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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Citations
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TL;DR: Investigation revealed that cells surviving glutamine withdrawal in particular, enhance expression and binding of BIM to BCL-2, consequently sensitizing these cells to the BH3 mimetic venetoclax, revealing a potent therapeutic strategy of metabolically driven synthetic lethality involving targeting glutamine metabolism for sensitization to venetClax in MM.
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Displacement of Bim by Bmf and Puma rather than increase in Bim level mediates paclitaxel-induced apoptosis in breast cancer cells.
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Bid, a Bcl2 Interacting Protein, Mediates Cytochrome c Release from Mitochondria in Response to Activation of Cell Surface Death Receptors
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Apaf-1, a Human Protein Homologous to C. elegans CED-4, Participates in Cytochrome c–Dependent Activation of Caspase-3
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