Journal Article10.1038/NCB1206-1317
Upgrading the BCL-2 network.
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TL;DR: New data delineate a multistep hierarchy of BCL-2-family protein interactions that are driven by signal-dependent pathways.
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Abstract: The BCL-2 oncogene promotes cancer progression by prohibiting cell death. BCL-2-related regulators were once thought to constitute a simple, two-class system of anti-death and pro-death factors. New data delineate a multistep hierarchy of BCL-2-family protein interactions that are driven by signal-dependent pathways.
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References
Bcl-2 gene promotes haemopoietic cell survival and cooperates with c-myc to immortalize pre-B cells.
TL;DR: Results argue that bcl-2 provided a distinct survival signal to the cell and may contribute to neoplasia by allowing a clone to persist until other oncogenes, such as c-myc, become activated.
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Differential targeting of prosurvival Bcl-2 proteins by their BH3-only ligands allows complementary apoptotic function
Lin Chen,Simon N. Willis,Andrew H. Wei,Brian J. Smith,Jamie I. Fletcher,Mark G. Hinds,Peter M. Colman,Catherine L. Day,Jerry M. Adams,David C.S. Huang +9 more
TL;DR: The results suggest that apoptosis relies on selective interactions between particular subsets of these proteins and that it should be feasible to discover BH3-mimetic drugs that inactivate specific prosurvival targets.
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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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Structure of Bcl-xL-Bak peptide complex: recognition between regulators of apoptosis.
Michael Sattler,Heng Liang,David G. Nettesheim,Robert P. Meadows,John E. Harlan,Matthias Eberstadt,Ho Sup Yoon,Suzanne B. Shuker,Brian S. Chang,Andy J. Minn,Craig B. Thompson,Stephen W. Fesik +11 more
TL;DR: The structure and binding affinities of mutant Bak peptides indicate that the Bak peptide adopts an amphipathic α helix that interacts with Bcl-xL through hydrophobic and electrostatic interactions.
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Mitochondria primed by death signals determine cellular addiction to antiapoptotic BCL-2 family members.
Michael Certo,Victoria Del Gaizo Moore,Mari Nishino,Guo Wei,Stanley J. Korsmeyer,Scott A. Armstrong,Anthony Letai +6 more
TL;DR: The data allow us to distinguish a cellular state the authors call "primed for death," which can be determined by BH3 profiling and which correlates with dependence on antiapoptotic family members for survival.
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