ArticleToxins2013
Difference in F-actin depolymerization induced by toxin B from the Clostridium difficile strain VPI 10463 and toxin B from the variant Clostridium difficile serotype F strain 1470.
Article in Toxins, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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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Who cites it
17 citing papers in PubMed, 29 citations in OpenAlex.
- MappingmBio · 2025Article
- Article
- Host Immunity and Immunization Strategies for Clostridioides difficile Infection.Clinical microbiology reviews · 2023Review
- The Essential Role of Rac1 Glucosylation inFrontiers in microbiology · 2022Article
- Tetrapyrrolic Pigments from Heme- and Chlorophyll Breakdown are Actin-Targeting Compounds.Angewandte Chemie (International ed. in English) · 2021Article
- Melittin fromAntibiotics (Basel, Switzerland) · 2020Article
- Human intestinal enteroids as a model ofAmerican journal of physiology. Gastrointestinal and liver physiology · 2020Article
- Low Density Lipoprotein Receptor-Related Protein-1 (LRP1) Is Involved in the Uptake ofFrontiers in cellular and infection microbiology · 2020Article
- Clostridium difficile toxins A and B decrease intestinal SLC26A3 protein expression.American journal of physiology. Gastrointestinal and liver physiology · 2018Article
- Difference in Mono-O-Glucosylation of Ras Subtype GTPases Between Toxin A and Toxin B FromFrontiers in microbiology · 2018Article
- The role of toxins in Clostridium difficile infection.FEMS microbiology reviews · 2017Review
- Chemical Genomics, Structure Elucidation, and in Vivo Studies of the Marine-Derived Anticlostridial Ecteinamycin.ACS chemical biology · 2017Article
- Omics Approaches to Identify Potential Biomarkers of Inflammatory Diseases in the Focal Adhesion Complex.Genomics, proteomics & bioinformatics · 2017Review
- Enteric glial cells are susceptible to Clostridium difficile toxin B.Cellular and molecular life sciences : CMLS · 2017Article
- Role of p38Toxins · 2016Article
- Metal Ion Activation of Clostridium sordellii Lethal Toxin and Clostridium difficile Toxin B.Toxins · 2016Article
- Rho-A prenylation and signaling link epithelial homeostasis to intestinal inflammation.The Journal of clinical investigation · 2016Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Clostridium difficile toxin A (TcdA) and toxin B (TcdB) are the causative agent of the C. difficile-associated diarrhea (CDAD) and its severe form, the pseudomembranous colitis (PMC). TcdB from the C. difficile strain VPI10463 mono-glucosylates (thereby inactivates) the small GTPases Rho, Rac, and Cdc42, while Toxin B from the variant C. difficile strain serotype F 1470 (TcdBF) specifically mono-glucosylates Rac but not Rho(A/B/C). TcdBF is related to lethal toxin from C. sordellii (TcsL) that glucosylates Rac1 but not Rho(A/B/C). In this study, the effects of Rho-inactivating toxins on the concentrations of cellular F-actin were investigated using the rhodamine-phalloidin-based F-actin ELISA. TcdB induces F-actin depolymerization comparable to the RhoA-inactivating exoenzyme C3 from C. limosum (C3-lim). In contrast, the Rac-glucosylating toxins TcdBF and TcsL did not cause F-actin depolymerization. These observations led to the conclusion that F-actin depolymerization depends on the toxin's capability of glucosylating RhoA. Furthermore, the integrity of focal adhesions (FAs) was analyzed using paxillin and p21-activated kinase (PAK) as FA marker proteins. Paxillin dephosphorylation was observed upon treatment of cells with TcdB, TcdBF, or C3-lim. In conclusion, the Rho-inactivating toxins induce loss of cell shape by either F-actin depolymerization (upon RhoA inactivation) or the disassembly of FAs (upon Rac1 inactivation).
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Registered trials
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