ArticleInfection and immunity2009
The long-lived nature of clostridium perfringens iota toxin in mammalian cells induces delayed apoptosis.
Article in Infection and immunity, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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
20 citing papers in PubMed, 31 citations in OpenAlex.
- MAP4Ks drive cell death in response tomBio · 2026Article
- Convergent mechanisms of epithelial cell structure manipulation by intestinal pathogens.PLoS pathogens · 2025Review
- Clostridial Myonecrosis: A Comprehensive Review of Toxin Pathophysiology and Management Strategies.Microorganisms · 2024Review
- Salmonella pSLT-encoded effector SpvB promotes RIPK3-dependent necroptosis in intestinal epithelial cells.Cell death discovery · 2022Article
- Pathogenicity and virulence ofVirulence · 2021Article
- An update on the human and animal enteric pathogen Clostridium perfringens.Emerging microbes & infections · 2018Review
- Mechanisms of Action and Cell Death Associated withToxins · 2018Review
- Combined Pharmacological Inhibition of Cyclophilins, FK506-Binding Proteins, Hsp90, and Hsp70 Protects Cells FromFrontiers in pharmacology · 2018Article
- Article
- Challenging the roles of CD44 and lipolysis stimulated lipoprotein receptor in conveying Clostridium perfringens iota toxin cytotoxicity in breast cancer.Molecular cancer · 2014Article
- Toxin plasmids of Clostridium perfringens.Microbiology and molecular biology reviews : MMBR · 2013Review
- 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
- Article
- Lipolysis-stimulated lipoprotein receptor (LSR) is the host receptor for the binary toxin Clostridium difficile transferase (CDT).Proceedings of the National Academy of Sciences of the United States of America · 2011Article
- A therapeutic chemical chaperone inhibits cholera intoxication and unfolding/translocation of the cholera toxin A1 subunit.PloS one · 2011Article
- Exploring the role of host cell chaperones/PPIases during cellular up-take of bacterial ADP-ribosylating toxins as basis for novel pharmacological strategies to protect mammalian cells against these virulence factors.Naunyn-Schmiedeberg's archives of pharmacology · 2011Review
- Article
- Clostridial binary toxins: iota and C2 family portraits.Frontiers in cellular and infection microbiology · 2011Review
- Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mono-ADP ribosylation of actin by bacterial toxins, such as Clostridium perfringens iota or Clostridium botulinum C2 toxins, results in rapid depolymerization of actin filaments and cell rounding. Here we report that treatment of African green monkey kidney (Vero) cells with iota toxin resulted in delayed caspase-dependent death. Unmodified actin did not reappear in toxin-treated cells, and enzyme-active toxin was detectable in the cytosol for at least 24 h. C2 toxin showed comparable, long-lived effects in cells, while a C2 toxin control lacking ADP-ribosyltransferase activity did not induce cell death. To address whether the remarkable stability of the iota and C2 toxins in cytosol was crucial for inducing cell death, we treated cells with C/SpvB, the catalytic domain of Salmonella enterica SpvB. Although C/SpvB also mono-ADP ribosylates actin as do the iota and C2 toxins, cells treated with a cell-permeating C/SpvB fusion toxin became rounded but recovered and remained viable. Moreover, unmodified actin reappeared in these cells, and ADP-ribosyltransferase activity due to C/SpvB was not detectable in the cytosol after 24 h, a result most likely due to degradation of C/SpvB. Repeated application of C/SpvB prevented recovery of cells and reappearance of unmodified actin. In conclusion, a complete but transient ADP ribosylation of actin was not sufficient to trigger apoptosis, implying that long-term stability of actin-ADP-ribosylating toxins, such as iota and C2, in the cytosol is crucial for inducing delayed, caspase-dependent 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.