Journal
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR CELL RESEARCH
Volume 1813, Issue 4, Pages 623-633Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.bbamcr.2010.08.007
Keywords
Mitochondria; Mitophagy; Neurodegeneration; Parkinson's disease; Parkin; PINK1
Categories
Funding
- MRC [G0700183, MC_G1000735] Funding Source: UKRI
- Medical Research Council [G0700183, MC_G1000735] Funding Source: researchfish
- Parkinson's UK [G-0612] Funding Source: researchfish
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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. (C) 2010 Elsevier B.V. All rights reserved.
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