McKee P A, Andersen J C, Switzer M E
Ann N Y Acad Sci. 1975 Jan 20;240:8-33. doi: 10.1111/j.1749-6632.1975.tb53319.x.
Neither normal nor hemophilic factor VIII protein enters a 5% sosium dodecyl sulfate gel; on reduction, however, a single 195 000-molecular-weight peptide is observed. Hemophilic and normal factor VIII contain carbohydrate and appear identical in subunit molecular weight, electrical charge, and major antigenic determinants. Thrombin activation and inactivation of factor VIII does not detectably change the subunit molecular weight. Trypsin causes similar activity changes and obviously cleaves the factor VIII subunit. Human plasmin destroys factor VIII procoagulant activity and degrades the factor VIII subunit to 103 000-, 88 000-, and 17 000-molecular-weight peptides. Both normal and hemophilic factor VIII as well as thrombin-inactivated factor VIII support ristocetin-induced platelet aggregation. Purified factor VIII chromatographed on 4% agarose in 1.0 M sodium chloride shows no dissociation of the procoagulant activity from the void volume protein. Gel chromatography on 4% agarose in 0.25 M calcium chloride results in a procoagulant activity peak removed from the void volume protein; both peaks contain protein which does not enter a 5% SDS gel, but on reduction a 195 000-molecular-weight subunit band is observed for each. Both the void volume protein peak and the procoagulant activity peak from the 0.25 M calcium chloride-agarose gel column support ristocetin-induced platelet aggregation. After removal of calcium, a small amount of procoagulant activity is present only in the void volume peak. These data suggest that both the procoagulant and von Willebrand activities are on the same molecule. Thus our previous conclusion remains the same: human factor VIII is a large glycoprotein composed of identical 195 000-molecular-weight subunits jointed by disulfide bonds and is responsible for both antihemophilic and von Willebrand activities in human plasma.
正常和血友病因子VIII蛋白均不能进入5%十二烷基硫酸钠凝胶;然而,经还原后,可观察到一条单一的195000分子量的肽段。血友病和正常因子VIII均含有碳水化合物,且在亚基分子量、电荷和主要抗原决定簇方面表现相同。凝血酶对因子VIII的激活和失活并未显著改变其亚基分子量。胰蛋白酶引起类似的活性变化,并明显切割因子VIII亚基。人纤溶酶破坏因子VIII促凝活性,并将因子VIII亚基降解为103000、88000和17000分子量的肽段。正常和血友病因子VIII以及凝血酶失活的因子VIII均支持瑞斯托霉素诱导的血小板聚集。在1.0M氯化钠中于4%琼脂糖上进行层析的纯化因子VIII,其促凝活性与空体积蛋白未发生解离。在0.25M氯化钙中于4%琼脂糖上进行凝胶层析,导致促凝活性峰与空体积蛋白分离;两个峰均含有不能进入5%SDS凝胶的蛋白质,但经还原后,每个峰均观察到一条195000分子量的亚基带。0.25M氯化钙-琼脂糖凝胶柱的空体积蛋白峰和促凝活性峰均支持瑞斯托霉素诱导的血小板聚集。去除钙后,仅在空体积峰中存在少量促凝活性。这些数据表明促凝活性和血管性血友病活性均存在于同一分子上。因此,我们先前的结论仍然成立:人因子VIII是一种由相同的195000分子量亚基通过二硫键连接而成的大型糖蛋白,在人血浆中负责抗血友病和血管性血友病活性。