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钙信号传导与线粒体运动

Calcium signalling and mitochondrial motility.

作者信息

Hajnóczky György, Saotome Masao, Csordás György, Weaver David, Yi Muqing

机构信息

Department of Pathology, Anatomy and Cell Biology, Thomas Jefferson University, Philadelphia, PA 19107, USA.

出版信息

Novartis Found Symp. 2007;287:105-17; discussion 117-21. doi: 10.1002/9780470725207.ch8.

Abstract

Intracellular Ca2+ is able to control numerous cellular responses through complex spatial and temporal organization. For the effective handling of intracellular Ca2+, endoplasmic reticulum (ER) Ca2+ mobilization and plasma membrane Ca2+ entry have to be complemented by strategic and dynamic positioning of an energy source that is usually provided by mitochondrial ATP production. Mitochondria also participate in the transport of Ca2+. Mitochondria are dynamically distributed in cells and utilize cytoskeletal tracks and motor proteins for their movements. Recent studies have reported that Ca2+ inhibits mitochondrial motility providing a mechanism to retain mitochondria at Ca2+ signalling sites. Here we discuss the control of the mitochondrial distribution by cell signalling mechanisms, the spatial relationship among individual mitochondria and ER domains, and the possible implications of mitochondrial movements in the Ca(2+)-dependent cell survival and cell death mechanisms.

摘要

细胞内钙离子能够通过复杂的时空组织来控制众多细胞反应。为了有效处理细胞内钙离子,内质网(ER)钙离子动员和质膜钙离子内流必须通过通常由线粒体ATP生成提供的能量源的策略性和动态定位来补充。线粒体也参与钙离子的运输。线粒体在细胞中动态分布,并利用细胞骨架轨道和运动蛋白进行移动。最近的研究报道,钙离子抑制线粒体运动,提供了一种将线粒体保留在钙离子信号位点的机制。在这里,我们讨论细胞信号机制对线粒体分布的控制、单个线粒体与内质网结构域之间的空间关系,以及线粒体运动在钙离子依赖性细胞存活和细胞死亡机制中的可能影响。

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