Journal
TRENDS IN BIOCHEMICAL SCIENCES
Volume 39, Issue 12, Pages 587-593Publisher
ELSEVIER SCIENCE LONDON
DOI: 10.1016/j.tibs.2014.10.003
Keywords
programmed necrosis; pseudokinase; mixed lineage kinase domain-like protein (MLKL); necroptosis; necrosis inhibitors; necrosis biomarker
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Funding
- Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences
- One Hundred Talents Program of Chinese Academy of Sciences
- National Basic Science 973 grant from the Ministry of Science and Technology of China [2010CB835400]
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Classically, there are two major forms of cell death: necrosis, an unregulated digestion of cellular components; and apoptosis, a programmed mechanism that is promoted by caspases. However, another form of cell death has recently been identified that is inhibited by caspases, and yet occurs through a regulated mechanism, termed programmed necrosis or necroptosis. The biochemical basis of this program has begun to emerge, with the discovery of the receptor-interacting kinase RIP3 and its substrate, the pseudokinase mixed lineage kinase domain-like protein (MLKL), as core components. Furthermore, animal models have revealed significant functions for RIP3/MLKL-mediated necrotic cell death in immune responses against microbial infection and in the etiology of diseases involving tissue damage. This review discusses recent advances in our understanding of the mechanistic details and physiological functions of programmed necrosis.
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