Antisense-induced multiexon skipping for Duchenne muscular dystrophy makes more sense. - Wikidata - awgldk - TriplyDB

Antisense-induced multiexon skipping for Duchenne muscular dystrophy makes more sense.

Antisense-induced multiexon skipping for Duchenne muscular dystrophy makes more sense.

http://www.wikidata.org/entity/Q41944520

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Antisense-mediated exon skipping: a versatile tool with therapeutic and research applications Dystrophin and the two related genetic diseases, Duchenne and Becker muscular dystrophies Splicing therapy for neuromuscular disease Differentiation of mammary tumors and reduction in metastasis upon Malat1 lncRNA loss.Rescue of cardiomyopathy through U7snRNA-mediated exon skipping in Mybpc3-targeted knock-in mice Antisense PMO found in dystrophic dog model was effective in cells from exon 7-deleted DMD patient Generation and analysis of the expressed sequence tags from the mycelium of Ganoderma lucidum Antisense-induced exon skipping for duplications in Duchenne muscular dystrophy Dynamics of co-transcriptional pre-mRNA folding influences the induction of dystrophin exon skipping by antisense oligonucleotides.Nanopolymers improve delivery of exon skipping oligonucleotides and concomitant dystrophin expression in skeletal muscle of mdx mice.Assessment of the feasibility of exon 45-55 multiexon skipping for Duchenne muscular dystrophy A duchenne muscular dystrophy gene hot spot mutation in dystrophin-deficient cavalier king charles spaniels is amenable to exon 51 skipping.Cationic PMMA nanoparticles bind and deliver antisense oligoribonucleotides allowing restoration of dystrophin expression in the mdx mouse Whole transcriptome analysis: what are we still missing?Dual exon skipping in myostatin and dystrophin for Duchenne muscular dystrophy.Dystrophin isoform induction in vivo by antisense-mediated alternative splicing.Therapeutic exon skipping for dysferlinopathies?Personalized exon skipping strategies to address clustered non-deletion dystrophin mutations.Mammalian models of Duchenne Muscular Dystrophy: pathological characteristics and therapeutic applications.Antisense-mediated isoform switching of steroid receptor coactivator-1 in the central nucleus of the amygdala of the mouse brain.Body-wide gene therapy of Duchenne muscular dystrophy in the mdx mouse model.Gene therapy progress and prospects: Duchenne muscular dystrophy.Potential of oligonucleotide-mediated exon-skipping therapy for Duchenne muscular dystrophy.Induction of revertant fibres in the mdx mouse using antisense oligonucleotides Bi-specific splice-switching PMO oligonucleotides conjugated via a single peptide active in a mouse model of Duchenne muscular dystrophy.The TREAT-NMD DMD Global Database: analysis of more than 7,000 Duchenne muscular dystrophy mutations.Non-sequential and multi-step splicing of the dystrophin transcript.Duchenne muscular dystrophy and dystrophin: pathogenesis and opportunities for treatment Modulating the expression of disease genes with RNA-based therapy.Multi-exon Skipping Using Cocktail Antisense Oligonucleotides in the Canine X-linked Muscular Dystrophy.Molecular-targeted therapy for Duchenne muscular dystrophy: progress and potential.Delivery of bifunctional RNAs that target an intronic repressor and increase SMN levels in an animal model of spinal muscular atrophy.Splice-switching antisense oligonucleotides as therapeutic drugs Polymersome delivery of siRNA and antisense oligonucleotides.Therapeutic potential of splice-switching oligonucleotides.Exon 32 Skipping of Dysferlin Rescues Membrane Repair in Patients' Cells Progress in therapeutic antisense applications for neuromuscular disorders.New insights in gene-derived therapy: the example of Duchenne muscular dystrophy.Opportunities and challenges for the development of antisense treatment in neuromuscular disorders.The function of dog models in developing gene therapy strategies for human health.

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Antisense-induced multiexon skipping for Duchenne muscular dystrophy makes more sense.

http://www.wikidata.org/entity/Q41944520

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Antisense-induced multiexon skipping for Duchenne muscular dystrophy makes more sense.

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Antisense-induced multiexon skipping for Duchenne muscular dystrophy makes more sense.

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Antisense-induced multiexon skipping for Duchenne muscular dystrophy makes more sense.

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P1433

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P1433

American Journal of Human Genetics

P1476

Antisense-induced multiexon skipping for Duchenne muscular dystrophy makes more sense.

@en

P2093

Anneke A M Janson

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

Johan T den Dunnen

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Judith C T van Deutekom

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Mattie Bremmer-Bout

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Wendy E Kaman

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P2860

Morpholino antisense oligonucleotides: tools for investigating vertebrate development.

The complete sequence of dystrophin predicts a rod-shaped cytoskeletal protein

Glycoprotein complex anchoring dystrophin to sarcolemma

Effective targeted gene 'knockdown' in zebrafish

Dystrophin: the protein product of the Duchenne muscular dystrophy locus

Listening to silence and understanding nonsense: exonic mutations that affect splicing

The mutational spectrum of single base-pair substitutions in mRNA splice junctions of human genes: causes and consequences

Exploiting the natural diversity in adenovirus tropism for therapy and prevention of disease.

Specific removal of the nonsense mutation from the mdx dystrophin mRNA using antisense oligonucleotides.

Chimeric snRNA molecules carrying antisense sequences against the splice junctions of exon 51 of the dystrophin pre-mRNA induce exon skipping and restoration of a dystrophin synthesis in Delta 48-50 DMD cells

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83-92

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10.1086/381039

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1

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P478

74

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Annemieke Aartsma-Rus

Gert-Jan van Ommen

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2003-12-16T00:00:00Z

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8953587

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14681829

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1181915

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