The INDRA Database: Results
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"Loss of Tsc1 and Tsc2 activates mTOR and disrupts PI3K-Akt signaling through downregulation of PDGFR."
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"In the presence of growth factors such as insulin or insulin like growth factors, stimulated Akt and extracellular signal regulated protein kinases 1 and 2 (ERK1/2) can phosphorylate and disrupt the tuberous sclerosis complex 1/2 (TSC1 and TSC2), which activates mTOR inhibition and thus inhibiting autophagy [XREF_BIBR]."
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"When either PTEN or TSC1 were silenced in order to reactivate the mTOR pathway, it led to induction of extensive axon regeneration in adult neurons."
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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 wild-type adult mice, the regeneration failure may be contributable to the suppression of mTOR activity and new protein synthesis in axotomized RGCs, since reactivating this pathway by conditional knockout of TSC1, which negatively regulate the mTOR pathway, leads to axon regeneration [XREF_BIBR]."
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"Loss of TSC1 or TSC2 leads to hyperactive mTOR signaling, which is the main cause of tumor growth in TSC patients, and the decreased AKT1 activity due to the negative feedback regulation of mTOR may account for the benign nature of TSC tumors."
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"When upstream signals are activated, TSC1 and TSC2 is inhibited by AKT, allowing mTOR activation."
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"Once activated, the TSC1 and TSC2 complex inhibits mTOR resulting in a decrease in protein synthesis."
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"Tuberous sclerosis complex 1 (TSC1) and TSC2 form a heterodimer that negatively regulates mTOR, preventing the phosphorylation of S6K."
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"The TSC1 and TSC2 complex inactivates Rheb to inhibit mTOR signaling XREF_BIBR, XREF_BIBR."
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"In particular, hamartin and tuberin, proteins encoded by the TSC1 and TSC2 genes, form a complex that normally inhibits the mTOR pathway via inhibition of the intermediary GTP binding protein Rheb."
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"TSC2 is phosphorylated and inactivated by Akt and the TSC1 and TSC2 complex negatively regulates the kinase mTOR."
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"Their protein products, hamartin and tuberin, respectively, form a dimer that acts via the GAP protein Rheb (Ras homolog enhanced in brain) to directly inhibit mTOR, again resulting in upregulation."
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"Since the TSC1 and TSC2 complex negatively regulates mTOR activity, the enlarged neurons of cortical tubers have high mTOR activity as measured by increased ribosomal protein S6 phosphorylation."
bel
"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"
bel
"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]."