Modification of phosphoinositides by the Shigella effector IpgD during host cell infection.
Autor: | Tran Van Nhieu G; Institute for Integrative Biology of the Cell - Centre National de la Recherche Scientifique (CNRS) UMR9198 - Institut National de la Santé et de la Recherche Médicale (Inserm) U1280, Team Calcium Signaling and Microbial Infections, Gif-sur-Yvette, France., Latour-Lambert P; Institut Pasteur, Unité Dynamique des interactions hôtes-pathogènes and Centre National de la Recherche Scientifique (CNRS) UMR3691, Université de Paris Cité, Paris, France., Enninga J; Institut Pasteur, Unité Dynamique des interactions hôtes-pathogènes and Centre National de la Recherche Scientifique (CNRS) UMR3691, Université de Paris Cité, Paris, France. |
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Jazyk: | angličtina |
Zdroj: | Frontiers in cellular and infection microbiology [Front Cell Infect Microbiol] 2022 Oct 27; Vol. 12, pp. 1012533. Date of Electronic Publication: 2022 Oct 27 (Print Publication: 2022). |
DOI: | 10.3389/fcimb.2022.1012533 |
Abstrakt: | Shigella , the causative agent of bacillary dysentery, subvert cytoskeletal and trafficking processes to invade and replicate in epithelial cells using an arsenal of bacterial effectors translocated through a type III secretion system. Here, we review the various roles of the type III effector IpgD, initially characterized as phosphatidylinositol 4,5 bisphosphate (PI4,5P Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. (Copyright © 2022 Tran Van Nhieu, Latour-Lambert and Enninga.) |
Databáze: | MEDLINE |
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