摘要
多聚Clq与人T细胞系Jurkat、B细胞系Ran和Mφ系U937细胞表面ClqR相互作用,诱导45Ca2+跨膜快速内流,刺激[Ca2+]i迅速增高,前者可为质膜Ca2+通道阻滞剂Verapamil所阻断,后者能被胞外Ca2+络合剂EGTA部分抑制,被蛋白酪氨酸激酶(PTK)抑制剂Genistein完全消除。资料表明,Clq/ClqR系统介导的信号转导机制涉及内Ca2+和外Ca2+两者的动员,且与PTK有关。
The interaction between aggregated Clq and the Clq receptor(ClqR)on the human Jurkat T cell line,Ran B cell line and U937 macrophaqe cell line elicited a rapid increase of transmembrane 45Ca2+ influx which could be blocked by Verapamil,aninhibitor of Ca2+ channel in plasma membrane,and induced a quick rise in[Ca2+]iwhich could be inhibited partly by the Ca2+ chelator EGTA and completely by the inhibitor of protein tyrosine kinase(PTK)Genistein.These observations suggest thatthe signalling pathway mediated by the Clq/ClqR system involves the mobilizationof both internal and external Ca2+,which relates to PTK.
出处
《上海免疫学杂志》
CSCD
北大核心
1996年第4期206-209,共4页
Shanghai Journal of Immunology
基金
全军"八五"基金
关键词
多聚Clq
免疫细胞
ClqR
信号转导
Ca2+moibilization signal transduction Clq/ClqR system immune cells