe inflammation and heightened proliferation and apoptosis are not dependent on MMP-7-mediated bacterial eradication |
-, 707992 |
| 3.4.24.23 | malfunction |
MMP-7 is involved in gastrointestinal cancer cell invasiveness |
708011 |
| 3.4.24.23 | malfunction |
MMP-7 knockout mice experience higher mortality, elevated serum creatinine, and more severe histologic lesions after ischemic or toxic insults. Tubular apoptosis and interstitial inflammation are more prominent in MMP-7 knockout kidneys, accompanied by increased expression of FasL and other components of the extrinsic apoptotic pathway, as well as increased expression of pro-inflammatory chemokines. Ablation of MMP-7 promotes tubular cell apoptosis after acute kidney injury (AKI) augmenting renal inflammation, phenotype, overview. Exogenous MMP-7 ameliorates kidney injury in MMP-7 knockout mice after ischemia/reperfusion, mechanism underlying renal protection of MMP-7 in AKI. MMP-7 augmentes c-fos and PCNA expression induced by mitogens-rich serum in renal tubules ex vivo |
754565 |
| 3.4.24.23 | malfunction |
MMP-7 polymorphisms are involved in colorectal cancer progression, overview |
710694 |
