ArticleInfection and immunity2006
The cholera toxin A1(3) subdomain is essential for interaction with ADP-ribosylation factor 6 and full toxic activity but is not required for translocation from the endoplasmic reticulum to the cytosol.
Article in Infection and immunity, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
24 citing papers in PubMed, 37 citations in OpenAlex.
- Article
- MVA-Spike encoding the A subunit of dmLT safely enhances systemic and mucosal immune responses.Frontiers in immunology · 2026Article
- A binding motif for Hsp90 in the A chains of ADP-ribosylating toxins that move from the endoplasmic reticulum to the cytosol.Cellular microbiology · 2019Article
- HSC70 and HSP90 chaperones perform complementary roles in translocation of the cholera toxin A1 subunit from the endoplasmic reticulum to the cytosol.The Journal of biological chemistry · 2019Article
- The plasma membrane as a capacitor for energy and metabolism.American journal of physiology. Cell physiology · 2016Review
- 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
- Co- and post-translocation roles for HSP90 in cholera Intoxication.The Journal of biological chemistry · 2014Article
- ADP-ribosylation factor 6 acts as an allosteric activator for the folded but not disordered cholera toxin A1 polypeptide.Molecular microbiology · 2014Article
- Substrate-induced unfolding of protein disulfide isomerase displaces the cholera toxin A1 subunit from its holotoxin.PLoS pathogens · 2014Article
- Toxin instability and its role in toxin translocation from the endoplasmic reticulum to the cytosol.Biomolecules · 2013Article
- Lipid rafts alter the stability and activity of the cholera toxin A1 subunit.The Journal of biological chemistry · 2012Article
- Cholera toxin activates nonconventional adjuvant pathways that induce protective CD8 T-cell responses after epicutaneous vaccination.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- Detection of toxin translocation into the host cytosol by surface plasmon resonance.Journal of visualized experiments : JoVE · 2012Article
- Insights on the trafficking and retro-translocation of glycosphingolipid-binding bacterial toxins.Frontiers in cellular and infection microbiology · 2012Review
- Structural and functional interactions between the cholera toxin A1 subunit and ERdj3/HEDJ, a chaperone of the endoplasmic reticulum.Infection and immunity · 2011Article
- Protein-disulfide isomerase displaces the cholera toxin A1 subunit from the holotoxin without unfolding the A1 subunit.The Journal of biological chemistry · 2011Article
- A therapeutic chemical chaperone inhibits cholera intoxication and unfolding/translocation of the cholera toxin A1 subunit.PloS one · 2011Article
- Characterization of a mutant Escherichia coli heat-labile toxin, LT(R192G/L211A), as a safe and effective oral adjuvant.Clinical and vaccine immunology : CVI · 2011Article
- Contribution of subdomain structure to the thermal stability of the cholera toxin A1 subunit.Biochemistry · 2010Article
- Stabilization of the tertiary structure of the cholera toxin A1 subunit inhibits toxin dislocation and cellular intoxication.Journal of molecular biology · 2009Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Cholera toxin (CT) moves from the plasma membrane to the endoplasmic reticulum (ER) by retrograde vesicular traffic. In the ER, the catalytic CTA1 polypeptide dissociates from the rest of the toxin and enters the cytosol by a process that involves the quality control mechanism of ER-associated degradation (ERAD). The cytosolic CTA1 then ADP ribosylates Gsalpha, resulting in adenylate cyclase activation and intoxication of the target cell. It is hypothesized that the C-terminal A1(3) subdomain of CTA1 plays two crucial roles in the intoxication process: (i) it contains a hydrophobic domain that triggers the ERAD mechanism and (ii) it facilitates interaction with the cytosolic ADP-ribosylation factors (ARFs) that serve as allosteric activators of CTA1. In this study, we examined the role(s) of the CTA1(3) subdomain in CT intoxication. Full-length CTA1 constructs and truncated CTA1 constructs lacking the A1(3) subdomain were generated and used to conduct two-hybrid studies of interactions with ARF6, in vitro enzyme assays, in vivo toxicity assays, and in vivo processing/degradation assays. Direct, plasmid-mediated expression of CTA1 constructs in the ER or cytosol of transfected CHO cells was used to perform the in vivo assays. With these methods, we found that the A1(3) subdomain of CTA1 is important both for interaction with ARF6 and for full expression of enzyme activity in vivo. Surprisingly, however, the A1(3) subdomain was not required for ERAD-mediated passage of CTA1 from the ER to the cytosol. A possible alternative trigger for CTA1 to activate the ERAD mechanism is discussed.
Indexed as
Identifiers
What OpenQuestion holds
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.