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首页> 外文期刊>Cancer Cell >Mitochondria primed by death signals determine cellular addiction to antiapoptotic BCL-2 family members.
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Mitochondria primed by death signals determine cellular addiction to antiapoptotic BCL-2 family members.

机译：由死亡信号引发的线粒体决定了细胞对抗凋亡BCL-2家族成员的依赖。

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摘要

We show that the antiapoptotic proteins BCL-2, BCL-XL, MCL-1, BFL-1, and BCL-w each bear a unique pattern of interaction with a panel of peptides derived from BH3 domains of BH3-only proteins. Cellular dependence on an antiapoptotic protein for survival can be decoded based on the pattern of mitochondrial sensitivity to this peptide panel, a strategy that we call BH3 profiling. Dependence on antiapoptotic proteins correlates with sequestration of activator BH3-only proteins like BID or BIM by antiapoptotic proteins. Sensitivity to the cell-permeable BCL-2 antagonist ABT-737 is also related to priming of BCL-2 by activator BH3-only molecules. Our data allow us to distinguish a cellular state we call "primed for death," which can be determined by BH3 profiling and which correlates with dependence on antiapoptotic family members for survival.
机译：我们表明，抗凋亡蛋白BCL-2，BCL-XL，MCL-1，BFL-1和BCL-w各自具有与衍生自仅BH3蛋白的BH3域的一组肽相互作用的独特模式。细胞对抗凋亡蛋白生存的依赖性可以基于线粒体对该肽组的敏感性模式进行解码，我们将这种策略称为BH3分析。对抗凋亡蛋白的依赖与通过抗凋亡蛋白螯合仅激活剂BH3的蛋白（如BID或BIM）相关。对细胞可渗透的BCL-2拮抗剂ABT-737的敏感性还与仅活化剂BH3的分子引发BCL-2有关。我们的数据使我们能够区分称为“死亡致死”的细胞状态，该状态可以通过BH3分析来确定，并且与抗凋亡家族成员的存活相关。

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