RIP3: a molecular switch for necrosis and inflammation
- Department of Pathology, Immunology and Microbiology Program, University of Massachusetts Medical School, Worcester, Massachusetts 01605, USA
Abstract
The 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.
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↵1 Corresponding author
E-mail francis.chan{at}umassmed.edu
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Article is online at http://www.genesdev.org/cgi/doi/10.1101/gad.223321.113.
- Copyright © 2013 by Cold Spring Harbor Laboratory Press