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The mitochondrial kinase PINK 1: functions beyond mitophagy
Author(s) -
Voigt Aaron,
Berlemann Lena A.,
Winklhofer Konstanze F.
Publication year - 2016
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/jnc.13655
Subject(s) - mitophagy , pink1 , mitochondrion , microbiology and biotechnology , kinase , biology , neuroscience , chemistry , genetics , autophagy , apoptosis
Abstract Mutations in the genes encoding the mitochondrial kinase PINK 1 and the E3 ubiquitin ligase Parkin cause autosomal recessive Parkinson's disease ( PD ). Pioneering work in Drosophila melanogaster revealed that the loss of PINK 1 or Parkin function causes similar phenotypes including dysfunctional mitochondria. Further research showed that PINK 1 can act upstream of Parkin in a mitochondrial quality control pathway to induce removal of damaged mitochondria in a process called mitophagy. Albeit the PINK 1/Parkin‐induced mitophagy pathway is well established and has recently been elucidated in great detail, its pathophysiological relevance is being debated. Mounting evidence indicates that PINK 1 has additional functions, for example, in regulating complex I activity and maintaining neuronal viability in response to stress. Here, we discuss mitophagy‐dependent and ‐independent functions of PINK 1 and their possible role in PD pathogenesis.Mutations in the PINK1 gene, encoding a mitochondrial kinase, are associated with autosomal recessive Parkinson's disease. In this review, we summarize and discuss the functional roles of PINK1 in maintaining mitochondrial integrity, eliminating damaged mitochondria, and promoting cell survival. This article is part of a special issue on Parkinson disease .