Friedreich's ataxia–associated GAA repeats induce replication-fork reversal and unusual molecular junctions
Author:
Publisher
Springer Science and Business Media LLC
Subject
Molecular Biology,Structural Biology
Link
http://www.nature.com/articles/nsmb.2520.pdf
Reference50 articles.
1. McMurray, C.T. Mechanisms of trinucleotide repeat instability during human development. Nat. Rev. Genet. 11, 786–799 (2010).
2. Mirkin, S.M. Expandable DNA repeats and human disease. Nature 447, 932–940 (2007).
3. Schmucker, S. & Puccio, H. Understanding the molecular mechanisms of Friedreich's ataxia to develop therapeutic approaches. Hum. Mol. Genet. 19, R103–R110 (2010).
4. Gacy, A.M. et al. GAA instability in Friedreich's Ataxia shares a common, DNA-directed and intraallelic mechanism with other trinucleotide diseases. Mol. Cell 1, 583–593 (1998).
5. Sakamoto, N. et al. Sticky DNA: self-association properties of long GAA.TTC repeats in R.R.Y triplex structures from Friedreich's ataxia. Mol. Cell 3, 465–475 (1999).
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