期刊
FEBS JOURNAL
卷 286, 期 5, 页码 874-881出版社
WILEY
DOI: 10.1111/febs.14681
关键词
bacterial toxin; cancers; Clostridium difficile; Clostridium difficile infection; frizzled; host-pathogen interactions; Wnt signaling
资金
- National Institute of Health (NIH) [R01 AI125704, R21 AI123920, R01 NS080833, R01 AI132387, R01 AI139087]
- NIH [P30DK034854]
- Boston Children's Hospital Intellectual and Developmental Disabilities Research Center [P30HD18655]
- Burroughs Wellcome Fund
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.
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