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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Proapoptotic BH3-only Bcl-2 family members induce cytochrome c release, but not mitochondrial membrane potential loss, and do not directly modulate voltage-dependent anion channel activity
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Proapoptotic BH3-only Bcl-2 family members induce cytochrome c release, but not mitochondrial membrane potential loss, and do not directly modulate voltage-dependent anion channel activity

机译：仅凋亡的BH3 Bcl-2家族成员诱导细胞色素c释放，但不诱导线粒体膜电位损失，并且不直接调节电压依赖性阴离子通道活性

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摘要

Through direct interaction with the voltage-dependent anion channel (VDAC), proapoptotic BcI-2 family members such as Bax and Bak induce apoptogenic mitochondrial cytochrome c release and membrane potential loss in isolated mitochondria. Using isolated mitochondria, we showed that Bid and Bik, BH3-only proteins from the BcI-2 family, induced cytochrome c release but not A+ loss. Unlike Bax/Bak, the cytochrome c release induced by Bid/Bik was Ca~2+-independent, cyclosporin A-insensitive, and res- piration-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 with- out Ath loss, whereas Bax induced apoptosis with △ψ loss. These findings indicated the involvement of a different mechanism in BH3-only, protein-induced apoptogenic cytochrome m release.
机译：通过与电压依赖性阴离子通道（VDAC）的直接相互作用，促凋亡的BcI-2家族成员（例如Bax和Bak）诱导凋亡的线粒体细胞色素c释放和分离的线粒体中的膜电位损失。使用分离的线粒体，我们显示来自Bcl-2家族的Bid和Bik（仅BH3的蛋白）诱导细胞色素c释放，但不诱导A +丢失。与Bax / Bak不同，Bid / Bik诱导的细胞色素C释放不依赖Ca〜2 +，对环孢菌素A不敏感且不依赖于复制。此外。与Bax / Bak相反。 Bid / Bik既不与VDAC相互作用，也不直接影响脂质体中VDAC的活性。一致。 Bid / Bik诱导凋亡而无Ath损失，而Bax诱导凋亡而使△ψ损失。这些发现表明，仅BH3蛋白诱导的凋亡性细胞色素m释放涉及不同的机制。

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