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Redox susceptibility of SOD1 mutants is associated with the differential response to CCS over-expression in vivo

Over-expression of CCS in G93A SOD1 mice accelerates neurological disease and enhances mitochondrial pathology. We studied the effect of CCS over-expression in transgenic mice expressing G37R, G86R or L126Z SOD1 mutations in order to understand factors which influence mitochondrial dysfunction. Over...

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Detalhes bibliográficos
Main Authors: Son, Marjatta, Fu, Qiao, Puttaparthi, Krishna, Matthews, Christina M., Elliott, Jeffrey L.
Formato: Artigo
Idioma:Inglês
Publicado em: 2009
Assuntos:
Acesso em linha:https://ncbi.nlm.nih.gov/pmc/articles/PMC2835407/
https://ncbi.nlm.nih.gov/pubmed/19320055
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