Therapeutic potential of antisense oligonucleotides as modulators of alternative splicing
J. Clin. Invest. Peter Sazani, et al. 112:481 doi:10.1172/JCI19547 [Go to this article.]

Figure 1
Modification of splicing by antisense oligonucleotides. Aberrant splicing in thalassemic β-globin pre-mRNA or in certain splice mutants in CFTR is prevented, and correct splicing is restored, by oligonucleotides (dark red bars) that block aberrant 5′ or 3′ cryptic splice sites (a). Similarly, oligonucleotides induce skipping of a normal exon (gray) (b) or force selection of an alternative 5′ splice site (c) by antisense oligonucleotides targeted to appropriate splice sites.