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A more recent version of this article appeared on October 15, 2004
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M408025200v1
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Papers In Press, published online ahead of print August 5, 2004
J. Biol. Chem, 10.1074/jbc.M408025200
Submitted on July 15, 2004
Revised on August 5, 2004
Accepted on August 5, 2004

Suppression of uracil-DNA glycosylase induces neuronal apoptosis

Inna I. Kruman, Elena Schwartz, Yuri Kruman, Roy Cutler, Xiaoxiang Zhu, Nigel H. Greig, and Mark M. Mattson

Sun Health Research Institute, Sun City, AZ 85351

Corresponding Author: inna.kruman{at}sunhealth.org

A chronic imbalance in DNA precursors, caused by one carbon metabolism (OCM) impairment, can result in a deficiency of DNA repair and increased DNA damage. Although indirect evidence suggests that DNA damage plays a role in neuronal apoptosis and in the pathogenesis of neurodegenerative disorders, the underlying mechanisms are poorly understood. In particular, very little is known about the role of base excision repair of misincorporated uracil in neuronal survival. To test the hypothesis that repair of DNA damage associated with uracil misincorporation is critical for neuronal survival, we employed an antisense (AS) oligonucleotide directed against uracil-DNA glycosylase encoded by the UNG gene, to deplete UNG in cultured rat


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