ArticleThe Journal of cell biology1997
Subtle neuromuscular defects in 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 68 papers.
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Who cites it
68 citing papers in PubMed, 212 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
- SH3BP2 deficiency in skeletal muscle leads to neuromuscular junction abnormalities and decreased muscle strength.Frontiers in molecular neuroscience · 2026Article
- 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
- 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
- Post-synaptic specialization of the neuromuscular junction: junctional folds formation, function, and disorders.Cell & bioscience · 2022Review
- 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
- Vezatin is required for the maturation of the neuromuscular synapse.Molecular biology of the cell · 2019Article
- Distinct mechanical properties in homologous spectrin-like repeats of utrophin.Scientific reports · 2019Article
- Alternative utrophin mRNAs contribute to phenotypic differences between dystrophin-deficient mice and Duchenne muscular dystrophy.FEBS letters · 2018Article
- Spatial distribution and molecular dynamics of dystrophin glycoprotein components at the neuromuscular junctionJournal of cell science · 2017Article
- From pluripotency to myogenesis: a multistep process in the dish.Journal of muscle research and cell motility · 2015Review
- VEGF induces stress fiber formation in fibroblasts isolated from dystrophic muscle.Journal of cell communication and signaling · 2015Article
- DNA methylation changes in the placenta are associated with fetal manganese exposure.Reproductive toxicology (Elmsford, N.Y.) · 2015Article
- Nonmechanical Roles of Dystrophin and Associated Proteins in Exercise, Neuromuscular Junctions, and Brains.Brain sciences · 2015Article
- Utrophin regulates modal gating of mechanosensitive ion channels in dystrophic skeletal muscle.The Journal of physiology · 2014Article
- Role of exercise in maintaining the integrity of the neuromuscular junction.Muscle & nerve · 2014Review
- Post-natal induction of PGC-1α protects against severe muscle dystrophy independently of utrophin.Skeletal muscle · 2014Article
- VBP15, a novel anti-inflammatory and membrane-stabilizer, improves muscular dystrophy without side effects.EMBO molecular medicine · 2013Article
8 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Utrophin is a large cytoskeletal protein that is homologous to dystrophin, the protein mutated in Duchenne and Becker muscular dystrophy. In skeletal muscle, dystrophin is broadly distributed along the sarcolemma whereas utrophin is concentrated at the neuromuscular junction. This differential localization, along with studies on cultured cells, led to the suggestion that utrophin is required for synaptic differentiation. In addition, utrophin is present in numerous nonmuscle cells, suggesting that it may have a more generalized role in the maintenance of cellular integrity. To test these hypotheses we generated and characterized utrophin-deficient mutant mice. These mutant mice were normal in appearance and behavior and showed no obvious defects in muscle or nonmuscle tissue. Detailed analysis, however, revealed that the density of acetylcholine receptors and the number of junctional folds were reduced at the neuromuscular junctions in utrophin-deficient skeletal muscle. Despite these subtle derangements, the overall structure of the mutant synapse was qualitatively normal, and the specialized characteristics of the dystrophin-associated protein complex were preserved at the mutant neuromuscular junction. These results point to a predominant role for other molecules in the differentiation and maintenance of the postsynaptic membrane.
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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.