Journal ArticleDOI
Mitochondria and apoptosis
Douglas R. Green,John C. Reed +1 more
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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.read more
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
Jerry M. Adams,Suzanne Cory +1 more
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
Peng Li,Deepak Nijhawan,Imawati Budihardjo,Srinivasa M. Srinivasula,Manzoor Ahmad,Emad S. Alnemri,Xiaodong Wang +6 more
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
Jie Yang,Xuesong Liu,Xuesong Liu,Kapil N. Bhalla,Caryn Naekyung Kim,Ana Maria Ibrado,Jiyang Cai,Tsung I. Peng,Dean P. Jones,Xiaodong Wang,Xiaodong Wang +10 more
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
Keisuke Kuida,Timothy S. Zheng,Songqing Na,Chia-Yi Kuan,Di Yang,Hajime Karasuyama,Pasko Rakic,Richard A. Flavell +7 more
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
Darci J. Kane,Theodore A. Sarafian,Rein Anton,Hejin Hahn,Edith Butler Gralla,Joan Selverstone Valentine,Tonis Ord,Dale E. Bredesen +7 more
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.