Developed by Dr. Takeda’s group at NCNP, Japan, the MDX-23 mutation does not disrupt the expression of four other shorter isoforms that are also expressed from the dystrophin gene through differential promoter usage. The skeletal muscles are hypertrophic, and the muscles exhibit variations in fiber size, with evidence of necrosis and regeneration. C57BL/6 mice are the wild-type controls for this model.

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