Artificial microRNA suppresses C9ORF72 variants and decreases toxic dipeptide repeat proteins in vivo
Author:
Publisher
Springer Science and Business Media LLC
Subject
Genetics,Molecular Biology,Molecular Medicine
Link
https://www.nature.com/articles/s41434-023-00418-w.pdf
Reference60 articles.
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2. Wijesekera LC, Leigh PN. Amyotrophic lateral sclerosis. Orphanet J Rare Dis. 2009;4:3.
3. DeJesus-Hernandez M, Mackenzie IRR, Boeve BFF, Boxer ALL, Baker M, Rutherford NJJ, et al. Expanded GGGGCC hexanucleotide repeat in noncoding region of C9ORF72 causes chromosome 9p-Linked FTD and ALS. Neuron. 2011;72:245–56.
4. Majounie E, Renton AE, Mok K, Dopper EGPP, Waite A, Rollinson S, et al. Frequency of the C9orf72 hexanucleotide repeat expansion in patients with amyotrophic lateral sclerosis and frontotemporal dementia: a cross-sectional study. Lancet Neurol. 2012;11:323–30.
5. Renton AE, Majounie E, Waite A, Simón-Sánchez J, Rollinson S, Gibbs JR, et al. A hexanucleotide repeat expansion in C9ORF72 is the cause of chromosome 9p21-linked ALS-FTD. Neuron. 2011;72:257–68.
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1. Dual-targeting CRISPR-CasRx reducesC9orf72ALS/FTD sense and antisense repeat RNAs in vitro and in vivo;2024-01-28
2. A high-fidelity CRISPR-Cas13 system improves abnormalities associated with C9ORF72-linked ALS/FTD;2023-12-12
3. Aberrant splicing exonizesC9ORF72repeat expansion in ALS/FTD;2023-11-14
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