ReviewThe FEBS journal2023
Receptor binding mechanisms of Clostridioides difficile toxin B and implications for therapeutics development.
Review in The FEBS journal, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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
9 citing papers in PubMed, 14 citations in OpenAlex.
- Integrating machine learning and WGCNA to identify core candidate genes and decipher immune-related molecular networks in TcdA/TcdB-associated CDI.Antonie van Leeuwenhoek · 2026Article
- Development of Peptide Glucosyltransferase Inhibitors With Comprehensive Coverage Across Clostridioides difficile Toxin B Sub-Types.Biotechnology and bioengineering · 2026Article
- CD44 is a macrophage receptor for TcdB fromGut microbes · 2025Article
- C. difficile Infection in Colorectal Cancer: Risk Determinants, Outcomes, and Evolving Management Approaches.Journal of gastrointestinal cancer · 2025Review
- Exploring the Toxin-Mediated Mechanisms inMicroorganisms · 2024Review
- Gaining New Insights into Fundamental Biological Pathways by Bacterial Toxin-Based Genetic Screens.Bioengineering (Basel, Switzerland) · 2023Review
- Identification of TFPI as a receptor reveals recombination-driven receptor switching in Clostridioides difficile toxin B variants.Nature communications · 2022Article
- Structure and conformational dynamics ofLife science alliance · 2022Article
- Neutralizing epitopes onFrontiers in immunology · 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
2 authors at 1 institution in 1 country.
Funding
Abstract
Clostridioides difficile is classified as an urgent antibiotic resistance threat by the Centers for Disease Control and Prevention (CDC). C. difficile infection (CDI) is mainly caused by the C. difficile exotoxin TcdB, which invades host cells via receptor-mediated endocytosis. However, many natural variants of TcdB have been identified including some from the hypervirulent strains, which pose significant challenges for developing effective CDI therapies. Here, we review the recent research progress on the molecular mechanisms by which TcdB recognizes Frizzed proteins (FZDs) and chondroitin sulfate proteoglycan 4 (CSPG4) as two major host receptors. We suggest that the receptor-binding sites and several previously identified neutralizing epitopes on TcdB are ideal targets for the development of broad-spectrum inhibitors to protect against diverse TcdB variants.
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.