Targeted disruption of exon 52 in the mouse dystrophin gene induced muscle degeneration similar to that observed in Duchenne muscular dystrophy.

@article{Araki1997TargetedDO,
  title={Targeted disruption of exon 52 in the mouse dystrophin gene induced muscle degeneration similar to that observed in Duchenne muscular dystrophy.},
  author={E. Araki and K. Nakamura and K. Nakao and S. Kameya and O. Kobayashi and I. Nonaka and T. Kobayashi and M. Katsuki},
  journal={Biochemical and biophysical research communications},
  year={1997},
  volume={238 2},
  pages={
          492-7
        }
}
Duchenne muscular dystrophy (DMD) is a degenerative disorder of the skeletal muscle in human and is caused by mutations in the dystrophin gene. The mdx mouse is a spontaneous mutant and an animal model for DMD. It has a point mutation in exon 23 of the dystrophin gene that eliminates the expression of dystrophin. However, this mutation does not disrupt the expression of four other shorter isoforms that are also expressed from the dystrophin gene through differential promoter usage. We generated… Expand
A dystrophic Duchenne mouse model for testing human antisense oligonucleotides
In-frame dystrophin following exon 51-skipping improves muscle pathology and function in the exon 52-deficient mdx mouse.
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