Skeletal muscle specific AMPKalpha1/2 deletion during hindlimb unloading
The primary goal of this study was to determine the role of AMPKalpha during disuse atrophy. Skeletal muscle-specific tamoxifen-inducible AMPKlpha1/alpha2 double knockout (KO) mice were generated and KO was induced for 4 weeks. After 2 weeks of KO, mice were hindlimb unloaded (HU) for 2 weeks to induce atrophy or maintained ambulatory (AMB). We observed that AMPKalpha double KO impaired skeletal muscle transcriptional profiles that may have carried over with HU. Overall design: Comparative gene expression profiling analysis of RNA-seq data for AMPKalpha double knock out soleus muscle samples with 7-8 replicates per group