Nishioka J, Suzuki K
Department of Molecular Biology on Genetic Disease, Mie University School of Medicine, Japan.
J Biol Chem. 1992 Nov 5;267(31):22224-9.
To elucidate the role of the COOH-terminal region of antithrombin III, we studied the effects of synthetic peptides corresponding to its sequence on the amidolytic and proteolytic activities of thrombin and Factor Xa in the presence or absence of the inhibitor, antithrombin III. The peptides ANRPFLVFI and IIFMGRVANP corresponding to residues Ala404 to Ile412 and Ile420 to Pro429, respectively, blocked the inhibition by antithrombin III. The effect of IIFMGRVANP was reduced in the presence of heparin. Both peptides at a concentration of 1 mM blocked complex formation between antithrombin III and thrombin or Factor Xa. The two peptides, particularly IIFMGRVANP, directly enhanced the amidolytic activity of thrombin and Factor Xa on the synthetic substrate Boc-Ala-Gly-Arg-MCA (where Boc is t-butoxycarbonyl and MCA is 4-methylcoumarin), which corresponds to residues P3-P1 of the reactive site of antithrombin III, and also on other substrates due to increased Vmax. IIFMGRVANP also shortened the thrombin-induced fibrinogen clotting time, whereas ANRPFLVFI inhibited the thrombin-catalyzed activation of protein C both in the presence and absence of thrombomodulin. The direct effect of ANRPFLVFI and IIFMGRVANP on thrombin was confirmed by enhancement of the incorporation of dansylarginine-N-(3-ethyl-1,5-pentanediyl)amide into thrombin. These findings suggest that the COOH-terminal region of antithrombin III interacts with thrombin and Factor Xa to increase the reactivity of the enzyme, which may enhance acyl-bond formation between the inhibitor and the enzyme.
为阐明抗凝血酶III羧基末端区域的作用,我们研究了与其序列对应的合成肽在有或没有抑制剂抗凝血酶III存在的情况下,对凝血酶和因子Xa的酰胺水解及蛋白水解活性的影响。分别对应于Ala404至Ile412和Ile420至Pro429残基的肽ANRPFLVFI和IIFMGRVANP可阻断抗凝血酶III的抑制作用。在肝素存在的情况下,IIFMGRVANP的作用减弱。两种肽在浓度为1 mM时均可阻断抗凝血酶III与凝血酶或因子Xa之间的复合物形成。这两种肽,尤其是IIFMGRVANP,可直接增强凝血酶和因子Xa对合成底物Boc-Ala-Gly-Arg-MCA(其中Boc为叔丁氧羰基,MCA为4-甲基香豆素)的酰胺水解活性,该底物对应于抗凝血酶III反应位点的P3-P1残基,并且由于Vmax增加,对其他底物也有增强作用。IIFMGRVANP还缩短了凝血酶诱导的纤维蛋白原凝血时间,而ANRPFLVFI在有或没有血栓调节蛋白的情况下均抑制凝血酶催化的蛋白C活化。通过增强丹磺酰精氨酸-N-(3-乙基-1,5-戊二基)酰胺掺入凝血酶,证实了ANRPFLVFI和IIFMGRVANP对凝血酶的直接作用。这些发现表明,抗凝血酶III的羧基末端区域与凝血酶和因子Xa相互作用以增加酶的反应性,这可能增强抑制剂与酶之间的酰基键形成。