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Cadherin‐mediated host–pathogen interactions
Cellular Microbiology ( IF 3.4 ) Pub Date : 2021-02-05 , DOI: 10.1111/cmi.13316
Sagarika Dash 1 , Kheerthana Duraivelan 1 , Dibyendu Samanta 1
Affiliation  

Cell adhesion molecules mediate cell‐to‐cell and cell‐to‐matrix adhesions and play an immense role in a myriad of physiological processes during the growth and development of a multicellular organism. Cadherins belong to a major group of membrane‐bound cell surface proteins that, in coordination with nectins, drive the formation and maintenance of adherens junctions for mediating cell to cell adhesion, cellular communication and signalling. Alongside adhesive function, the involvement of cadherins in mediating host–pathogen interactions has been extensively explored in recent years. In this review, we provide an in‐depth understanding of microbial pathogens and their virulence factors that exploit cadherins for their strategical invasion into the host cell. Furthermore, macromolecular interactions involving cadherins and various microbial factors such as secretory toxins and adhesins lead to the disintegration of host cell junctions followed by the entry of the pathogen or triggering downstream signalling pathways responsible for successful invasion of the pathogenic microbes are discussed. Besides providing a comprehensive insight into some of the structural complexes involving cadherins and microbial factors to offer the mechanistic details of host–pathogen interactions, the current review also highlights novel constituents of various cell signalling events such as endocytosis machinery elicited upon microbial infections.

中文翻译:

钙粘蛋白介导的宿主-病原体相互作用

细胞粘附分子介导细胞与细胞和细胞与基质的粘附,并在多细胞生物的生长和发育过程中的无数生理过程中发挥巨大作用。钙粘蛋白属于一大类膜结合细胞表面蛋白,与连接蛋白协同驱动粘附连接的形成和维持,以介导细胞间粘附、细胞通讯和信号传导。除了粘附功能外,近年来还广泛探索了钙粘蛋白在介导宿主 - 病原体相互作用中的作用。在这篇综述中,我们深入了解了微生物病原体及其利用钙粘蛋白战略入侵宿主细胞的毒力因子。此外,讨论了涉及钙粘蛋白和各种微生物因素(如分泌性毒素和粘附素)的大分子相互作用导致宿主细胞连接解体,随后病原体进入或触发下游信号通路负责致病微生物的成功入侵。除了提供对涉及钙粘蛋白和微生物因子的一些结构复合物的全面了解以提供宿主 - 病原体相互作用的机制细节外,本综述还强调了各种细胞信号事件的新成分,例如微生物感染引起的内吞作用机制。
更新日期:2021-04-12
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