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Akt Phosphorylation - U.S. Department of Veterans Affairs

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Last Updated: 13 February 2022

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Plk1 phosphorylation of IRS2 prevents premature mitotic exit via AKT inactivation.

Insulin receptor substrate proteins play a vital role in transducing signals from transmembrane receptors on growth factor stimulation by acting as a platform for transmembrane receptor substrates. Although tyrosine phosphorylation of IRS proteins is a key component of signal transduction, phosphorylation of IRS proteins on serine/threonine residues is thought to play various regulatory roles in IRS protein function. Phosphorylation of IRS2 at these two serine residues by Plk1 stops the PI3K pathway from being activated by growth factor stimulation by reducing the interaction between IRS2 and the PI3K pathway components and increasing the rate of IRS2 protein degradation.

Source link: https://doi.org/10.1021/acs.biochem.5b00016


Rescuing 3T3-L1 adipocytes from insulin resistance induced by stimulation of Akt-mammalian target of rapamycin/p70 S6 kinase (S6K1) pathway and serine phosphorylation of insulin receptor substrate-1: effect of reduced expression of p85alpha subunit of phosphatidylinositol 3-kinase and S6K1 kinase.

Phosphorylation of insulin receptor substrate-1 on serine residues has been recognized as a factor responsible for a decrease in insulin action and insulin resistance. Implication with and/or decrease in the expression of certain signaling intermediates that participate in insulin resistance's pathogenesis can lead to insulin resistance's sensitivity. We then reduced the expression of the PI 3-kinase regulatory subunit, p85alpha, or expression of S6K1 kinase using small interfering RNA transfections, resulting in a decrease in p85alpha expression at 48 h and S6K1 of 49 percent.

Source link: https://doi.org/10.1210/en.2008-0437

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions