ArticlePloS one2012
The DMD locus harbours multiple long non-coding RNAs which orchestrate and control transcription of muscle dystrophin mRNA isoforms.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
39 citing papers in PubMed, 55 citations in OpenAlex.
- Inhibited Differentiation and Growth of Myocyte Associated With Sarcopenia: The Key Role of the lncRNA A430093F15Rik/microRNA-337-3p/Fam168a Pathway.Journal of cellular and molecular medicine · 2026Article
- Local Non-Coding Regulatory Elements in Muscular Dystrophies.International journal of molecular sciences · 2025Review
- Exploring lncRNA-Mediated Mechanisms in Muscle Regulation and Their Implications for Duchenne Muscular Dystrophy.International journal of molecular sciences · 2025Review
- Functions and Therapeutic Potentials of Long Noncoding RNA in Skeletal Muscle Atrophy and Dystrophy.Journal of cachexia, sarcopenia and muscle · 2025Review
- Deletion of exons 45 to 55 in the DMD gene: from the therapeutic perspective to the in vitro model.Skeletal muscle · 2024Article
- Article
- Ion Channels of the Sarcolemma and Intracellular Organelles in Duchenne Muscular Dystrophy: A Role in the Dysregulation of Ion Homeostasis and a Possible Target for Therapy.International journal of molecular sciences · 2023Review
- Dystrophinopathy Phenotypes and Modifying Factors in DMD Exon 45-55 Deletion.Annals of neurology · 2022Article
- Review
- LncRNAs as a new regulator of chronic musculoskeletal disorder.Cell proliferation · 2021Review
- Autism Spectrum Disorder and Duchenne Muscular Dystrophy: A Clinical Case on the Potential Role of the Dystrophin in Autism Neurobiology.Journal of clinical medicine · 2021Article
- Inhibition of lncRNA MAAT Controls Multiple Types of Muscle Atrophy by cis- and trans-Regulatory Actions.Molecular therapy : the journal of the American Society of Gene Therapy · 2021Article
- The lncRNA 44s2 Study Applicability to the Design of 45-55 Exon Skipping Therapeutic Strategy for DMD.Biomedicines · 2021Article
- Myogenesis modelled by human pluripotent stem cells: a multi-omic study of Duchenne myopathy early onset.Journal of cachexia, sarcopenia and muscle · 2021Article
- Noncoding RNAs in Duchenne and Becker muscular dystrophies: role in pathogenesis and future prognostic and therapeutic perspectives.Cellular and molecular life sciences : CMLS · 2020Review
- Premature termination codons in theProceedings of the National Academy of Sciences of the United States of America · 2020Article
- Clinical value of non-coding RNAs in cardiovascular, pulmonary, and muscle diseases.American journal of physiology. Cell physiology · 2020Review
- Functions and Regulatory Mechanisms of lncRNAs in Skeletal Myogenesis, Muscle Disease and Meat Production.Cells · 2019Review
- MicroRNAs and Long Non-coding RNAs in Genetic Diseases.Molecular diagnosis & therapy · 2019Review
- Importance of Long Non-coding RNAs in the Development and Disease of Skeletal Muscle and Cardiovascular Lineages.Frontiers in cell and developmental biology · 2019Review
Corrections and comments
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
Abstract
The 2.2 Mb long dystrophin (DMD) gene, the largest gene in the human genome, corresponds to roughly 0.1% of the entire human DNA sequence. Mutations in this gene cause Duchenne muscular dystrophy and other milder X-linked, recessive dystrophinopathies. Using a custom-made tiling array, specifically designed for the DMD locus, we identified a variety of novel long non-coding RNAs (lncRNAs), both sense and antisense oriented, whose expression profiles mirror that of DMD gene. Importantly, these transcripts are intronic in origin and specifically localized to the nucleus and are transcribed contextually with dystrophin isoforms or primed by MyoD-induced myogenic differentiation. Furthermore, their forced ectopic expression in both human muscle and neuronal cells causes a specific and negative regulation of endogenous dystrophin full length isoforms and significantly down-regulate the activity of a luciferase reporter construct carrying the minimal promoter regions of the muscle dystrophin isoform. Consistent with this apparently repressive role, we found that, in muscle samples of dystrophinopathic female carriers, lncRNAs expression levels inversely correlate with those of muscle full length DMD isoforms. Overall these findings unveil an unprecedented complexity of the transcriptional pattern of the DMD locus and reveal that DMD lncRNAs may contribute to the orchestration and homeostasis of the muscle dystrophin expression pattern by either selective targeting and down-modulating the dystrophin promoter transcriptional activity.
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Registered trials
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