ArticleInfection and immunity2008
ADP-ribosylation of actin by the Clostridium botulinum C2 toxin in mammalian cells results in delayed caspase-dependent apoptotic cell death.
Article in Infection and immunity, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed.
- Novel endogenous protein-based strategies to inhibit clinically relevant bacterial AB-type toxins including pertussis toxin.Archives of toxicology · 2026Review
- MAP4Ks drive cell death in response tomBio · 2026Article
- A host defense role for Fibrinogen by direct binding of Clostridium botulinum C2 toxin.Cellular and molecular life sciences : CMLS · 2026Article
- Convergent mechanisms of epithelial cell structure manipulation by intestinal pathogens.PLoS pathogens · 2025Review
- An Updated View on the Cellular Uptake and Mode-of-Action of Clostridioides difficile Toxins.Advances in experimental medicine and biology · 2024Article
- Repurposing FDA-approved disulfiram for targeted inhibition of diphtheria toxin and the binary protein toxins ofFrontiers in pharmacology · 2024Article
- TheToxins · 2023Article
- The Pore-Forming Subunit C2IIa of the BinaryFrontiers in pharmacology · 2022Article
- Posttranslational modifications of the cytoskeleton.Cytoskeleton (Hoboken, N.J.) · 2021Review
- Avian intestinal ultrastructure changes provide insight into the pathogenesis of enteric diseases and probiotic mode of action.Scientific reports · 2021Article
- Caspase-3 cleavage of Salmonella type III secreted effector protein SifA is required for localization of functional domains and bacterial dissemination.Gut microbes · 2019Article
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- Retargeting the Clostridium botulinum C2 toxin to the neuronal cytosol.Scientific reports · 2016Article
- The tuberculosis necrotizing toxin kills macrophages by hydrolyzing NAD.Nature structural & molecular biology · 2015Article
- The Neisseria meningitidis ADP-Ribosyltransferase NarE Enters Human Epithelial Cells and Disrupts Epithelial Monolayer Integrity.PloS one · 2015Article
- Bacterial secreted effectors and caspase-3 interactions.Cellular microbiology · 2014Review
- Cationic PAMAM dendrimers as pore-blocking binary toxin inhibitors.Biomacromolecules · 2014Article
- Host cell cytotoxicity and cytoskeleton disruption by CerADPr, an ADP-ribosyltransferase of Bacillus cereus G9241.Biochemistry · 2013Article
- A cell-permeable fusion protein based on Clostridium botulinum C2 toxin for delivery of p53 tumorsuppressor into cancer cells.PloS one · 2013Article
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4 authors.
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No grant is acknowledged in the PubMed record.
Abstract
The binary C2 toxin from Clostridium botulinum mono-ADP-ribosylates G-actin in the cytosol of eukaryotic cells. This modification leads to depolymerization of actin filaments accompanied by cell rounding within 3 h of incubation but does not immediately induce cell death. Here we investigated the long-term responses of mammalian cell lines (HeLa and Vero) following C2 toxin treatment. Cells stayed round even though the toxin was removed from the medium after its internalization into the cells. No unmodified actin reappeared in the C2 toxin-treated cells within 48 h. Despite actin being completely ADP-ribosylated after about 7 h, no obvious decrease in the overall amount of actin was observed for at least 48 h. Therefore, ADP-ribosylation was not a signal for an accelerated degradation of actin in the tested cell lines. C2 toxin treatment resulted in delayed apoptotic cell death that became detectable about 15 to 24 h after toxin application in a portion of the cells. Poly(ADP)-ribosyltransferase 1 (PARP-1) was cleaved in C2 toxin-treated cells, an indication of caspase 3 activation and a hallmark of apoptosis. Furthermore, specific caspase inhibitors prevented C2 toxin-induced apoptosis, implying that caspases 8 and 9 were activated in C2 toxin-treated cells. C2I, the ADP-ribosyltransferase component of the C2 toxin, remained active in the cytosol for at least 48 h, and no extensive degradation of C2I was observed. From our data, we conclude that the long-lived nature of C2I in the host cell cytosol was essential for the nonreversible cytotoxic effect of C2 toxin, resulting in delayed apoptosis of the tested mammalian cells.
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