ArticleNucleic acids research2014
Converging pathways involving microRNA-206 and the RNA-binding protein KSRP control post-transcriptionally utrophin A expression in skeletal muscle.
Article in Nucleic acids research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 29 citations in OpenAlex.
- CRISPR-Cas9-mediated upregulation of utrophin ameliorates Duchenne muscular dystrophy.Molecular therapy : the journal of the American Society of Gene Therapy · 2026Article
- The miR-206-3p/Cpeb1 axis delays acetylcholine receptor degradation and preserves neuromuscular junction stability in denervation-induced muscle atrophy.Cellular and molecular life sciences : CMLS · 2026Article
- The RNA-Binding Protein KSRP Is a Negative Regulator of Innate Immunity.Biomolecules · 2025Review
- RNA signaling in skeletal muscle: the central role of microRNAs and exosomal microRNAs.Frontiers in cell and developmental biology · 2025Review
- Regulation of miR-206 in denervated and dystrophic muscles, and its effect on acetylcholine receptor clustering.Journal of cell science · 2024Article
- The Role of KH-Type Splicing Regulatory Protein (KSRP) for Immune Functions and Tumorigenesis.Cells · 2022Review
- Poly C Binding Protein 2 dependent nuclear retention of the utrophin-A mRNA in C2C12 cells.RNA biology · 2021Article
- Targeting IRES-dependent translation as a novel approach for treating Duchenne muscular dystrophy.RNA biology · 2021Review
- HDAC inhibitors tune miRNAs in extracellular vesicles of dystrophic muscle-resident mesenchymal cells.EMBO reports · 2020Article
- High-throughput identification of post-transcriptional utrophin up-regulators for Duchenne muscle dystrophy (DMD) therapy.Scientific reports · 2020Article
- miR-424 Promotes Bovine Adipogenesis Through an Unconventional Post-Transcriptional Regulation ofFrontiers in genetics · 2020Article
- Circulating microRNAs as potential biomarkers and therapeutic targets in spinal muscular atrophy.Therapeutic advances in neurological disorders · 2020Review
- Review
- Embryonic myosin is a regeneration marker to monitor utrophin-based therapies for DMD.Human molecular genetics · 2019Article
- MicroRNA-17-92 regulates myoblast proliferation and differentiation by targeting the ENH1/Id1 signaling axis.Cell death and differentiation · 2016Article
- Tadalafil Treatment Delays the Onset of Cardiomyopathy in Dystrophin-Deficient Hearts.Journal of the American Heart Association · 2016Article
- Competing Interactions of RNA-Binding Proteins, MicroRNAs, and Their Targets Control Neuronal Development and Function.Biomolecules · 2015Review
- Roles of the canonical myomiRs miR-1, -133 and -206 in cell development and disease.World journal of biological chemistry · 2015Review
- HuR Mediates Changes in the Stability of AChR β-Subunit mRNAs after Skeletal Muscle Denervation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- MiR-206, a key modulator of skeletal muscle development and disease.International journal of biological sciences · 2015Review
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Several reports have previously highlighted the potential role of miR-206 in the post-transcriptional downregulation of utrophin A in cultured cells. Along those lines, we recently identified K-homology splicing regulator protein (KSRP) as an important negative regulator in the post-transcriptional control of utrophin A in skeletal muscle. We sought to determine whether these two pathways act together to downregulate utrophin A expression in skeletal muscle. Surprisingly, we discovered that miR-206 overexpression in cultured cells and dystrophic muscle fibers causes upregulation of endogenous utrophin A levels. We further show that this upregulation of utrophin A results from the binding of miR-206 to conserved sites located in the 3'-UTR (untranslated region) of KSRP, thus causing the subsequent inhibition of KSRP expression. This miR-206-mediated decrease in KSRP levels leads, in turn, to an increase in the expression of utrophin A due to a reduction in the activity of this destabilizing RNA-binding protein. Our work shows that miR-206 can oscillate between direct repression of utrophin A expression via its 3'-UTR and activation of its expression through decreased availability of KSRP and interactions with AU-rich elements located within the 3'-UTR of utrophin A. Our study thus reveals that two apparent negative post-transcriptional pathways can act distinctively as molecular switches causing repression or activation of utrophin A expression.
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