Fig. 4.

Possible mechanisms of Akt activation by β-AR signaling. IGF-I activates Akt, which stimulates protein synthesis via activating mTOR and inhibits muscle-specific ubiquitin ligase expression via repressive phosphorylation of FoxO transcription factors. β₂-AR signaling leads to muscle hypertrophy, which is accompanied by activation of Akt, activation of protein synthesis, and inhibition of proteolysis. PKA signaling induces calpastatin transcription and inhibits calpains by an unknown mechanism. β₂-AR signaling also activates Akt by an unknown mechanism, possibly mediated by Gβγ subunits, β-arrestin, or PKA (dashed arrows). Not shown: Wnt7a-Fzd7-Gα_s activates PI 3-kinase directly.