ArticleMolecular biology of the cell2010
The Ero1alpha-PDI redox cycle regulates retro-translocation of cholera toxin.
Article in Molecular biology of the cell, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 37 citations in OpenAlex.
- Targeting Lipophagy in Liver Diseases: Impact on Oxidative Stress and Steatohepatitis.Antioxidants (Basel, Switzerland) · 2025Review
- Effects of ricin on primary pulmonary alveolar macrophages.The Journal of international medical research · 2019Article
- Toxins Utilize the Endoplasmic Reticulum-Associated Protein Degradation Pathway in Their Intoxication Process.International journal of molecular sciences · 2019Review
- Exploring the cross talk between ER stress and inflammation in age-related macular degeneration.PloS one · 2017Article
- The nucleotide exchange factors Grp170 and Sil1 induce cholera toxin release from BiP to enable retrotranslocation.Molecular biology of the cell · 2015Article
- Identification of protein disulfide isomerase 1 as a key isomerase for disulfide bond formation in apolipoprotein B100.Molecular biology of the cell · 2015Article
- A bacterial toxin and a nonenveloped virus hijack ER-to-cytosol membrane translocation pathways to cause disease.Critical reviews in biochemistry and molecular biology · 2015Review
- Apolipoprotein B100 quality control and the regulation of hepatic very low density lipoprotein secretion.Journal of biomedical research · 2014Article
- Protein Disulfide Isomerase Superfamily in Disease and the Regulation of Apoptosis.Endoplasmic reticulum stress in diseases · 2014Article
- ERAD and how viruses exploit it.Frontiers in microbiology · 2014Review
- The ERdj5-Sel1L complex facilitates cholera toxin retrotranslocation.Molecular biology of the cell · 2013Article
- How viruses use the endoplasmic reticulum for entry, replication, and assembly.Cold Spring Harbor perspectives in biology · 2013Review
- Stepwise assembly of fibrinogen is assisted by the endoplasmic reticulum lectin-chaperone system in HepG2 cells.PloS one · 2013Article
- Article
- SOD1 aggregation in astrocytes following ischemia/reperfusion injury: a role of NO-mediated S-nitrosylation of protein disulfide isomerase (PDI).Journal of neuroinflammation · 2012Article
- Endoplasmic reticulum-dependent redox reactions control endoplasmic reticulum-associated degradation and pathogen entry.Antioxidants & redox signaling · 2012Review
- The delicate balance between secreted protein folding and endoplasmic reticulum-associated degradation in human physiology.Physiological reviews · 2012Review
- Protein disulfide isomerases contribute differentially to the endoplasmic reticulum-associated degradation of apolipoprotein B and other substrates.Molecular biology of the cell · 2012Article
- A guide to taming a toxin--recombinant immunotoxins constructed from Pseudomonas exotoxin A for the treatment of cancer.The FEBS journal · 2011Review
- Structural and functional interactions between the cholera toxin A1 subunit and ERdj3/HEDJ, a chaperone of the endoplasmic reticulum.Infection and immunity · 2011Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Cholera toxin (CT) is transported from the plasma membrane of host cells to the endoplasmic reticulum (ER) where the catalytic CTA1 subunit retro-translocates to the cytosol to induce toxicity. Our previous analyses demonstrated that the ER oxidoreductase protein disulfide isomerase (PDI) acts as a redox-dependent chaperone to unfold CTA1, a reaction postulated to initiate toxin retro-translocation. In its reduced state, PDI binds and unfolds CTA1; subsequent oxidation of PDI by Ero1alpha enables toxin release. Whether this in vitro model describes events in cells that control CTA1 retro-translocation is unknown. Here we show that down-regulation of Ero1alpha decreases retro-translocation of CTA1 by increasing reduced PDI and blocking efficient toxin release. Overexpression of Ero1alpha also attenuates CTA1 retro-translocation, an effect due to increased PDI oxidation, which prevents PDI from engaging the toxin effectively. Interestingly, Ero1alpha down-regulation increases interaction between PDI and Derlin-1, an ER membrane protein that is a component of the retro-translocation complex. These findings demonstrate that an appropriate Ero1alpha-PDI ratio is critical for regulating the binding-release cycle of CTA1 by PDI during retro-translocation, and implicate PDI's redox state in targeting it to the retro-translocon.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.