The molecular regulation of programmed necrotic cell injury

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...

Full description

Saved in:
Bibliographic Details
Published in:Trends in biochemical sciences (Amsterdam. Regular ed.) 2010-08, Vol.35 (8), p.434-441
Main Authors: Moquin, David, Chan, Francis Ka-Ming
Format: Article
Language:English
Subjects:
Animals
Apoptosis - physiology
Caspases - metabolism
Humans
Metazoa
Necrosis
Phosphorylation
Receptor-Interacting Protein Serine-Threonine Kinases - metabolism
Ubiquitination
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary: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.
ISSN:0968-0004
1362-4326
DOI:10.1016/j.tibs.2010.03.001