IndraLab

Statements

MTORC1 decreases the amount of IRS1. 16 / 16
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"Chronic activation of S6K1 and mTORC1 promotes IRS-1 degradation via phosphorylation of Ser265, 307, 522, and 636 and inhibits IRS-1 transcription (Copps and White, 2012)."
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"Akt signaling activates mTORC1 and S6K, which then suppresses IRS1 expression, serving as an additional regulatory mechanism (44)."
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"Consistent with previous studies demonstrating that chronic mTORC1 activation decreases both the expression and stability of IRS-1 and IRS-2 XREF_BIBR, XREF_BIBR, XREF_BIBR, we find that 24 h treatment with rapamycin increases Irs-1 and Irs-2 transcript levels and IRS-1 protein levels in Tsc2 -/- adipocytes, albeit to levels still significantly lower than Tsc2 +/+ adipocytes (XREF_SUPPLEMENTARY, panels A and B)."
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"Direct inhibition of mTORC1 with rapamycin blocks S6Kinase dependent feedback inhibition of IRS-1 expression and activates IGF-1R signaling."
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"AMPK inhibits mTORC1 via raptor or TSC phosphorylations [XREF_BIBR, XREF_BIBR] and supports IRS-1 and Akt expressions."
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"Further, AKT activates TORC1 and S6K, which repress IRS1 expression in order to regulate pathway signaling output."
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"The continuous activation of mTORC1 in cultured cells suppresses insulin dependent activation of PI3K by downregulating IRS1 (insulin receptor substrate-1) gene expression or by inhibitory phosphorylation of IRS-1."
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"Inhibition of mTORC1 with rapamycin has been known to increase IRS-1 levels and induce AKT phosphorylation and downstream signaling [XREF_BIBR]."
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"First, S6K, a substrate of mTORC1, decreases the activity and protein levels of IRS1 by phosphorylating it (Harrington et al., 2004; Um et al., 2004; Shah et al., 2004)."
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"8 This may be in part due to the presence of a negative feedback mechanism, whereby inhibition of mTORC1 induces insulin receptor substrate IRS-1 expression leading to upregulation of IGF1R-dependent [MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"Moreover, inhibition of mTORC1 with either rapamycin or raptor knockdown did not elevate IRS-1 levels, despite potently increasing Akt phosphorylation."
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"The feedback observed in EGFR and HER2 driven cancers is distinct from a well described feedback mechanism in which mTORC1 inhibition leads to increased IRS-1 expression and up-regulation of IGF-IR and IRS signaling."
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"Specifically, mTORC1 impairs PI3K activation in response to growth factors by downregulating the expression of Insulin Receptor Substrate 1 and 2 (IRS-1/2) and Platelet Derived Growth Factor Receptor-Beta (PDGFR-beta) (reviewed in)."
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"AKT activation also leads to activation of TORC1 and S6K which inhibits IRS1 expression, resulting in reduced signalling.With the use of PI3K inhibitors, the phosphorylation of FOXO by AKT is suppressed, leading to the stimulation of RTKs and partial restoration of PIP3 activity."
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"Notably, rapalog-mediated inhibition of mTORC1/S6K1 signaling increases the level of insulin receptor substrate-1 (IRS1) and facilitates hyperactivation of the survival-promoting PI3K/AKT pathway [65]."
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"Consistent with previous findings [XREF_BIBR], inhibition of mTORC1 by raptor knockdown or short-term rapamycin treatment slightly enhanced IRS-1 expression."
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