抑制Rho、Rac和Cdc42的试剂不会阻断感染肠致病性大肠杆菌的HeLa细胞中肌动蛋白基座的形成。
Agents that inhibit Rho, Rac, and Cdc42 do not block formation of actin pedestals in HeLa cells infected with enteropathogenic Escherichia coli.
作者信息
Ben-Ami G, Ozeri V, Hanski E, Hofmann F, Aktories K, Hahn K M, Bokoch G M, Rosenshine I
机构信息
Department of Molecular Genetics and Biotechnology, Faculty of Medicine, The Hebrew University, Jerusalem, Israel.
出版信息
Infect Immun. 1998 Apr;66(4):1755-8. doi: 10.1128/IAI.66.4.1755-1758.1998.
Abstract
Enteropathogenic Escherichia coli (EPEC) induces formation of actin pedestals in infected host cells. Agents that inhibit the activity of Rho, Rac, and Cdc42, including Clostridium difficile toxin B (ToxB), compactin, and dominant negative Rho, Rac, and Cdc42, did not inhibit formation of actin pedestals. In contrast, treatment of HeLa cells with ToxB inhibited EPEC invasion. Thus, Rho, Rac, and Cdc42 are not required for assembly of actin pedestals; however, they may be involved in EPEC uptake by HeLa cells.
摘要
肠致病性大肠杆菌（EPEC）可诱导感染的宿主细胞中形成肌动蛋白基座。包括艰难梭菌毒素B（ToxB）、洛伐他汀和显性负性Rho、Rac及Cdc42在内的抑制Rho、Rac和Cdc42活性的试剂，并未抑制肌动蛋白基座的形成。相反，用ToxB处理HeLa细胞可抑制EPEC的侵袭。因此，肌动蛋白基座的组装不需要Rho、Rac和Cdc42；然而，它们可能参与HeLa细胞对EPEC的摄取。
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