When the AMP:ATP ratio increases, AMPK phosphorylates TSC2 and RAPTOR, leading to inhibition of mTORC1

The activity of mTORC1 appears to be regulated through a dynamic interaction between mTOR and Raptor, one which is mediated by GβL.^[9]^[10] Raptor and mTOR share a strong N-terminal interaction and a weaker C-terminal interaction near mTOR\'s kinase domain.^[9] When stimulatory signals are sensed, such as high nutrient/energy levels, the mTOR-Raptor C-terminal interaction is weakened and possibly completely lost, allowing mTOR kinase activity to be turned on. When stimulatory signals are withdrawn, such as low nutrient levels, the mTOR-Raptor C-terminal interaction is strengthened, essentially shutting off kinase function of mTOR

Pathways of Gene regulation