IndraLab

Statements


TSC1 inhibits MTOR. 10 / 174
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"In this regard, S6K is regulated by mTor, which is inactivated by the TSC1 and TSC2 tumor suppressors (Inoki et al., 2005; Manning and Cantley, 2003; Nobukini and Thomas, 2004)."

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"Nevertheless, the ability of the Rheb-GAP, TSC1 and TSC2, to inhibit mTOR signaling in vivo is consistent with the inference that Rheb-GDP provides a less effective stimulus than Rheb-GTP."

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"Loss of TSC1 leads to mTOR mediated inhibition of PI3K-AKT in naive CD8 + T cells."

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"XREF_BIBR Both sestrins can trigger the AMPK and target it to phosphorylate and activate TSC1 and TSC2 complex, thereby inhibiting the signaling of mTOR, a critical autophagy inhibitor of cells, XREF_BIBR, XREF_BIBR and so CX-5461-induced autophagy through AMPK and mTOR signaling pathway in U2-OS cells might arise from the upregulation of Sesn1/2 by p53."

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"This mechanism of p53-induced autophagy involves activation of 5′ AMP-activated protein kinase (AMPK) as well as the tuberus sclerosis complex kinases, TSC1 and TSC2, which finally inhibit mTOR kinase."

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"In the majority of cells under stress conditions, activation of AMPK phosphorylates TSC2 leading to TSC1 and TSC2 dependent suppression of mTOR to inhibit cell proliferation [XREF_BIBR, XREF_BIBR]."

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"Interestingly, in 2001 and 2002, TSC1 and TSC2 were shown to canonically modulate the serine threonine kinase mechanistic target of rapamycin (mTOR), within the insulin growth factor (IGF) signaling pathway."

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"Constitutive mTOR activation by loss of TSC1 and TSC2 rapidly stimulates the targets of both PERK and IRE1, which UPR activation could not be observed in combined treatment of TSC1 and TSC2 depletion and rapamycin addition."

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"Two of these genes, TSC1 and TSC2, are downstream of AMPK and negatively regulate mTOR in response to cellular energy deficits."

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"AKT activation leads to cell growth by activating mTOR through TSC1/2 phosphorylation, while increased levels of TSC1 and TSC2 inhibit the mTOR pathway; mTOR positively regulates 4E-BP1 and p70S6k, which are activated in a variety of cancers."
TSC1 bound to TSC2 inhibits MTOR. 10 / 51
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"TSC2 forms a heterodimeric complex with TSC1 and negatively regulates mTOR."

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"The TSC1 and TSC2 complex inactivates Rheb to inhibit mTOR signaling XREF_BIBR, XREF_BIBR."

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"TSC1 and TSC2 complex inhibits mTOR activity by activating the GTPase activity of Rheb, and both Akt and AMPK converged at TSC1 and TSC2 to regulate mTOR activity."

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"Activation of the TSC1 and TSC2 complex by AMPK can negatively regulate the mTOR pathway not only by inhibiting mTOR activation via Rheb, a member of the Ras family of GTPases, but also by mediating phosphorylation of the mTORC1 partner Raptor."

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"The TSC1 and TSC2 complex inactivates Rheb to inhibit mTOR signaling."

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"As the hamartin and tuberin complex normally inhibits the mTOR pathway, mutation of either TSC1 or TSC2 leads to abnormal disinhibition of the mTOR pathway."

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"Akt mediated phosphory lation of TSC2 disrupts the TSC1 and TSC2 complex, allowing unrestrained mTOR kinase activity."

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"The proteins hamartin and tuberin, respectively, encoded by the TSC1 and TSC2 genes, form a complex that downregulates the mTOR pathway."

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"We may add that activated AMPK is also known to downregulate the mTOR-p70S6K-S6 ribosomal protein phosphorylation cascade by phosphorylating TSC2 and increasing the activity of the TSC1 and TSC2 compl[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"Overexpression of constitutively activated Akt or disruption of TSC1 and TSC2 complex by small interfering RNA or gene knockout only partially restored curcumin mediated inhibition of mTOR and downstream signaling, indicating that they are not the primary effectors of curcumin mediated inhibition of Akt and mTOR signaling."
Catalytically active TSC1 bound to TSC2 inhibits MTOR. 3 / 3
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"Akt then phosphorylates several substrates, one of which is the tuberous sclerosis complex (TSC1/2), a GTPase activating protein complex that suppresses Rheb, a GTPase that contributes directly to the activation of mTOR"

"Genetic support for a linear Akt1-mTOR-p70S6K pathway has recently come from reports demonstrating that the tuberous sclerosis complex 1 and 2 proteins (Tsc1 and Tsc2) can inhibit mTOR (Fig. 1). Akt1 phosphorylates Tsc2, thereby activating mTOR at least in part by disrupting the Tsc1-Tsc2 complex [54]."

"TSC2, in a complex with TSC1, normally represses signalling through mTOR, and phosphorylation by Akt/PKB inhibits this function of TSC2 (for review, see Manning & Cantley, 2003)."
TSC1 bound to sclerosis complex 1 inhibits MTOR. 1 / 1
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"Tuberous sclerosis complex 1 (TSC1) and TSC2 form a heterodimer that negatively regulates mTOR, preventing the phosphorylation of S6K."
TSC1 bound to TSC2 inhibits MTOR. 1 / 1
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"The TSC1-TSC2 complex is a critical negative regulator of mTORC1."
TSC1 bound to TSC1 inhibits MTOR. 1 / 1
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"Hamartin and tuberin, the TSC1 and TSC2 gene products, form a complex that inhibits mammalian target of rapamycin (mTOR) in a conserved cellular signaling pathway (PI3kinase- Akt-mTOR pathway) that regulates nutrient uptake, growth and protein translation [9], [10], [11]."
Mutated TSC1 inhibits MTOR. 1 / 1
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"The inactive mutation of TSC1 or TSC2 is found in patients with LAM to activate the crucial mammalian target of rapamycin (mTOR) signaling pathway and result in enhanced cell proliferation and migration."