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血管性血友病因子前体的蛋白水解切割对于多聚体形成并非必不可少。

Proteolytic cleavage of the precursor of von Willebrand factor is not essential for multimer formation.

作者信息

Verweij C L, Hart M, Pannekoek H

机构信息

Department of Molecular Biology, the Netherlands Red Cross Blood Transfusion Service, Amsterdam.

出版信息

J Biol Chem. 1988 Jun 15;263(17):7921-4.

PMID:3131331
Abstract

Monkey kidney cells (COS-1), transfected with full-length human von Willebrand factor (vWF) cDNA encoding the precursor of vWF (pro-vWF), mimic the characteristics of the biosynthesis and of the constitutive secretory pathway, displayed by cultured vascular endothelial cells. Such heterologous transfected cells are able to cleave pro-vWF, generating the propolypeptide and mature vWF, and to assemble pro-vWF dimers into a series of multimers, similarly to endothelial cells. Evidence is presented showing that proteolytic processing of pro-vWF by COS-1 cells occurs at the peptide bond between arginine and serine in the sequence Lys762-Arg763-Ser764, identical to endothelial cell-associated proteolysis. This conclusion stems from the observation that substitution of Arg763 by a glycine residue completely abolishes proteolytic processing. As a result, transfection of COS-1 with the mutant vWF-Gly763 cDNA does not significantly affect the multimeric organization of secreted vWF molecules. Consequently, we conclude that proteolytic processing of pro-vWF is not required for multimer formation. Pulse-chase labeling of COS-1 cells transfected with full-length vWF cDNA reveals pro-vWF exclusively in cell lysates, whereas both pro-vWF and mature vWF are encountered in the conditioned medium. These observations indicate that proteolytic processing of pro-vWF is a "late" event during intracellular routing of these molecules or may occur extracellularly.

摘要

用编码血管性血友病因子前体(pro-vWF)的全长人血管性血友病因子(vWF)cDNA转染的猴肾细胞(COS-1),模拟了培养的血管内皮细胞所表现出的生物合成和组成型分泌途径的特征。这种异源转染细胞能够切割pro-vWF,产生前肽和成熟的vWF,并将pro-vWF二聚体组装成一系列多聚体,这与内皮细胞类似。有证据表明,COS-1细胞对pro-vWF的蛋白水解加工发生在序列Lys762-Arg763-Ser764中精氨酸和丝氨酸之间的肽键处,这与内皮细胞相关的蛋白水解相同。这一结论源于以下观察结果:将Arg763替换为甘氨酸残基会完全消除蛋白水解加工。因此,用突变体vWF-Gly763 cDNA转染COS-1对分泌的vWF分子的多聚体组织没有显著影响。因此,我们得出结论,pro-vWF的蛋白水解加工不是多聚体形成所必需的。用全长vWF cDNA转染的COS-1细胞的脉冲追踪标记显示,pro-vWF仅存在于细胞裂解物中,而在条件培养基中同时存在pro-vWF和成熟的vWF。这些观察结果表明,pro-vWF的蛋白水解加工是这些分子细胞内运输过程中的一个“晚期”事件,或者可能发生在细胞外。

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