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血小板膜糖蛋白Ib的血管性血友病因子结合结构域。通过单克隆抗体和蛋白水解片段的部分氨基酸序列分析进行表征。

The von Willebrand factor-binding domain of platelet membrane glycoprotein Ib. Characterization by monoclonal antibodies and partial amino acid sequence analysis of proteolytic fragments.

作者信息

Handa M, Titani K, Holland L Z, Roberts J R, Ruggeri Z M

出版信息

J Biol Chem. 1986 Sep 25;261(27):12579-85.

PMID:2943738
Abstract

The glycoprotein Ib (GPIb), a two-chain integral platelet membrane protein, acts as a receptor for von Willebrand factor. In order to obtain information on the domain involved in this function, as well as on the structural organization of GPIb, the protein has been purified and submitted to limited proteolysis using three different enzymes. The resulting fragments were topographically oriented by means of partial NH2-terminal sequence analysis and immunological identification using monoclonal antibodies. One of these antibodies (LJ-Ib1) inhibited the von Willebrand factor-GPIb interaction completely, one (LJ-P3) partially, and one (LJ-Ib10) had no inhibitory effect. Three distinct fragments, the 38-kDa fragment produced by Serratia marcescens protease as well as the 45- and 35-kDa fragments produced by trypsin, had the same NH2 terminus as the intact GPIb alpha-chain (apparent molecular mass = 140 kDa). These fragments and the alpha-chain reacted with the inhibitory antibodies. On the other hand, three fragments produced by Staphylococcus aureus V8 protease, one of 92 kDa similar to the previously described "macroglycopeptide" and two others of 52 and 45 kDa, had NH2-terminal sequences different from that of the GPIb alpha-chain and reacted only with the noninhibitor monoclonal antibody LJIb10. Thus, the binding domain for von Willebrand factor resides near the NH2 terminus of the GPIb alpha-chain, whereas the carbohydrate-rich region is part of the innermost portion of GPIb and does not appear to be involved in the von Willebrand factor binding function.

摘要

糖蛋白Ib(GPIb)是一种双链整合血小板膜蛋白,作为血管性血友病因子的受体。为了获得有关该功能所涉及结构域以及GPIb结构组织的信息,已对该蛋白进行纯化,并使用三种不同的酶进行有限的蛋白酶解。通过部分NH2末端序列分析和使用单克隆抗体的免疫鉴定,对所得片段进行拓扑定位。其中一种抗体(LJ-Ib1)完全抑制血管性血友病因子与GPIb的相互作用,一种(LJ-P3)部分抑制,一种(LJ-Ib10)没有抑制作用。三个不同的片段,即粘质沙雷氏菌蛋白酶产生的38 kDa片段以及胰蛋白酶产生的45 kDa和35 kDa片段,与完整的GPIbα链(表观分子量=140 kDa)具有相同的NH2末端。这些片段和α链与抑制性抗体发生反应。另一方面,金黄色葡萄球菌V8蛋白酶产生的三个片段,一个92 kDa的片段类似于先前描述的“大糖肽”,另外两个分别为52 kDa和45 kDa,其NH2末端序列与GPIbα链不同,并且仅与非抑制性单克隆抗体LJ-Ib10发生反应。因此,血管性血友病因子的结合结构域位于GPIbα链的NH2末端附近,而富含碳水化合物的区域是GPIb最内部的一部分,似乎不参与血管性血友病因子的结合功能。

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