Just I, Wille M, Chaponnier C, Aktories K
Institut für Pharmakologie und Toxikologie, Universität des Saarlandes, Homburg-Saar, Germany.
Eur J Pharmacol. 1993 Aug 15;246(3):293-7. doi: 10.1016/0922-4106(93)90045-b.
The gelsolin-actin complex was ADP-ribosylated by Clostridium botulinum C2 toxin and Clostridium perfringens iota toxin in lysates of human platelets and human neutrophils. When [32P]orthophosphate-labelled human neutrophils were treated with C. botulinum C2 toxin, [32P]ADP-ribosylated gelsolin-actin was precipitated with anti-gelsolin antibody. Stimulation of neutrophils by formyl-methionine-leucine-phenylalanine decreased the interaction of gelsolin with ADP-ribosylated actin in toxin-treated cells. The data indicate that the gelsolin-actin complex is a pathophysiological substrate for actin-ADP-ribosylating toxins.
凝溶胶蛋白 - 肌动蛋白复合物在人血小板和人中性粒细胞裂解物中被肉毒杆菌C2毒素和产气荚膜梭菌iota毒素进行ADP核糖基化。当用[32P]正磷酸盐标记的人中性粒细胞用肉毒杆菌C2毒素处理时,[32P] ADP核糖基化的凝溶胶蛋白 - 肌动蛋白用抗凝溶胶蛋白抗体沉淀。甲酰甲硫氨酸 - 亮氨酸 - 苯丙氨酸对中性粒细胞的刺激降低了毒素处理细胞中凝溶胶蛋白与ADP核糖基化肌动蛋白的相互作用。数据表明,凝溶胶蛋白 - 肌动蛋白复合物是肌动蛋白ADP核糖基化毒素的病理生理底物。