RIP kinases initiate programmed necrosis.
Some lethal stimuli can induce either apoptosis or necrosis, depending on the cell type and/or experimental setting. Until recently, the molecular bases of this phenomenon were largely unknown. Now, two members of the receptor-interacting serine-threonine kinase (RIP) family, RIP1 and RIP3, have been demonstrated to control the switch between apoptotic and necrotic cell death. Some mechanistic details, however, remain controversial.
Galluzzi
Lorenzo
L
INSERM, Villejuif, France.
Kepp
Oliver
O
Kroemer
Guido
G
D000818:Animals; D017209:Apoptosis; D053078:Membrane Potential, Mitochondrial; D051379:Mice; D008928:Mitochondria / Q000201:enzymology / Q000473:pathology; D009336:Necrosis / Q000201:enzymology*; D017382:Reactive Oxygen Species / Q000378:metabolism; D053422:Receptor-Interacting Protein Serine-Threonine Kinases / Q000378:metabolism*
D017382:Reactive Oxygen Species; D053422:Receptor-Interacting Protein Serine-Threonine Kinases