Goethe University Medical School, Institute of Biochemistry II and Frankfurt Institute for Molecular Life Sciences, Theodor-Stern-Kai 7, Frankfurt a.M., D-60590, Germany.
Nat Cell Biol. 2010 Feb;12(2):104-6. doi: 10.1038/ncb0210-104.
Recent studies have revealed a prominent role of mitochondrial dysfunction in the development of one of the most common neurodegenerative disorders, Parkinson's disease. The ubiquitin ligase Parkin and the protein kinase PINK1, whose mutations are associated with Parkinson's disease, function in a pathway that links ubiquitylation with selective autophagy of damaged mitochondria.
最近的研究表明,线粒体功能障碍在最常见的神经退行性疾病之一帕金森病的发展中起着重要作用。泛素连接酶 Parkin 和蛋白激酶 PINK1 的突变与帕金森病有关,它们在一条通路中发挥作用,这条通路将泛素化与受损线粒体的选择性自噬联系起来。