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• W2081690888 startingPage "577" @default.
• W2081690888 abstract "Through direct interaction with the voltage-dependent anion channel (VDAC), proapoptotic Bcl-2 family members such as Bax and Bak induce apoptogenic mitochondrial cytochrome c release and membrane potential (Deltapsi) loss in isolated mitochondria. Using isolated mitochondria, we showed that Bid and Bik, BH3-only proteins from the Bcl-2 family, induced cytochrome c release but not Deltapsi loss. Unlike Bax/Bak, the cytochrome c release induced by Bid/Bik was Ca(2+)-independent, cyclosporin A-insensitive, and respiration-independent. Furthermore, in contrast to Bax/Bak, Bid/Bik neither interacted with VDAC nor directly affected the VDAC activity in liposomes. Consistently, Bid/Bik induced apoptosis without Deltapsi loss, whereas Bax induced apoptosis with Deltapsi loss. These findings indicated the involvement of a different mechanism in BH3-only, protein-induced apoptogenic cytochrome c release." @default.
• W2081690888 created "2016-06-24" @default.
• W2081690888 creator A5006956477 @default.
• W2081690888 creator A5038136910 @default.
• W2081690888 date "2000-01-18" @default.
• W2081690888 modified "2023-10-14" @default.
• W2081690888 title "Proapoptotic BH3-only Bcl-2 family members induce cytochrome<i>c</i>release, but not mitochondrial membrane potential loss, and do not directly modulate voltage-dependent anion channel activity" @default.
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• W2081690888 doi "https://doi.org/10.1073/pnas.97.2.577" @default.
• W2081690888 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/15372" @default.
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