| Literature DB >> 30347517 |
Peng Chen1, Liang Tao2,3,4, Zheng Liu1, Min Dong2,3,4, Rongsheng Jin1.
Abstract
The incidence of Clostridium difficile infection (CDI) has increased significantly worldwide, causing substantial morbidity and mortality. One of the major virulence factor, TcdB, manages to enter the colonic epithelia via the human frizzled proteins (FZDs), which are physiological receptors for Wnt morphogens. Binding of TcdB to FZDs inhibits Wnt signaling, which may contribute to pathogenesis of CDI. Here, we review the structural mechanism by which TcdB exploits to recognize FZDs for cell entry and inhibiting Wnt signaling, which reveals new strategies to modulate Wnt signaling for therapeutic interventions.Entities:
Keywords: zzm321990Clostridium difficilezzm321990; Clostridium difficile infection; Wnt signaling; bacterial toxin; cancers; frizzled; host-pathogen interactions
Mesh:
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Year: 2018 PMID: 30347517 PMCID: PMC6399045 DOI: 10.1111/febs.14681
Source DB: PubMed Journal: FEBS J ISSN: 1742-464X Impact factor: 5.542