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A novel variant of human SOD1 harboring ALS-associated and experimental mutations in metal-binding residues and free cysteines lacks toxicity in vivo
Mutations in SOD1 cause FALS. The Cu binding capacity of SOD1 has spawned hypotheses that implicate metal-mediated production of reactive species as a potential mechanism of toxicity. In past experiments, we have tested such hypotheses by mutating residues in SOD1 that normally coordinate the bindin...
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| Główni autorzy: | , , , , , |
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| Format: | Artigo |
| Język: | Inglês |
| Wydane: |
2012
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| Hasła przedmiotowe: | |
| Dostęp online: | https://ncbi.nlm.nih.gov/pmc/articles/PMC3705958/ https://ncbi.nlm.nih.gov/pubmed/22332887 https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1111/j.1471-4159.2012.07690.x |
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