IndraLab

Statements


RPS6KB1 decreases the amount of IRS1. 8 / 8
3 | 5

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"The mechanism behind this may be that suppression of S6K (p70S6K) activity stabilizes IRS-1 and increases IRS-1 adapter protein levels, which in turn induces Akt activity."

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"Similar results were reported in mice, that is, S6K1 mRNA was elevated, thereby inhibiting the expression of IRS-1 by inducing IRS-1 degradation 21."

"In this report, we identified insulin receptor substrate 1 (IRS-1), a critical mediator of the insulin/insulin-like growth factor 1 signaling, as a proteolytic target of the CUL7 E3 ligase in a manner that depends on mammalian target of rapamycin and the p70 S6 kinase activities.Elimination of phosphorylation at S307/S312/S527/S636/S639 renders V5-IRS-1 partially resistant to degradation by Fbw8"

"In this report, we identified insulin receptor substrate 1 (IRS-1), a critical mediator of the insulin/insulin-like growth factor 1 signaling, as a proteolytic target of the CUL7 E3 ligase in a manner that depends on mammalian target of rapamycin and the p70 S6 kinase activities.Elimination of phosphorylation at S307/S312/S527/S636/S639 renders V5-IRS-1 partially resistant to degradation by Fbw8"

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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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"Loss-of-function and pharmacological inhibition studies have shown that the mTOR target S6K1, for instance, inhibits and desensitizes insulin-PI3K signaling by phosphorylating IRS1 protein and suppressing IRS1 gene transcription."

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"These data suggest that the physiological activation of S6K1 does not mediate the decrease of IRS-1 protein level during myoblast differentiation and has no effect on myotube formation."

"In this report, we identified insulin receptor substrate 1 (IRS-1), a critical mediator of the insulin/insulin-like growth factor 1 signaling, as a proteolytic target of the CUL7 E3 ligase in a manner that depends on mammalian target of rapamycin and the p70 S6 kinase activities.Elimination of phosphorylation at S307/S312/S527/S636/S639 renders V5-IRS-1 partially resistant to degradation by Fbw8"