Morpholino oligomer-mediated exon skipping averts the onset of dystrophic pathology in the mdx mouse (Q80501077)

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1 January 2020

title

Morpholino oligomer-mediated exon skipping averts the onset of dystrophic pathology in the mdx mouse (English)

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1 January 2020

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Patrick L Iversen

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author name string

Kaite Honeyman

2

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Abbie M Fall

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Penny L Harding

4

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Russell D Johnsen

5

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Joshua P Steinhaus

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Hong M Moulton

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Stephen D Wilton

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publication date

19 June 2007

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volume

15

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issue

9

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page(s)

1587-1592

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RNA splicing manipulation: strategies to modify gene expression for a variety of therapeutic outcomes.

1 January 2020

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Massive idiosyncratic exon skipping corrects the nonsense mutation in dystrophic mouse muscle and produces functional revertant fibers by clonal expansion

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Revertant fibres: a possible genetic therapy for Duchenne muscular dystrophy?

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Immunohistological evidence for second or somatic mutations as the underlying cause of dystrophin expression by isolated fibres in Xp21 muscular dystrophy of Duchenne-type severity

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Comparative analysis of antisense oligonucleotide analogs for targeted DMD exon 46 skipping in muscle cells

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Dystrophin expression in the mdx mouse after localised and systemic administration of a morpholino antisense oligonucleotide

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Terminal antisense oligonucleotide modifications can enhance induced exon skipping

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Morpholino antisense oligonucleotide induced dystrophin exon 23 skipping in mdx mouse muscle.

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Systemic delivery of morpholino oligonucleotide restores dystrophin expression bodywide and improves dystrophic pathology

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Functional amounts of dystrophin produced by skipping the mutated exon in the mdx dystrophic mouse

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Muscular weakness in the mdx mouse

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Vectorization of morpholino oligomers by the (R-Ahx-R)4 peptide allows efficient splicing correction in the absence of endosomolytic agents.

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Antisense oligonucleotide-induced exon skipping restores dystrophin expression in vitro in a canine model of DMD.

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X chromosome-linked muscular dystrophy (mdx) in the mouse

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Identifiers

DOI

10.1038/SJ.MT.6300245

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1 January 2020

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