ArticleThe Journal of biological chemistry2010
Cytolethal distending toxin family members are differentially affected by alterations in host glycans and membrane cholesterol.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04557215 (Evaluation of the Efficacy and Safety of Rifaximin in Combination With N-acetylcysteine), which is not on this map. Cited by 44 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.
Evaluation of the Efficacy and Safety of Rifaximin in Combination With N-acetylcysteine (NAC) in Adult Patients With Irritable Bowel Syndrome With Diarrhea
Who cites it
44 citing papers in PubMed, 76 citations in OpenAlex.
- TM9SF4 acts as a receptor mediatingFrontiers in cellular and infection microbiology · 2026Article
- Cytolethal distending toxin from Glaesserella parasuis induces ferroptosis in porcine alveolar macrophages and mice.Veterinary research · 2025Article
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- Cellugyrin (synaptogyrin-2) dependent pathways are used by bacterial cytolethal distending toxin and SARS-CoV-2 virus to gain cell entry.Frontiers in cellular and infection microbiology · 2024Article
- Presence of Functionally Active Cytolethal Distending Toxin Genes on a Conjugative Plasmid in a Clinical Isolate of Providencia rustigianii.Infection and immunity · 2023Article
- Targeting the Inside of Cells with Biologicals: Toxin Routes in a Therapeutic Context.BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy · 2023Review
- Revisiting bacterial cytolethal distending toxin structure and function.Frontiers in cellular and infection microbiology · 2023Article
- Delivery, structure, and function of bacterial genotoxins.Virulence · 2022Review
- The Active Subunit of the Cytolethal Distending Toxin, CdtB, Derived From BothFrontiers in cellular and infection microbiology · 2021Article
- From DNA Damage to Cancer Progression: Potential Effects of Cytolethal Distending Toxin.Frontiers in immunology · 2021Review
- Functional Study ofToxins · 2020Article
- Rapamycin Re-Directs Lysosome Network, Stimulates ER-Remodeling, Involving Membrane CD317 and Affecting Exocytosis, inInternational journal of molecular sciences · 2020Article
- Internalization and Intoxication of Human Macrophages by the Active Subunit of theFrontiers in immunology · 2020Article
- Review
- Genome-Wide Identification of Host Genes Required for Toxicity of Bacterial Cytolethal Distending Toxin in a Yeast Model.Frontiers in microbiology · 2019Article
- Internalization of the Active Subunit of theFrontiers in cellular and infection microbiology · 2017Article
- Cytolethal Distending Toxin FromJundishapur journal of microbiology · 2016Article
- Review
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Cytolethal distending toxins (CDTs) are tripartite protein exotoxins produced by a diverse group of pathogenic Gram-negative bacteria. Based on their ability to induce DNA damage, cell cycle arrest, and apoptosis of cultured cells, CDTs are proposed to enhance virulence by blocking cellular division and/or directly killing epithelial and immune cells. Despite the widespread distribution of CDTs among several important human pathogens, our understanding of how these toxins interact with host cells is limited. Here we demonstrate that CDTs from Haemophilus ducreyi, Aggregatibacter actinomycetemcomitans, Escherichia coli, and Campylobacter jejuni differ in their abilities to intoxicate host cells with defined defects in host factors previously implicated in CDT binding, including glycoproteins, and glycosphingolipids. The absence of cell surface sialic acid sensitized cells to intoxication by three of the four CDTs tested. Surprisingly, fucosylated N-linked glycans and glycolipids, previously implicated in CDT-host interactions, were not required for intoxication by any of the CDTs tested. Finally, altering host-cellular cholesterol, also previously implicated in CDT binding, affected intoxication by only a subset of CDTs tested. The findings presented here provide insight into the molecular and cellular basis of CDT-host interactions.
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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.