ReviewAnaerobe2016
The interaction of Clostridium perfringens enterotoxin with receptor claudins.
Review in Anaerobe, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
37 citing papers in PubMed, 52 citations in OpenAlex.
- Structure-forward targeting of claudins with synthetic binders.FEBS letters · 2026Review
- Article
- Biomimetic Protein Materials for Adjuvant-Free Dermal Penetration.ACS materials letters · 2026Article
- Claudins in ovarian cancer: emerging biomarkers and therapeutic targets.Tissue barriers · 2026Review
- Unlocking the Potential of Polysaccharides for the Treatment of Lung Cancer.Anti-cancer agents in medicinal chemistry · 2026Review
- Orally Administered Zinc Gluconate Induces Tight Junctional Remodeling and Reduces Passive Transmucosal Permeability Across Human Intestine in a Patient-Based Study.International journal of molecular sciences · 2025Article
- Cryo-EM structures of Clostridium perfringens enterotoxin bound to its human receptor, claudin-4.Structure (London, England : 1993) · 2024Article
- Biophysics of claudin proteins in tight junction architecture: Three decades of progress.Biophysical journal · 2024Review
- Clostridial Myonecrosis: A Comprehensive Review of Toxin Pathophysiology and Management Strategies.Microorganisms · 2024Review
- Structural and biophysical insights into targeting of claudin-4 by a synthetic antibody fragment.Communications biology · 2024Article
- Overview of Bacterial Protein Toxins from Pathogenic Bacteria: Mode of Action and Insights into Evolution.Toxins · 2024Review
- Micronutrients at Supplemental Levels, Tight Junctions and Epithelial Barrier Function: A Narrative Review.International journal of molecular sciences · 2024Review
- Structural Basis ofToxins · 2023Article
- Review
- Role of the gut microbiota in anticancer therapy: from molecular mechanisms to clinical applications.Signal transduction and targeted therapy · 2023Review
- Claudin-4: A New Molecular Target for Epithelial Cancer Therapy.International journal of molecular sciences · 2023Review
- Characterizing the Contributions of Various Clostridium perfringens Enterotoxin Properties tomSphere · 2022Article
- Necrotic Enteritis in Broiler Chickens: A Review on the Pathogen, Pathogenesis, and Prevention.Microorganisms · 2022Review
- Application of C-Terminal Clostridium Perfringens Enterotoxin in Treatment of Brain Metastasis from Breast Cancer.Cancers · 2022Review
- Epicardium-derived cells organize through tight junctions to replenish cardiac muscle in salamanders.Nature cell biology · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Clostridium perfringens enterotoxin (CPE) has significant medical importance due to its involvement in several common human gastrointestinal diseases. This 35 kDa single polypeptide toxin consists of two domains: a C-terminal domain involved in receptor binding and an N-terminal domain involved in oligomerization, membrane insertion and pore formation. The action of CPE starts with its binding to receptors, which include certain members of the claudin tight junction protein family; bound CPE then forms a series of complexes, one of which is a pore that causes the calcium influx responsible for host cell death. Recent studies have revealed that CPE binding to claudin receptors involves interactions between the C-terminal CPE domain and both the 1st and 2nd extracellular loops (ECL-1 and ECL-2) of claudin receptors. Of particular importance for this binding is the docking of ECL-2 into a pocket present in the C-terminal domain of the toxin. This increased understanding of CPE interactions with claudin receptors is now fostering the development of receptor decoy therapeutics for CPE-mediated gastrointestinal disease, reagents for cancer therapy/diagnoses and enhancers of drug delivery.
Indexed as
Identifiers
What OpenQuestion holds
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.