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UCP2 overexpression worsens mitochondrial dysfunction and accelerates disease progression in a mouse model of amyotrophic lateral sclerosis
Mitochondrial dysfunction leading to deficits in energy production, Ca(2+) uptake capacity, and free radical generation has been implicated in the pathogenesis of familial amyotrophic lateral sclerosis (ALS) caused by mutations in Cu, Zn superoxide dismutase (SOD1). Numerous studies link UCP2, a mem...
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| Autors principals: | , , , , , |
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| Format: | Artigo |
| Idioma: | Inglês |
| Publicat: |
2013
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| Matèries: | |
| Accés en línia: | https://ncbi.nlm.nih.gov/pmc/articles/PMC3891658/ https://ncbi.nlm.nih.gov/pubmed/24141050 https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1016/j.mcn.2013.10.002 |
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