Segers Kenneth, Dahlbäck Björn, Bock Paul E, Tans Guido, Rosing Jan, Nicolaes Gerry A F
Department of Biochemistry, Cardiovascular Research Institute Maastricht, Maastricht University, Maastricht, The Netherlands.
J Biol Chem. 2007 Nov 23;282(47):33915-24. doi: 10.1074/jbc.M701123200. Epub 2007 Sep 18.
Human blood coagulation Factor V (FV) is a plasma protein with little procoagulant activity. Limited proteolysis at Arg(709), Arg(1018), and Arg(1545) by thrombin or Factor Xa (FXa) results in the generation of activated FV, which serves as a cofactor of FXa in prothrombin activation. Both thrombin exosites I and II have been reported to be involved in FV activation, but the relative importance of these regions in the individual cleavages remains unclear. To investigate the role of each exosite in FV activation, we have used recombinant FV molecules with only one of the three activation cleavage sites available, in combination with exosite I- or II-specific aptamers. In addition, structural requirements for exosite interactions located in the B-domain of FV were probed using FV B-domain deletion mutants and comparison with FV activating enzymes from the venom of Russell's viper (RVV-V) and of Levant's viper (LVV-V) known to activate FV by specific cleavage at Arg(1545). Our results indicate that thrombin exosite II is not involved in cleavage at Arg(709) and that both thrombin exosites are important for recognition and cleavage at Arg(1545). Efficient thrombin-catalyzed FV activation requires both the N- and C-terminal regions of the B-domain, whereas only the latter is required by RVV-V and LVV-V. This indicates that proteolysis of FV by thrombin at Arg(709), Arg(1018), and Arg(1545) show different cleavage requirements with respect to interactions mediated by thrombin exosites and areas that surround the respective cleavage sites. In addition, interactions between exosite I of thrombin and FV are primarily responsible for the different cleavage site specificity as compared with activation by RVV-V or LVV-V.
人凝血因子V(FV)是一种几乎没有促凝血活性的血浆蛋白。凝血酶或因子Xa(FXa)在精氨酸(709)、精氨酸(1018)和精氨酸(1545)处进行有限的蛋白水解,导致生成活化的FV,其在凝血酶原激活中作为FXa的辅因子。据报道,凝血酶的外位点I和II均参与FV激活,但这些区域在各个裂解过程中的相对重要性仍不清楚。为了研究每个外位点在FV激活中的作用,我们使用了仅具有三个激活裂解位点之一的重组FV分子,并结合外位点I或II特异性适体。此外,使用FV B结构域缺失突变体,并与已知通过在精氨酸(1545)处特异性裂解来激活FV的锯鳞蝰蛇(RVV-V)和黎凡特蝰蛇(LVV-V)毒液中的FV激活酶进行比较,探究了位于FV B结构域中外位点相互作用的结构要求。我们的结果表明,凝血酶外位点II不参与精氨酸(709)处的裂解,并且凝血酶的两个外位点对于精氨酸(1545)处的识别和裂解都很重要。有效的凝血酶催化的FV激活需要B结构域的N端和C端区域,而RVV-V和LVV-V仅需要后者。这表明凝血酶在精氨酸(709)、精氨酸(1018)和精氨酸(1545)处对FV的蛋白水解在凝血酶外位点介导的相互作用以及各个裂解位点周围区域方面表现出不同的裂解要求。此外,与RVV-V或LVV-V激活相比,凝血酶外位点I与FV之间的相互作用主要负责不同的裂解位点特异性。