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Journal ArticleDOI

Mitochondria and apoptosis

Douglas R. Green, +1 more
- 28 Aug 1998 - 
- Vol. 281, Iss: 5381, pp 1309-1312
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TLDR
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.
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.

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Citations
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Journal ArticleDOI

The hallmarks of cancer.

TL;DR: This work has been supported by the Department of the Army and the National Institutes of Health, and the author acknowledges the support and encouragement of the National Cancer Institute.
Journal ArticleDOI

The biochemistry of apoptosis

TL;DR: The basic components of the death machinery are reviewed, how they interact to regulate apoptosis in a coordinated manner is described, and the main pathways that are used to activate cell death are discussed.
Journal ArticleDOI

Caspases: Enemies Within

TL;DR: This work has shown that understanding caspase regulation is intimately linked to the ability to rationally manipulate apoptosis for therapeutic gain.
Journal ArticleDOI

The Bcl-2 Protein Family: Arbiters of Cell Survival

TL;DR: Bcl-2 and related cytoplasmic proteins are key regulators of apoptosis, the cell suicide program critical for development, tissue homeostasis, and protection against pathogens.
Journal ArticleDOI

Cellular survival: a play in three Akts

TL;DR: The mechanisms by which survival factors regulate the PI3K/c-Akt cascade, the evidence that activation of the PI 3K/ c-AKT pathway promotes cell survival, and the current spectrum of c- akt targets and their roles in mediating c- Akt-dependent cell survival are reviewed.
References
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Book ChapterDOI

Cell death : the significance of apoptosis

TL;DR: It has proved feasible to categorize most if not all dying cells into one or the other of two discrete and distinctive patterns of morphological change, which have, generally, been found to occur under disparate but individually characteristic circumstances.
Journal ArticleDOI

Cytochrome c and dATP-Dependent Formation of Apaf-1/Caspase-9 Complex Initiates an Apoptotic Protease Cascade

TL;DR: Mutation of the active site of caspase-9 attenuated the activation of cazase-3 and cellular apoptotic response in vivo, indicating that casp enzyme-9 is the most upstream member of the apoptotic protease cascade that is triggered by cytochrome c and dATP.
Journal ArticleDOI

Prevention of Apoptosis by Bcl-2: Release of Cytochrome c from Mitochondria Blocked

TL;DR: One possible role of Bcl-2 in prevention of apoptosis is to block cytochrome c release from mitochondria, which is normally located in the mitochondrial intermembrane space.
Journal ArticleDOI

Decreased apoptosis in the brain and premature lethality in CPP32-deficient mice

TL;DR: CPP32 is shown to play a critical role during morphogenetic cell death in the mammalian brain during embryonic day 12, resulting in a variety of hyperplasias and disorganized cell deployment.
Journal ArticleDOI

Bcl-2 inhibition of neural death : decreased generation of reactive oxygen species

TL;DR: The proto-oncogene bcl-2 inhibits apoptotic and necrotic neural cell death by decreasing the net cellular generation of reactive oxygen species and lipid peroxides as discussed by the authors.
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