Proteomics

Dataset Information

0

Proteome analysis of skeletal muscle samples from a porcine model of Duchenne muscular dystrophy treated by somatic gene editing

ABSTRACT: Duchenne muscular dystrophy (DMD) is caused by genetic deficiency of dystrophin and characterized by massive structural and functional changes of skeletal muscle tissue, leading to terminal muscle failure. In this project, proteomics data from skeletal muscle of a genetically engineered DMD pig model treated by somatic gene editing are shown.

INSTRUMENT(S): Q Exactive

ORGANISM(S): Sus Scrofa Domesticus (domestic Pig)

TISSUE(S): Skeletal Muscle

DISEASE(S): Duchenne Muscular Dystrophy

SUBMITTER: Thomas Fröhlich  

LAB HEAD: Thomas Fröhlich

PROVIDER: PXD014893 | Pride | 2020-02-05

REPOSITORIES: Pride

Json Xml

Dataset's files

Source:
Action DRS
OxidationMSites.txt Txt
allPeptides.txt Txt
evidence.txt Txt
modificationSpecificPeptides.txt Txt
msScans.txt Txt
Items per page:
1 - 5 of 36
altmetric image

Publications

Somatic gene editing ameliorates skeletal and cardiac muscle failure in pig and human models of Duchenne muscular dystrophy.

Moretti A A   Fonteyne L L   Giesert F F   Hoppmann P P   Meier A B AB   Bozoglu T T   Baehr A A   Schneider C M CM   Sinnecker D D   Klett K K   Fröhlich T T   Rahman F Abdel FA   Haufe T T   Sun S S   Jurisch V V   Kessler B B   Hinkel R R   Dirschinger R R   Martens E E   Jilek C C   Graf A A   Krebs S S   Santamaria G G   Kurome M M   Zakhartchenko V V   Campbell B B   Voelse K K   Wolf A A   Ziegler T T   Reichert S S   Lee S S   Flenkenthaler F F   Dorn T T   Jeremias I I   Blum H H   Dendorfer A A   Schnieke A A   Krause S S   Walter M C MC   Klymiuk N N   Laugwitz K L KL   Wolf E E   Wurst W W   Kupatt C C  

Nature medicine 20200127 2

Frameshift mutations in the DMD gene, encoding dystrophin, cause Duchenne muscular dystrophy (DMD), leading to terminal muscle and heart failure in patients. Somatic gene editing by sequence-specific nucleases offers new options for restoring the DMD reading frame, resulting in expression of a shortened but largely functional dystrophin protein. Here, we validated this approach in a pig model of DMD lacking exon 52 of DMD (DMDΔ52), as well as in a corresponding patient-derived induced pluripoten  ...[more]

Similar Datasets

Proteomics Proteome analysis of skeletal muscle samples from a porcine model of Duchenne muscular dystrophy
2020-01-09 | PXD016003 | Pride
Proteomics A scalable, clinically severe pig model for Duchenne muscular dystrophy
2021-12-01 | PXD027772 | Pride
Transcriptomics The microRNA, miR-133b, functions to slow Duchenne muscular dystrophy pathogenesis
2020-08-15 | GSE156267 | GEO
Proteomics Systemic deletion of DMD exon 51 rescues clinically severe Duchenne muscular dystrophy in a pig model lacking DMD exon 52
2023-07-11 | PXD039533 | Pride
Transcriptomics DMD vs. AGING
2011-11-01 | E-GEOD-32720 | biostudies-arrayexpress
Transcriptomics Gene expression data from Duchenne muscular dystrophy patients versus controls
2016-07-01 | E-GEOD-38417 | biostudies-arrayexpress
Proteomics Myogenesis modelled by human pluripotent stem cells uncovers Duchenne muscular dystrophy phenotypes prior to skeletal muscle commitment
2021-09-08 | PXD015355 | Pride
Transcriptomics miR-486 is an epigenetic modulator of Duchenne muscular dystrophy pathologies [RNA-seq]
2022-10-01 | GSE178772 | GEO
Other MicroRNA-486 is an epigenetic modulator of Duchenne muscular dystrophy pathologies [eCLIP-seq]
2022-05-04 | GSE173821 | GEO
Transcriptomics Gene expression data from Duchenne muscular dystrophy patients versus controls
2016-07-01 | GSE38417 | GEO