ArticlePloS one2012
Oligomerization of Clostridium perfringens epsilon toxin is dependent upon caveolins 1 and 2.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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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.
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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.
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Who cites it
28 citing papers in PubMed, 48 citations in OpenAlex.
- Caveolin 1 is a conserved host factor mediating Bacillus cereus hemolysin BL toxin cytolytic toxicity.PLoS biology · 2026Article
- Novel genotypes, phenotypes, and triggers in humans with OTULIN haploinsufficiency.Journal of human immunity · 2025Article
- Effect ofNAM journal · 2025Article
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- Systematic evaluation of membrane-camouflaged nanoparticles in neutralizing Clostridium perfringens ε-toxin.Journal of nanobiotechnology · 2023Article
- New Mutants of Epsilon Toxin fromToxins · 2022Article
- Phenotypic and Genotypic Characterization ofVeterinary sciences · 2022Article
- Article
- The Na/K-ATPase α1 and c-Src form signaling complex under native condition: A crosslinking approach.Scientific reports · 2020Article
- Gut Microbiota in Neurological Disorders.Archivum immunologiae et therapiae experimentalis · 2019Review
- Clostridium perfringens epsilon toxin induces blood brain barrier permeability via caveolae-dependent transcytosis and requires expression of MAL.PLoS pathogens · 2019Article
- Clostridium perfringens Epsilon Toxin Compromises the Blood-Brain Barrier in a Humanized Zebrafish Model.iScience · 2019Article
- Article
- Inhibition of bacterial toxin recognition of membrane components as an anti-virulence strategy.Journal of biological engineering · 2019Review
- A Novel Panel of Rabbit Monoclonal Antibodies and Their Diverse Applications Including Inhibition ofAntibodies (Basel, Switzerland) · 2018Article
- Evaluation of plant-producedThe Onderstepoort journal of veterinary research · 2017Article
- Bacterial Signaling to the Nervous System through Toxins and Metabolites.Journal of molecular biology · 2017Review
- Does the Gut Microbiota Influence Immunity and Inflammation in Multiple Sclerosis Pathophysiology?Journal of immunology research · 2017Review
- Characterization of a caveolin-1 mutation associated with both pulmonary arterial hypertension and congenital generalized lipodystrophy.Traffic (Copenhagen, Denmark) · 2016Article
- Immunization with a novel Clostridium perfringens epsilon toxin mutant rETX(Y196E)-C confers strong protection in mice.Scientific reports · 2016Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Evidence from multiple studies suggests that Clostridium perfringens ε-toxin is a pore-forming toxin, assembling into oligomeric complexes in the plasma membrane of sensitive cells. In a previous study, we used gene-trap mutagenesis to identify mammalian factors contributing to toxin activity, including caveolin-2 (CAV2). In this study, we demonstrate the importance of caveolin-2 and its interaction partner, caveolin-1 (CAV1), in ε-toxin-induced cytotoxicity. Using CAV2-specific shRNA in a toxin-sensitive human kidney cell line, ACHN, we confirmed that cells deficient in CAV2 exhibit increased resistance to ε-toxin. Similarly, using CAV1-specific shRNA, we demonstrate that cells deficient in CAV1 also exhibit increased resistance to the toxin. Immunoprecipitation of CAV1 and CAV2 from ε-toxin-treated ACHN cells demonstrated interaction of both CAV1 and -2 with the toxin. Furthermore, blue-native PAGE indicated that the toxin and caveolins were components of a 670 kDa protein complex. Although ε-toxin binding was only slightly perturbed in caveolin-deficient cells, oligomerization of the toxin was dramatically reduced in both CAV1- and CAV2-deficient cells. These results indicate that CAV1 and -2 potentiate ε-toxin induced cytotoxicity by promoting toxin oligomerization - an event which is requisite for pore formation and, by extension, cell death.
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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.