Gene interactions and pathways from curated databases and text-mining

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AKT1 — ARHGEF7

Protein-Protein interactions - manually collected from original source literature:

Studies that report less than 10 interactions are marked with *

Text-mined interactions from Literome

Lu-Kuo et al., J Biol Chem 2000 : In contrast, p85alpha gene products were not required for FcepsilonRI initiated exocytosis and phosphorylation of Akt
Wang et al., J Biol Chem 2000 : Expression of a dominant negative mutant of p85 ( regulatory component of PI3-K ) and treatment with inhibitors of PI3-K ( wortmannin and LY294002 ) prevented H ( 2 ) O ( 2 ) -induced Akt activation
Lee et al., Cancer Res 2001 (Breast Neoplasms) : p85-sErbB3 inhibits HRG induced phosphorylation of ErbB2, ErbB3, and ErbB4 in breast carcinoma derived cell lines and can also block HRG stimulated activation of mitogen activated protein kinase, Akt , and association of ErbB3 with the phosphatidylinositol 3'-kinase p85 regulatory subunit
Sithanandam et al., Carcinogenesis 2003 (Adenocarcinoma...) : Serum treatment increased the pErbB3/p85 complexes and also stimulated phosphorylation of Akt and GSK3beta, increase in cyclin D1 and cell cycle progression, and these events were blocked by the Akt activation inhibitor LY294002
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
Bridgewater et al., Kidney Int 2005 : IGF-1 stimulation resulted in the formation of the insulin receptor substrate (IRS)-1-p85 complex, an increase in PI3 kinase activity, and activation of protein kinase B ( AKT/PKB ) and the bcl-2 family member bad ... IGF-1 stimulation resulted in the formation of the insulin receptor substrate (IRS)-1-p85 complex, an increase in PI3 kinase activity, and activation of protein kinase B ( AKT/PKB ) and the bcl-2 family member bad
Kubo et al., Biochem J 2005 : Specific role for p85/p110beta in GTP-binding-protein mediated activation of Akt
Xu et al., Hippocampus 2007 (Brain Infarction...) : W-13, an active CaM inhibitor, prevented the combination of CaM and p85 and subsequent Akt activation
Jaiswal et al., Cancer Cell 2009 (Cell Transformation, Neoplastic...) : The p85alpha mutants promote cell survival, AKT activation, anchorage independent cell growth, and oncogenesis in a p110 dependent manner
Cooper et al., PloS one 2011 : Similarly, depletion of the PI3K regulatory subunits p85a and p85ß by RNAi had no inhibitory effect on SopB dependent Akt phosphorylation