UMass Chan AffiliationsDepartment of Pathology
Gene Expression Regulation
Protein Processing, Post-Translational
Receptor-Interacting Protein Serine-Threonine Kinases
Cellular and Molecular Physiology
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AbstractThe receptor-interacting protein kinase 3 (RIP3/RIPK3) has emerged as a critical regulator of programmed necrosis/necroptosis, an inflammatory form of cell death with important functions in pathogen-induced and sterile inflammation. RIP3 activation is tightly regulated by phosphorylation, ubiquitination, and caspase-mediated cleavage. These post-translational modifications coordinately regulate the assembly of a macromolecular signaling complex termed the necrosome. Recently, several reports indicate that RIP3 can promote inflammation independent of its pronecrotic activity. Here, we review our current understanding of the mechanisms that drive RIP3-dependent necrosis and its role in different inflammatory diseases.
SourceGenes Dev. 2013 Aug 1;27(15):1640-9. doi: 10.1101/gad.223321.113. Link to article on publisher's site
Permanent Link to this Itemhttp://hdl.handle.net/20.500.14038/30281
Related ResourcesLink to Article in PubMed
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