The molecular regulation of programmed necrotic cell injury.

Published

Journal Article (Review)

Proper regulation of cell death is essential for metazoan development and functions. Unlike apoptosis, necrosis is a more inflammatory form of cell death that might contribute to antiviral immunity. Indeed, necrotic cell injury is distinguished from apoptosis by extensive organelle and cell swelling and plasma membrane rupture. Recent evidence indicates that an elaborate biochemical network emanating from receptors in the TNF superfamily can induce apoptosis as well as necrotic cell death. The induction of necrosis by TNF-like cytokines requires biochemical components that are distinct from those involved in apoptosis. Specifically, serine/threonine protein kinases in the receptor interacting protein (RIP) family are required for "programmed" necrotic cell injury. In this review, we discuss the molecular crosstalk between apoptosis and programmed necrosis, with a special emphasis on how caspases, protein ubiquitylation and phosphorylation regulate the induction of necrotic cell injury.

Full Text

Duke Authors

Cited Authors

  • Moquin, D; Chan, FK-M

Published Date

  • August 2010

Published In

Volume / Issue

  • 35 / 8

Start / End Page

  • 434 - 441

PubMed ID

  • 20346680

Pubmed Central ID

  • 20346680

International Standard Serial Number (ISSN)

  • 0968-0004

Digital Object Identifier (DOI)

  • 10.1016/j.tibs.2010.03.001

Language

  • eng

Conference Location

  • England