| Literature DB >> 21220178 |
Stéphanie Millecamps1, Séverine Boillée, Elodie Chabrol, William Camu, Cécile Cazeneuve, François Salachas, Pierre-François Pradat, Véronique Danel-Brunaud, Nadia Vandenberghe, Philippe Corcia, Nadine Le Forestier, Lucette Lacomblez, Gaëlle Bruneteau, Danielle Seilhean, Alexis Brice, Josué Feingold, Vincent Meininger, Eric LeGuern.
Abstract
Mutations in OPTN gene encoding optineurin have recently been identified at the homozygote and heterozygote state in Japanese families with slowly progressive amyotrophic lateral sclerosis (ALS). OPTN had previously been involved in adult primary open angle glaucoma (POAG). We sequenced the coding exons of OPTN in 126 French patients with familial ALS (FALS). We identified, at the heterozygote state, the nonsense c.382_383insAG variant (also called 691_692insAG), alternatively reported as a causative mutation for primary open angle glaucoma (POAG) or a rare polymorphism and the new p.Arg96Leu variant in a family with dominant ALS. Western blot experiments on the patients' lymphoblasts showed that the former variant led to a loss of function and the latter did not cause protein accumulation. Our results do not confirm the contribution of OPTN in ALS.Entities:
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Year: 2011 PMID: 21220178 DOI: 10.1016/j.neurobiolaging.2010.11.005
Source DB: PubMed Journal: Neurobiol Aging ISSN: 0197-4580 Impact factor: 4.673