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.


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


  • Cholera Toxin