PINK1 import regulation; a fine system to convey mitochondrial stress to the cytosol

被引：249

作者：

Sekine, Shiori ^{[1
]}

Youle, Richard J. ^{[1
]}

机构：

[1] NINDS, Biochem Sect, Surg Neurol Branch, NIH, Bldg 36,Rm 4D04, Bethesda, MD 20892 USA

来源：

BMC BIOLOGY | 2018年 / 16卷

基金：

日本学术振兴会;

关键词：

END RULE PATHWAY; PARKINSONS-DISEASE; RHOMBOID PROTEASE; DAMAGED MITOCHONDRIA; PINK1/PARKIN-MEDIATED MITOPHAGY; INTRAMEMBRANE PROTEOLYSIS; SUBCELLULAR-LOCALIZATION; RECESSIVE PARKINSONISM; UBIQUITIN LIGASES; ACTIVATE PARKIN;

D O I：

10.1186/s12915-017-0470-7

中图分类号：

Q [生物科学];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

Insights from inherited forms of parkinsonism suggest that insufficient mitophagy may be one etiology of the disease. PINK1/Parkin-dependent mitophagy, which helps maintain a healthy mitochondrial network, is initiated by activation of the PINK1 kinase specifically on damaged mitochondria. Recent investigation of this process reveals that import of PINK1 into mitochondria is regulated and yields a stress-sensing mechanism. In this review, we focus on the mechanisms of mitochondrial stress-dependent PINK1 activation that is exerted by regulated import of PINK1 into different mitochondrial compartments and how this offers strategies to pharmacologically activate the PINK1/Parkin pathway.

引用

页数：12

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