FACTOR-XI ACTIVATION IN A REVISED MODEL OF BLOOD-COAGULATION

被引：662

作者：

GAILANI, D ^{[1
]}

BROZE, GJ ^{[1
]}

机构：

[1] WASHINGTON UNIV, JEWISH HOSP ST LOUIS,MED CTR,DEPT MED, DIV HEMATOL ONCOL, ST LOUIS, MO 63110 USA

来源：

SCIENCE | 1991年 / 253卷 / 5022期

关键词：

D O I：

10.1126/science.1652157

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

Coagulation factor XI is activated in vitro by factor XIIa in the presence of high molecular weight kininogen (HMWK) and a negatively charged surface. Factor XII deficiency is not associated with bleeding, which suggests that another mechanism for factor XI activation exists in vivo. A revised model of coagulation is proposed in which factor XI is activated by thrombin. In the absence of cofactors, thrombin is more effective (k(cat)/K(m) = 1.6 X 10(5)) than factor XIIa (1.7 X 10(4)) in activating factor XI. Dextran sulfate enhances activation of factor XI by thrombin 2000-fold; part of this effect is due to autoactivation of factor XI by activated factor XI.

引用

页码：909 / 912

页数：4

共 27 条

[1] INHERITANCE AND BLEEDING IN FACTOR-XI DEFICIENCY [J].