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BimS-induced apoptosis requires mitochondrial localization but not interaction with anti-apoptotic Bcl-2 proteins
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TOM22, a core component of the mitochondria outer membrane protein translocation pore, is a mitochondrial receptor for the proapoptotic protein Bax
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Role of Bax and Bak in mitochondrial morphogenesis
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Cell death provoked by loss of interleukin-3 signaling is independent of Bad, Bim, and PI3 kinase, but depends in part on Puma
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Mitochondrial factors with dual roles in death and survival
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Mitochondria primed by death signals determine cellular addiction to antiapoptotic BCL-2 family members
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Proapoptotic Bak is sequestered by Mcl-1 and Bcl-xL, but not Bcl-2, until displaced by BH3-only proteins
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BH3 domains of BH3-only proteins differentially regulate bax-mediated mitochondrial membrane permeabilization both directly and indirectly
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JNK promotes Bax translocation to mitochondria through phosphorylation of 14-3-3 proteins
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Bcl-xL sequesters its C-terminal membrane anchor in soluble, cytosolic homodimers
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VDAC2 inhibits BAK activation and mitochondrial apoptosis
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Elimination of Mcl-1 is required for the initiation of apoptosis following ultraviolet irradiation
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Humanin peptide suppresses apoptosis by interfering with Bax activation
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