Mitochondrial protein phosphorylation as a regulatory modality: implications for mitochondrial dysfunction in heart failure.
Mitochondrial protein phosphorylation as a regulatory modality: implications for mitochondrial dysfunction in heart failure.
复制标题
DOI：
10.1111/j.1751-7133.2011.00266.x
复制
发表时间：
2011-11-01
期刊：
影响因子：
--
通讯作者：
Foster, D Brian
中科院分区：
文献类型：
--
作者：
O'Rourke, Brian;Van Eyk, Jennifer E;Foster, D Brian
线粒体蛋白的磷酸化已经被认识了几十年，并且丙酮酸和支链α -酮酸脱氢酶通过非典型激酶/磷酸酶级联的调节已经得到了很好的证实。最近，基于质谱的新技术的发展导致在各种线粒体靶点上发现了许多新的磷酸化位点。有证据表明，主要种类的激酶和几种磷酸酶可能存在于线粒体外膜、膜间空间、内膜和基质中，但关于这些磷酸化事件的位置、时间和可逆性以及它们是否在功能上相关，仍有许多问题有待解答。作者回顾了磷酸化作为一种线粒体调控策略，并强调了其在心脏肥大和衰竭的病理生理学中的可能作用。
Phosphorylation of mitochondrial proteins has been recognized for decades, and the regulation of pyruvate- and branched-chain alpha-ketoacid dehydrogenases by an atypical kinase/phosphatase cascade is well established. More recently, the development of new mass spectrometry-based technologies has led to the discovery of many novel phosphorylation sites on a variety of mitochondrial targets. The evidence suggests that the major classes of kinase and several phosphatases may be present at the mitochondrial outer membrane, intermembrane space, inner membrane, and matrix, but many questions remain to be answered as to the location, timing, and reversibility of these phosphorylation events and whether they are functionally relevant. The authors review phosphorylation as a mitochondrial regulatory strategy and highlight its possible role in the pathophysiology of cardiac hypertrophy and failure.