Overexpression Of The Htsc1 Muscular Atrophy Mouse Model To Establish Its Molecular Mechanism

Skeletal muscle atrophy accompanies with many diseases, such as cancer, diabetes and AIDS. Regulation of muscle mass is correlated with the activity of Insulin/IGF pathway. The Tuberous Sclerosis (TSC) complex, which consists of two components — TSC1 and TSC2, works as a suppressor of the Insulin/IGF pathway. Here we report that specific overexpression of hTSC1 in mouse skeletal muscle causes obvious atrophy phenotype. Ectopically expressed hTSC1 stabilizes endogenous mouse TSC2, thus resulting in an increase at the intracellular level of the TSC complex. Furthermore results also show that the hTSC1-mTSC2 hetero-complex can be regulated by Insulin stimulation in vivo, and respond normally to nutrition signals.