Humphries, Fiachra and Yang, Shuo and Wang, Bingwei and Moynagh, Paul N. (2015) RIP kinases: key decision makers in cell death and innate immunity. Cell Death and Differentiation, 22. pp. 225-236. ISSN 1476-5403

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Abstract

Innate immunity represents the first line of defence against invading pathogens. It consists of an initial inflammatory response that recruits white blood cells to the site of infection in an effort to destroy and eliminate the pathogen. Some pathogens replicate within host cells, and cell death by apoptosis is an important effector mechanism to remove the replication niche for such microbes. However, some microbes have evolved evasive strategies to block apoptosis, and in these cases host cells may employ further countermeasures, including an inflammatory form of cell death know as necroptosis. This review aims to highlight the importance of the RIP kinase family in controlling these various defence strategies. RIP1 is initially discussed as a key component of death receptor signalling and in the context of dictating whether a cell triggers a pathway of pro-inflammatory gene expression or cell death by apoptosis. The molecular and functional interplay of RIP1 and RIP3 is described, especially with respect to mediating necroptosis and as key mediators of inflammation. The function of RIP2, with particular emphasis on its role in NOD signalling, is also explored. Special attention is given to emphasizing the physiological and pathophysiological contexts for these various functions of RIP kinases.

Item Type:	Article
Keywords:	RIP kinases; cell death; innate immunity; RIP kinase family;
Academic Unit:	Faculty of Science and Engineering > Biology
Item ID:	11032
Identification Number:	https://doi.org/10.1038/cdd.2014.126
Depositing User:	Professor Paul Moynagh
Date Deposited:	10 Sep 2019 15:50
Journal or Publication Title:	Cell Death and Differentiation
Publisher:	Springer Nature
Refereed:	Yes
Funders:	Science Foundation Ireland (SFI)
URI:	https://www.nature.com
Use Licence:	This item is available under a Creative Commons Attribution Non Commercial Share Alike Licence (CC BY-NC-SA). Details of this licence are available here

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