Czachor Alexander, Failla Athena, Lockey Richard, Kolliputi Narasaiah
Division of Allergy and Immunology, Department of Internal Medicine, Morsani College of Medicine, University of South Florida, Tampa, Florida.
Division of Allergy and Immunology, Department of Internal Medicine, Morsani College of Medicine, University of South Florida, Tampa, Florida
Am J Physiol Cell Physiol. 2016 Apr 15;310(8):C625-8. doi: 10.1152/ajpcell.00292.2015. Epub 2016 Jan 28.
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 Ca(2+)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.
在本综述中，我们讨论了线粒体支架蛋白AKAP121（也称为AKAP1，人类同源物为AKAP149）研究中的一些最新进展，重点是其在线粒体生理学中的作用。AKAP121已被确定为多种线粒体事件中的关键调节分子，包括氧化磷酸化、膜电位控制、裂变诱导的细胞凋亡、线粒体Ca(2+)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，我们讨论了缺氧在引发细胞应激和损伤中的作用，已证明缺氧介导AKAP121的蛋白酶体降解，导致活性氧产生增加、线粒体功能障碍，最终导致细胞死亡。
