Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA407979 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR6058523_1.fastq.gz | Fastqsanger.gz | |||
| SRR6058523_2.fastq.gz | Fastqsanger.gz | |||
| SRR6058543_1.fastq.gz | Fastqsanger.gz | |||
| SRR6058543_2.fastq.gz | Fastqsanger.gz | |||
| SRR6058524_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 16 |
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Project description:We performed RNA-seq analysis for C2C12 myoblasts as a function of differentiation. Cells were treated with either DMSO or family VIII bromodomain-specific inhibitor PFI-3 at a concentration of 50uM. We find that PFI-3 treatment affects proper differentiation of myoblasts as compared to DMSO-treated C2C12 cells. We conclude that function of mammalian SWI/SNF bromodomains is important for regulation of myoblast differentiation.
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Project description:PFI-7 is a GID4 specific inhibitor. In order to verify the specificity of GID4 towards the target, a chemoproteomic competition experiment was performed. The biotinylated adduct of PFI-7, NB716, is used to enrich for potential target proteins of PFI-7. When PFI-7 is added in excess, the inhibitor competes with NB716 for target binding. We demonstrate that GID4 is the only protein that is affected by addition of PFI-7, and we observe no effects when adding the negative control to PFI-7, PFI-7N.
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Project description:The homeodomain transcription factor Prep1 was previously shown to regulate insulin sensitivity. Our aim was to study the specific role of Prep1 for the regulation of energy metabolism in skeletal muscle. Muscle specific ablation of Prep1 resulted in increased expression of respiratory chain subunits. This finding was consistent with an increase in mitochondrial enzyme activity without affecting mitochondrial volume fraction as assessed by electron microscopy. Metabolic phenotyping revealed no differences in daily energy expenditure or body composition. However, during treadmill exercise challenge, Prep1 ablation resulted in a higher maximal oxidative capacity and better endurance. Elevated PGC-1α expression was identified as a cause for increased mitochondrial capacity in Prep1-ablated mice. Prep1 stabilizes p160 Mybbp1a, a known inhibitor of PGC-1α activity. Thereby, P160 protein levels were significantly lower in muscle of Prep1-ablated mice. By a ChIPseq approach, PREP1-binding sites in genes encoding mitochondrial components (e.g. Ndufs2) were identified that might be responsible for elevated OXPHOS proteins in the muscle of Prep1 nullmutants. These results suggest that Prep1 exhibits additional direct effects on regulation of mitochondrial proteins. We therefore conclude that Prep1 is a regulator of oxidative phosphorylation components via direct and indirect mechanisms. Consequence of Prep1 ablation in skeletal muscle was investigated in Prep1deltaSM mice and compared to Prep1 flox mice, both on C57BL/6 background. 4 mice of each genotype were used to extract RNA from the tibialis anterior muscle.
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