Pivotal role of AKAP121 in mitochondrial physiology
Pivotal role of AKAP121 in mitochondrial physiology
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DOI：
10.1152/ajpcell.00292.2015
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发表时间：
2016-04-15
影响因子：
5.5
通讯作者：
Kolliputi, Narasaiah
中科院分区：
文献类型：
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作者：
Czachor, Alexander;Failla, Athena;Kolliputi, Narasaiah
在这一观点中，我们讨论了线粒体支架蛋白AKAP121（也称为AKAP1，或AKAP149作为人类同源物）研究的一些最新进展，重点是其在线粒体生理学中的作用。AKAP121已被确定为几个线粒体事件的关键调控分子，包括氧化磷酸化、膜电位的控制、裂变诱导的凋亡、线粒体Ca2+稳态的维持以及各种线粒体呼吸链底物分子的磷酸化。此外，我们讨论了缺氧在促进细胞应激和损伤中的作用，这已被证明可以介导AKAP121的蛋白体降解，导致活性氧产生增加，线粒体功能障碍，最终导致细胞死亡。
In this Perspective, we discuss some recent developments in the study of the mitochondrial scaffolding protein AKAP121 (also known as AKAP1, or AKAP149 as the human homolog), with an emphasis on its role in mitochondrial physiology. AKAP121 has been identified to function as a key regulatory molecule in several mitochondrial events including oxidative phosphorylation, the control of membrane potential, fission-induced apoptosis, maintenance of mitochondrial Ca2+ homeostasis, and the phosphorylation of various mitochondrial respiratory chain substrate molecules. Furthermore, we discuss the role of hypoxia in prompting cellular stress and damage, which has been demonstrated to mediate the proteosomal degradation of AKAP121, leading to an increase in reactive oxgyen species production, mitochondrial dysfunction, and ultimately cell death.