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Membrane traffic and the cellular uptake of cholera toxin

Authors
Journal
Biochimica et Biophysica Acta (BBA) - Molecular Cell Research
0167-4889
Publisher
Elsevier
Publication Date
Volume
1450
Issue
3
Identifiers
DOI: 10.1016/s0167-4889(99)00070-1
Keywords
  • Cholera Toxin
  • E. Coliheat Labile Toxin
  • Ganglioside Gm1
  • Retrograde Vesicular Traffic
  • Caveolae
Disciplines
  • Medicine

Abstract

Abstract 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.

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