Metformin-induced mitochondrial function and ABCD2 up-regulation in X-linked adrenoleukodystrophy involves AMP-activated protein kinase
Author:
Affiliation:
1. Department of Neurology; Henry Ford Health System; Detroit Michigan USA
2. Department of Pathology; Henry Ford Health System; Detroit Michigan USA
Funder
Henry Ford Health System Proposal Development
Mentored Scientist Grant
Publisher
Wiley
Subject
Cellular and Molecular Neuroscience,Biochemistry
Link
http://onlinelibrary.wiley.com/wol1/doi/10.1111/jnc.13562/fullpdf
Reference76 articles.
1. Decreased expression of ABCD4 and BG1 genes early in the pathogenesis of X-linked adrenoleukodystrophy;Asheuer;Hum. Mol. Genet.,2005
2. Pathophysiology of X-linked adrenoleukodystrophy;Berger;Biochimie,2014
3. Low concentrations of metformin suppress glucose production in hepatocytes through AMP-activated protein kinase (AMPK);Cao;J. Biol. Chem.,2014
4. AMPKalpha1 deficiency amplifies proinflammatory myeloid APC activity and CD40 signaling;Carroll;J. Leukoc. Biol.,2013
5. Hematopoietic stem cell gene therapy with a lentiviral vector in X-linked adrenoleukodystrophy;Cartier;Science,2009
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