University of Massachusetts Medical School Faculty Publications

UMMS Affiliation

Department of Pathology

Publication Date

2013-08-01

Document Type

Article

Subjects

Animals; Embryonic Development; Gene Expression Regulation; Humans; Inflammation; Necrosis; Neoplasms; Protein Processing, Post-Translational; Receptor-Interacting Protein Serine-Threonine Kinases; Signal Transduction

Disciplines

Cellular and Molecular Physiology | Developmental Biology | Immunopathology | Molecular Genetics | Pathology

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.

Keywords

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

10.1101/gad.223321.113

Source

Genes Dev. 2013 Aug 1;27(15):1640-9. doi: 10.1101/gad.223321.113. Link to article on publisher's site

Related Resources

Link to Article in PubMed

Journal/Book/Conference Title

Genes and development

PubMed ID

23913919

Creative Commons License

Creative Commons Attribution-Noncommercial 4.0 License
This work is licensed under a Creative Commons Attribution-Noncommercial 4.0 License

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