Rafting With Cholera Toxin: Endocytosis and Trafficking From Plasma Membrane to ER

FEMS Microbiol Lett. 2007 Jan;266(2):129-37. doi: 10.1111/j.1574-6968.2006.00545.x. Epub 2006 Nov 29.

Abstract

Cholera toxin (CT), and members of the AB(5) family of toxins enter host cells and hijack the cell's endogenous pathways to induce toxicity. CT binds to a lipid receptor on the plasma membrane (PM), ganglioside GM1, which has the ability to associate with lipid rafts. The toxin can then enter the cell by various modes of receptor-mediated endocytosis and traffic in a retrograde manner from the PM to the Golgi and the endoplasmic reticulum (ER). Once in the ER, a portion of the toxin is unfolded and retro-translocated to the cytosol so as to induce disease. GM1 is the vehicle that carries CT from PM to ER. Thus, the toxin pathway from PM to ER is a lipid-based sorting pathway, which is potentially meditated by the determinants of the GM1 ganglioside structure itself.

Publication types

  • Research Support, N.I.H., Extramural
  • Review

MeSH terms

  • Animals
  • Cell Membrane / metabolism*
  • Cholera Toxin / metabolism*
  • Endocytosis / physiology*
  • Endoplasmic Reticulum / metabolism*
  • Humans
  • Models, Biological
  • Protein Transport / physiology

Substances

  • Cholera Toxin