ArticleThe Journal of cell biology1997
Postsynaptic abnormalities at the neuromuscular junctions of utrophin-deficient mice.
Article in The Journal of cell biology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers.
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Who cites it
73 citing papers in PubMed, 217 citations in OpenAlex.
- Cytoplasmic region of beta-dystroglycan is essential for postsynaptic maturation and neuromuscular function in mice.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Skeletal muscle-specific PGC-1α-b overexpression prevents eccentric contraction-induced muscle injury through an utrophin-independent pathway in mice.Physiological reports · 2026Article
- Integrative phosphoproteomic analysis identifies functional roles of TRPM7 phosphosites in oncogenesis.Frontiers in bioinformatics · 2026Article
- Respiratory pathology in the mdx/utrn -/- mouse: A murine model for Duchenne Muscular Dystrophy (DMD).PloS one · 2025Article
- Upregulation of utrophin improves the phenotype of Duchenne muscular dystrophy hiPSC-derived CMs.Molecular therapy. Nucleic acids · 2024Article
- NMJ-related diseases beyond the congenital myasthenic syndromes.Frontiers in cell and developmental biology · 2023Review
- A genome-wide association study (GWAS) of the personality constructs in CPAI-2 in Taiwanese Hakka populations.PloS one · 2023Article
- Proteins implicated in muscular dystrophy and cancer are functional constituents of the centrosome.Life science alliance · 2022Article
- Distinct roles of the dystrophin-glycoprotein complex: α-dystrobrevin and α-syntrophin in the maintenance of the postsynaptic apparatus of the neuromuscular synapse.Human molecular genetics · 2022Article
- Therapeutic aspects of cell signaling and communication in Duchenne muscular dystrophy.Cellular and molecular life sciences : CMLS · 2021Review
- Improved Bone Quality and Bone Healing of Dystrophic Mice by Parabiosis.Metabolites · 2021Article
- Microutrophin expression in dystrophic mice displays myofiber type differences in therapeutic effects.PLoS genetics · 2020Article
- Recent insights into neuromuscular junction biology in Duchenne muscular dystrophy: Impacts, challenges, and opportunities.EBioMedicine · 2020Review
- The role of the dystrophin glycoprotein complex on the neuromuscular system.Neuroscience letters · 2020Review
- Mouse models for muscular dystrophies: an overview.Disease models & mechanisms · 2020Review
- NAD+ improves neuromuscular development in a zebrafish model of FKRP-associated dystroglycanopathy.Skeletal muscle · 2019Review
- The potential of utrophin and dystrophin combination therapies for Duchenne muscular dystrophy.Human molecular genetics · 2019Article
- Distinct mechanical properties in homologous spectrin-like repeats of utrophin.Scientific reports · 2019Article
- A role for Regulator of G protein Signaling-12 (RGS12) in the balance between myoblast proliferation and differentiation.PloS one · 2019Article
- Utrophin up-regulation by artificial transcription factors induces muscle rescue and impacts the neuromuscular junction in mdx mice.Biochimica et biophysica acta. Molecular basis of disease · 2018Article
13 more citing papers are in PubMed but not listed here.
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
Utrophin is a dystrophin-related cytoskeletal protein expressed in many tissues. It is thought to link F-actin in the internal cytoskeleton to a transmembrane protein complex similar to the dystrophin protein complex (DPC). At the adult neuromuscular junction (NMJ), utrophin is precisely colocalized with acetylcholine receptors (AChRs) and recent studies have suggested a role for utrophin in AChR cluster formation or maintenance during NMJ differentiation. We have disrupted utrophin expression by gene targeting in the mouse. Such mice have no utrophin detectable by Western blotting or immunocytochemistry. Utrophin-deficient mice are healthy and show no signs of weakness. However, their NMJs have reduced numbers of AChRs (alpha-bungarotoxin [alpha-BgTx] binding reduced to approximately 60% normal) and decreased postsynaptic folding, though only minimal electrophysiological changes. Utrophin is thus not essential for AChR clustering at the NMJ but may act as a component of the postsynaptic cytoskeleton, contributing to the development or maintenance of the postsynaptic folds. Defects of utrophin could underlie some forms of congenital myasthenic syndrome in which a reduction of postsynaptic folds is observed.
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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.