ArticleScientific reports2015
Nuclear retention of full-length HTT RNA is mediated by splicing factors MBNL1 and U2AF65.
Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
34 citing papers in PubMed, 55 citations in OpenAlex.
- Nuclear MBL-1 modulates mitochondrial morphology through carnitine palmitoyltransferase inProceedings of the National Academy of Sciences of the United States of America · 2026Article
- Stick-slip unfolding favors self-association of expanded HTT mRNA.Nature communications · 2024Article
- Stick-slip unfolding favors self-association of expandedbioRxiv : the preprint server for biology · 2024Article
- Lowering mutant huntingtin by small molecules relieves Huntington's disease symptoms and progression.EMBO molecular medicine · 2024Article
- CAG repeat expansions create splicing acceptor sites and produce aberrant repeat-containing RNAs.Molecular cell · 2024Article
- Subcellular RNA distribution and its change during human embryonic stem cell differentiation.Stem cell reports · 2024Article
- Bidirectional Transcription at the PPP2R2B Gene Locus in Spinocerebellar Ataxia Type 12.Movement disorders : official journal of the Movement Disorder Society · 2023Article
- CAG repeat expansions create splicing acceptor sites and produce aberrant repeat-containing RNAs.bioRxiv : the preprint server for biology · 2023Article
- Native functions of short tandem repeats.eLife · 2023Article
- Repeat-associated non-AUG translation induces cytoplasmic aggregation of CAG repeat-containing RNAs.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Partners in crime: Proteins implicated in RNA repeat expansion diseases.Wiley interdisciplinary reviews. RNA · 2022Review
- Interaction of huntingtin with PRMTs and its subsequent arginine methylation affects HTT solubility, phase transition behavior and neuronal toxicity.Human molecular genetics · 2022Article
- Article
- Emerging Therapies for Huntington's Disease - Focus on N-Terminal Huntingtin and Huntingtin Exon 1.Biologics : targets & therapy · 2022Review
- Oxidative stress alters transcript localization of disease-associated genes in the retinal pigment epithelium.Molecular vision · 2022Article
- Mutant huntingtin messenger RNA forms neuronal nuclear clusters in rodent and human brains.Brain communications · 2022Article
- Localization of RNAs in the nucleus:RNA biology · 2021Review
- RNA Toxicity and Perturbation of rRNA Processing in Spinocerebellar Ataxia Type 2.Movement disorders : official journal of the Movement Disorder Society · 2021Article
- A high-throughput screening to identify small molecules that suppress huntingtin promoter activity or activate huntingtin-antisense promoter activity.Scientific reports · 2021Article
- Review
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
Abstract
Huntington's disease (HD) is caused by a CAG repeat expansion in the huntingtin (HTT) gene. Recent evidence suggests that HD is a consequence of multimodal, non-mutually exclusive mechanisms of pathogenesis that involve both HTT protein- and HTT RNA-triggered mechanisms. Here we provide further evidence for the role of expanded HTT (expHTT) RNA in HD by demonstrating that a fragment of expHTT is cytotoxic in the absence of any translation and that the extent of cytotoxicity is similar to the cytotoxicity of an expHTT protein fragment encoded by a transcript of similar length and with a similar repeat size. In addition, full-length (FL) expHTT is retained in the nucleus. Overexpression of the splicing factor muscleblind-like 1 (MBNL1) increases nuclear retention of expHTT and decreases the expression of expHTT protein in the cytosol. The splicing and nuclear export factor U2AF65 has the opposite effect, decreasing expHTT nuclear retention and increasing expression of expHTT protein. This suggests that MBNL1 and U2AF65 play a role in nuclear export of expHTT RNA.
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Registered trials
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.