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Parkin 介导的选择性线粒体自噬,即 mitophagy:Parkin 从重要的线粒体网络中清除受损的细胞器。

Parkin-mediated selective mitochondrial autophagy, mitophagy: Parkin purges damaged organelles from the vital mitochondrial network.

机构信息

Biochemistry Section, Surgical Neurology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892-3704, USA.

出版信息

FEBS Lett. 2010 Apr 2;584(7):1386-92. doi: 10.1016/j.febslet.2010.02.060. Epub 2010 Feb 25.

Abstract

Cellular homeostasis is linked tightly to mitochondrial functions. Some damage to mitochondrial proteins and nucleic acids can lead to the depolarization of the inner mitochondrial membrane, thereby sensitizing impaired mitochondria for selective elimination by autophagy. Mitochondrial dysfunction is one of the key aspects of the pathobiology of neurodegenerative disease. Parkin, an E3 ligase located in the cytosol and originally discovered as mutated in monogenic forms of Parkinson's disease (PD), was found recently to translocate specifically to uncoupled mitochondria and to induce their autophagy.

摘要

细胞内环境稳态与线粒体功能密切相关。线粒体蛋白和核酸的某些损伤可导致线粒体内膜去极化,从而使受损的线粒体对自噬的选择性消除变得敏感。线粒体功能障碍是神经退行性疾病病理生物学的关键方面之一。Parkin 是一种位于细胞质中的 E3 连接酶,最初在帕金森病(PD)的单基因形式中发现其发生突变,最近发现它可特异性转位到解偶联的线粒体并诱导其自噬。

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PINK1-dependent recruitment of Parkin to mitochondria in mitophagy.PINK1 依赖性募集 Parkin 到线粒体进行线粒体自噬。
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