"Phosphorylation of TSC2 by AMPK can increase the GAP activity of TSC2, stabilize the TSC2 and TSC1 complex, and inactivate Rheb, resulting in the inactivation of mTORC1 and the initiation of autophagy XREF_BIBR."
"Activation of IIS inhibits TSC1 and TSC2, a heterodimer that negatively regulates Rheb, an activator of the TOR complex."
"Indeed, in the scientific paper corpus we have used, this inhibition of Rheb by Tsc2 was not demonstrated."
"TSC2 inhibits Rheb, the upstream activator of mTORC1, while AKT and AMPK can activate or inhibit mTORC1 function by inhibiting or activating TSC2, respectively ( xref , xref )."
"Akt activates mTORC1 through phosphorylation and inhibition of tumor-suppressor protein TSC2 (tuberin) thus releasing TSC2 inhibition of Rheb, which subsequently leads to mTORC1 activation [XREF_BIBR - XREF_BIBR]."
"These phosphorylation events release TSC2 mediated inhibition of the GTPase Ras homolog enriched in brain (RHEB), thus allowing RHEB to activate mTORC1 [XREF_BIBR]."
"TSC2 then inactivates Rheb, which impairs the interaction of mTOR with Rheb and Rag proteins."
"Phosphorylation of TSC2 by AKT inactivates its Rheb GTPase activity, leading to activation of mTOR Complex 1 (mTORC1)."
"TSC2 inhibits RheB through its GAP activity and thus functions as negative regulator of mTORC1 signaling."
"This includes the inhibition of mTOR through the phosphorylation of the tumor suppressor TSC2, which inactivates Rheb and dampens mTOR activity."