Membrane traffic and the cellular uptake of cholera toxin

被引：209

作者：

Lencer, WI

Hirst, TR

Holmes, RK

机构：

[1] Childrens Hosp, Combined Program Pediat Gastroenterol & Nutr, Boston, MA 02115 USA

[2] Harvard Univ, Sch Med, Dept Pediat, Boston, MA 02115 USA

[3] Harvard Univ, Ctr Digest Dis, Boston, MA 02115 USA

[4] Univ Bristol, Sch Med Sci, Dept Pathol & Microbiol, Bristol BS8 1TD, Avon, England

[5] Univ Colorado, Hlth Sci Ctr, Dept Microbiol, Denver, CO USA

来源：

BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR CELL RESEARCH | 1999年 / 1450卷 / 03期

关键词：

cholera toxin; E. coli heat labile toxin; ganglioside GM1; retrograde vesicular traffic; caveolae;

D O I：

10.1016/S0167-4889(99)00070-1

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

In nature, cholera toxin (CT) and the structurally related E. coli heat labile toxin type I (LTI) must breech the epithelial barrier of the intestine to cause the massive diarrhea seen in cholera. This requires endocytosis of toxin-receptor complexes into the apical endosome, retrograde transport into Golgi cisternae or endoplasmic reticulum (ER), and finally transport of toxin across the cell to its site of action on the basolateral membrane. Targeting into this pathway depends on toxin binding ganglioside GM1 and association with caveolae-like membrane domains. Thus to cause disease, both CT and LTI co-opt the molecular machinery used by the host cell to sort, move, and organize their cellular membranes and substituent components. (C) 1999 Elsevier Science B.V. All rights reserved.

引用

页码：177 / 190

页数：14

共 152 条

[1] POTOCYTOSIS - SEQUESTRATION AND TRANSPORT OF SMALL MOLECULES BY CAVEOLAE [J].