ArticleRNA biology2017
Antisense transcription of the myotonic dystrophy locus yields low-abundant RNAs with and without (CAG)n repeat.
Article in RNA biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 31 citations in OpenAlex.
- RNA cargo profiling of muscle extracellular vesicles identifies candidate biomarkers of disease activity and muscle degeneration in FSHD.Journal of translational medicine · 2026Article
- Short CAG repeat variation as a regulatory factor in health and disease.Frontiers in genetics · 2026Review
- Local Non-Coding Regulatory Elements in Muscular Dystrophies.International journal of molecular sciences · 2025Review
- Multisystem Symptoms in Myotonic Dystrophy Type 1: A Management and Therapeutic Perspective.International journal of molecular sciences · 2025Review
- Comparative Analysis of Splicing Alterations in Three Muscular Dystrophies.Biomedicines · 2025Article
- RNA gain-of-function mechanisms in short tandem repeat diseases.RNA (New York, N.Y.) · 2025Review
- RNA dysregulation in neurodegenerative diseases.The EMBO journal · 2025Review
- Transcriptome changes in DM1 patients' tissues are governed by the RNA interference pathway.Frontiers in molecular biosciences · 2022Article
- Characterization of RAN Translation and Antisense Transcription in Primary Cell Cultures of Patients with Myotonic Dystrophy Type 1.Journal of clinical medicine · 2021Article
- RNA Targeting in Inherited Neuromuscular Disorders: Novel Therapeutic Strategies to Counteract Mis-Splicing.Cells · 2021Review
- Transcriptome Analysis in a Primary Human Muscle Cell Differentiation Model for Myotonic Dystrophy Type 1.International journal of molecular sciences · 2021Article
- Regulatory Potential of Competing Endogenous RNAs in Myotonic Dystrophies.International journal of molecular sciences · 2021Review
- Brain Pathogenesis and Potential Therapeutic Strategies in Myotonic Dystrophy Type 1.Frontiers in aging neuroscience · 2021Review
- The Biomarker Potential of miRNAs in Myotonic Dystrophy Type I.Journal of clinical medicine · 2020Review
- HNRNPA1-induced spliceopathy in a transgenic mouse model of myotonic dystrophy.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Intrinsic Myogenic Potential of Skeletal Muscle-Derived Pericytes from Patients with Myotonic Dystrophy Type 1.Molecular therapy. Methods & clinical development · 2019Article
- CRISPR/Cas Applications in Myotonic Dystrophy: Expanding Opportunities.International journal of molecular sciences · 2019Review
- Therapeutic Genome Editing for Myotonic Dystrophy Type 1 Using CRISPR/Cas9.Molecular therapy : the journal of the American Society of Gene Therapy · 2018Article
- Quantitative Methods to Monitor RNA Biomarkers in Myotonic Dystrophy.Scientific reports · 2018Article
- Oligonucleotides targeting TCF4 triplet repeat expansion inhibit RNA foci and mis-splicing in Fuchs' dystrophy.Human molecular genetics · 2018Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
The unstable (CTG·CAG)n trinucleotide repeat in the myotonic dystrophy type 1 (DM1) locus is bidirectionally transcribed from genes with terminal overlap. By transcription in the sense direction, the DMPK gene produces various alternatively spliced mRNAs with a (CUG)n repeat in their 3' UTR. Expression in opposite orientation reportedly yields (CAG)n-repeat containing RNA, but both structure and biologic significance of this antisense gene (DM1-AS) are largely unknown. Via a combinatorial approach of computational and experimental analyses of RNA from unaffected individuals and DM1 patients we discovered that DM1-AS spans >6 kb, contains alternative transcription start sites and uses alternative polyadenylation sites up- and downstream of the (CAG)n repeat. Moreover, its primary transcripts undergo alternative splicing, whereby the (CAG)n segment is removed as part of an intron. Thus, in patients a mixture of DM1-AS RNAs with and without expanded (CAG)n repeat are produced. DM1-AS expression appears upregulated in patients, but transcript abundance remains very low in all tissues analyzed. Our data suggest that DM1-AS transcripts belong to the class of long non-coding RNAs. These and other biologically relevant implications for how (CAG)n-expanded transcripts may contribute to DM1 pathology can now be explored experimentally.
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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.