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线粒体膜水平的细胞凋亡调控。

Apoptosis regulation at the mitochondria membrane level.

机构信息

Institute for Genetics, CECAD Research Center, University of Cologne, Germany.

Institute for Genetics, CECAD Research Center, University of Cologne, Germany.

出版信息

Biochim Biophys Acta Biomembr. 2021 Dec 1;1863(12):183716. doi: 10.1016/j.bbamem.2021.183716. Epub 2021 Jul 31.

Abstract

Mitochondrial outer membrane permeabilization (MOMP) is a key checkpoint in apoptosis that activates the caspase cascade and irreversibly causes the majority of cells to die. The proteins of the Bcl-2 family are master regulators of apoptosis that form a complex interaction network within the mitochondrial membrane that determines the induction of MOMP. This culminates in the activation of the effector members Bax and Bak, which permeabilize the mitochondrial outer membrane to mediate MOMP. Although the key role of Bax and Bak has been established, many questions remain unresolved regarding molecular mechanisms that control the apoptotic pore. In this review, we discuss the recent progress in our understanding of the regulation of Bax/Bak activity within the mitochondrial membrane.

摘要

线粒体膜通透性改变(MOMP)是细胞凋亡的一个关键检查点,它激活了半胱氨酸天冬氨酸蛋白酶(caspase)级联反应,导致大多数细胞不可逆地死亡。Bcl-2 家族蛋白是细胞凋亡的主要调节因子,它们在线粒体膜内形成了一个复杂的相互作用网络,决定了 MOMP 的诱导。这最终导致效应因子 Bax 和 Bak 的激活,它们使线粒体膜通透性改变,从而介导 MOMP。尽管 Bax 和 Bak 的关键作用已经确立,但关于控制凋亡孔的分子机制仍有许多问题尚未解决。在这篇综述中,我们讨论了在理解 Bax/Bak 在线粒体膜内活性调节方面的最新进展。

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