ArticleMolecular biology of the cell2002
Utrophin binds laterally along actin filaments and can couple costameric actin with sarcolemma when overexpressed in dystrophin-deficient muscle.
Article in Molecular biology of the cell, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
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Who cites it
52 citing papers in PubMed, 100 citations in OpenAlex.
- The atomic structure of human dystrophin spectrin-like repeat 24.Acta crystallographica. Section F, Structural biology communications · 2026Article
- Bidirectional role of Costameres in the pathophysiology of mdx skeletal muscles.Human molecular genetics · 2025Article
- Review
- Evolution and developmental functions of the dystrophin-associated protein complex: beyond the idea of a muscle-specific cell adhesion complex.Frontiers in cell and developmental biology · 2023Review
- Dystrophin involvement in peripheral circadian SRF signalling.Life science alliance · 2021Article
- Ixazomib, an oral proteasome inhibitor, exhibits potential effect in dystrophin-deficient mdx mice.International journal of experimental pathology · 2021Article
- Variable cytoplasmic actin expression impacts the sensitivity of different dystrophin-deficient mdx skeletal muscles to eccentric contraction.The FEBS journal · 2019Article
- The utrophin-beta 2 syntrophin complex regulates adipocyte lipid droplet size independent of adipogenesis.Molecular and cellular biochemistry · 2019Article
- Protein disulfide isomerase as a prosurvival factor in cell therapy for muscular and vascular diseases.Stem cell research & therapy · 2018Article
- Article
- Disease-proportional proteasomal degradation of missense dystrophins.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Inhibition of muscle fibrosis results in increases in both utrophin levels and the number of revertant myofibers in Duchenne muscular dystrophy.Oncotarget · 2015Article
- Creatine kinase B is necessary to limit myoblast fusion during myogenesis.American journal of physiology. Cell physiology · 2015Article
- Microtubule binding distinguishes dystrophin from utrophin.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Calpain-mediated proteolysis of tropomodulin isoforms leads to thin filament elongation in dystrophic skeletal muscle.Molecular biology of the cell · 2014Article
- An ex vivo gene therapy approach to treat muscular dystrophy using inducible pluripotent stem cells.Nature communications · 2013Article
- Impacts of dystrophin and utrophin domains on actin structural dynamics: implications for therapeutic design.Journal of molecular biology · 2012Article
- Thermodynamic stability, unfolding kinetics, and aggregation of the N-terminal actin-binding domains of utrophin and dystrophin.Proteins · 2012Article
- Adaptive strength gains in dystrophic muscle exposed to repeated bouts of eccentric contraction.Journal of applied physiology (Bethesda, Md. : 1985) · 2011Article
- Large-scale opening of utrophin's tandem calponin homology (CH) domains upon actin binding by an induced-fit mechanism.Proceedings of the National Academy of Sciences of the United States of America · 2011Article
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
Dystrophin is widely thought to mechanically link the cortical cytoskeleton with the muscle sarcolemma. Although the dystrophin homolog utrophin can functionally compensate for dystrophin in mice, recent studies question whether utrophin can bind laterally along actin filaments and anchor filaments to the sarcolemma. Herein, we have expressed full-length recombinant utrophin and show that the purified protein is fully soluble with a native molecular weight and molecular dimensions indicative of monomers. We demonstrate that like dystrophin, utrophin can form an extensive lateral association with actin filaments and protect actin filaments from depolymerization in vitro. However, utrophin binds laterally along actin filaments through contribution of acidic spectrin-like repeats rather than the cluster of basic repeats used by dystrophin. We also show that the defective linkage between costameric actin filaments and the sarcolemma in dystrophin-deficient mdx muscle is rescued by overexpression of utrophin. Our results demonstrate that utrophin and dystrophin are functionally interchangeable actin binding proteins, but that the molecular epitopes important for filament binding differ between the two proteins. More generally, our results raise the possibility that spectrin-like repeats may enable some members of the plakin family of cytolinkers to laterally bind and stabilize actin filaments.
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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.