The BCL-2 family of proteins control a key checkpoint in apoptosis, that of mitochondrial outer membrane permeabilization or, simply, mitochondrial poration. The family consists of three subgroups: BH3-only initiators that respond to apoptotic stimuli; antiapoptotic guardians that protect against cell death; and the membrane permeabilizing effectors BAX, BAK, and BOK. On activation, effector proteins are converted from inert monomers into membrane permeabilizing oligomers. For many years, this process has been poorly understood at the molecular level, but a number of recent advances have provided important insights. We review the regulation of these effectors, their activation, subsequent conformational changes, and the ensuing oligomerization events that enable mitochondrial poration, which initiates apoptosis through release of key signaling factors such as cytochrome c We highlight the mysteries that remain in understanding these important proteins in an endeavor to provide a comprehensive picture of where the field currently sits and where it is moving toward.

中文翻译：

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BAX、BAK 和 BOK：BCL-2 家族效应蛋白的成熟。

BCL-2 蛋白家族控制细胞凋亡中的一个关键检查点，即线粒体外膜通透性或简单的线粒体穿孔。该家族由三个亚组组成：对凋亡刺激作出反应的仅 BH3 引发剂；防止细胞死亡的抗凋亡监护人；以及膜透化效应子 BAX、BAK 和 BOK。激活后，效应蛋白从惰性单体转化为膜透化寡聚体。多年来，在分子水平上对这一过程知之甚少，但最近的一些进展提供了重要的见解。我们回顾了这些效应器的调节、它们的激活、随后的构象变化，以及随后使线粒体穿孔的寡聚化事件，