UMass Chan Affiliations
Department of PathologyDocument Type
Journal ArticlePublication Date
2013-08-01Keywords
AnimalsEmbryonic Development
Gene Expression Regulation
Humans
Inflammation
Necrosis
Neoplasms
Protein Processing, Post-Translational
Receptor-Interacting Protein Serine-Threonine Kinases
Signal Transduction
FADD
MLKL
PGAM5
RIP1
caspase 8
inflammation
Cellular and Molecular Physiology
Developmental Biology
Immunopathology
Molecular Genetics
Pathology
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Show full item recordAbstract
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.Source
Genes Dev. 2013 Aug 1;27(15):1640-9. doi: 10.1101/gad.223321.113. Link to article on publisher's siteDOI
10.1101/gad.223321.113Permanent Link to this Item
http://hdl.handle.net/20.500.14038/30281PubMed ID
23913919Related Resources
Link to Article in PubMedRights
Publisher PDF posted as allowed by the publisher's author rights policy at http://genesdev.cshlp.org/site/misc/terms.xhtml.Distribution License
http://creativecommons.org/licenses/by-nc/4.0/ae974a485f413a2113503eed53cd6c53
10.1101/gad.223321.113
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Except where otherwise noted, this item's license is described as Publisher PDF posted as allowed by the publisher's author rights policy at http://genesdev.cshlp.org/site/misc/terms.xhtml.