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. Comparative gene expression profiling analysis of RNA-seq data for AMPKalpha double knock out soleus muscle samples with 7-8 replicates per group