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LRRK2 in Transcription and Translation Regulation: Relevance for Parkinson’s Disease
Parkinson’s disease (PD) is the most common neurodegenerative movement disorder and is characterized by the selective loss of dopaminergic neurons and the presence of Lewy bodies. Mutations in the leucine-rich repeat kinase 2 (LRRK2) gene are the most frequent cause of both familial and sporadic PD....
Autores principales: | , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Frontiers Research Foundation
2012
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3276974/ https://www.ncbi.nlm.nih.gov/pubmed/22363314 http://dx.doi.org/10.3389/fneur.2012.00012 |
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author | Dorval, Véronique Hébert, Sébastien S. |
author_facet | Dorval, Véronique Hébert, Sébastien S. |
author_sort | Dorval, Véronique |
collection | PubMed |
description | Parkinson’s disease (PD) is the most common neurodegenerative movement disorder and is characterized by the selective loss of dopaminergic neurons and the presence of Lewy bodies. Mutations in the leucine-rich repeat kinase 2 (LRRK2) gene are the most frequent cause of both familial and sporadic PD. One critical question is how PD-associated LRRK2 mutations cause neurodegeneration. Here, we discuss recent findings related to LRRK2-mediated regulation of gene expression and translation and provide a critical assessment of the current models that are used to address the impact of LRRK2 on the transcriptome. A better understanding of these mechanisms could provide important new clues into the function of LRRK2 during both normal and pathological conditions. |
format | Online Article Text |
id | pubmed-3276974 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2012 |
publisher | Frontiers Research Foundation |
record_format | MEDLINE/PubMed |
spelling | pubmed-32769742012-02-23 LRRK2 in Transcription and Translation Regulation: Relevance for Parkinson’s Disease Dorval, Véronique Hébert, Sébastien S. Front Neurol Neuroscience Parkinson’s disease (PD) is the most common neurodegenerative movement disorder and is characterized by the selective loss of dopaminergic neurons and the presence of Lewy bodies. Mutations in the leucine-rich repeat kinase 2 (LRRK2) gene are the most frequent cause of both familial and sporadic PD. One critical question is how PD-associated LRRK2 mutations cause neurodegeneration. Here, we discuss recent findings related to LRRK2-mediated regulation of gene expression and translation and provide a critical assessment of the current models that are used to address the impact of LRRK2 on the transcriptome. A better understanding of these mechanisms could provide important new clues into the function of LRRK2 during both normal and pathological conditions. Frontiers Research Foundation 2012-02-10 /pmc/articles/PMC3276974/ /pubmed/22363314 http://dx.doi.org/10.3389/fneur.2012.00012 Text en Copyright © 2012 Dorval and Hébert. http://www.frontiersin.org/licenseagreement This is an open-access article distributed under the terms of the Creative Commons Attribution Non Commercial License, which permits non-commercial use, distribution, and reproduction in other forums, provided the original authors and source are credited. |
spellingShingle | Neuroscience Dorval, Véronique Hébert, Sébastien S. LRRK2 in Transcription and Translation Regulation: Relevance for Parkinson’s Disease |
title | LRRK2 in Transcription and Translation Regulation: Relevance for Parkinson’s Disease |
title_full | LRRK2 in Transcription and Translation Regulation: Relevance for Parkinson’s Disease |
title_fullStr | LRRK2 in Transcription and Translation Regulation: Relevance for Parkinson’s Disease |
title_full_unstemmed | LRRK2 in Transcription and Translation Regulation: Relevance for Parkinson’s Disease |
title_short | LRRK2 in Transcription and Translation Regulation: Relevance for Parkinson’s Disease |
title_sort | lrrk2 in transcription and translation regulation: relevance for parkinson’s disease |
topic | Neuroscience |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3276974/ https://www.ncbi.nlm.nih.gov/pubmed/22363314 http://dx.doi.org/10.3389/fneur.2012.00012 |
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