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在细胞凋亡过程中,心磷脂参与tBID诱导的BAX激活。

Involvement of cardiolipin in tBID-induced activation of BAX during apoptosis.

作者信息

Raemy Etienne, Martinou Jean-Claude

机构信息

Department of Cell Biology, University of Geneva, 30 Quai Ernest Ansermet, 1211 Geneva 4, Switzerland.

Department of Cell Biology, University of Geneva, 30 Quai Ernest Ansermet, 1211 Geneva 4, Switzerland.

出版信息

Chem Phys Lipids. 2014 Apr;179:70-4. doi: 10.1016/j.chemphyslip.2013.12.002. Epub 2013 Dec 12.

Abstract

Permeabilization of the outer mitochondrial membrane constitutes an essential step in response to a wide range of apoptotic stimuli. Pro-apoptotic members of the BCL-2 family such as BAX and BAK are responsible for disrupting the integrity of the mitochondrial outer membrane, thereby allowing the release of apoptogenic factors including cytochrome c, which activate caspases in the cytosol. How BAX and BAK are activated during apoptosis is still not fully understood. Cooperation between tBID and the mitochondrial-specific phospholipid cardiolipin has been suggested to promote BAX or BAK oligomerization. Here we review the evidence for and against a role for cardiolipin in BAX and BAK activation and in the subsequent onset of apoptosis.

摘要

线粒体外膜的通透化是对多种凋亡刺激作出反应的关键步骤。BCL-2家族的促凋亡成员,如BAX和BAK,负责破坏线粒体外膜的完整性,从而使包括细胞色素c在内的凋亡因子得以释放,细胞色素c可激活细胞质中的半胱天冬酶。目前仍未完全了解BAX和BAK在凋亡过程中是如何被激活的。有研究表明,tBID与线粒体特异性磷脂心磷脂之间的协同作用可促进BAX或BAK的寡聚化。在此,我们综述了支持和反对心磷脂在BAX和BAK激活以及随后凋亡发生中起作用的证据。

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