Display Settings:

Format

Send to:

Choose Destination
Toxins (Basel). 2010 Mar;2(3):310-25. doi: 10.3390/toxins2030310. Epub 2010 Mar 5.

Cholera toxin: an intracellular journey into the cytosol by way of the endoplasmic reticulum.

Author information

  • 1GI Cell Biology, Children's Hospital (and Harvard Medical School), Boston, MA, USA. Naomi.Wernick@childrens.harvard.edu

Abstract

Cholera toxin (CT), an AB(5)-subunit toxin, enters host cells by binding the ganglioside GM1 at the plasma membrane (PM) and travels retrograde through the trans-Golgi Network into the endoplasmic reticulum (ER). In the ER, a portion of CT, the enzymatic A1-chain, is unfolded by protein disulfide isomerase and retro-translocated to the cytosol by hijacking components of the ER associated degradation pathway for misfolded proteins. After crossing the ER membrane, the A1-chain refolds in the cytosol and escapes rapid degradation by the proteasome to induce disease by ADP-ribosylating the large G-protein Gs and activating adenylyl cyclase. Here, we review the mechanisms of toxin trafficking by GM1 and retro-translocation of the A1-chain to the cytosol.

KEYWORDS:

ERAD; cholera toxin; lipid rafts; retro-translocation; retrograde pathway

PMID:
22069586
[PubMed - indexed for MEDLINE]
PMCID:
PMC3153193
Free PMC Article

Images from this publication.See all images (4)Free text

Figure 1
Figure 2
Figure 3
Figure 4
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Icon for Multidisciplinary Digital Publishing Institute (MDPI) Icon for PubMed Central
    Loading ...
    Write to the Help Desk