Pathological impact of SMN2 mis-splicing in adult SMA mice - Wikidata - awgldk - TriplyDB

Pathological impact of SMN2 mis-splicing in adult SMA mice

Pathological impact of SMN2 mis-splicing in adult SMA mice

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Repeated low doses of morpholino antisense oligomer: an intermediate mouse model of spinal muscular atrophy to explore the window of therapeutic response Peripheral androgen receptor gene suppression rescues disease in mouse models of spinal and bulbar muscular atrophy.Protective effects of butyrate-based compounds on a mouse model for spinal muscular atrophy.Efficient SMN Rescue following Subcutaneous Tricyclo-DNA Antisense Oligonucleotide Treatment A sensitive assay system to test antisense oligonucleotides for splice suppression therapy in the mouse liver.Motor neuron cell-nonautonomous rescue of spinal muscular atrophy phenotypes in mild and severe transgenic mouse models Motor neuron disease. SMN2 splicing modifiers improve motor function and longevity in mice with spinal muscular atrophy.Splice-switching antisense oligonucleotides as therapeutic drugs RNA-sequencing of a mouse-model of spinal muscular atrophy reveals tissue-wide changes in splicing of U12-dependent introns.SMN deficiency in severe models of spinal muscular atrophy causes widespread intron retention and DNA damage Pharmacologically induced mouse model of adult spinal muscular atrophy to evaluate effectiveness of therapeutics after disease onset.SMA-causing missense mutations in survival motor neuron (Smn) display a wide range of phenotypes when modeled in Drosophila.The Antisense Transcript SMN-AS1 Regulates SMN Expression and Is a Novel Therapeutic Target for Spinal Muscular Atrophy.Silencing neuronal mutant androgen receptor in a mouse model of spinal and bulbar muscular atrophy.

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Pathological impact of SMN2 mis-splicing in adult SMA mice

http://www.wikidata.org/entity/Q30551534

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2013 nî lūn-bûn

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2013 թուականի Սեպտեմբերին հրատարակուած գիտական յօդուած

@hyw

2013 թվականի սեպտեմբերին հրատարակված գիտական հոդված

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2013年の論文

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2013年論文

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2013年論文

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2013年論文

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2013年論文

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2013年論文

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2013年论文

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name

Pathological impact of SMN2 mis-splicing in adult SMA mice

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Pathological impact of SMN2 mis-splicing in adult SMA mice

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Pathological impact of SMN2 mis-splicing in adult SMA mice

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Pathological impact of SMN2 mis-splicing in adult SMA mice

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Pathological impact of SMN2 mis-splicing in adult SMA mice

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Pathological impact of SMN2 mis-splicing in adult SMA mice

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EMBO Molecular Medicine

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Pathological impact of SMN2 mis-splicing in adult SMA mice

@en

P2093

C Frank Bennett

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

Chien-Ping Ko

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

David Xu

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

Frank Rigo

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Gene Hung

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John Erby Wilkinson

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Karen K Y Ling

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Kentaro Sahashi

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Richard Z Lin

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Ya-Ping Jiang

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P2860

Synaptic defects in the spinal and neuromuscular circuitry in a mouse model of spinal muscular atrophy

SAHA ameliorates the SMA phenotype in two mouse models for spinal muscular atrophy

Early heart failure in the SMNDelta7 model of spinal muscular atrophy and correction by postnatal scAAV9-SMN delivery

Congenital heart disease is a feature of severe infantile spinal muscular atrophy

Arrhythmia and cardiac defects are a feature of spinal muscular atrophy model mice.

A role for SMN exon 7 splicing in the selective vulnerability of motor neurons in spinal muscular atrophy

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

The power of automated high-resolution behavior analysis revealed by its application to mouse models of Huntington's and prion diseases.

Postsymptomatic restoration of SMN rescues the disease phenotype in a mouse model of severe spinal muscular atrophy.

Enhancement of SMN2 exon 7 inclusion by antisense oligonucleotides targeting the exon.

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1586-1601

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scholarly article

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10.1002/EMMM.201302567

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10

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5

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Adrian Robert Krainer

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2013-09-09T00:00:00Z

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256469807

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3799581

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