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ANXA6 — IRS1

Text-mined interactions from Literome

Ishibashi et al., J Clin Invest 2001 : Chronic ET-1 treatment inhibited insulin stimulated tyrosine phosphorylation of G alpha q/11 and IRS-1, as well as their association with PI3-kinase and blocked the activation of PI3-kinase activity and phosphorylation of AKT : In addition, chronic ET-1 treatment caused IRS-1 degradation, which could be blocked by inhibitors of PI3-kinase or p70 S6-kinase
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
Obata et al., Circ Res 1996 : In this study, we observed that > or = 1 nmol/L insulin stimulated tyrosine phosphorylation of insulin receptor substrate-1 (IRS-1) and activated IRS-1 dependent phosphatidylinositol 3'-kinase ( PI 3'-kinase ) and p70 S6 kinase (p70S6K) but not MAP kinase ( extracellular signal regulated kinase 2 ) and p90 S6 kinase ( p90RSK )
Sharma et al., Mol Cell Biol 1997 : In both cell types, overexpression of either the PTB or the SAIN protein caused a significant decrease in insulin induced tyrosine phosphorylation of IRS-1 and Shc proteins, IRS-1 associated phosphatidylinositol 3-kinase (PI 3-K) enzymatic activity, p70s6k activation , and p44 and p42 mitogen activated protein kinase ( MAPK ) phosphorylation ... Thus, interference with the IRS-1-IR interaction inhibits insulin stimulated IRS-1 and Shc phosphorylation, PI 3-K enzymatic activity, p70s6k activation, MAPK phosphorylation and cell cycle progression