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IRS1 — NOS3

Text-mined interactions from Literome

Kim et al., Arterioscler Thromb Vasc Biol 2005 : Insulin receptor substrate-1 (IRS-1) regulation is critical for activation of endothelial nitric oxide synthase (eNOS) in response to stimulation by insulin or fluid shear stress
Sugita et al., J Biol Chem 2005 : Inducible nitric-oxide synthase and NO donor induce insulin receptor substrate-1 degradation in skeletal muscle cells
Kim et al., J Mol Cell Cardiol 2005 : Since activation of endothelial nitric oxide synthase (eNOS) is dependent on IRS-1/PI3-kinase signaling, we hypothesized that activation of IKKbeta may contribute to the effect of glucose to impair NO production
Xu et al., Mol Endocrinol 2007 (Insulin Resistance...) : Recombinant CRP suppressed insulin induced NO production, inhibited the phosphorylation of Akt and endothelial nitric oxide synthase , and stimulated the phosphorylation of IRS-1 at the Ser307 site in a dose dependent manner
Kim et al., Am J Physiol Endocrinol Metab 2012 : ANG II increased phosphorylation of insulin receptor substrate-1 (IRS-1) at Ser ( 636/639 ) and inhibited the insulin stimulated phosphorylation of endothelial nitric oxide synthase (eNOS)
Maeno et al., J Biol Chem 2012 (Metabolic Diseases) : Thr-86 of p85/PI3K was identified to be phosphorylated by PKC activation and confirmed to affect IRS1 mediated activation of Akt/eNOS by insulin and VEGF using a deletion mutant of the Thr-86 region of p85/PI3K