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RIPK 3 in cell death and inflammation: the good, the bad, and the ugly
Author(s) -
Orozco Susana,
Oberst Andrew
Publication year - 2017
Publication title -
immunological reviews
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.839
H-Index - 223
eISSN - 1600-065X
pISSN - 0105-2896
DOI - 10.1111/imr.12536
Subject(s) - necroptosis , biology , programmed cell death , inflammation , microbiology and biotechnology , apoptosis , signal transduction , context (archaeology) , ubiquitin , receptor , caspase , immunology , genetics , gene , paleontology
Summary Necroptosis is a form of cell death that can be observed downstream of death receptor or pattern recognition receptor signaling under certain cellular contexts, or in response to some viral and bacterial infections. The receptor interacting protein kinases‐1 ( RIPK 1) and RIPK 3 are at the core of necroptotic signaling, among other proteins. Because this pathway is normally halted by the pro‐apoptotic protease caspase‐8 and the IAP ubiquitin ligases, how and when necroptosis is triggered in physiological settings are ongoing questions. Interestingly, accumulating evidence suggests that RIPK 3 has functions beyond the induction of necroptotic cell death, especially in the areas of tissue injury and sterile inflammation. Here, we will discuss the role of RIPK 3 in a variety of physiological conditions, including necroptotic and non‐necroptotic cell death, in the context of viral and bacterial infections, tissue damage, and inflammation.