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C500140200v1
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Papers In Press, published online ahead of print October 5, 2005
J. Biol. Chem, 10.1074/jbc.C500140200
Submitted on March 28, 2005
Revised on September 23, 2005
Accepted on October 5, 2005

Mitochondrial creb mediates mitochondrial gene expression and neuronal survival

Junghee Lee, Chun-Hyung Kim, David K Simon, Lyaylya Aminova, Alexander Andreyev, Yulia Kushnareva, Anne A Murphy, Bonnie E Lonze, Kwang-Soo Kim, DAvid D. Ginty, Robert J. Ferrante, Hoon Ryu, and Rajiv R. Ratan

Boston University School of Medicine, Bedford, MA 01730

Corresponding Author: hoonryu{at}bu.edu

Cyclic AMP response element binding protein (CREB) is a widely expressed transcription factor whose role in neuronal protection is now well established. Here we report that CREB is present in the mitochondrial matrix of neurons, and that it binds directly to cyclic AMP response elements (CREs) found within the mitochondrial genome. Disruption of CREB activity in the mitochondria decreases the expression of subset of mitochondrial genes, including the ND5 subunit of complex I, down regulates complex-I dependent mitochondrial respiration, and increases susceptibility to 3-nitropropionic acid, a mitochondrial toxin that induces a clinical and pathological phenotype similar to HD. These results demonstrate that regulation of mitochondrial gene expression by mitochondrial CREB, in part, underlies the protective effects of CREB, and raise the possibility that decreased mitochondrial CREB activity contributes to the mitochondrial dysfunction and neuronal loss associated with neurodegenerative disorders.


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