A novel SOD1-ALS mutation separates central and peripheral effects of mutant SOD1 toxicity

Transgenic mouse models expressing mutant superoxide dismutase 1 (SOD1) have been critical in furthering our understanding of amyotrophic lateral sclerosis (ALS). However, such models generally overexpress the mutant protein, which may give rise to phenotypes not directly relevant to the disorder. H...

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Veröffentlicht in:	Human molecular genetics 2015-04, Vol.24 (7), p.1883-1897
Hauptverfasser:	Joyce, Peter I, Mcgoldrick, Philip, Saccon, Rachele A, Weber, William, Fratta, Pietro, West, Steven J, Zhu, Ning, Carter, Sarah, Phatak, Vinaya, Stewart, Michelle, Simon, Michelle, Kumar, Saumya, Heise, Ines, Bros-Facer, Virginie, Dick, James, Corrochano, Silvia, Stanford, Macdonnell J, Luong, Tu Vinh, Nolan, Patrick M, Meyer, Timothy, Brandner, Sebastian, Bennett, David L H, Ozdinler, P Hande, Greensmith, Linda, Fisher, Elizabeth M C, Acevedo-Arozena, Abraham
Format:	Artikel
Sprache:	eng
Schlagworte:	Amyotrophic Lateral Sclerosis - enzymology Amyotrophic Lateral Sclerosis - genetics Animals Disease Models, Animal Humans Mice Mice, Inbred C57BL Motor Neurons - enzymology Mutation, Missense Point Mutation Superoxide Dismutase - genetics Superoxide Dismutase - metabolism Superoxide Dismutase - toxicity Superoxide Dismutase-1
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