ArticleScientific reports2020
Silencing Srsf6 does not modulate incomplete splicing of the huntingtin gene in Huntington's disease models.
Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 25 citations in OpenAlex.
- Human-specific sequence features in HTT exon 1 promote toxic misprocessing via splicing factor SRSF7.Nature communications · 2026Article
- Enhancing the detection of HTT1a with neoepitope antibodies in mouse models of Huntington's disease.Brain communications · 2026Article
- A collaborative network analysis for the interpretation of transcriptomics data in Huntington's disease.Scientific reports · 2025Article
- mEMBO reports · 2024Article
- Regulation ofInternational journal of molecular sciences · 2024Review
- Article
- Alternative splicing in neurodegenerative disease and the promise of RNA therapies.Nature reviews. Neuroscience · 2023Review
- Towards understandings of serine/arginine-rich splicing factors.Acta pharmaceutica Sinica. B · 2023Review
- Alternative processing of human HTT mRNA with implications for Huntington's disease therapeutics.Brain : a journal of neurology · 2022Article
- SRSF6 balances mitochondrial-driven innate immune outcomes through alternative splicing of BAX.eLife · 2022Article
- Review
- Emerging Therapies for Huntington's Disease - Focus on N-Terminal Huntingtin and Huntingtin Exon 1.Biologics : targets & therapy · 2022Review
- Review
- Role and Perspective of Molecular Simulation-Based Investigation of RNA-Ligand Interaction: From Small Molecules and Peptides to Photoswitchable RNA Binding.Molecules (Basel, Switzerland) · 2021Review
- The heat shock response, determined by QuantiGene multiplex, is impaired in HD mouse models and not caused by HSF1 reduction.Scientific reports · 2021Article
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
We have previously shown that the incomplete splicing of exon 1 to exon 2 of the HTT gene results in the production of a small polyadenylated transcript (Httexon1) that encodes the highly pathogenic exon 1 HTT protein. There is evidence to suggest that the splicing factor SRSF6 is involved in the mechanism that underlies this aberrant splicing event. Therefore, we set out to test this hypothesis, by manipulating SRSF6 levels in Huntington's disease models in which an expanded CAG repeat had been knocked in to the endogenous Htt gene. We began by generating mice that were knocked out for Srsf6, and demonstrated that reduction of SRSF6 to 50% of wild type levels had no effect on incomplete splicing in zQ175 knockin mice. We found that nullizygosity for Srsf6 was embryonic lethal, and therefore, to decrease SRSF6 levels further, we established mouse embryonic fibroblasts (MEFs) from wild type, zQ175, and zQ175::Srsf6
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