Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA239719 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:A commercially available gene array (SABiosciences array PAMM-029ZD-12) was used to assay gene expression in skeletal muscle of SMA mice and control littermates. The Taiwanese severe SMA mouse model was used (Hsieh-Li et al. 2000). The array included 84 genes associated with DNA damage detection, DNA repair, apoptosis, cell cycle, and other functions.
2014-03-03 | GSE55481 | GEO
Project description:A commercially available gene array (SABiosciences array PAMM-029ZD-12) was used to assay gene expression in skeletal muscle of SMA mice and control littermates. The Taiwanese severe SMA mouse model was used (Hsieh-Li et al. 2000). The array included 84 genes associated with DNA damage detection, DNA repair, apoptosis, cell cycle, and other functions. SMA group (n=3) vs. control group (n=3) - single technical replicates, triple biological replicates
2014-03-03 | E-GEOD-55481 | biostudies-arrayexpress
Project description:Replacing skeletal muscle alpha-actin with cardiac actin in mouse skeletal muscle
| PRJNA110869 | ENA
Project description:Exon array data from neuromuscular junction (NMJ) in mouse skeletal muscle.
| PRJNA357461 | ENA
Project description:Mutations in genes encoding nuclear envelope proteins lead to diseases known as nuclear envelopathies, characterized by skeletal muscle and heart abnormalities, such as Emery-Dreifuss Muscular Dystrophy (EDMD). The tissue-specific role of the nuclear envelope in the etiology of these diseases has not been extensively explored. We previously showed that global deletion of the muscle-specific nuclear envelope protein NET39 in mice leads to neonatal lethality due to skeletal muscle dysfunction. To study the potential role of the Net39 gene in adulthood, we generated a muscle-specific conditional knockout (cKO) of Net39 in mice. cKO mice recapitulated key skeletal muscle features of EDMD, including muscle wasting, impaired muscle contractility, abnormal myonuclear morphology, and DNA damage. The loss of Net39 rendered myoblasts hypersensitive to mechanical stretch, resulting in stretch-induced DNA damage. Net39 was downregulated in a mouse model of congenital myopathy, and restoration of Net39 expression through AAV gene delivery extended lifespan and ameliorated the muscle abnormalities. These findings establish NET39 as a direct contributor to the pathogenesis of EDMD by protecting against mechanical stress and DNA damage.
2023-06-08 | GSE232046 | GEO
Project description:Mutations in genes encoding nuclear envelope proteins lead to diseases known as nuclear envelopathies, characterized by skeletal muscle and heart abnormalities, such as Emery-Dreifuss Muscular Dystrophy (EDMD). The tissue-specific role of the nuclear envelope in the etiology of these diseases has not been extensively explored. We previously showed that global deletion of the muscle-specific nuclear envelope protein NET39 in mice leads to neonatal lethality due to skeletal muscle dysfunction. To study the potential role of the Net39 gene in adulthood, we generated a muscle-specific conditional knockout (cKO) of Net39 in mice. cKO mice recapitulated key skeletal muscle features of EDMD, including muscle wasting, impaired muscle contractility, abnormal myonuclear morphology, and DNA damage. The loss of Net39 rendered myoblasts hypersensitive to mechanical stretch, resulting in stretch-induced DNA damage. Net39 was downregulated in a mouse model of congenital myopathy, and restoration of Net39 expression through AAV gene delivery extended lifespan and ameliorated the muscle abnormalities. These findings establish NET39 as a direct contributor to the pathogenesis of EDMD by protecting against mechanical stress and DNA damage.
2023-06-08 | GSE232048 | GEO
Project description:Mutations in genes encoding nuclear envelope proteins lead to diseases known as nuclear envelopathies, characterized by skeletal muscle and heart abnormalities, such as Emery-Dreifuss Muscular Dystrophy (EDMD). The tissue-specific role of the nuclear envelope in the etiology of these diseases has not been extensively explored. We previously showed that global deletion of the muscle-specific nuclear envelope protein NET39 in mice leads to neonatal lethality due to skeletal muscle dysfunction. To study the potential role of the Net39 gene in adulthood, we generated a muscle-specific conditional knockout (cKO) of Net39 in mice. cKO mice recapitulated key skeletal muscle features of EDMD, including muscle wasting, impaired muscle contractility, abnormal myonuclear morphology, and DNA damage. The loss of Net39 rendered myoblasts hypersensitive to mechanical stretch, resulting in stretch-induced DNA damage. Net39 was downregulated in a mouse model of congenital myopathy, and restoration of Net39 expression through AAV gene delivery extended lifespan and ameliorated the muscle abnormalities. These findings establish NET39 as a direct contributor to the pathogenesis of EDMD by protecting against mechanical stress and DNA damage.
2023-06-08 | GSE232047 | GEO
Project description:SILAC based protein correlation profiling using size exclusion of protein complexes derived from Mus musculus tissues (Heart, Liver, Lung, Kidney, Skeletal Muscle, Thymus)
2021-05-05 | PXD022309 | Pride