Regulatory mechanisms of incomplete huntingtin mRNA splicing
Author:
Publisher
Springer Science and Business Media LLC
Subject
General Physics and Astronomy,General Biochemistry, Genetics and Molecular Biology,General Chemistry
Link
http://www.nature.com/articles/s41467-018-06281-3.pdf
Reference62 articles.
1. Bates, G. P. et al. Huntington disease. Nat. Rev. Dis. Prim. 1, 15005 (2015).
2. The Huntington’s Disease Collaborative Research Group. A novel gene containing a trinucleotide repeat that is expanded and unstable on Huntington’s disease chromosomes. The Huntington’s Disease Collaborative Research Group. Cell 72, 971–983 (1993).
3. Romo, L., Ashar-Patel, A., Pfister, E. & Aronin, N. Alterations in mRNA 3′ UTR isoform abundance accompany gene expression changes in human Huntington’s disease brains. Cell Rep. 20, 3057–3070 (2017).
4. Lin, B. et al. Differential 3′ polyadenylation of the Huntington disease gene results in two mRNA species with variable tissue expression. Hum. Mol. Genet 2, 1541–1545 (1993).
5. Xu, H., An, J. J. & Xu, B. Distinct cellular toxicity of two mutant huntingtin mRNA variants due to translation regulation. PLoS One 12, e0177610 (2017).
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