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通过泛素系统调节沙门氏菌与宿主细胞的相互作用。

Regulation of Salmonella-host cell interactions via the ubiquitin system.

机构信息

Institute of Biochemistry II, Goethe University Frankfurt - Medical Faculty, University Hospital, 60590 Frankfurt am Main, Germany.

Institute of Biochemistry II, Goethe University Frankfurt - Medical Faculty, University Hospital, 60590 Frankfurt am Main, Germany; Buchmann Institute for Molecular Life Sciences, Goethe University Frankfurt, Riedberg Campus, 60438 Frankfurt am Main, Germany.

出版信息

Int J Med Microbiol. 2018 Jan;308(1):176-184. doi: 10.1016/j.ijmm.2017.11.003. Epub 2017 Nov 6.

Abstract

Salmonella infections cause acute intestinal inflammatory responses through the action of bacterial effector proteins secreted into the host cytosol. These proteins promote Salmonella survival, amongst others, by deregulating the host innate immune system and interfering with host cell ubiquitylation signaling. This review describes the recent findings of dynamic changes of the host ubiquitinome during pathogen infection, how bacterial effector proteins modulate the host ubiquitin system and how the host innate immune system counteracts Salmonella invasion by using these pathogens as signaling platforms to initiate immune responses.

摘要

沙门氏菌感染通过将细菌效应蛋白分泌到宿主细胞质中而引起急性肠道炎症反应。这些蛋白质通过扰乱宿主固有免疫系统和干扰宿主细胞泛素化信号来促进沙门氏菌的存活。本综述描述了宿主泛素组在病原体感染过程中动态变化的最新发现,细菌效应蛋白如何调节宿主泛素系统,以及宿主固有免疫系统如何通过利用这些病原体作为信号平台来启动免疫反应来抵抗沙门氏菌入侵。

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