C9orf72 expansion disrupts ATM-mediated chromosomal break repair
Author:
Publisher
Springer Science and Business Media LLC
Subject
General Neuroscience
Link
http://www.nature.com/articles/nn.4604.pdf
Reference54 articles.
1. Schottlaender, L.V. et al. Analysis of C9orf72 repeat expansions in a large series of clinically and pathologically diagnosed cases with atypical Parkinsonism. Neurobiol. Aging 36, 1221.e1–1221.e6 (2015).
2. Rutherford, N.J. et al. Length of normal alleles of C9ORF72 GGGGCC repeat do not influence disease phenotype. Neurobiol. Aging 33, 2950.e5–2950.e7 (2012).
3. DeJesus-Hernandez, M. et al. Expanded GGGGCC hexanucleotide repeat in noncoding region of C9ORF72 causes chromosome 9p-linked FTD and ALS. Neuron 72, 245–256 (2011).
4. Groh, M. & Gromak, N. Out of balance: R-loops in human disease. PLoS Genet. 10, e1004630 (2014).
5. Roy, D., Yu, K. & Lieber, M.R. Mechanism of R-loop formation at immunoglobulin class switch sequences. Mol. Cell. Biol. 28, 50–60 (2008).
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