Mitochondria as the central control point of apoptosis.
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Summary
The current view of the mechanisms that lead to the efflux of many proteins from mitochondria during apoptosis and the role played by Bcl-2 family proteins in the control of this event are summarized.
- Type
- review
- Published
- 2000-09-01
- Cited by
- 1,990
- References
- 69
- OpenAlex
- https://openalex.org/W1974980101
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:44889030
Keywords
Biology, Bcl-2 family, Mitochondrion, Apoptosis, Cytochrome c
References
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- Bid-deficient mice are resistant to Fas-induced hepatocellular apoptosis
- Injected cytochrome c induces apoptosis
- How BAD phosphorylation is good for survival
- Bcl-2 family proteins regulate the release of apoptogenic cytochrome c by the mitochondrial channel VDAC
- Bcl-2 prolongs cell survival after Bax-induced release of cytochrome c
- X-ray and NMR structure of human Bcl-xL, an inhibitor of programmed cell death
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- The mitochondrial permeability transition pore and its role in cell death.
- Bcl-xL regulates the membrane potential and volume homeostasis of mitochondria.
- Prevention of Apoptosis by Bcl-2: Release of Cytochrome c from Mitochondria Blocked
- The proapoptotic activity of the Bcl-2 family member Bim is regulated by interaction with the dynein motor complex.
- Bax interacts with the permeability transition pore to induce permeability transition and cytochrome c release in isolated mitochondria.
- Mitochondrial Proliferation and Paradoxical Membrane Depolarization during Terminal Differentiation and Apoptosis in a Human Colon Carcinoma Cell Line
- Bax, but not Bcl-xL, decreases the lifetime of planar phospholipid bilayer membranes at subnanomolar concentrations.
- Cell-free apoptosis in Xenopus egg extracts: inhibition by Bcl-2 and requirement for an organelle fraction enriched in mitochondria.
- Bcl-2 family proteins as ion-channels
Cited by
- Study of intracellular signaling pathways triggered by natural antioxidants in human endothelial cells
- Characterization of the Role of Mitochondrial Function During Tumor Development and Muscle Wasting
- Apoptotic Cleavage of Cytoplasmic Dynein Intermediate Chain and P150GluedStops Dynein-Dependent Membrane Motility
- Electrical stimulation of cerebellar fastigial nucleus protects rat brain, in vitro, from staurosporine‐induced apoptosis
- Active, phosphorylation-dependent mitogen-activated protein kinase (MAPK/ERK), stress-activated protein kinase/c-Jun N-terminal kinase (SAPK/JNK), and p38 kinase expression in Parkinson's disease and Dementia with Lewy bodies
- Protective effects of rilmenidine and AGN 192403 on oxidative cytotoxicity and mitochondrial inhibitor-induced cytotoxicity in astrocytes.
- Glutathione disulfide induces apoptosis in U937 cells by a redox‐mediated p38 mitogen‐activated protein kinase pathway
- H9c2 cardiac myoblasts undergo apoptosis in a model of ischemia consisting of serum deprivation and hypoxia: inhibition by PMA
- Significance of endothelial cell survival programs for renal transplantation.
- Respiratory inhibition of isolated mammalian mitochondria by salivary antifungal peptide histatin-5.
- Induction of the mitochondrial permeability transition by selenium compounds mediated by oxidation of the protein thiol groups and generation of the superoxide.
- Astrocyte apoptosis: implications for neuroprotection.
- Bax Does Not Directly Participate in the Ca2+-induced Permeability Transition of Isolated Mitochondria*
- Dehydrocrotonin and its derivative, dimethylamide-crotonin induce apoptosis with lipid peroxidation and activation of caspases-2, -6 and -9 in human leukemic cells HL60.
- Genistein Induces Apoptosis in T Lymphoma Cells via Mitochondrial Damage
- The Effect of Mild and Severe Hypoxia on Rat Cortical Synaptosomes
- The cell cycle inhibitor p57Kip2 promotes cell death via the mitochondrial apoptotic pathway
- Trichinella spiralis: nurse cell formation with emphasis on analogy to muscle cell repair
- Formosanin C‐induced apoptosis requires activation of caspase‐2 and change of mitochondrial membrane potential
- Mollugin induces apoptosis in human Jurkat T cells through endoplasmic reticulum stress-mediated activation of JNK and caspase-12 and subsequent activation of mitochondria-dependent caspase cascade regulated by Bcl-xL.
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