ArticleProceedings of the National Academy of Sciences of the United States of America2014
Microtubule binding distinguishes dystrophin from utrophin.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 99 papers, 1 of them a synthesis that pooled it.
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Who cites it
99 citing papers in PubMed, 1 synthesis or guideline pooled it, 152 citations in OpenAlex.
- Muscle and cardiac therapeutic strategies for Duchenne muscular dystrophy: past, present, and future.Pharmacological reports : PR · 2020Pooled it
- 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
- Weak protein-bicelle binding quantification via surface-based DNA nanolevers.European biophysics journal : EBJ · 2026Article
- Dystrophins DP71 and DP427 determine cell viability during proliferation and myofibre differentiation.Cell death & disease · 2026Article
- Deaths in gene therapy of Duchenne muscular dystrophy and other diseases: Underlying mechanisms and mitigating strategies.Molecular therapy : the journal of the American Society of Gene Therapy · 2026Review
- Myonuclear Domain-Associated and Central Nucleation-Dependent Spatial Restriction of Dystrophin Protein Expression.Journal of cachexia, sarcopenia and muscle · 2026Article
- Multiple modes of AFM reveal distinct mechanical properties for dystrophin and utrophin not manifest by small fragments.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Embedding muscle fibers in hydrogel improves viability and preserves contractile function during prolonged ex vivo culture.The Journal of general physiology · 2026Article
- (Z)-Endoxifen as a Potential Modulator of Utrophin Pathways in Duchenne Muscular Dystrophy: A Mechanistic and Transcriptomic Perspective.Degenerative neurological and neuromuscular disease · 2026Review
- Intrinsic dysfunction in muscle stem cells lacking dystrophin begins during secondary myogenesis.Nature communications · 2025Article
- Bidirectional role of Costameres in the pathophysiology of mdx skeletal muscles.Human molecular genetics · 2025Article
- Review
- Embedding muscle fibers in hydrogel improves viability and preserves contractile function during prolongedbioRxiv : the preprint server for biology · 2025Article
- Advances in Duchenne Muscular Dystrophy: Diagnostic Techniques and Dystrophin Domain Insights.International journal of molecular sciences · 2025Review
- Histone deacetylase 6 inhibition promotes microtubule acetylation and facilitates autophagosome-lysosome fusion in dystrophin-deficient mdx mice.Acta physiologica (Oxford, England) · 2025Article
- The Dystrophin-Dystroglycan complex ensures cytokinesis efficiency in Drosophila epithelia.EMBO reports · 2025Article
- Coupling of Spectrin Repeat Modules for the Assembly of Nanorods and Presentation of Protein Domains.ACS nano · 2024Article
- Review
- Decreasing microtubule detyrosination modulates Nav1.5 subcellular distribution and restores sodium current in mdx cardiomyocytes.Cardiovascular research · 2024Article
39 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 3 countries.
Funding
Abstract
Dystrophin and utrophin are highly similar proteins that both link cortical actin filaments with a complex of sarcolemmal glycoproteins, yet localize to different subcellular domains within normal muscle cells. In mdx mice and Duchenne muscular dystrophy patients, dystrophin is lacking and utrophin is consequently up-regulated and redistributed to locations normally occupied by dystrophin. Transgenic overexpression of utrophin has been shown to significantly improve aspects of the disease phenotype in the mdx mouse; therefore, utrophin up-regulation is under intense investigation as a potential therapy for Duchenne muscular dystrophy. Here we biochemically compared the previously documented microtubule binding activity of dystrophin with utrophin and analyzed several transgenic mouse models to identify phenotypes of the mdx mouse that remain despite transgenic utrophin overexpression. Our in vitro analyses revealed that dystrophin binds microtubules with high affinity and pauses microtubule polymerization, whereas utrophin has no activity in either assay. We also found that transgenic utrophin overexpression does not correct subsarcolemmal microtubule lattice disorganization, loss of torque production after in vivo eccentric contractions, or physical inactivity after mild exercise. Finally, our data suggest that exercise-induced inactivity correlates with loss of sarcolemmal neuronal NOS localization in mdx muscle, whereas loss of in vivo torque production after eccentric contraction-induced injury is associated with microtubule lattice disorganization.
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