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Mitophagy and Parkinson's disease: The PINK1–parkin link()
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 diso...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Elsevier Pub. Co
2011
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3925795/ https://www.ncbi.nlm.nih.gov/pubmed/20736035 http://dx.doi.org/10.1016/j.bbamcr.2010.08.007 |
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author | Deas, Emma Wood, Nicholas W. Plun-Favreau, Hélène |
author_facet | Deas, Emma Wood, Nicholas W. Plun-Favreau, Hélène |
author_sort | Deas, Emma |
collection | PubMed |
description | 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. |
format | Online Article Text |
id | pubmed-3925795 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2011 |
publisher | Elsevier Pub. Co |
record_format | MEDLINE/PubMed |
spelling | pubmed-39257952014-02-21 Mitophagy and Parkinson's disease: The PINK1–parkin link() Deas, Emma Wood, Nicholas W. Plun-Favreau, Hélène Biochim Biophys Acta Review 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. Elsevier Pub. Co 2011-04 /pmc/articles/PMC3925795/ /pubmed/20736035 http://dx.doi.org/10.1016/j.bbamcr.2010.08.007 Text en © 2011 Elsevier B.V. https://creativecommons.org/licenses/by/4.0/This work is licensed under a Creative Commons Attribution 4.0 International License (https://creativecommons.org/licenses/by/4.0/) , which allows reusers to distribute, remix, adapt, and build upon the material in any medium or format, so long as attribution is given to the creator. The license allows for commercial use. |
spellingShingle | Review Deas, Emma Wood, Nicholas W. Plun-Favreau, Hélène Mitophagy and Parkinson's disease: The PINK1–parkin link() |
title | Mitophagy and Parkinson's disease: The PINK1–parkin link() |
title_full | Mitophagy and Parkinson's disease: The PINK1–parkin link() |
title_fullStr | Mitophagy and Parkinson's disease: The PINK1–parkin link() |
title_full_unstemmed | Mitophagy and Parkinson's disease: The PINK1–parkin link() |
title_short | Mitophagy and Parkinson's disease: The PINK1–parkin link() |
title_sort | mitophagy and parkinson's disease: the pink1–parkin link() |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3925795/ https://www.ncbi.nlm.nih.gov/pubmed/20736035 http://dx.doi.org/10.1016/j.bbamcr.2010.08.007 |
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