MitoTALEN reduces mutant mtDNA load and restores tRNAAla levels in a mouse model of heteroplasmic mtDNA mutation
Author:
Publisher
Springer Science and Business Media LLC
Subject
General Biochemistry, Genetics and Molecular Biology,General Medicine
Link
http://www.nature.com/articles/s41591-018-0166-8.pdf
Reference27 articles.
1. Craven, L., Alston, C. L., Taylor, R. W. & Turnbull, D. M. Recent advances in mitochondrial disease. Annu. Rev. Genomics Hum. Genet. 18, 257–275 (2017).
2. Kauppila, J. H. et al. A phenotype-driven approach to generate mouse models with pathogenic mtDNA mutations causing mitochondrial disease. Cell Rep. 16, 2980–2990 (2016).
3. Bacman, S. R., Williams, S. L., Pinto, M., Peralta, S. & Moraes, C. T. Specific elimination of mutant mitochondrial genomes in patient-derived cells by mitoTALENs. Nat. Med. 19, 1111–1113 (2013).
4. Hashimoto, M. et al. MitoTALEN: a general approach to reduce mutant mtDNA Loads and restore oxidative phosphorylation function in mitochondrial diseases. Mol. Ther. 23, 1592–1599 (2015).
5. Gammage, P. A. et al. Near-complete elimination of mutant mtDNA by iterative or dynamic dose-controlled treatment with mtZFNs. Nucleic Acids Res. 44, 7804–7816 (2016).
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