The Overexpression of Bax Produces Cell Death upon Induction of the Mitochondrial Permeability Transition
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It is concluded that Bax induces the mitochondrial permeability transition (MPT), a critical event in the loss of cell viability, and mediates other typical manifestations of apoptosis in this model, namely release of cytochrome c, caspase activation with PARP cleavage, and DNA fragmentation.About:
This article is published in Journal of Biological Chemistry.The article was published on 1998-03-27 and is currently open access. It has received 593 citations till now. The article focuses on the topics: Bcl-2-associated X protein & Mitochondrial permeability transition pore.read more
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Bid, a Bcl2 Interacting Protein, Mediates Cytochrome c Release from Mitochondria in Response to Activation of Cell Surface Death Receptors
TL;DR: The purification of a cytosolic protein that induces cytochrome c release from mitochondria in response to caspase-8, the apical caspases activated by cell surface death receptors such as Fas and TNF is reported.
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BCL-2 family members and the mitochondria in apoptosis
TL;DR: As the BCL-2 family members reside upstream of irreversible cellular damage and focus much of their efforts at the level of mitochondria, they play a pivotal role in deciding whether a cell will live or die, and it is argued that the amphipathic a-helical BH3 domain serves as a critical death domain in the pro-apoptotic members.
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Ischemic Cell Death in Brain Neurons
TL;DR: A major unifying thread of the review is a consideration of how the changes occurring during and after ischemia conspire to produce damaging levels of free radicals and peroxynitrite to activate calpain and other Ca(2+)-driven processes that are damaging, and to initiate the apoptotic process.
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Biochemical Pathways of Caspase Activation During Apoptosis
TL;DR: This review focuses on the two most well-studied pathways of caspase activation: the cell surface death receptor pathway and the mitochondria-initiated pathway.
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Loss of cyclophilin D reveals a critical role for mitochondrial permeability transition in cell death
Christopher P. Baines,Robert A. Kaiser,Nicole H. Purcell,N. Scott Blair,Hanna Osinska,Michael Hambleton,Eric W. Brunskill,M. Richard Sayen,Roberta A. Gottlieb,Gerald W. Dorn,Jeffrey Robbins,Jeffery D. Molkentin +11 more
TL;DR: Cyclophilin D and the mitochondrial permeability transition are required for mediating Ca2+- and oxidative damage-induced cell death, but not Bcl-2 family member-regulated death.
References
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Bcl-2 heterodimerizes in vivo with a conserved homolog, Bax, that accelerates programed cell death
TL;DR: Overexpressed Bax accelerates apoptotic death induced by cytokine deprivation in an IL-3-dependent cell line and counters the death repressor activity of B cl-2, suggesting a model in which the ratio of Bcl-2 to Bax determines survival or death following an apoptotic stimulus.
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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.
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Glucocorticoid-induced thymocyte apoptosis is associated with endogenous endonuclease activation
TL;DR: It is shown here that this morphological change is closely associated with excision of nucleosome chains from nuclear chromatin, apparently through activation of an intracellular, but non-lysosomal, endonuclease.
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Identification and inhibition of the ICE/CED-3 protease necessary for mammalian apoptosis
Donald W. Nicholson,Ambereen Ali,Nancy A. Thornberry,John P. Vaillancourt,C K Ding,Michel Gallant,Yves Gareau,Patrick R. Griffin,Marc Labelle,Yuri Lazebnik +9 more
TL;DR: A potent peptide aldehyde inhibitor has been developed and shown to prevent apoptotic events in vitro, suggesting that apopain/CPP32 is important for the initiation of apoptotic cell death.
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Calcineurin is a common target of cyclophilin-cyclosporin A and FKBP-FK506 complexes
Jun Liu,Jesse D. Farmer,Willam S. Lane,Jeffrey S. Friedman,Irving L. Weissman,Stuart L. Schreiber +5 more
TL;DR: The results suggest that calcineurin is involved in a common step associated with T cell receptor and IgE receptor signaling pathways and that cyclophilin and FKBP mediate the actions of CsA and Fk506 by forming drug-dependent complexes with and altering the activity of calcineURin-calmodulin.