Effective rescue of dystrophin improves cardiac function in dystrophin-deficient mice by a modified morpholino oligomer. - Wikidata - wikimedia - TriplyDB

Effective rescue of dystrophin improves cardiac function in dystrophin-deficient mice by a modified morpholino oligomer.

Effective rescue of dystrophin improves cardiac function in dystrophin-deficient mice by a modified morpholino oligomer.

http://www.wikidata.org/entity/Q36897347

about

A chemical view of oligonucleotides for exon skipping and related drug applications Proteomic profiling of the dystrophin-deficient mdx phenocopy of dystrophinopathy-associated cardiomyopathy Antisense oligonucleotides: treating neurodegeneration at the level of RNA Splicing therapy for neuromuscular disease Current understanding of molecular pathology and treatment of cardiomyopathy in duchenne muscular dystrophy Animal models of Duchenne muscular dystrophy: from basic mechanisms to gene therapy Targeted skipping of human dystrophin exons in transgenic mouse model systemically for antisense drug development Silencing disease genes in the laboratory and the clinic Prevention of dystrophic pathology in severely affected dystrophin/utrophin-deficient mice by morpholino-oligomer-mediated exon-skipping.Rescue of severely affected dystrophin/utrophin-deficient mice through scAAV-U7snRNA-mediated exon skipping Prevention of exercised induced cardiomyopathy following Pip-PMO treatment in dystrophic mdx mice.Guanine analogues enhance antisense oligonucleotide-induced exon skipping in dystrophin gene in vitro and in vivo.Long-term improvement in mdx cardiomyopathy after therapy with peptide-conjugated morpholino oligomers.Effects of systemic multiexon skipping with peptide-conjugated morpholinos in the heart of a dog model of Duchenne muscular dystrophy.Context Dependent Effects of Chimeric Peptide Morpholino Conjugates Contribute to Dystrophin Exon-skipping Efficiency Evaluation of Tris[2-(acryloyloxy)ethyl]isocyanurate cross-linked polyethylenimine as antisense morpholino oligomer delivery vehicle in cell culture and dystrophic mdx mice Long-term treatment with naproxcinod significantly improves skeletal and cardiac disease phenotype in the mdx mouse model of dystrophy Octa-guanidine morpholino restores dystrophin expression in cardiac and skeletal muscles and ameliorates pathology in dystrophic mdx mice.Chronic administration of membrane sealant prevents severe cardiac injury and ventricular dilatation in dystrophic dogs.Emerging genetic therapies to treat Duchenne muscular dystrophy Gene and cell-mediated therapies for muscular dystrophy.Proteomic Profiling of the Dystrophin-Deficient MDX Heart Reveals Drastically Altered Levels of Key Metabolic and Contractile Proteins.Gene knockdowns in adult animals: PPMOs and vivo-morpholinos.Splice-correcting oligonucleotides restore BTK function in X-linked agammaglobulinemia model In vivo MRI characterization of progressive cardiac dysfunction in the mdx mouse model of muscular dystrophy.Exon skipping restores dystrophin expression, but fails to prevent disease progression in later stage dystrophic dko mice RNA therapeutics: beyond RNA interference and antisense oligonucleotides.Sildenafil reverses cardiac dysfunction in the mdx mouse model of Duchenne muscular dystrophy.Local in vivo GSK3β knockdown promotes pancreatic β cell and acinar cell regeneration in 90% pancreatectomized rat Anti-tumor activity of splice-switching oligonucleotides.The status of exon skipping as a therapeutic approach to duchenne muscular dystrophy Chronic systemic therapy with low-dose morpholino oligomers ameliorates the pathology and normalizes locomotor behavior in mdx mice.Antisense therapy in neurology One-year treatment of morpholino antisense oligomer improves skeletal and cardiac muscle functions in dystrophic mdx mice.Inhibition of nonsense-mediated mRNA decay by antisense morpholino oligonucleotides restores functional expression of hERG nonsense and frameshift mutations in long-QT syndrome Progress in muscular dystrophy research with special emphasis on gene therapy.Therapeutic approaches to muscular dystrophy.Current status of pharmaceutical and genetic therapeutic approaches to treat DMD.Duchenne muscular dystrophy gene therapy: Lost in translation?Restoring dystrophin expression in duchenne muscular dystrophy muscle progress in exon skipping and stop codon read through.

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P2860

Effective rescue of dystrophin improves cardiac function in dystrophin-deficient mice by a modified morpholino oligomer.

http://www.wikidata.org/entity/Q36897347

description

2008 nî lūn-bûn

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2008年の論文

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2008年論文

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2008年論文

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2008年論文

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2008年論文

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2008年論文

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2008年论文

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2008年论文

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2008年论文

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name

Effective rescue of dystrophin ...... modified morpholino oligomer.

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type

label

Effective rescue of dystrophin ...... modified morpholino oligomer.

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prefLabel

Effective rescue of dystrophin ...... modified morpholino oligomer.

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PNAS.0805676105

P1433

Proceedings of the National Academy of Sciences of the United States of America

P1476

Effective rescue of dystrophin ...... modified morpholino oligomer.

@en

P2093

Alfredo D Guerron

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Arpana Sali

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Bo Wu

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Christopher F Spurney

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Hong M Moulton

http://www.w3.org/2001/XMLSchema#string

Jianbin Li

http://www.w3.org/2001/XMLSchema#string

Jiangang Jiang

http://www.w3.org/2001/XMLSchema#string

Juan Li

http://www.w3.org/2001/XMLSchema#string

Patrick L Iversen

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Peijuan Lu

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P2860

TAT-mediated intracellular delivery of purine nucleoside phosphorylase corrects its deficiency in mice

Cell-penetrating peptides as transporters for morpholino oligomers: effects of amino acid composition on intracellular delivery and cytotoxicity

Morpholino antisense oligomers: design, preparation, and properties

Inhibition of influenza A H3N8 virus infections in mice by morpholino oligomers

Rescue of dystrophic muscle through U7 snRNA-mediated exon skipping

Dystrophin: the protein product of the Duchenne muscular dystrophy locus

Systemic delivery of antisense oligoribonucleotide restores dystrophin expression in body-wide skeletal muscles

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

Systemic delivery of genes to striated muscles using adeno-associated viral vectors.

Very mild muscular dystrophy associated with the deletion of 46% of dystrophin.

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14814-14819

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scholarly article

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10.1073/PNAS.0805676105

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39

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105

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Kanneboyina Nagaraju

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2008-09-19T00:00:00Z

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23269990

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18806224

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2546441

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