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• W2172287346 startingPage "871" @default.
• W2172287346 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." @default.
• W2172287346 created "2016-06-24" @default.
• W2172287346 creator A5018912234 @default.
• W2172287346 creator A5079314793 @default.
• W2172287346 creator A5091813085 @default.
• W2172287346 date "1997-02-24" @default.
• W2172287346 modified "2023-09-26" @default.
• W2172287346 title "Subtle Neuromuscular Defects in Utrophin-deficient Mice" @default.
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• W2172287346 doi "https://doi.org/10.1083/jcb.136.4.871" @default.
• W2172287346 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2132496" @default.
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• W2172287346 hasPublicationYear "1997" @default.
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