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. Author manuscript; available in PMC: 2015 Mar 1.
Published in final edited form as: Trends Endocrinol Metab. 2013 Dec 24;25(3):156–164. doi: 10.1016/j.tem.2013.11.004

Figure 1.

Figure 1

Regulation of autophagy by mTOR and AMPK

Insulin and growth factors signal through phosphoinositide 3-kinase (PI3K) and Akt to inhibit the tuberous sclerosis (TSC)1/2 complex. Inhibition of this complex allows active Ras homolog enriched in brain (RHEB)-GTP to activate mTOR in the mTORC1 complex, leading to phosphorylation of the ULK1 complex and inhibition of autophagy. Amino acids can also activate the mTORC1 complex by a separate mechanism. AMPK responds to low cellular energy levels by activating ULK1 via phosphorylation, resulting in activation of autophagy. Additionally, AMPK can initiate autophagy by disrupting Bcl-2 inhibition of Beclin 1, by activating forkhead box protein O (FoxO) transcription factors, and by directly activating TSC1/2 and Beclin 1.