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INSR — PI3

Text-mined interactions from Literome

Benzeroual et al., Biochim Biophys Acta 2000 : Our data demonstrate that the stimulation of PI 3-kinase activity by the activated insulin receptor , but not the phosphorylation of IR beta-subunit and IRS-1, requires an influx of Ca ( 2+ )
Goldfine et al., Metabolism 2000 (Diabetes Mellitus, Type 2) : Vanadyl modifies proteins in human skeletal muscle involved in early insulin signaling, including basal insulin receptor and substrate tyrosine phosphorylation and activation of PI 3-kinase , and is not additive or synergistic with insulin at these steps
Hers et al., Biochem J 2002 : Furthermore, insulin induced insulin receptor tyrosine phosphorylation, phosphorylation of Tyr ( 1158 ) and insulin receptor tyrosine kinase activity were all reduced by inhibition of PI 3-kinase at later time points ( > or=20 min )
Ogihara et al., Hypertension 2002 (Hyperinsulinism...) : Despite the insulin resistance, insulin induced tyrosine phosphorylation of the insulin receptor and insulin receptor substrates, activation of phosphatidylinositol (PI) 3-kinase , and phosphorylation of Akt were all enhanced by AII infusion
Kanda et al., Biochem Biophys Res Commun 2003 : However, VEGFR-2, insulin receptor substrate-1, and c-Src were also involved in VEGF-A induced activation of PI3-kinase , resulting in the compensation in cells expressing kinase-inactive c-Fes
Fisslthaler et al., Nitric Oxide 2003 : Insulin applied to native porcine aortic endothelial cells elicited the tyrosine phosphorylation of the insulin receptor and receptor substrate, the subsequent activation of phosphatidylinositol 3-kinase (PI 3-K) , Akt ( protein kinase B ), and ERK1/2
Rajala et al., Mol Neurobiol 2003 : This article, describes recent studies that link the photobleaching of rhodopsin to tyrosine phosphorylation of the insulin receptor and subsequent activation of phosphoinositide 3- kinase (PI3K)
Chang et al., J Biol Chem 1995 : We conclude that ( i ) transgenic expression of kinase-defective insulin receptors exerts dominant negative effects at the level of receptor auto-phosphorylation and kinase activation ; ( ii ) insulin receptor tyrosine kinase activity is required for in vivo insulin stimulated IRS-1 phosphorylation, IRS-1 associated PI 3-kinase activation, phosphorylation of mitogen activated protein kinase, and c-fos gene induction in skeletal muscle ; ( iii ) hybrid receptor formation is likely to contribute to the in vivo dominant negative effects of kinase-defective receptor expression
Yenush et al., Mol Cell Biol 1996 : IRS-1 was required by the human insulin receptor to activate PI 3-kinase and p70s6k, whereas hDIR associated with PI 3-kinase and activated p70s6k without IRS-1