Department of Pathology
Animals; Embryonic Development; Gene Expression Regulation; Humans; Inflammation; Necrosis; Neoplasms; Protein Processing, Post-Translational; Receptor-Interacting Protein Serine-Threonine Kinases; Signal Transduction
Cellular and Molecular Physiology | Developmental Biology | Immunopathology | Molecular Genetics | Pathology
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.
FADD, MLKL, PGAM5, RIP1, caspase 8, inflammation
Rights and Permissions
Publisher PDF posted as allowed by the publisher's author rights policy at http://genesdev.cshlp.org/site/misc/terms.xhtml.
DOI of Published Version
Genes Dev. 2013 Aug 1;27(15):1640-9. doi: 10.1101/gad.223321.113. Link to article on publisher's site
Genes and development
Moriwaki K, Chan FK. (2013). RIP3: a molecular switch for necrosis and inflammation. University of Massachusetts Medical School Faculty Publications. https://doi.org/10.1101/gad.223321.113. Retrieved from https://escholarship.umassmed.edu/faculty_pubs/534
Creative Commons License
This work is licensed under a Creative Commons Attribution-Noncommercial 4.0 License