reviewTop 1% cited
Mitochondria and Apoptosis
Science · 1998 · Vol. 281(5381) · pp. 1309–1312
Douglas R. Green✉(La Jolla Institute for Immunology)John C. Reed(La Jolla Institute for Immunology)
Abstract
A variety of key events in apoptosis focus on mitochondria, including the release of caspase activators (such as cytochrome c), changes in electron transport, loss of mitochondrial transmembrane potential, altered cellular oxidation-reduction, and participation of pro- and antiapoptotic Bcl-2 family proteins. The different signals that converge on mitochondria to trigger or inhibit these events and their downstream effects delineate several major pathways in physiological cell death.
Cell death mechanisms and regulationMitochondrial Function and PathologyNeuroscience and Neuropharmacology ResearchMitochondrionApoptosisCell biologyCytochrome cBcl-2 familyElectron transport chainProgrammed cell deathCaspaseBiologyChemistry
MeSH terms
AnimalsCysteine EndopeptidasesCytochrome c GroupElectron TransportHumansIntracellular MembranesIon ChannelsMembrane PotentialsMitochondriaOxidation-ReductionPermeabilityApoptosisProto-Oncogene Proteins c-bcl-2
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References
Mitochondrial cytochrome c release in apoptosis occurs upstream of DEVD-specific caspase activation and independently of mitochondrial transmembrane depolarization
The EMBO Journal · 1998 · 1,231 citations
Cytochrome c and dATP-Dependent Formation of Apaf-1/Caspase-9 Complex Initiates an Apoptotic Protease Cascade
Cell · 1997 · 7,227 citations
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