Mitochondria and Apoptosis
- 28 August 1998
- journal article
- review article
- Published by American Association for the Advancement of Science (AAAS) in Science
- Vol. 281 (5381), 1309-1312
- https://doi.org/10.1126/science.281.5381.1309
Abstract
REVIEW 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.Keywords
This publication has 44 references indexed in Scilit:
- Apoptosis Induction by Caspase-8 Is Amplified through the Mitochondrial Release of Cytochrome cOnline Journal of Public Health Informatics, 1998
- Commitment to cell death measured by loss of clonogenicity is separable from the appearance of apoptotic markersCell Death & Differentiation, 1998
- The apoptosis-necrosis paradox. Apoptogenic proteases activated after mitochondrial permeability transition determine the mode of cell deathOncogene, 1997
- Origin of eukaryotic programmed cell death: A consequence of aerobic metabolism?BioEssays, 1997
- Inhibition of Bax Channel-Forming Activity by Bcl-2Science, 1997
- Bcl-xL forms an ion channel in synthetic lipid membranesNature, 1997
- Inhibitors of permeability transition interfere with the disruption of the mitochondrial transmembrane potential during apoptosisFEBS Letters, 1996
- Mitochondrial control of nuclear apoptosis.The Journal of Experimental Medicine, 1996
- Bcl‐2 Protects Neural Cells from Cyanide/Aglycemia‐Induced Lipid Oxidation, Mitochondrial Injury, and Loss of ViabilityJournal of Neurochemistry, 1995
- Toward the molecular structure of the mitochondrial channel, VDACJournal of Bioenergetics and Biomembranes, 1992