Excess α-synuclein worsens disease in mice lacking ubiquitin carboxy-terminal hydrolase L1

Mutations in α-synuclein (αSN) and ubiquitin carboxy-terminal hydrolase L1 (UCH-L1) have been linked to familial Parkinson's disease (PD). Physical and functional interactions between these two proteins have been described. Whether they act additively in vivo to influence disease has remained c...

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Detalles Bibliográficos
Autores principales: Shimshek, Derya R., Schweizer, Tatjana, Schmid, Peter, van der Putten, P. Herman
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group 2012
Materias:
Article
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3278044/
https://www.ncbi.nlm.nih.gov/pubmed/22355774
http://dx.doi.org/10.1038/srep00262

Internet

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3278044/
https://www.ncbi.nlm.nih.gov/pubmed/22355774
http://dx.doi.org/10.1038/srep00262

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