IndraLab

Statements

TSC2 inhibits RHEB. 10 / 186
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"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 )."
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"Liver kinase B1 ( LKB1 , tumour suppressor ) , an upstream kinase of AMP-activated protein kinase ( AMPK ) induces AMPK phosphorylation of tuberous sclerosis complex 2 ( TSC2 ) to suppress Ras homolog enriched in brain ( Rheb ) and inhibit mTOR ."
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"Tuberous sclerosis complex 2 (TSC2), a GTPase-activating protein (GAP) for Rheb, together with its partner TSC1, inactivates Rheb GTPase (Inoki et al., 2003)."
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"TSC2 then inactivates Rheb, which impairs the interaction of mTOR with Rheb and Rag proteins."
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"The activation of EPH receptor leads to inhibition of MAPK1, in turn, allowing TSC2 to inhibit RHEB and MTOR."
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"This includes the inhibition of mTOR through the phosphorylation of the tumor suppressor TSC2, which inactivates Rheb and dampens mTOR activity."
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"AMPK is known to be phosphorylated by the serine/threonine kinase LKB1 (Liver kinase B1) and to phosphorylate TSC2 (Tuberous Sclerosis Complex 2), a GAP (GTPase activating protein) domain containing protein, which inactivates the Rheb GTPase, a direct activator of MTORC1 (XREF_FIG)."
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"Thus, AKT phosphorylates and inhibits the tumor suppressor proteins TSC1 and TSC2 that in turn inhibit Rheb, a GTPase that is an important regulatory component of the mTOR complex."
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"Therefore, Wnt mediated inactivation of Gsk3 alleviates Tsc2 driven inhibition of Rheb and results in TOR activation."
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"Phosphorylated TSC2 inactivates the GTP binding protein, Rheb, and prevents Rheb from promoting mTOR ( xref )."
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TSC2 bound to TSC1 inhibits RHEB. 10 / 25
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"On the other hand, it has been found that TORC1 is activated by the Ras family Rheb GTPase, which is negatively regulated by the Tsc1 and Tsc2 complex that acts as Rheb GTPase activating protein (GAP) [XREF_BIBR]."
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"TSC1 and TSC2 form a complex that inhibits Rheb directed mTOR activation through a GTPase activating protein (GAP) domain in the TSC2 C terminus."
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"TSC2 phosphorylation by Akt represses GAP activity of the TSC1 and TSC2 complex, allowing Rheb to accumulate in a GTP bound state."
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"TSC2 phosphorylation by Akt represses GAP activity of the TSC1 and TSC2 complex, allowing Rheb to accumulate in a GTP bound state."
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"The tuberous sclerosis 1 (TSC1) and TSC2 form a complex that inactivates RHEB through its GAP (GTPase activating protein) activity, thereby suppressing mTORC1 activity."
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"The TSC1 and TSC2 complex normally suppresses the GTPase Rheb [XREF_BIBR]."
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"For example, the TSC1 and TSC2 complex inhibits mTOR functions by inactivating Rheb; Rheb binds and activates mTOR only when the former is in its GTP bound form."
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"TSC2 phosphorylation by Akt represses GAP activity of the TSC1 and TSC2 complex, allowing Rheb to accumulate in a GTP bound state."
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"The TSC1 and TSC2 complex inactivates Rheb to inhibit mTOR signaling, which would lead to autophagy."
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"The major downstream effector of LKB1 in response to energy stress is the TSC2 and TSC1 complex, which inhibits Rheb GTPase, a mTOR activator."
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TSC2 bound to TSC1 inhibits RHEB. 1 / 1
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"The phosphorylated TSC1 and TSC2 complex inactivates the Rheb GTP component needed for mTOR signaling."
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Phosphorylated TSC2 inhibits RHEB. 1 / 1
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"Phosphorylation of TSC2 by AKT results in the activation of mTORC1, as the phosphorylated TSC2 no longer inhibits the Ras homolog enriched in brain (Rheb) protein that is critically required for mTORC1 functions 40."
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