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幽门螺杆菌致病机制中CagA的SagA

SagA of CagA in Helicobacter pylori pathogenesis.

作者信息

Hatakeyama Masanori

机构信息

Division of Molecular Oncology, Institute for Genetic Medicine, Hokkaido University, Sapporo, Japan.

出版信息

Curr Opin Microbiol. 2008 Feb;11(1):30-7. doi: 10.1016/j.mib.2007.12.003. Epub 2008 Feb 20.

DOI:10.1016/j.mib.2007.12.003
PMID:18243773
Abstract

Much attention has recently been given to the role of the Helicobacter pylori CagA protein, the only as yet identified H. pylori protein that is delivered into the host gastric epithelial cells by a type IV secretion system, in the development of H. pylori-associated diseases, including gastric carcinoma. This review summarizes the latest advances in our understanding of pathogenic actions of H. pylori CagA, particularly focusing on the molecular mechanisms underlying CagA entry into the host cells as well as CagA-mediated perturbation of host cell signaling involved in proliferation, motility, differentiation, and polarity, which contributes malignant transformation of mammalian cells.

摘要

最近,幽门螺杆菌CagA蛋白在幽门螺杆菌相关疾病(包括胃癌)发展中的作用备受关注。CagA蛋白是目前唯一已确定的通过IV型分泌系统递送至宿主胃上皮细胞的幽门螺杆菌蛋白。本综述总结了我们对幽门螺杆菌CagA致病作用理解的最新进展,特别关注CagA进入宿主细胞的分子机制,以及CagA介导的对宿主细胞增殖、运动、分化和极性相关信号传导的干扰,这些干扰促使哺乳动物细胞发生恶性转化。

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