Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA389697 | ENA |
REPOSITORIES: ENA
Similar Datasets
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
Project description:SILAC based protein correlation profiling using size exclusion of protein complexes derived from seven Mus musculus tissues (Heart, Brain, Liver, Lung, Kidney, Skeletal Muscle, Thymus)
2018-04-24 | PXD007288 | Pride
Project description:Calorie restriction (CR) is a dietary intervention that extends lifespan and healthspan in a variety of organisms. CR improves mitochondrial energy production, fuel oxidation and reactive oxygen species scavenging in skeletal muscle and other tissues, and these processes are thought to be critical to the benefits of CR. PGC-1a is a transcriptional coactivator that regulates mitochondrial function and is induced by CR. Consequently, many of the mitochondrial and metabolic benefits of CR are attributed to increased PGC-1a activity. To test this model for the first time, we examined the metabolic and mitochondrial response to CR in mice lacking skeletal muscle PGC-1a (MKO). Surprisingly, MKO mice demonstrated a normal improvement in glucose homeostasis in response to CR, indicating that skeletal muscle PGC-1a is dispensable for the whole-body benefits of CR. In contrast, gene expression profiling and electron microscopy demonstrated that PGC-1a is required for the full CR-induced increases in mitochondrial gene expression and mitochondrial density in skeletal muscle. These results demonstrate that PGC-1a is a major regulator of the mitochondrial response to CR in skeletal muscle, but surprisingly show that neither PGC-1a nor mitochondrial biogenesis in skeletal muscle are required for the metabolic benefits of CR. Control (FLOX) and PGC-1a skeletal muscle specific knock out (MKO) mice were placed on a control diet [C] or a calorie restriction diet [CR] for 12 weeks. RNA was isolated from TA/EDL muscles for microarray analysis. The following numbers of mice were analyzed from each group: C FLOX: n = 6; C MKO: n = 7; CR FLOX: n = 6; CR MKO: n = 7. Mice were mixed C57/BL6 and 129 background.
2012-02-04 | E-GEOD-34773 | biostudies-arrayexpress
Project description:Transcriptomic profiling of skeletal muscle in cFeimin MKO mice during exercise
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Project description:ATF4 is a fasting-induced trascription factor that promotes skeletal muscle atrophy. The goal of these studies was to determine how of loss of ATF4 affects skeletal muscle mRNA expression. For additional details see Ebert et al, Stress-Induced Skeletal Muscle Gadd45a Expression Reprograms Myonuclei and Causes Muscle Atrophy. JBC epub. June 12, 2012. Muscle-specfic ATF4 knockout (ATF4 mKO) mice and littermate controls were fasted for 24 hours and then tibialis anterior muscles were harvested. mRNA levels in ATF4 mKO muscles were normalized to levels in littermate control muscles.
2012-09-15 | E-GEOD-39193 | biostudies-arrayexpress
Project description:Effect of muscle-specific ATF4 gene knockout (ATF4 mKO) on skeletal muscle mRNA levels in aged mice.
| PRJNA294603 | ENA
Project description:We generated and analyzed a conditional Dystrophin flox52/Y: human alpha-skeletal actin muscle knockout (Dmd flox52/Y: HSA mKO) model by targeting exon 52 deletion in the Dystrophin gene to study the consequences of dystrophin loss in skeletal muscle lineages. The generated DMD mouse model ablates dystrophin protein expression after mating with a Cre recombinase transgenic mouse under the control of HSA promoter element that is restricted to the skeletal muscle. The resulting Dmd mKO mice have been assessed using histopathological, phenotypical, functional and biochemical assays based on TRET-NMD standard operating protocols (SOPs) for mdx mouse models. Phenotypic analysis of these conditional Dmd mKO mice revealed a significant decline in locomotor activity and reduced muscle force, motor and muscular function. The histochemical analysis revealed an increase in centralized myonuclei and fibrotic area similar to mdx mice. Immunoassays including western blot and immunohistochemistry confirmed low expression levels of dystrophin in skeletal muscles of Dmd mKO mice. Bulk RNA sequencing analysis revealed that dystrophin loss in myofiber significantly disrupted the expression of cytokines and extracellular matrix genes.
2024-12-25 | GSE284723 | GEO
Project description:For additional details see Ebert et al, Identification and Small Molecule Inhibition of an ATF4-dependent Pathway to Age-related Skeletal Muscle Weakness and Atrophy. Quadriceps femoris muscles were harvested from 22-month-old muscle-specfic ATF4 knockout (ATF4 mKO) mice and littermate controls. mRNA levels in ATF4 mKO muscles were normalized to levels in littermate control muscles.
2015-09-03 | E-GEOD-72658 | biostudies-arrayexpress
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)
2024-11-07 | MSV000096332 | MassIVE
Project description:SILAC based protein correlation profiling using size exclusion of protein complexes derived from seven Mus musculus tissues (Heart, Brain, Liver, Lung, Kidney, Skeletal Muscle, Thymus)
2024-11-07 | MSV000096331 | MassIVE