帕金蛋白与PTEN诱导激酶1：远不止于线粒体自噬
Parkin and PINK1: much more than mitophagy.
作者信息
Scarffe Leslie A, Stevens Daniel A, Dawson Valina L, Dawson Ted M
机构信息
Neuroregeneration and Stem Cell Programs, Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA; Solomon H. Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA; Adrienne Helis Malvin Medical Research Foundation, New Orleans, LA 70130-2685, USA.
Neuroregeneration and Stem Cell Programs, Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA; Solomon H. Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.
出版信息
Trends Neurosci. 2014 Jun;37(6):315-24. doi: 10.1016/j.tins.2014.03.004. Epub 2014 Apr 13.
Parkinson's disease (PD) is a progressive neurodegenerative disease that causes a debilitating movement disorder. Although most cases of PD appear to be sporadic, rare Mendelian forms have provided tremendous insight into disease pathogenesis. Accumulating evidence suggests that impaired mitochondria underpin PD pathology. In support of this theory, data from multiple PD models have linked Phosphatase and tensin homolog (PTEN)-induced putative kinase 1 (PINK1) and parkin, two recessive PD genes, in a common pathway impacting mitochondrial health, prompting a flurry of research to identify their mitochondrial targets. Recent work has focused on the role of PINK1 and parkin in mediating mitochondrial autophagy (mitophagy); however, emerging evidence casts parkin and PINK1 as key players in multiple domains of mitochondrial health and quality control.
帕金森病（PD）是一种进行性神经退行性疾病，会导致使人衰弱的运动障碍。尽管大多数帕金森病病例似乎是散发性的，但罕见的孟德尔形式为疾病发病机制提供了深刻见解。越来越多的证据表明，线粒体功能受损是帕金森病病理的基础。支持这一理论的是，来自多个帕金森病模型的数据将磷酸酶和张力蛋白同源物（PTEN）诱导的假定激酶1（PINK1）和帕金蛋白这两个隐性帕金森病基因，联系到一条影响线粒体健康的共同途径中，引发了一系列研究以确定它们的线粒体靶点。最近的研究工作集中在PINK1和帕金蛋白在介导线粒体自噬（mitophagy）中的作用；然而，新出现的证据表明，帕金蛋白和PINK1是线粒体健康和质量控制多个领域的关键参与者。
Zotero 插件