Slow mitochondrial repair of 5′-AMP renders mtDNA susceptible to damage in APTX deficient cells
Author:
Publisher
Springer Science and Business Media LLC
Subject
Multidisciplinary
Link
http://www.nature.com/articles/srep12876.pdf
Reference47 articles.
1. Kijas, A. W., Harris, J. L., Harris, J. M. & Lavin, M. F. Aprataxin forms a discrete branch in the HIT (histidine triad) superfamily of proteins with both DNA/RNA binding and nucleotide hydrolase activities. J Biol Chem 281, 13939–13948 (2006).
2. Caldecott, K. W. Single-strand break repair and genetic disease. Nat Rev Genet 9, 619–631 (2008).
3. Date, H. et al. Early-onset ataxia with ocular motor apraxia and hypoalbuminemia is caused by mutations in a new HIT superfamily gene. Nat Genet 29, 184–188 (2001).
4. Moreira, M. C. et al. The gene mutated in ataxia-ocular apraxia 1 encodes the new HIT/Zn-finger protein aprataxin. Nat Genet 29, 189–193 (2001).
5. Ahel, I. et al. The neurodegenerative disease protein aprataxin resolves abortive DNA ligation intermediates. Nature 443, 713–716 (2006).
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