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Journal ArticleDOI

Targeted exon skipping as a potential gene correction therapy for Duchenne muscular dystrophy.

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TLDR
This study has identified antisense oligoribonucleotides with which the skipping of 11 other Duchenne muscular dystrophy exons could be induced in cultured human muscle cells and would allow correction of over 50% of deletions and 22% of duplications reported in the Leiden DMD-mutation Database.
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This article is published in Neuromuscular Disorders.The article was published on 2002-10-01. It has received 231 citations till now. The article focuses on the topics: Exon skipping & Duchenne muscular dystrophy.

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Citations
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Journal ArticleDOI

Dystrophin and mutations: one gene, several proteins, multiple phenotypes

TL;DR: Current understanding of the genotype-phenotype relation for mutations in the dystrophin gene and their implications for gene functions are focused on.
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Local Dystrophin Restoration with Antisense Oligonucleotide PRO051

TL;DR: Intramuscular injection of antisense oligonucleotide PRO051 induced dystrophin synthesis in four patients with Duchenne's muscular dystrophy who had suitable mutations, suggesting that further studies might be feasible.
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Systemic delivery of morpholino oligonucleotide restores dystrophin expression bodywide and improves dystrophic pathology

TL;DR: It is shown that weekly intravenous injections of morpholino phosphorodiamidate (morpholino) AONs induce expression of functional levels of dystrophin in body-wide skeletal muscles of the dystrophic mdx mouse, with resulting improvement in muscle function.
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Antisense oligonucleotides: the next frontier for treatment of neurological disorders

TL;DR: With the rapid development of improved next-generation ASOs toward clinical application, this technology now holds the potential to have a dramatic effect on the treatment of many neurological conditions in the near future.
References
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Journal ArticleDOI

Dystrophin: The protein product of the duchenne muscular dystrophy locus

TL;DR: The identification of the mdx mouse as an animal model for DMD has important implications with regard to the etiology of the lethal DMD phenotype, and the protein dystrophin is named because of its identification via the isolation of the Duchenne muscular dystrophy locus.
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Expanded sequence dependence of thermodynamic parameters improves prediction of RNA secondary structure.

TL;DR: An improved dynamic programming algorithm is reported for RNA secondary structure prediction by free energy minimization and experimental constraints, derived from enzymatic and flavin mononucleotide cleavage, improve the accuracy of structure predictions.
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The Complete Sequence of Dystrophin Predicts a Rod-Shaped Cytoskeletal Protein

TL;DR: The complete sequence of the human Duchenne muscular dystrophy cDNA has been determined and dystrophin shares many features with the cytoskeletal protein spectrin and alpha-actinin and is likely to adopt a rod shape about 150 nm in length.
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Membrane organization of the dystrophin-glycoprotein complex

TL;DR: It is demonstrated that dystrophin and its 59 kd associated protein are cytoskeletal elements that are tightly linked to a 156 kd extracellular glycoprotein by way of a complex of transmembrane proteins.
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The molecular basis of muscular dystrophy in the mdx mouse: a point mutation

TL;DR: Sequence analysis of the amplification products showed that the mdx mouse has a single base substitution within an exon, which causes premature termination of the polypeptide chain.
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