Proapoptotic BH3-only Bcl-2 family members induce cytochromecrelease, but not mitochondrial membrane potential loss, and do not directly modulate voltage-dependent anion channel activity | Zendy

Shigeomi Shimizu | Zendy; Yoshihide Tsujimoto | Zendy

Open Access

Proapoptotic BH3-only Bcl-2 family members induce cytochromecrelease, but not mitochondrial membrane potential loss, and do not directly modulate voltage-dependent anion channel activity

Author(s) -

Shigeomi Shimizu,

Yoshihide Tsujimoto

Publication year - 2000

Publication title -

proceedings of the national academy of sciences

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 5.011

H-Index - 771

eISSN - 1091-6490

pISSN - 0027-8424

DOI - 10.1073/pnas.97.2.577

Subject(s) - voltage dependent anion channel , cytochrome c , mitochondrial apoptosis induced channel , bcl 2 family , mitochondrion , membrane potential , apoptosis , microbiology and biotechnology , chemistry , cytochrome , bcl 2 associated x protein , inner mitochondrial membrane , biology , bacterial outer membrane , biochemistry , programmed cell death , caspase 3 , enzyme , escherichia coli , gene

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.

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