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
reading

MTOR inhibits IRS1. 10 / 35
7 | 5 21
reach
"Inhibition of mTOR has been shown to inhibit proteasomal degradation of IRS-1 enhancing signaling through the PI-3 kinase and Akt pathway."
reach
"Rapamycin has been reported to have alternate effects on Akt phosphorylation; prolonged rapamycin exposure has been shown to inhibit assembly of mTORC2, thereby inhibiting Akt, and mTOR inhibition has also been described to induce insulin receptor substrate-1 (IRS-1), leading to Akt activation."
reach
"O'Reilly et al. provide evidence that poor tumor response to rapamycins is the result of relieving mTOR mediated feedback inhibition of insulin receptor substrate 1, and activation of Akt mediated survival."
reach
"XREF_BIBR - XREF_BIBR Recent data suggest that the inhibition of mTOR relieves negative feedback regulation of IRS-1, resulting in increased IRS-1 expression and activation of AKT."
reach
"In these cells, Shh upregulates IRS-1 by interfering with mTOR mediated IRS-1 degradation, and by enhancing IRS-1 translation."
reach
"A negative feedback loop has been described, whereby mTOR and S6K1 activation attenuates PI3K signaling by suppressing insulin receptor substrate-1 (IRS1) function, a mediator of insulin receptor- dependent activation of PI3K."
reach
"Thus, the CUL7 E3 appears to be responsible for mediating mTOR dependent degradation of IRS-1, thereby functioning as a critical component of the mTOR and IRS -1 negative feedback loop, which fine-tunes the PI3K activity in accordance with the magnitude and duration of mTOR and S6K activities."
signor
"Mtor induced the serine phosphorylation of irs-1 (ser-636/639), and such phosphorylation was inhibited by rapamycin. These results suggest that tnf impairs insulin signaling through irs-1 by activation of a pi 3-kinase/akt/mtor pathway, which is antagonized by pten"
sparser
"For example, mTOR and its downstream S6K can inhibit the upstream insulin signaling molecule IRS-1 to regulate glucose uptake and protein synthesis [ xref , xref ]."
reach
"In early studies mTOR inhibition led to p70 ribosomal protein S6 kinase (S6K) suppression, IRS1 upregulation, and PI3K-AKT activation 181."
Kinase-active MTOR inhibits IRS1. 1 / 1
1 |
bel
"Here, we demonstrate that nutrients suppress phosphatidylinositol 3 (PI3)-kinase/Akt signaling via Raptor-dependent mTOR (mammalian target of rapamycin)-mediated phosphorylation of insulin receptor substrate 1 (IRS-1). Raptor directly binds to and serves as a scaffold for mTOR-mediated phosphorylation of IRS-1 on Ser636/639"