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. Author manuscript; available in PMC: 2018 Jan 1.
Published in final edited form as: Biochim Biophys Acta. 2016 Oct 17;1863(1):33–42. doi: 10.1016/j.bbadis.2016.10.009

Fig. 4. Schematic diagram of mTOR signaling and proposed activation mechanisms by elevated GABA.

Fig. 4

This diagram is presented to provide guidance in the interpretation of the data of Table 1. Upstream activation of the mTOR complexes (mTORC1/mTORC2) can occur through tyrosine kinase receptors, insulin/Akt (protein kinase B), growth factors, and amino acids. AMPK (5′ AMP-activated protein kinase) modulates low energy status signals and inhibits mTOR through activation of TSC1/2 (tuberous sclerosis complexes). Additional abbreviations: Rheb, ras homolog enriched in brain; PI3K, phosphatidylinositol-4,5-bisphosphate 3-kinase; PIP3, phosphatidylinositol (3,4,5)-trisphosphate; PIP2, phosphatidylinositol 4,5-bisphosphate; PTEN, phosphate and tensin homolog; S6K, ribosomal protein S6 kinase; 4EBP, factor 4E binding protein; ULK, Unc-51 like autophagy activating kinase; PKC, protein kinase C; SGK1, serum and glucocorticoid-regulated kinase 1; Rag A-D, Ras-related GTP binding proteins A, B, C and D. Solid bars attached to lines indicate inhibition, wherease arrows indicate activation.