In-frame Dystrophin Following Exon 51-Skipping Improves Muscle Pathology and Function in the Exon 52–Deficient mdx Mouse-Reference-Cited by-同舟云学术

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In-frame Dystrophin Following Exon 51-Skipping Improves Muscle Pathology and Function in the Exon 52–Deficient mdx Mouse

Published:2010-11 Issue:11 Volume:18 Page:1995-2005
ISSN:1525-0016
Container-title:Molecular Therapy
language:en
Short-container-title:Molecular Therapy

Author:

Aoki Yoshitsugu,Nakamura Akinori,Yokota Toshifumi,Saito Takashi,Okazawa Hitoshi,Nagata Tetsuya,Takeda Shin'ichi

Publisher

Elsevier BV

Subject

Drug Discovery,Pharmacology,Genetics,Molecular Biology,Molecular Medicine

Reference51 articles.

1. Dystrophin: the protein product of the Duchenne muscular dystrophy locus;Hoffman;Cell,1987

2. An explanation for the phenotypic differences between patients bearing partial deletions of the DMD locus;Monaco;Genomics,1988

3. Antisense oligonucleotide-induced exon skipping across the human dystrophin gene transcript;Wilton;Mol Ther,2007

4. Targeted exon skipping as a potential gene correction therapy for Duchenne muscular dystrophy;Aartsma-Rus;Neuromuscul Disord,2002

5. Exon skipping during splicing of dystrophin mRNA precursor due to an intraexon deletion in the dystrophin gene of Duchenne muscular dystrophy kobe;Matsuo;J Clin Invest,1991

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2. Phase I/II Trial of Brogidirsen: Dual-Targeting Antisense Oligonucleotides for Exon 44 Skipping in Duchenne Muscular Dystrophy;2024-08-30

3. Establishment of a Triple Quadrupole HPLC-MS Quantitation Method for Dystrophin Protein in Mouse and Human Skeletal Muscle;International Journal of Molecular Sciences;2023-12-25

4. Exon 44 skipping in Duchenne muscular dystrophy: NS-089/NCNP-02, a dual-targeting antisense oligonucleotide;Molecular Therapy - Nucleic Acids;2023-12

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