KDEL receptor (Erd2p)-mediated retrograde transport of the cholera toxin A subunit from the Golgi involves COPI, p23, and the COOH terminus of Erd2p

被引:122
作者
Majoul, I
Sohn, K
Wieland, FT
Pepperkok, R
Pizza, M
Hillemann, J
Söling, HD
机构
[1] Max Planck Inst Biophys Chem, D-37077 Gottingen, Germany
[2] Univ Gottingen, Abt Klin Biochem, D-37070 Gottingen, Germany
[3] Univ Heidelberg, Inst Biochem 1, D-69120 Heidelberg, Germany
[4] European Mol Biol Lab, D-69012 Heidelberg, Germany
[5] IRIS, Chiron Vaccines Immunobiol Res Inst, I-53100 Siena, Italy
关键词
cholera toxin; COPI; KDEL-receptor; p23; p53;
D O I
10.1083/jcb.143.3.601
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
A:cholera toxin mutant (CTX-K63) unable to raise cAMP levels was used to study in Vero cells the retrograde transport of the toxin A subunit (CTX-A-K63), which possesses a COOH-terminal KDEL retrieval signal. Microinjected GTP-gamma-S inhibits the internalization as well as Golgi-ER transport of CTX-A-K63. The appearance of CTX-A-K63 in the Golgi induces a marked dispersion of Erd2p and p53 but not of the Golgi marker giantin. Erd2p is translocated under these conditions most likely to the intermediate compartment as indicated by an increased colocalization of Erd2p with mSEC13, a member of the mammalian coat protein II complex. IgGs as well as F-ab fragments directed against Erd2p, beta-COP, or p23, a new member of the p24 protein family, inhibit or block retrograde transport of CTX-A-K63 from the Golgi with out affecting its internalization or its transport to the Golgi. Anti-Erd2p antibodies do not affect the binding of CTX-A to Erd2p, but inhibit the CTX-K63-induced translocation of Erd2p and p53.
引用
收藏
页码:601 / 612
页数:12
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