ArticleInternational journal of molecular sciences2019
Removal of the Polyglutamine Repeat of Ataxin-3 by Redirecting pre-mRNA Processing.
Article in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 15 citations in OpenAlex.
- Expansion of Splice-Switching Therapy with Antisense Oligonucleotides.International journal of molecular sciences · 2025Review
- Down syndrome and DYRK1A overexpression: relationships and future therapeutic directions.Frontiers in molecular neuroscience · 2024Review
- Polyglutamine Ataxias: Our Current Molecular Understanding and What the Future Holds for Antisense Therapies.Biomedicines · 2021Review
- CRISPR/Cas9 mediated gene correction ameliorates abnormal phenotypes in spinocerebellar ataxia type 3 patient-derived induced pluripotent stem cells.Translational psychiatry · 2021Article
- Induction of cryptic pre-mRNA splice-switching by antisense oligonucleotides.Scientific reports · 2021Article
- Antisense Oligonucleotide-Mediated Exon-skipping Therapies: Precision Medicine Spreading from Duchenne Muscular Dystrophy.JMA journal · 2021Review
- Proof-of-Concept: Antisense Oligonucleotide Mediated Skipping of Fibrillin-1 Exon 52.International journal of molecular sciences · 2021Article
- Repeat RNA expansion disorders of the nervous system: post-transcriptional mechanisms and therapeutic strategies.Critical reviews in biochemistry and molecular biology · 2021Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Spinocerebellar ataxia type 3 (SCA3) is a devastating neurodegenerative disease for which there is currently no cure, nor effective treatment strategy. One of nine polyglutamine disorders known to date, SCA3 is clinically heterogeneous and the main feature is progressive ataxia, which in turn affects speech, balance and gait of the affected individual. SCA3 is caused by an expanded polyglutamine tract in the ataxin-3 protein, resulting in conformational changes that lead to toxic gain of function. The expanded glutamine tract is located at the 5' end of the penultimate exon (exon 10) of
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Registered trials
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