ArticleHuman molecular genetics2011
A natural antisense transcript at the Huntington's disease repeat locus regulates HTT expression.
Article in Human molecular genetics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 121 papers.
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Who cites it
121 citing papers in PubMed, 191 citations in OpenAlex.
- RAN proteins and RNA foci from antisense transcripts in C9ORF72 ALS and frontotemporal dementia.Proceedings of the National Academy of Sciences of the United States of America · 2013Trial
- Regulation of PHOX2B gene expression by the long non-coding natural antisense RNA PHOX2B-AS1.The FEBS journal · 2026Article
- Metformin improves RAN protein pathology, alternative splicing, and behavioral phenotypes in SCA8 mice.Life science alliance · 2026Article
- Long non-coding RNAs in neurodegenerative diseases - Molecular mechanisms, liquid biopsy biomarkers, and therapeutic targets: A review.Biomolecules & biomedicine · 2026Review
- MBNL proteins in health, disease, and therapeutic applications.Nucleic acids research · 2026Review
- Repeat-associated non-AUG translation as a common mechanism for the polyGln ataxias.Cell reports · 2026Article
- An antisense-long-noncoding-RNA modulates p75iScience · 2025Article
- Regulation ofInternational journal of molecular sciences · 2024Review
- Therapeutic targeting of RNA for neurological and neuromuscular disease.Genes & development · 2024Review
- Article
- Emerging Perspectives on Prime Editor Delivery to the Brain.Pharmaceuticals (Basel, Switzerland) · 2024Review
- Huntington disease-like 2: insight into neurodegeneration from an African disease.Nature reviews. Neurology · 2024Review
- Therapeutic potential of natural antisense transcripts and various mechanisms involved for clinical applications and disease prevention.RNA biology · 2024Review
- Hidden regulators: the emerging roles of lncRNAs in brain development and disease.Frontiers in neuroscience · 2024Review
- Bidirectional Transcription at the PPP2R2B Gene Locus in Spinocerebellar Ataxia Type 12.Movement disorders : official journal of the Movement Disorder Society · 2023Article
- Review
- From Pathogenesis to Therapeutics: A Review of 150 Years of Huntington's Disease Research.International journal of molecular sciences · 2023Review
- Distinct regulatory functions and biological roles of lncRNA splice variants.Molecular therapy. Nucleic acids · 2023Review
- Review
- Current Diagnostic Methods and Non-Coding RNAs as Possible Biomarkers in Huntington's Disease.Genes · 2022Review
61 more citing papers are in PubMed but not listed here.
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Huntington's disease (HD) is a progressive neurodegenerative disorder caused by a CAG repeat expansion in exon 1 of huntingtin (HTT). Relatively little attention has been directed to the genomic features of the antisense strand at the HD locus, though the presence of a transcript from this strand has been suggested by a survey of the entire transcriptome and the existence of several EST tags. In this study, we identified huntingtin antisense (HTTAS), a natural antisense transcript at the HD repeat locus that contain the repeat tract. HTTAS is 5' capped, poly (A) tailed and contains three exons, alternatively spliced into HTTAS_v1 (exons 1 and 3) and HTTAS_v2 (exons 2 and 3). Exon 1 includes the repeat. HTTAS_v1 has a weak promoter, and is expressed at low levels in multiple tissue types and throughout the brain. Reporter assays indicate that while efficient promoter activity requires a short repeat, repeat expansion reduces promoter efficiency. Consistent with the reporter assays, levels of HTTAS_v1 are reduced in human HD frontal cortex. In cell systems, overexpression of HTTAS_v1 specifically reduces endogenous HTT transcript levels, while siRNA knockdown of HTTAS_v1 increases HTT transcript levels. Minigene constructs of the HD locus confirm the regulatory effect of HTTAS_v1 on HTT, and demonstrate that the effect is dependent on repeat length and is at least partially Dicer dependent. Together, these findings provide strong evidence for the existence of a gene antisense to HTT, with properties that include regulation of HTT expression.
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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.