Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.24.17 (MMP-3)
 3,419 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The function of many transmembrane molecules can be altered by cleavage and subsequent release of their ectodomains. We have investigated ectodomain cleavage of the cell-cell adhesion and signal-transducing molecule E-cadherin. The E-cadherin ectodomain is constitutively shed from the surface of MCF-7 and MDCKts.srcC12 cells in culture. Release of the 80 kDa soluble E-cadherin fragment is stimulated by phorbol-12-myristate-13-acetate and is inhibited by overexpression of the tissue inhibitor of metalloproteinases-2. The metalloproteinases matrilysin and stromelysin-1 both cleave E-cadherin at the cell surface and release sE-CAD into the medium. The soluble E-cadherin fragment thus released inhibits E-cadherin functions in a paracrine way, as indicated by induction of invasion into collagen type I and inhibition of E-cadherin-dependent cell aggregation. Our results, therefore, suggest a novel mechanism by which metalloproteinases can influence invasion.
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PMID:Release of an invasion promoter E-cadherin fragment by matrilysin and stromelysin-1. 1111 95

Apart from coronary artery bypass grafting, percutaneous transluminal coronary angioplasty (PTCA) and intracoronary stent placement are well established treatment strategies for CAD. Substantial differences exist in the mechanisms of restenosis between conventional PTCA and stenting. Arterial remodeling is the main contributor to lumen re-narrowing after PTCA, whereas neointimal hyperplasia is almost the sole mechanism of restenosis after stenting. Several reports have demonstrated that genetic factors may be involved in the pathogenesis of restenosis after PTCA and in-stent restenosis. In this review the candidate genes involved in the pathogenesis of restenosis are analyzed as potential genetic markers of restenosis after PTCA and in-stent restenosis. The I/D angiotensin-I converting enzyme gene polymorphism, gene polymorphisms of the endothelial nitric oxide synthase (Glu298Asp, -786T>C), the glycoprotein IIIa PlA1/A2 gene polymorphism, gene polymorphism of the estrogen (PvuII), allele 2 of the interleukin-1ra gene, and the GT repeats in heme oxygenase-1 gene promoter may be used as genetic markers for in-stent-restenosis. On the other hand, only the stromelysin-1 5A/6A gene polymorphism and allele 2 of the interleukin-1ra gene may be used as a genetic marker for restenosis after PTCA.
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PMID:Genetic markers of restenosis after coronary angioplasty and after stent implantation. 1579 9