Loss of the m-AAA protease subunit AFG3L2 causes mitochondrial transport defects and tau hyperphosphorylation

The m-AAA protease subunit AFG3L2 is involved in degradation and processing of substrates in the inner mitochondrial membrane. Mutations in AFG3L2 are associated with spinocerebellar ataxia SCA28 in humans and impair axonal development and neuronal survival in mice. The loss of AFG3L2 causes fragmen...

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Main Authors: Kondadi, Arun Kumar, Wang, Shuaiyu, Montagner, Sara, Kladt, Nikolay, Korwitz, Anne, Martinelli, Paola, Herholz, David, Baker, Michael J, Schauss, Astrid C, Langer, Thomas, Rugarli, Elena I
Formato: Artigo
Idioma:Inglês
Publicado: BlackWell Publishing Ltd 2014
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Articles
Acceso en liña:https://ncbi.nlm.nih.gov/pmc/articles/PMC4193934/
https://ncbi.nlm.nih.gov/pubmed/24681487
https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1002/embj.201387009
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