Matrix metalloproteinases in angiogenesis: a moving target for therapeutic intervention.
作者信息
Stetler-Stevenson W G
机构信息
Laboratory of Pathology, Division of Clinical Sciences, National Cancer Institute, Bethesda, Maryland 20892,
出版信息
J Clin Invest. 1999 May;103(9):1237-41. doi: 10.1172/JCI6870.
Abstract
摘要
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本文引用的文献
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Identification of the tissue inhibitor of metalloproteinases-2 (TIMP-2) binding site on the hemopexin carboxyl domain of human gelatinase A by site-directed mutagenesis. The hierarchical role in binding TIMP-2 of the unique cationic clusters of hemopexin modules III and IV.通过定点诱变鉴定人明胶酶A的血红素结合蛋白羧基结构域上金属蛋白酶组织抑制剂-2（TIMP-2）的结合位点。血红素结合蛋白模块III和IV的独特阳离子簇在结合TIMP-2中的层级作用。
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Matrix metalloproteinases generate angiostatin: effects on neovascularization.基质金属蛋白酶生成血管抑素：对新血管形成的影响。
J Immunol. 1998 Dec 15;161(12):6845-52.
3
Matrix metalloproteinases regulate neovascularization by acting as pericellular fibrinolysins.基质金属蛋白酶通过作为细胞周纤维蛋白溶解酶来调节新血管形成。
Cell. 1998 Oct 30;95(3):365-77. doi: 10.1016/s0092-8674(00)81768-7.
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MMP-9/gelatinase B is a key regulator of growth plate angiogenesis and apoptosis of hypertrophic chondrocytes.基质金属蛋白酶-9/明胶酶B是生长板血管生成和肥大软骨细胞凋亡的关键调节因子。
Cell. 1998 May 1;93(3):411-22. doi: 10.1016/s0092-8674(00)81169-1.
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Three-dimensional type I collagen lattices induce coordinate expression of matrix metalloproteinases MT1-MMP and MMP-2 in microvascular endothelial cells.三维I型胶原晶格诱导微血管内皮细胞中基质金属蛋白酶MT1-MMP和MMP-2的协同表达。
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10
Stromelysin-3 is induced in tumor/stroma cocultures and inactivated via a tumor-specific and basic fibroblast growth factor-dependent mechanism.基质溶解素-3在肿瘤/基质共培养物中被诱导，并通过一种肿瘤特异性且依赖碱性成纤维细胞生长因子的机制失活。
J Biol Chem. 1998 Jan 2;273(1):618-26. doi: 10.1074/jbc.273.1.618.
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