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ARHGEF7 — PI3

Text-mined interactions from Literome

Jiang et al., Diabetes 1999 : Pretreatment of cells with ET-1 ( 10 nmol/l ) inhibited insulin stimulated PI 3-kinase activity associated with IRS-2 by 50-60 % and inhibited the association of p85 subunit of PI 3-kinase to IRS-2
Gillooly et al., Biochem J 1999 : A p85 dependent PI 3-kinase was shown to be involved in the initial phase of FcgammaRI mediated endocytosis, but not in the trafficking of immune complexes for degradation or the activation of phospholipase D
Ueki et al., Mol Cell Biol 2000 : Expression of a p85alpha mutant lacking the p110 binding site ( Deltap85 ) also inhibited phosphotyrosine associated PI 3-kinase activity but not p110 associated activity
Arribas et al., J Biol Chem 2003 : In brown adipocytes expressing the IRS-3F4 mutant, the association of the p85alpha regulatory subunit via Src homology 2 binding was lost, but insulin nevertheless induced PI 3-kinase activity and Akt phosphorylation in a wortmannin dependent manner
Serve et al., J Biol Chem 1994 : These results indicate that tyrosine 719 within the 719YMDM motif in the kinase insert plays an important role in binding of p85 and that its phosphorylation is a prerequisite for binding of p85 and the subsequent activation of PI 3-kinase
Klippel et al., Mol Cell Biol 1994 : We also show that the association of p85 and p110 mediated by these domains is critical for PI 3-kinase activity
Cerboni et al., Eur J Immunol 1998 : CD16 mediated activation of phosphatidylinositol-3 kinase (PI-3K) in human NK cells involves tyrosine phosphorylation of Cbl and its association with Grb2, Shc, pp36 and p85 PI-3K subunit