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A dystrophic Duchenne mouse model for testing human antisense oligonucleotides

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By Marcel Veltrop, Laura van Vliet, Margriet Hulsker, Jill Claassens
| PLOS
Duchenne muscular dystrophy (DMD) is a severe muscle-wasting disease generally caused by reading frame disrupting mutations in the DMD gene resulting in loss of functional dystrophin protein. The reading frame can be restored by antisense oligonucleotide (AON)-mediated exon skipping, allowing production of internally deleted, but partially functional dystrophin proteins as found in the less severe Becker muscular dystrophy.
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