FACTOR-XI ACTIVATION IN A REVISED MODEL OF BLOOD-COAGULATION
FACTOR-XI ACTIVATION IN A REVISED MODEL OF BLOOD-COAGULATION
复制标题
DOI：
10.1126/science.1652157
复制
发表时间：
1991-08-23
期刊：
影响因子：
56.9
通讯作者：
BROZE, GJ
中科院分区：
文献类型：
--
作者：
GAILANI, D;BROZE, GJ
凝血因子XI在高分子量激肽原（HMWK）和带负电荷的表面存在下，在体外被因子XIIa激活。因子XII缺乏与出血无关，这表明体内存在因子XI激活的另一种机制。提出了一种修正的凝血模型，其中因子XI被凝血酶激活。在没有辅因子的情况下，凝血酶在活化因子XI方面比因子XIIa（1.7 × 10（4））更有效（k（cat）/K（m）= 1.6 × 10（5））。硫酸葡聚糖可使凝血酶对因子XI的活化增强2000倍;这种作用的一部分是由于活化因子XI对因子XI的自活化。
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.