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RPS6KB1 phosphorylates IRS1 on S636. 15 / 15
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"IRS-1 S302 and S632 (S307 and S636, respectively, in humans) are directly phosphorylated by S6K1 and mTORC1, respectively (Copps and White, 2012)."

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"In addition, when mTORC1 is activated, S6K1 could directly phosphorylate Insulin receptor substrate 1 (IRS1; S307 and S636 and S639) and promote its degradation, which subsequently blunts phosphoinositide 3-kinase (PI3K)-AKT activation and its downstream effects such as glucose uptake and glycogen accumulation."

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"Together, this may suggest that T-cad upregulation in SHR might be a characteristic feature of hypertensive and insulin resistant VSMC phenotype.Attenuation of insulin signaling is achieved through a [MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

No evidence text available

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"P70S6K phosphorylates IRS-1 on S312 and/or S636 and S639."

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"Moreover, mTORC1 and S6K1 activation directly mediated the hyperphosphorylation of IRS-1 Ser636 upon alpha-Syn overexpression, while PP2A activation reversed this process in SK-N-SH cells and transgen[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

"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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"These results indicate that alpha-Syn overexpression negatively regulates IRS-1 at least in part by stimulating IRS-1 Ser636 phosphorylation and tyrosine dephosphorylation by mTORC1 and S6K1."

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"When mTORC1 is activated, S6K1 could directly phosphorylate IRS1 (S307 and S636/S639) and promote its degradation, which subsequently blunts PI3K-AKT activation and its downstream effects such as glucose uptake, glycogen accumulation, etc. [2,3]."

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"Inhibition of mTOR and S6K1 by HM-chromanone significantly reduced IRS-1 Ser307 and IRS-1 Ser632 phosphorylation, leading to insulin resistance."

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"IRS-1 S302 and S632 (S307 and S636, respectively, in humans) are directly phosphorylated by S6K1 and mTORC1, respectively ( Copps and White, 2012 )."

"Nevertheless, s6k1-deficient mice remain sensitive to insulin owing to the apparent loss of a negative feedback loop from s6k1 to insulin receptor substrate 1 (irs1), which blunts s307 and s636/s639 phosphorylation; thus under conditions of nutrient satiation s6k1 negatively regulatesinsulin."

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"IRS-1 is phosphorylated at Ser636 by S6K1 which is activated by mTOR."

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"P70S6K can phosphorylate IRS-1 on S312 and/or S636 and S639."

No evidence text available