Gailani D, Broze G J
Department of Medicine, Jewish Hospital, Washington University Medical Center, St. Louis, MO 63110.
Science. 1991 Aug 23;253(5022):909-12. doi: 10.1126/science.1652157.
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 (kcat/Km = 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.
在高分子量激肽原（HMWK）和带负电荷表面存在的情况下，凝血因子XI在体外被因子XIIa激活。因子XII缺乏与出血无关，这表明体内存在另一种激活因子XI的机制。提出了一种修订的凝血模型，其中因子XI被凝血酶激活。在没有辅因子的情况下，凝血酶在激活因子XI方面比因子XIIa更有效（催化常数与米氏常数之比为1.6×10⁵）（因子XIIa为1.7×10⁴）。硫酸葡聚糖可使凝血酶对因子XI的激活增强2000倍；这种作用部分归因于活化的因子XI对因子XI的自身激活。
