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CBFA2T2 — PI3

Text-mined interactions from Literome

Hakak et al., Oncogene 2000 : Activation of PI3-kinase by v-Src may be mediated by the association of the adapter protein Cbl with the p85 subunit
Bilderback et al., J Neurochem 2001 : NGF stimulated PI 3-kinase activity was necessary for inhibition of acid SMase but was not required for ligand induced association of the p85 subunit of PI 3-kinase with the phospholipase
Rieusset et al., FEBS Lett 2001 : Up-regulation of p85alphaPI-3K gene expression resulted in a rise in p85alphaPI-3K protein level and in an increase in insulin induced PI3-kinase activity
Hers et al., Biochem J 2002 : In contrast, inhibition of PI 3-kinase led to a decrease in insulin stimulated p85 binding to IRS-3, but had no effect on SHP-2 binding
Hill et al., Biochim Biophys Acta 2004 : The dose-response relationships at 10-min insulin ( 10 to 300 nM ) stimulation showed that IRS-1 and pY-IRS-1 responded to 100 and 300 nM insulin, and the p85 PI3-kinase response peaked at 30 nM insulin
Komori et al., Clinical calcium 2006 : Phosphoinositide 3-kinase (PI3K)-Akt signaling enhances DNA binding of Runx2 and Runx2 dependent transcription, and Runx2 upregulates PI3K subunits ( p85 and p110 beta ) and Akt
Matheu et al., J Immunol 2007 : Our results show, for the first time, that class IA PI3Ks play an important role in regulating basal lymphocyte motility and that p85alpha regulatory subunit expression is required to maintain B cell morphology in a manner independent of PI3K catalytic function
Adochio et al., Endocrinology 2009 (Insulin Resistance) : Reduction in expression of either p85alpha or S6K1 achieved with small interfering RNA in the presence of myristoylated Akt rescued 3T3-L1 adipocytes from the insulin resistance induced by serine phosphorylation of IRS-1 and completely restored insulin stimulated activation of PI 3-kinase and glucose uptake
Wu et al., Proc Natl Acad Sci U S A 2009 : Regulation of Class IA PI 3-kinases : C2 domain-iSH2 domain contacts inhibit p85/p110alpha and are disrupted in oncogenic p85 mutants
Liu et al., Mol Cell Biol 1993 : These results suggest that the v-Src SH3 domain may mediate an interaction between the v-Src tyrosine kinase and PI 3'-kinase , by direct binding to p85
al-Shami et al., Blood 1997 : The simultaneous treatment of the cells with GM-CSF and phorbol esters such as phorbol 12-myristate 13-acetate ( PMA ) and phorbol 12,13-dibutyrate ( PDBu ) significantly inhibited both the tyrosine phosphorylation of p85 and the activation of PI3-kinase ... The results suggest that the activation of PI3-kinase by GM-CSF is mediated by the tyrosine phosphorylation of p85 and that this activation is downregulated by PKC possibly via the inhibition of lyn