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利用重组嵌合体对凝血因子V第二个C型结构域内功能重要表位进行定位。

Localization of functionally important epitopes within the second C-type domain of coagulation factor V using recombinant chimeras.

作者信息

Ortel T L, Quinn-Allen M A, Keller F G, Peterson J A, Larocca D, Kane W H

机构信息

Department of Medicine, Duke University Medical Center, Durham, North Carolina 27710.

出版信息

J Biol Chem. 1994 Jun 3;269(22):15898-905.

PMID:7515064
Abstract

Coagulation factor V, an integral component of the prothrombinase complex, possesses two C-type domains at the carboxyl-terminal end of the molecule. Homologous C-type domains are present in factor VIII as well as several non-coagulation proteins. Deletion of the second C-type domain of factor V results in the loss of procoagulant activity and the ability to bind phosphatidylserine. We now report the effect of substitution of all or a portion of the C2 domain of factor V with the corresponding regions of factor VIII or the human breast carcinoma protein BA46. Substitution of the entire domain with a heterologous C2 domain does not restore significant procoagulant activity, although smaller, exon-size substitutions do result in chimeras with partial activity (approximately 10% of factor Va). Using chimeras with partial substitutions, we determined that the amino-terminal region of the domain is involved in binding to phosphatidylserine. In contrast, the central region of the domain is not involved in phosphatidylserine binding, but an antibody binding at or near this site inhibits procoagulant activity, suggesting that this region is involved in a separate function. Lastly, the molecular basis for the light chain doublet, which is important in the expression of full procoagulant activity, is located within the carboxyl-terminal region of the C2 domain.

摘要

凝血因子V是凝血酶原酶复合物的一个组成部分,在分子的羧基末端具有两个C型结构域。因子VIII以及几种非凝血蛋白中也存在同源的C型结构域。凝血因子V的第二个C型结构域缺失会导致促凝活性丧失以及结合磷脂酰丝氨酸的能力丧失。我们现在报告用因子VIII或人乳腺癌蛋白BA46的相应区域替换凝血因子V的全部或部分C2结构域的效果。用异源C2结构域替换整个结构域并不能恢复显著的促凝活性,尽管较小的外显子大小的替换确实会产生具有部分活性的嵌合体(约为因子Va活性的10%)。使用具有部分替换的嵌合体,我们确定该结构域的氨基末端区域参与与磷脂酰丝氨酸的结合。相比之下,该结构域的中央区域不参与磷脂酰丝氨酸结合,但在此位点或其附近结合的抗体可抑制促凝活性,这表明该区域参与了一种独立的功能。最后,轻链双峰的分子基础(在完整促凝活性的表达中很重要)位于C2结构域的羧基末端区域内。

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