BCL-2, BCL-XL Sequester BH3 Domain-Only Molecules Preventing BAX- and BAK-Mediated Mitochondrial Apoptosis
Emily H. Cheng,Michael C. Wei,Solly Weiler,Richard A. Flavell,Tak W. Mak,Tullia Lindsten,Stanley J. Korsmeyer +6 more
TL;DR: In mammals, BH3 domain-only molecules activate multidomain proapoptotic members to trigger a mitochondrial pathway, which both releases cytochrome c to activate caspases and initiates caspase-independent mitochondrial dysfunction.
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About: This article is published in Molecular Cell. The article was published on 01 Sep 2001. and is currently open access. The article focuses on the topics: Mitochondrial apoptosis-induced channel & Bcl-2-associated X protein.
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TL;DR: 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.
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Cytochrome c and dATP-Dependent Formation of Apaf-1/Caspase-9 Complex Initiates an Apoptotic Protease Cascade
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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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Apaf-1, a Human Protein Homologous to C. elegans CED-4, Participates in Cytochrome c–Dependent Activation of Caspase-3
TL;DR: The purification and cDNA cloning of Apaf-1, a novel 130 kd protein from HeLa cell cytosol that participates in the cytochrome c-dependent activation of caspase-3, leading to apoptosis is reported here.
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