A stop codon mutation in exon-23 of the dystrophin gene results in dystrophin deficiency. Mouse models with the same mutation are widely used as genetic and biochemical mouse models for DMD . The disease phenotype is mild. Skeletal muscle pathology develops around 3 weeks of age, with muscle weakness by 5-6 weeks. These mice are homozygous, and no genotyping is needed. C57BL/10ScSnJ mice are wild-type controls for this model. We have systematically phenotyped this model at multiple age groups.

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