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Fig. 6 | Molecular Medicine

Fig. 6

From: OTC intron 4 variations mediate pathogenic splicing patterns caused by the c.386G>A mutation in humans and spfash mice, and govern susceptibility to RNA-based therapies

Fig. 6

Cross-activity of the human and mouse tailored U1snRNAs. A Pre-mRNA sequences of the human and mouse OTC exon 4 exon–intron junctions, with exonic and intronic nucleotides in upper and lower cases, respectively. The regions targeted by the 5′ tail of the modified U1snRNAs are reported (solid line). The c.386G>A change is indicated in bold. B The bar plots report the splicing patterns in HepG2 or Hepa1-6 transiently transfected with the OTC-386Ah (left) or OTC-386Am (right) minigenes, respectively, and challenged with the U1 variants. Bar plots indicate the relative percentage of each transcript, and results are expressed as mean ± SD from three independent experiments

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