RIP3: a molecular switch for necrosis and inflammation.

Published

Journal Article (Review)

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.

Full Text

Duke Authors

Cited Authors

  • Moriwaki, K; Chan, FK-M

Published Date

  • August 1, 2013

Published In

Volume / Issue

  • 27 / 15

Start / End Page

  • 1640 - 1649

PubMed ID

  • 23913919

Pubmed Central ID

  • 23913919

Electronic International Standard Serial Number (EISSN)

  • 1549-5477

Digital Object Identifier (DOI)

  • 10.1101/gad.223321.113

Language

  • eng

Conference Location

  • United States