ArticleFrontiers in cellular neuroscience2017
Reduction of Huntington's Disease RNA Foci by CAG Repeat-Targeting Reagents.
Article in Frontiers in cellular neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
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Who cites it
14 citing papers in PubMed, 15 citations in OpenAlex.
- Molecular drivers of RNA phase separation.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- A peptide inhibitor that rescues polyglutamine-induced synaptic defects and cell death through suppressing RNA and protein toxicities.Molecular therapy. Nucleic acids · 2022Article
- Nuclear speckles - a driving force in gene expression.Journal of cell science · 2022Review
- Mutant huntingtin messenger RNA forms neuronal nuclear clusters in rodent and human brains.Brain communications · 2022Article
- Emerging Therapies for Huntington's Disease - Focus on N-Terminal Huntingtin and Huntingtin Exon 1.Biologics : targets & therapy · 2022Review
- Review
- Artificial miRNAs targeting CAG repeat expansion in ORFs cause rapid deadenylation and translation inhibition of mutant transcripts.Cellular and molecular life sciences : CMLS · 2021Article
- Repeat RNA expansion disorders of the nervous system: post-transcriptional mechanisms and therapeutic strategies.Critical reviews in biochemistry and molecular biology · 2021Review
- Potent and sustained huntingtin lowering via AAV5 encoding miRNA preserves striatal volume and cognitive function in a humanized mouse model of Huntington disease.Nucleic acids research · 2020Article
- A CRISPR-Cas13a Based Strategy That Tracks and Degrades Toxic RNA in Myotonic Dystrophy Type 1.Frontiers in genetics · 2020Article
- Curcumin Regulates the r(CGG)Frontiers in neuroscience · 2020Article
- Structural insights into synthetic ligands targeting A-A pairs in disease-related CAG RNA repeats.Nucleic acids research · 2019Article
- Trinucleotide Repeat Expansion Diseases, RNAi, and Cancer.Trends in cancer · 2018Review
- Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In several human polyglutamine diseases caused by expansions of CAG repeats in the coding sequence of single genes, mutant transcripts are detained in nuclear RNA foci. In polyglutamine disorders, unlike other repeat-associated diseases, both RNA and proteins exert pathogenic effects; therefore, decreases of both RNA and protein toxicity need to be addressed in proposed treatments. A variety of oligonucleotide-based therapeutic approaches have been developed for polyglutamine diseases, but concomitant assays for RNA foci reduction are lacking. Here, we show that various types of oligonucleotide-based reagents affect RNA foci number in Huntington's disease cells. We analyzed the effects of reagents targeting either CAG repeat tracts or specific
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.