RIP3, an Energy Metabolism Regulator That Switches TNF-Induced Cell Death from Apoptosis to Necrosis

• Published in: Science (American Association for the Advancement of Science) Vol. 325; no. 5938; pp. 332 - 336
• Main Authors: Zhang, Duan-Wu, Shao, Jing, Lin, Juan, Zhang, Na, Lu, Bao-Ju, Lin, Sheng-Cai, Dong, Meng-Qiu, Han, Jiahuai
• Format: Journal Article
• Language: English
• Published: Washington, DC American Association for the Advancement of Science 17.07.2009; The American Association for the Advancement of Science
• Subjects: 3T3 cells; Ageing, cell death; agonists; Amino Acid Chloromethyl Ketones - pharmacology; Animals; Apoptosis; biochemical pathways; Biological and medical sciences; caspases; Cell death; Cell Line; Cell lines; Cell physiology; Cells; death; death domain receptors; Energy Metabolism; Enzymes; Fundamental and applied biological sciences. Psychology; Gangrene; Gin; Glutamate Dehydrogenase - metabolism; Glutamate-Ammonia Ligase - metabolism; Glycogen Phosphorylase - metabolism; Kinases; Metabolism; Mice; Molecular and cellular biology; Molecular biology; Mortality; Necrosis; NIH 3T3 Cells; protein kinases; reactive oxygen species; Reactive Oxygen Species - metabolism; Receptor-Interacting Protein Serine-Threonine Kinases - genetics; Receptor-Interacting Protein Serine-Threonine Kinases - metabolism; RNA Interference; Tumor Necrosis Factor-alpha - pharmacology; tumor necrosis factors; Viability; Energy metabolism; Regulator; Tumor necrosis factor; Cell death; Apoptosis; Necrosis

Necrosis can be induced by stimulating death receptors with tumor necrosis factor (TNF) or other agonists; however, the underlying mechanism differentiating necrosis from apoptosis is largely unknown. We identified the protein kinase receptor-interacting protein 3 (RIP3) as a molecular switch betwee...