BRIEF REPORT - COMPLETE DEFICIENCY OF PLASMINOGEN-ACTIVATOR INHIBITOR TYPE-1 DUE TO A FRAME-SHIFT MUTATION

被引：224
作者：
FAY, WP
SHAPIRO, AD
SHIH, JL
SCHLEEF, RR
GINSBURG, D
机构：
[1] UNIV MICHIGAN, MED CTR,SCH MED,DEPT INTERNAL MED,4520 MSRB 1, 1150 W MED CTR DR, ANN ARBOR, MI 48109 USA
[2] ANN ARBOR VET AFFAIRS HOSP, DIV CARDIOL, ANN ARBOR, MI USA
[3] ANN ARBOR VET AFFAIRS HOSP, RES SERV, ANN ARBOR, MI USA
[4] INDIANA UNIV, MED CTR, INDIANAPOLIS, IN 46204 USA
[5] SCRIPPS RES INST, COMM VASC BIOL, LA JOLLA, CA USA
[6] UNIV MICHIGAN, SCH MED, DEPT HUMAN GENET, ANN ARBOR, MI 48104 USA
[7] UNIV MICHIGAN, SCH MED, HOWARD HUGHES MED INST, ANN ARBOR, MI 48104 USA
来源：
NEW ENGLAND JOURNAL OF MEDICINE | 1992年 / 327卷 / 24期
关键词：
D O I：
10.1056/NEJM199212103272406
中图分类号：
R5 [内科学];
学科分类号：
1002 ; 100201 ;
摘要：
THE process of plasminogen activation is considered a critical component of diverse biologic systems in humans. This reaction, which is catalyzed in vivo by tissue-type and urokinase-type plasminogen activators, results in the conversion of plasminogen to plasmin. Plasmin has an essential role in maintaining vascular patency by converting fibrin to soluble fibrin-degradation products. In addition, plasminogen activators have been implicated in the regulation of embryogenesis, angiogenesis, ovulation, inflammation, and tumor metastasis,1 suggesting that the plasminogen-activation system is an important mediator of tissue remodeling and cell migration. The activity of plasminogen activators is precisely regulated by several mechanisms.1 Critical among these… © 1992, Massachusetts Medical Society. All rights reserved.
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页码：1729 / 1733
页数：5
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