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本文引用的文献

1
PINK1 is selectively stabilized on impaired mitochondria to activate Parkin.PINK1 在功能失调的线粒体上选择性地稳定,以激活 Parkin。
PLoS Biol. 2010 Jan 26;8(1):e1000298. doi: 10.1371/journal.pbio.1000298.
2
PINK1/Parkin-mediated mitophagy is dependent on VDAC1 and p62/SQSTM1.PINK1/Parkin 介导的线粒体自噬依赖于 VDAC1 和 p62/SQSTM1。
Nat Cell Biol. 2010 Feb;12(2):119-31. doi: 10.1038/ncb2012. Epub 2010 Jan 24.
3
The PINK1/Parkin pathway: a mitochondrial quality control system?PINK1/Parkin 通路:一种线粒体质量控制系统?
J Bioenerg Biomembr. 2009 Dec;41(6):499-503. doi: 10.1007/s10863-009-9253-3.
4
The role of dopamine oxidation in mitochondrial dysfunction: implications for Parkinson's disease.多巴胺氧化在线粒体功能障碍中的作用:对帕金森病的影响。
J Bioenerg Biomembr. 2009 Dec;41(6):469-72. doi: 10.1007/s10863-009-9257-z.
5
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。
Proc Natl Acad Sci U S A. 2010 Jan 5;107(1):378-83. doi: 10.1073/pnas.0911187107. Epub 2009 Dec 4.
6
Progression of Parkinson's disease in the clinical phase: potential markers.帕金森病临床阶段的进展:潜在标志物
Lancet Neurol. 2009 Dec;8(12):1158-71. doi: 10.1016/S1474-4422(09)70291-1.
7
Atg32 is a mitochondrial protein that confers selectivity during mitophagy.Atg32是一种在线粒体自噬过程中赋予选择性的线粒体蛋白。
Dev Cell. 2009 Jul;17(1):98-109. doi: 10.1016/j.devcel.2009.06.014.
8
Mitochondria-anchored receptor Atg32 mediates degradation of mitochondria via selective autophagy.线粒体锚定受体Atg32通过选择性自噬介导线粒体的降解。
Dev Cell. 2009 Jul;17(1):87-97. doi: 10.1016/j.devcel.2009.06.013.
9
Parkin protects dopaminergic neurons from excessive Wnt/beta-catenin signaling.帕金蛋白可保护多巴胺能神经元免受过度的Wnt/β-连环蛋白信号传导的影响。
Biochem Biophys Res Commun. 2009 Oct 23;388(3):473-8. doi: 10.1016/j.bbrc.2009.07.014. Epub 2009 Jul 8.
10
Mitochondrial kinases in Parkinson's disease: converging insights from neurotoxin and genetic models.帕金森病中的线粒体激酶:来自神经毒素和遗传模型的综合见解
Mitochondrion. 2009 Sep;9(5):289-98. doi: 10.1016/j.mito.2009.06.001. Epub 2009 Jun 27.

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.

DOI:10.1016/j.febslet.2010.02.060
PMID:20188730
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2843751/
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。