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duchenne muscular dystrophy (10) 10
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Molecular Therapy - Nucleic Acids, ISSN 2162-2531, 2015, Volume 4, Issue 2, pp. e225 - e225
Antisense-mediated exon skipping, which can restore the reading frame, is a most promising therapeutic approach for Duchenne muscular dystrophy. Remaining... 
multiexon skipping | antisense therapeutics | mdx52 mouse | dystrophin | Vivo-Morpholinos | Duchenne muscular dystrophy | Antisense therapeutics | Dystrophin | Multiexon skipping | Mmdx52 mouse | MUSCLE PATHOLOGY | MEDICINE, RESEARCH & EXPERIMENTAL | CARDIAC-MUSCLE | RESTORATION | DETERMINES | THERAPY | RESCUE | IMPROVEMENT | DUCHENNE MUSCULAR-DYSTROPHY | SKELETAL | EXPRESSION | Original
Journal Article
Methods in Molecular Biology, ISSN 1064-3745, 2018, Volume 1828, pp. 275 - 292
Exon-skipping therapy is an emerging approach that uses synthetic DNA-like molecules called antisense oligonucleotides (ASOs) to splice out frame-disrupting... 
mdx | mdx52 | Exon skipping | Duchenne muscular dystrophy (DMD) | Eteplirsen (Exondys 51) | Vivo-morpholinos (vPMOs) | Dystrophin | Multiexon skipping | Becker muscular dystrophy (BMD) | Phosphorodiamidate morpholino oligomer (PMO) | Index Medicus
Journal Article
Molecular Therapy, ISSN 1525-0016, 11/2017, Volume 25, Issue 11, pp. 2561 - 2572
Duchenne muscular dystrophy (DMD), the most common lethal genetic disorder, is caused by mutations in the ( ) gene. Exon skipping is a therapeutic approach... 
mdx52 mice | Becker muscular dystrophy | Exondys 51 | eteplirsen | exon skipping | Duchenne muscular dystrophy | clinical trial candidate screening | BMD | antisense morpholino | drisapersen | machine learning | hDMD/Dmd-null mice | MEDICINE, RESEARCH & EXPERIMENTAL | DIAGNOSIS | DESIGN | EFFICACY | DMD GENE | RESTORATION | PHASE-2 | OLIGONUCLEOTIDES | THERAPY | BIOTECHNOLOGY & APPLIED MICROBIOLOGY | GENETICS & HEREDITY | MICE | ETEPLIRSEN | Exons | Humans | Oligonucleotides, Antisense - metabolism | Male | Muscle, Skeletal - metabolism | Reading Frames | Recovery of Function | RNA Splicing | Female | Muscular Dystrophy, Duchenne - therapy | Dystrophin - metabolism | Disease Models, Animal | Gene Expression | Morpholinos - genetics | Mice, Transgenic | Muscular Dystrophy, Duchenne - pathology | Morpholinos - metabolism | Animals | Oligonucleotides, Antisense - genetics | Dystrophin - genetics | Mice | Muscular Dystrophy, Duchenne - metabolism | Muscle, Skeletal - pathology | Muscular Dystrophy, Duchenne - genetics | Mutation | Genetic Therapy - methods | Performance evaluation | Medical research | Statistical analysis | Splicing | Antisense oligonucleotides | Muscular dystrophy | Proteins | Musculoskeletal system | Protein folding | Efficiency | Exon skipping | Duchenne's muscular dystrophy | Protein expression | Muscle function | Dystrophy | Dystrophin | Evacuations & rescues | Index Medicus | hDMD | Dmd-null mice | Original
Journal Article
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 04/2017, Volume 114, Issue 16, pp. 4213 - 4218
Duchenne muscular dystrophy (DMD) is a lethal genetic disorder caused by an absence of the dystrophin protein in bodywide muscles, including the heart.... 
Cardiac Purkinje fibers | Dystrophic dog model | Peptide-conjugated morpholinos | Duchenne muscular dystrophy | Exon skipping | MUSCLE PATHOLOGY | MULTIDISCIPLINARY SCIENCES | DMD GENE | CARDIOMYOPATHY | BODYWIDE | dystrophic dog model | peptide-conjugated morpholinos | MDX52 MICE | OLIGONUCLEOTIDES | RESCUE | exon skipping | LABORATORY-ANIMALS | cardiac Purkinje fibers | EXPRESSION | EXONS 45-55 | Genetic Therapy | Muscular Dystrophy, Animal - genetics | Exons | Male | Muscle, Skeletal - metabolism | Muscular Dystrophy, Animal - complications | Muscular Dystrophy, Duchenne - complications | Cardiomyopathies - etiology | Cardiomyopathies - therapy | Cell-Penetrating Peptides - pharmacology | Animals | Dogs | Morpholinos - pharmacology | Female | Muscular Dystrophy, Animal - therapy | Muscle, Skeletal - pathology | Muscular Dystrophy, Duchenne - genetics | Muscular Dystrophy, Duchenne - therapy | Dystrophin - metabolism | Disease Models, Animal | Heart | Physiological aspects | Health aspects | Conduction | Intravenous administration | Peptides | Toxicity | Cardiomyopathy | Effects | Muscular dystrophy | Fibers | Oligomers | Nerve conduction | Arginine | Duchenne's muscular dystrophy | Degeneration | Polymers | Heart diseases | Dystrophin | EKG | Cardiac muscle | Abnormalities | Muscles | Skeletal muscle | Purkinje fibers | Myocardium | Dystrophy | Index Medicus | Biological Sciences
Journal Article
Journal of Visualized Experiments, ISSN 1940-087X, 05/2016, Volume 2016, Issue 111
Journal Article
Clinical Neurology, ISSN 0009-918X, 2011, Volume 51, Issue 11, pp. 914 - 916
Journal Article
臨床神経学, ISSN 0009-918X, 2011, Volume 51, Issue 11, pp. 914 - 916
Duchenne muscular dystrophy (DMD) is caused by the lack of dystrophin at the sarcolemma. Exon skipping by antisense oligonucleotides is a novel method to... 
mdx52マウス | ジストロフィン | エクソン・スキッピング | Duchenne型筋ジストロフィー | 臨床治験
Journal Article
Journal of Neuromuscular Diseases, ISSN 2214-3599, 2016, Volume 3, Issue 1, pp. 29 - 48
Duchenne muscular dystrophy (DMD) is an X-linked genetic disorder characterized by progressive muscle degeneration. Mutations in the DMD gene result in the... 
DBA/2-mdx | mdx | exon skipping | C57BL/6-mdx | mdx52, hDMD | dko | Duchenne muscular dystrophy (DMD) | Cmah-mdx | DMD-null
Journal Article
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