A database built with INDRA combining content from numerous readers and databases. This page allows you to curate the loaded statements. For more information please see the manual.

IndraLab

Statements

databases
phosphosite cbn pc11 biopax bel_lc signor biogrid tas lincs_drug hprd trrust | geneways tees isi trips rlimsp medscan sparser reach
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"In cancer, there is an increase in the activity of PI3K-AKT axis, and TSC1 and TSC2 is inhibited by AKT, allowing mTORC1 activation and subsequently activation of P70S6K1 and EIF4e."
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"The ability of WISP1 to limit TSC2 (Ser 1387) phosphorylation appears to allow WISP1 to increase the activity of p70S6K."
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"Over-expression of TSC1 and TSC2 also markedly inhibited S6K1, positioning TSC1 and TSC2 upstream of S6K1."
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"Hamartin with alanine mutations in the three cyclin-dependent kinase 1 phosphorylation sites increased the inhibition of p70S6 kinase by the hamartin-tuberin complex."
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"Hamartin with alanine mutations in the three cyclin-dependent kinase 1 phosphorylation sites increased the inhibition of p70S6 kinase by the hamartin-tuberin complex."
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"The loss of TSC2, which is upstream of mTOR, activates S6K1, promotes cell growth and survival, activates mTOR kinase activities, inhibits mTORC1 and mTORC2 via mTOR inhibitors, and suppresses S6K1 and Akt."
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"Here we review recent findings demonstrating that the TSC1 and TSC2 inhibitory complex normally acts on Rheb to mediate mTOR and S6K1 signalling."
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"Under the condition of starvation, AMPK phosphorylates tuberous sclerosis 2 (TSC2), which inhibits mTOR and S6K1 pathway [XREF_BIBR] : phosphorylation of TSC2 by AMPK is critical in the process of mRNA translation and cell size regulation during energy deficiency (XREF_FIG)."
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"The ability of WISP1 to limit TSC2 (Ser 1387) phosphorylation appears to allow WISP1 to increase the activity of p70S6K, since gene silencing of TSC2 further enhances WISP1 phosphorylation of p70S6K."
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"Moreover, in mammalian cells in culture, co-overexpression of TSC1 and TSC2 prevents amino acid dependent activation of S6K1 [XREF_BIBR]."
Mutated TSC2 inhibits RPS6KB1. 2 / 2
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"Finally, we find that a tuberin mutant lacking the major PI3K dependent phosphorylation sites can block the activation of S6K1, suggesting a means by which the PI3K-Akt pathway regulates S6K1 activity."
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"Finally, a tuberin mutant lacking the major PI3K dependent phosphorylation sites blocked the activation of S6K1, suggesting a means by which the PI3K-Akt pathway regulates S6K1 activity [XREF_BIBR]."
TSC2 inhibits RPS6KB1. 1 / 1
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bel
"Tuberin interferes with insulin-like growth factor-1-induced BAD Ser136 phosphorylation and cell survival. Our work proposes a model in which tuberin-mediated inhibition of p70S6K activates BAD to heterodimerize with BCL-2 and BCL-XL to promote apoptosis. A mutation of TSC2--as it occurs in TSC patients--attenuates this proapoptotic potential, underscoring the relevance of our findings for human pathophysiology."
TSC2 inhibits RPS6KB1-S6K. 1 / 1
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"siRNA mediated knockdown of both TSC2 and Rictor elevates p70 S6K activation and induces differentiation of hESCs."
TSC2 bound to TSC1 inhibits RPS6KB1. 1 / 1
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"Loss of TSC2 GAP activity or disruption of the TSC1 and TSC2 complex dysregulates S6K1 activation, which leads to abnormal cell proliferation associated with LAM disease."
TSC2 phosphorylated on S1798 inhibits RPS6KB1. 1 / 1
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bel
"TSC2 S1798A mutant.Thi s mutant was used to prove that RSK-dependent phosphorylation of tuberin on Ser1798 inhibits its potential to turn off Rheb and to downregulate the activities of mTOR and p70S6K.Mu tation of Ser1798 inhibited most of tuberin phosphorylation and inactivation by RSK (Roux et al., 2004).Invest igating PARP cleavage, caspase 3 cleavage, the percentage of HOPI-positive cells and the percentage of subG1 cells demonstrated that the cell survival effects of activated Ras over tuberin-induced apoptosis are significantly diminished by this mutation in TSC2 (Figures 5a–c)."