ArticleScientific reports2017
Glucosyltransferase Activity of Clostridium difficile Toxin B Triggers Autophagy-mediated Cell Growth Arrest.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 12 citations in OpenAlex.
- Article
- STAT1-IFITM3 promotes autophagy in epithelial cells to controlLife science alliance · 2025Article
- Mechanisms ofFrontiers in cellular and infection microbiology · 2025Review
- Exploring the Toxin-Mediated Mechanisms inMicroorganisms · 2024Review
- Article
- The Essential Role of Rac1 Glucosylation inFrontiers in microbiology · 2022Article
- Genetically incorporated crosslinkers reveal NleE attenuates host autophagy dependent on PSMD10.eLife · 2021Article
- Cryptosporidium parvum infection induces autophagy in intestinal epithelial cells.Cellular microbiology · 2021Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Autophagy is a bulk cell-degradation process that occurs through the lysosomal machinery, and many reports have shown that it participates in microbial pathogenicity. However, the role of autophagy in Clostridium difficile infection (CDI), the leading cause of antibiotics-associated diarrhea, pseudomembranous colitis and even death in severe cases, is not clear. Here we report that the major virulent factor toxin B (TcdB) of Clostridium difficile elicits a strong autophagy response in host cells through its glucosyltransferase activity. Using a variety of autophagy-deficient cell lines, i.e. HeLa/ATG7
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