Journal ArticleDOI
Mitochondrial control of apoptosis
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TLDR
It is demonstrated that mitochondrial membrane permeabilization (MMP) constitutes a decisive step of the apoptotic process, and several apoptogenic proteins normally confined to mitochondria are released in the extra-mitochondrial space and participate in the suicidal dismantling of the cell.About:
This article is published in Immunology Today.The article was published on 1997-01-01. It has received 1466 citations till now. The article focuses on the topics: Effector.read more
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Mitochondrial Membrane Permeabilization in Cell Death
TL;DR: Once MMP has been induced, it causes the release of catabolic hydrolases and activators of such enzymes (including those of caspases) from mitochondria, meaning that mitochondria coordinate the late stage of cellular demise.
Journal ArticleDOI
Two CD95 (APO-1/Fas) signaling pathways
Carsten Scaffidi,Simone Fulda,Anu Srinivasan,Claudia Friesen,Feng Li,Kevin J. Tomaselli,Klaus-Michael Debatin,Peter H. Krammer,Marcus E. Peter +8 more
TL;DR: In the presence of caspase‐3 the amount of active casp enzyme‐8 generated at the DISC determines whether a mitochondria‐independent apoptosis pathway is used (type I cells) or not (type II cells).
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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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A model for p53-induced apoptosis
Kornelia Polyak,Kornelia Polyak,Yong Xia,Jay L. Zweier,Kenneth W. Kinzler,Bert Vogelstein,Bert Vogelstein +6 more
TL;DR: Examination of transcripts induced by p53 expression before the onset of apoptosis stimulated additional biochemical and pharmacological experiments suggesting that p53 results in apoptosis through a three-step process: the transcriptional induction of redox-related genes; the formation of reactive oxygen species; and the oxidative degradation of mitochondrial components, culminating in cell death.
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Mammalian thioredoxin is a direct inhibitor of apoptosis signal-regulating kinase (ASK) 1.
Masao Saitoh,Hideki Nishitoh,Makiko Fujii,Kohsuke Takeda,Kei Tobiume,Yasuhiro Sawada,Masahiro Kawabata,Kohei Miyazono,Hidenori Ichijo +8 more
TL;DR: Evidence that Trx is a negative regulator of ASK1 suggests possible mechanisms for redox regulation of the apoptosis signal transduction pathway as well as the effects of antioxidants against cytokine‐ and stress‐induced apoptosis.
References
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Journal ArticleDOI
Induction of apoptotic program in cell-free extracts : requirement for datp and cytochrome c
TL;DR: Cells undergoing apoptosis in vivo showed increased release of cy tochrome c to their cytosol, suggesting that mitochondria may function in apoptosis by releasing cytochrome c.
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Bcl-2 functions in an antioxidant pathway to prevent apoptosis
TL;DR: A model in which Bcl-2 regulates an antioxidant pathway at sites of free radical generation is proposed in which it protected cells from H2O2- and menadione-induced oxidative deaths and suppressed lipid peroxidation completely.
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Bcl-2 and the regulation of programmed cell death
TL;DR: The bcl-2 gene has emerged as a critical regulator of PCD in a variety of physiological and pathological contexts and can contribute to the pathogenesis of many diseases ranging from cancer to AIDS.
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Hypoxia-mediated selection of cells with diminished apoptotic potential in solid tumours
Thomas G. Graeber,Cynthia Osmanian,Tyler Jacks,David E. Housman,Cameron J. Koch,Scott W. Lowe,Scott W. Lowe,Amato J. Giaccia +7 more
TL;DR: It is proposed that hypoxia provides a physiological selective pressure in tumours for the expansion of variants that have lost their apoptotic potential, and in particular for cells acquiring p53mutations.