UCP2 overexpression worsens mitochondrial dysfunction and accelerates disease progression in a mouse model of amyotrophic lateral sclerosis-Reference-Cited by-同舟云学术

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UCP2 overexpression worsens mitochondrial dysfunction and accelerates disease progression in a mouse model of amyotrophic lateral sclerosis

Published:2013-11 Issue: Volume:57 Page:104-110
ISSN:1044-7431
Container-title:Molecular and Cellular Neuroscience
language:en
Short-container-title:Molecular and Cellular Neuroscience

Author:

Peixoto Pablo M.,Kim Hyun-Jeong,Sider Brittany,Starkov Anatoly,Horvath Tamas L.,Manfredi Giovanni

Publisher

Elsevier BV

Subject

Cell Biology,Cellular and Molecular Neuroscience,Molecular Biology

Reference52 articles.

1. Ghrelin promotes and protects nigrostriatal dopamine function via a UCP2-dependent mitochondrial mechanism;Andrews;J. Neurosci.,2009

2. Uncoupling protein-2 is critical for nigral dopamine cell survival in a mouse model of Parkinson's disease;Andrews;J. Neurosci.,2005

3. Uncoupling protein-2 regulates lifespan in mice;Andrews;Am. J. Physiol. Endocrinol. Metab.,2009

4. UCP2 mediates ghrelin/'s action on NPY/AgRP neurons by lowering free radicals;Andrews;Nature,2008

5. Disruption of the uncoupling protein-2 gene in mice reveals a role in immunity and reactive oxygen species production;Arsenijevic;Nat. Genet.,2000

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