ArticleInfection and immunity2007
Difference in the cytotoxic effects of toxin B from Clostridium difficile strain VPI 10463 and toxin B from variant Clostridium difficile strain 1470.
Article in Infection and immunity, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
What it found
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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.
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.
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Who cites it
39 citing papers in PubMed, 70 citations in OpenAlex.
- The Use of Bacteria and Their Toxins as Antitumor Agents: Present and Future.Microorganisms · 2026Review
- A sequence invariable region in TcdB2 is required for toxin escape fromJournal of bacteriology · 2024Article
- Exploring the Toxin-Mediated Mechanisms inMicroorganisms · 2024Review
- Review
- Clostridioides difficile toxin B alone and with pro-inflammatory cytokines induces apoptosis in enteric glial cells by activating three different signalling pathways mediated by caspases, calpains and cathepsin B.Cellular and molecular life sciences : CMLS · 2022Article
- TcdB ofInternational journal of molecular sciences · 2022Article
- Low-density lipoprotein receptor-related protein 1 is a CROPs-associated receptor for Clostridioides infection toxin B.Science China. Life sciences · 2022Article
- Structural basis for selective modification of Rho and Ras GTPases byScience advances · 2021Article
- Subtyping analysis reveals new variants and accelerated evolution of Clostridioides difficile toxin B.Communications biology · 2020Article
- Current Approaches for Combination Therapy of Cancer: The Role of Immunogenic Cell Death.Cancers · 2020Review
- Enterotoxic Clostridia:Microbiology spectrum · 2019Review
- Difference in Mono-O-Glucosylation of Ras Subtype GTPases Between Toxin A and Toxin B FromFrontiers in microbiology · 2018Article
- Enteric glial cells are susceptible to Clostridium difficile toxin B.Cellular and molecular life sciences : CMLS · 2017Article
- Clostridium difficile Toxins TcdA and TcdB Cause Colonic Tissue Damage by Distinct Mechanisms.Infection and immunity · 2016Article
- Clostridium difficile Toxins A and B: Insights into Pathogenic Properties and Extraintestinal Effects.Toxins · 2016Review
- Analysis of TcdB Proteins within the Hypervirulent Clade 2 Reveals an Impact of RhoA Glucosylation on Clostridium difficile Proinflammatory Activities.Infection and immunity · 2016Article
- Clinical Characteristics and Treatment Outcomes of Clostridium difficile Infections by PCR Ribotype 017 and 018 Strains.PloS one · 2016Article
- Article
- Review
- DXD motif-dependent and -independent effects of the chlamydia trachomatis cytotoxin CT166.Toxins · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glucosylation of RhoA, Rac1, and Cdc42 by Clostridium difficile toxin B from strain VPI 10463 (TcdB) results in actin reorganization (cytopathic effect) and apoptosis (cytotoxic effect). Toxin B from variant C. difficile strain 1470 serotype F (TcdBF) differs from TcdB with regard to substrate proteins, as it glucosylates Rac1 and R-Ras but not RhoA and Cdc42. In this study, we addressed the question of whether the cellular effects of the toxins depend on their protein substrate specificity. Rat basophilic leukemia (RBL) cells were synchronized using the thymidine double-block technique. We show that cells were most sensitive to the cytotoxic effect of TcdB in S phase, as analyzed in terms of phosphatidyl serine externalization, fragmentation of nuclei, and activation of caspase-3; in contrast, TcdBF induced only a marginal cytotoxic effect, suggesting that inactivation of RhoA (but not of Rac1) was required for the cytotoxic effect. The glucosylation of Rac1 was correlated to the cytopathic effect of either toxin, suggesting a close connection of the two effects. The cytotoxic effect of TcdB was executed by caspase-3, as it was responsive to inhibition by acetyl-Asp-Met-Gln-Asp-aldehyde (Ac-DMQD-CHO), an inhibitor of caspase-3. The viability of TcdB-treated RBL cells was reduced, whereas the viability of TcdBF-treated cells was unchanged, further confirming that inactivation of RhoA is required for the cytotoxic effect. In conclusion, the protein substrate specificity of the glucosylating toxins determines their biological activity.
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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.