LRRK2 in Transcription and Translation Regulation: Relevance for Parkinson’s Disease
Identifieur interne : 001214 ( Main/Merge ); précédent : 001213; suivant : 001215LRRK2 in Transcription and Translation Regulation: Relevance for Parkinson’s Disease
Auteurs : Véronique Dorval [Canada] ; Sébastien S. Hébert [Canada]Source :
- Frontiers in Neurology [ 1664-2295 ] ; 2012.
Abstract
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.
Url:
DOI: 10.3389/fneur.2012.00012
PubMed: 22363314
PubMed Central: 3276974
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Hébert</name><affiliation wicri:level="1"><nlm:aff id="aff1"><institution>Centre de Recherche du CHUQ, Axe Neurosciences, Université Laval</institution><country>Québec, QC, Canada</country></nlm:aff><country xml:lang="fr">Canada</country><wicri:regionArea></wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="aff2"><institution>Département de Psychiatrie et Neurosciences, Faculté de Médecine, Université Laval</institution><country>Québec, QC, Canada</country></nlm:aff><country xml:lang="fr">Canada</country><wicri:regionArea></wicri:regionArea></affiliation></author></analytic><series><title level="j">Frontiers in Neurology</title><idno type="eISSN">1664-2295</idno><imprint><date when="2012">2012</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>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.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Bagetta, V" uniqKey="Bagetta V">V. Bagetta</name></author><author><name sortKey="Ghiglieri, V" uniqKey="Ghiglieri V">V. Ghiglieri</name></author><author><name sortKey="Sgobio, C" uniqKey="Sgobio C">C. Sgobio</name></author><author><name sortKey="Calabresi, P" uniqKey="Calabresi P">P. 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Dawson</name></author><author><name sortKey="Dawson, T M" uniqKey="Dawson T">T. M. Dawson</name></author><author><name sortKey="Moore, D J" uniqKey="Moore D">D. J. Moore</name></author></analytic></biblStruct></listBibl></div1></back></TEI></record>Pour manipuler ce document sous Unix (Dilib)
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