ArticlePloS one2011
Translational regulation of utrophin by miRNAs.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 49 citations in OpenAlex.
- Duchenne muscular dystrophy: from gene to gene-ius therapies.Skeletal muscle · 2026Review
- CRISPR-Cas9-mediated upregulation of utrophin ameliorates Duchenne muscular dystrophy.Molecular therapy : the journal of the American Society of Gene Therapy · 2026Article
- Emerging roles of microRNAs and other non-coding transcriptome in muscular dystrophies.Inflammation and regeneration · 2026Review
- On RNA-programmable gene modulation as a versatile set of principles targeting muscular dystrophies.Molecular therapy : the journal of the American Society of Gene Therapy · 2024Review
- IL-1β Induces Human Endothelial Surface Expression of IL-15 by Relieving let-7c-3p Suppression of Protein Translation.Journal of immunology (Baltimore, Md. : 1950) · 2024Article
- Therapeutic approaches for Duchenne muscular dystrophy.Nature reviews. Drug discovery · 2023Review
- Promising therapeutic approaches of utrophin replacing dystrophin in the treatment of Duchenne muscular dystrophy.Fundamental research · 2022Review
- MicroRNAs in Dystrophinopathy.International journal of molecular sciences · 2022Review
- Poly C Binding Protein 2 dependent nuclear retention of the utrophin-A mRNA in C2C12 cells.RNA biology · 2021Article
- Utrophin modulator drugs as potential therapies for Duchenne and Becker muscular dystrophies.Neuropathology and applied neurobiology · 2021Article
- Targeting IRES-dependent translation as a novel approach for treating Duchenne muscular dystrophy.RNA biology · 2021Review
- PMO-based let-7c site blocking oligonucleotide (SBO) mediated utrophin upregulation in mdx mice, a therapeutic approach for Duchenne muscular dystrophy (DMD).Scientific reports · 2020Article
- Genome Editing-Mediated Utrophin Upregulation in Duchenne Muscular Dystrophy Stem Cells.Molecular therapy. Nucleic acids · 2020Article
- Noncoding RNAs in Duchenne and Becker muscular dystrophies: role in pathogenesis and future prognostic and therapeutic perspectives.Cellular and molecular life sciences : CMLS · 2020Review
- Identification of therapeutics that target eEF1A2 and upregulate utrophin A translation in dystrophic muscles.Nature communications · 2020Article
- High-throughput identification of post-transcriptional utrophin up-regulators for Duchenne muscle dystrophy (DMD) therapy.Scientific reports · 2020Article
- 6-Bromoindirubin-3'-oxime intercepts GSK3 signaling to promote and enhance skeletal muscle differentiation affecting miR-206 expression in mice.Scientific reports · 2019Article
- Repression-free utrophin-A 5'UTR variants.Molecular biology research communications · 2019Article
- sPIF promotes myoblast differentiation and utrophin expression while inhibiting fibrosis in Duchenne muscular dystrophy via the H19/miR-675/let-7 and miR-21 pathways.Cell death & disease · 2019Article
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Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundUtrophin is the autosomal homolog of dystrophin, the product of the Duchenne Muscular Dystrophy (DMD) locus. Its regulation is of therapeutic interest as its overexpression can compensate for dystrophin's absence in animal models of DMD. The tissue distribution and transcriptional regulation of utrophin have been characterized extensively, and more recently translational control mechanisms that may underlie its complex expression patterns have begun to be identified. METHODOLOGY/PRINCIPAL
findingsUsing a variety of bioinformatic, molecular and cell biology techniques, we show that the muscle isoform utrophin-A is predominantly suppressed at the translational level in C2C12 myoblasts. The extent of translational inhibition is estimated to be ~99% in C2C12 cells and is mediated by both the 5'- and 3'-UTRs of the utrophin-A mRNA. In this study we identify five miRNAs (let-7c, miR-150, miR-196b, miR-296-5p, miR-133b) that mediate the repression, and confirm repression by the previously identified miR-206. We demonstrate that this translational repression can be overcome by blocking the actions of miRNAs, resulting in an increased level of utrophin protein in C2C12 cells. CONCLUSIONS/SIGNIFICANCE: The present study has identified key inhibitory mechanisms featuring miRNAs that regulate utrophin expression, and demonstrated that these mechanisms can be targeted to increase endogenous utrophin expression in cultured muscle cells. We suggest that miRNA-mediated inhibitory mechanisms could be targeted by methods similar to those described here as a novel strategy to increase utrophin expression as a therapy for DMD.
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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.