ArticleEMBO reports2011
miR-31 modulates dystrophin expression: new implications for Duchenne muscular dystrophy therapy.
Article in EMBO reports, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 97 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
97 citing papers in PubMed, 153 citations in OpenAlex.
- Timing matters: Exon skipping therapy is most effective when initiated early in a mouse model of Duchenne muscular dystrophy.Molecular therapy. Nucleic acids · 2026Article
- Emerging roles of microRNAs and other non-coding transcriptome in muscular dystrophies.Inflammation and regeneration · 2026Review
- Myonuclear Domain-Associated and Central Nucleation-Dependent Spatial Restriction of Dystrophin Protein Expression.Journal of cachexia, sarcopenia and muscle · 2026Article
- Local Non-Coding Regulatory Elements in Muscular Dystrophies.International journal of molecular sciences · 2025Review
- Spatiotemporal analysis of dystrophin expression during muscle repair.Skeletal muscle · 2025Article
- MyomiRs Expression in Limb Girdle Muscular Dystrophy.IUBMB life · 2025Review
- Effects of Epicatechin on the Expression of MyomiRs-31, -133, -136, -206, -296, and -486 in the Skeletal Muscle of the Offspring of Obese Mothers.Cell biochemistry and biophysics · 2025Article
- Investigation of urinary miRNA profile changes in amphotericin B-induced nephrotoxicity in C57BL/6 mouse, Sprague-Dawley rats and Beagle dogs.Toxicological sciences : an official journal of the Society of Toxicology · 2025Article
- Functions and Therapeutic Potentials of Long Noncoding RNA in Skeletal Muscle Atrophy and Dystrophy.Journal of cachexia, sarcopenia and muscle · 2025Review
- Deletion of miR-146a enhances therapeutic protein restoration in model of dystrophin exon skipping.Molecular therapy. Nucleic acids · 2024Article
- Why is early-onset atrial fibrillation uncommon in patients with Duchenne muscular dystrophy? Insights from the mdx mouse.Cardiovascular research · 2024Article
- Transcription of microRNAs is regulated by developmental signaling pathways and transcription factors.Frontiers in cell and developmental biology · 2024Article
- Antisense oligonucleotides targeting the miR-29b binding site in the GRN mRNA increase progranulin translation.The Journal of biological chemistry · 2023Article
- Therapeutic approaches for Duchenne muscular dystrophy.Nature reviews. Drug discovery · 2023Review
- Modeling Duchenne Muscular Dystrophy Cardiomyopathy with Patients' Induced Pluripotent Stem-Cell-Derived Cardiomyocytes.International journal of molecular sciences · 2023Review
- miR-31-5p as a Potential Circulating Biomarker and Tracer of Clinical Improvement for Chronic Inflammatory Demyelinating Polyneuropathy.Oxidative medicine and cellular longevity · 2023Article
- Putting the "mi" in omics: discovering miRNA biomarkers for pediatric precision care.Pediatric research · 2023Review
- MFIDMA: A Multiple Information Integration Model for the Prediction of Drug-miRNA Associations.Biology · 2022Article
- MicroRNAs as serum biomarkers in Becker muscular dystrophy.Journal of cellular and molecular medicine · 2022Article
- MicroRNAs in Dystrophinopathy.International journal of molecular sciences · 2022Review
37 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Duchenne muscular dystrophy (DMD)--which is caused by mutations in the dystrophin gene-is one of the most severe myopathies. Among therapeutic strategies, exon skipping allows the rescue of dystrophin synthesis through the production of a shorter but functional messenger RNA. Here, we report the identification of a microRNA--miR-31--that represses dystrophin expression by targeting its 3' untranslated region. In human DMD myoblasts treated with exon skipping, we demonstrate that miR-31 inhibition increases dystrophin rescue. These results indicate that interfering with miR-31 activity can provide an ameliorating strategy for those DMD therapies that are aimed at efficiently recovering dystrophin synthesis.
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What OpenQuestion holds
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.