帕金
品脱1
粒体自噬
自噬
线粒体
泛素连接酶
细胞生物学
生物
泛素
帕金森病
遗传学
突变
疾病
基因
医学
细胞凋亡
病理
作者
Emma Deas,Nicholas William Wood,Hélène Plun‐Favreau
标识
DOI:10.1016/j.bbamcr.2010.08.007
摘要
The study of rare, inherited mutations underlying familial forms of Parkinson's disease has provided insight into the molecular mechanisms of disease pathogenesis. Mutations in these genes have been functionally linked to several key molecular pathways implicated in other neurodegenerative disorders, including mitochondrial dysfunction, protein accumulation and the autophagic-lysosomal pathway. In particular, the mitochondrial kinase PINK1 and the cytosolic E3 ubiquitin ligase parkin act in a common pathway to regulate mitochondrial function. In this review we discuss the recent evidence suggesting that the PINK1/parkin pathway also plays a critical role in the autophagic removal of damaged mitochondria-mitophagy. This article is part of a Special Issue entitled Mitochondria: the deadly organelle.
科研通智能强力驱动
Strongly Powered by AbleSci AI