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利用致病性大肠杆菌模拟跨膜受体信号传导。

Exploiting pathogenic Escherichia coli to model transmembrane receptor signalling.

作者信息

Hayward Richard D, Leong John M, Koronakis Vassilis, Campellone Kenneth G

机构信息

University of Cambridge, Department of Pathology, Tennis Court Road, Cambridge CB2 1QP, UK.

出版信息

Nat Rev Microbiol. 2006 May;4(5):358-70. doi: 10.1038/nrmicro1391.

Abstract

Many microbial pathogens manipulate the actin cytoskeleton of eukaryotic target cells to promote their internalization, intracellular motility and dissemination. Enteropathogenic and enterohaemorrhagic Escherichia coli, which both cause severe diarrhoeal disease, can adhere to mammalian intestinal cells and induce reorganization of the actin cytoskeleton into 'pedestal-like' pseudopods beneath the extracellular bacteria. As pedestal assembly is triggered by E. coli virulence factors that mimic several host cell-signalling components, such as transmembrane receptors, their cognate ligands and cytoplasmic adaptor proteins, it can serve as a powerful model system to study eukaryotic transmembrane signalling. Here, we consider the impact of recent data on our understanding of both E. coli pathogenesis and cell biology, and the rich prospects for exploiting these bacterial factors as versatile tools to probe cellular signalling pathways.

摘要

许多微生物病原体操纵真核靶细胞的肌动蛋白细胞骨架,以促进其内化、细胞内运动和传播。引起严重腹泻疾病的肠致病性大肠杆菌和肠出血性大肠杆菌,都能粘附于哺乳动物肠道细胞,并诱导肌动蛋白细胞骨架在细胞外细菌下方重组为“基座样”伪足。由于基座组装是由模仿几种宿主细胞信号成分(如跨膜受体、其同源配体和细胞质衔接蛋白)的大肠杆菌毒力因子触发的,它可以作为研究真核跨膜信号传导的强大模型系统。在这里,我们考虑了最新数据对我们理解大肠杆菌发病机制和细胞生物学的影响,以及利用这些细菌因子作为探测细胞信号通路的通用工具的丰富前景。

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