Title : Antisense oligonucleotide induced dystrophin exon 45 skipping at a low half-maximal effective concentration in a cell-free splicing system.

Pub. Date : 2011 Oct

PMID : 21967521






1 Functional Relationships(s)
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1 Antisense oligonucleotides (AOs) can facilitate the expression of internally deleted dystrophin in dystrophin-deficient Duchenne muscular dystrophy (DMD) by correcting the reading frame of the pre-mRNA with AO-mediated exon skipping. Oligonucleotides, Antisense dystrophin Homo sapiens