Green Douglas R
Department of Immunology, St. Jude Children's Research Hospital, Memphis, Tennessee 38105, USA.
Cancer Cell. 2006 May;9(5):328-30. doi: 10.1016/j.ccr.2006.05.004.
Apoptosis that proceeds via the mitochondrial pathway involves mitochondrial outer membrane permeabilization (MOMP), responsible for the release of cytochrome c and other proteins of the mitochondrial intermembrane space. This essential step is controlled and mediated by proteins of the Bcl-2 family. The proapoptotic proteins Bax and Bak are required for MOMP, while the antiapoptotic Bcl-2 proteins, including Bcl-2, Bcl-xL, Mcl-1, and others, prevent MOMP. Different proapoptotic BH3-only proteins act to interfere with the function of the antiapoptotic Bcl-2 members and/or activate Bax and Bak. Here, we discuss an emerging view, proposed by Certo et al. in this issue of Cancer Cell, on how these interactions result in MOMP and apoptosis.
通过线粒体途径进行的细胞凋亡涉及线粒体外膜通透性改变（MOMP），这一过程负责细胞色素c和线粒体膜间隙其他蛋白质的释放。这一关键步骤由Bcl-2家族蛋白控制和介导。促凋亡蛋白Bax和Bak是MOMP所必需的，而抗凋亡Bcl-2蛋白，包括Bcl-2、Bcl-xL、Mcl-1等，则可防止MOMP的发生。不同的仅含BH3结构域的促凋亡蛋白可干扰抗凋亡Bcl-2成员的功能和/或激活Bax和Bak。在此，我们将讨论Certo等人在本期《癌细胞》中提出的一种新观点，即这些相互作用如何导致MOMP和细胞凋亡。
