Biochemical properties of the kinase PINK1 as sensor protein for mitochondrial damage signalling. (7th April 2015)

• Record Type: Journal Article
• Authors: Rüb, Cornelia; Schröder, Nadja; Voos, Wolfgang
• Is Part Of: Biochemical Society transactions. Volume 43:Number 2(2015)
• Page Start: 287
• Page End: 291
• Publication Date: 2015-04-07
• Subjects: mitochondria -- mitophagy -- organellar quality control -- phosphatase and tensin homologue-induced kinase 1 (PINK1) -- protein import; Biochemistry -- Congresses; 572
• DOI: 10.1042/BST20150005
• Languages: English
• ISSNs: 0300-5127

Abstract

Abstract : Defects of mitochondrial functions have been implicated in many different human diseases, in particular neurodegenerative diseases. The kinase PINK1 [phosphatase and tensin homologue (PTEN)-induced kinase 1] has been identified as a crucial player in a specific damage signalling pathway, eliminating defective mitochondria by an autophagic process. Mutations in PINK1 have been shown to cause familial cases of Parkinson's disease. In this review, we summarize the biochemical mechanisms that underlie the association of PINK1 with mitochondria under normal and pathological conditions. This unconventional mitochondrial localization pathway is discussed in the context of the role of PINK1 as a sensor of mitochondrial damage and a causative factor in Parkinson's disease.