Gene interactions and pathways from curated databases and text-mining

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CSF2 — PI3

Text-mined interactions from Literome

Al-Shami et al., J Biol Chem 1999 : Here we report that pretreating the cells with a Jak2 inhibitor ( AG-490 ) abolishes tyrosine phosphorylation of the p85 subunit of PI3-kinase induced by GM-CSF ... These results suggest that stimulation of the activity of PI3-kinase induced by GM-CSF is mediated by Jak2 and that the association between Jak2 and p85 depends on an adaptor protein yet to be identified
Senokuchi et al., Atherosclerosis 2004 (Arteriosclerosis...) : Recombinant GM-CSF induced PI-3K activation and Akt phosphorylation were significantly inhibited by SB203580 but enhanced by PD98059
Dhar-Mascareno et al., Biochem Biophys Res Commun 2005 : PI3-kinase activation by GM-CSF in endothelium is upstream of Jak/Stat pathway : role of alphaGMR ... GM-CSF induced tube formation in human umbilical vein endothelial cells, as examined using Matrigel assay, was inhibited by specific inhibitors of PI3-kinase , wortmannin, and LY294002 ... These studies underscore the significance of the GM-CSF mediated PI3-kinase activation and its role in angiogenesis
Lasbury et al., Infect Immun 2009 (Pneumonia, Pneumocystis) : Calmodulin has been implicated in control of GM-CSF production and PI-3K activation in other immune cell types
Jücker et al., J Biol Chem 1995 (Leukemia, Erythroblastic, Acute) : Binding of human granulocyte/macrophage colony stimulating factor ( hGM-CSF ) to its receptor induces the rapid activation of phosphatidylinositol-3 kinase ( PI 3-kinase )
Gold et al., J Biol Chem 1994 : We show that interleukin-3 (IL-3), interleukin-4 (IL-4), interleukin-5 (IL-5), granulocyte-macrophage colony stimulating factor ( GM-CSF ), and steel factor ( SLF ) all activate PI 3-kinase
Yusoff et al., Growth Factors 1994 : GM-CSF also stimulated PI 3-kinase activity although to a lesser extent than CSF-1, correlating well with their degree of mitogenic activity on the BMM
Sato et al., EMBO J 1993 : GM-CSF increased phosphatidylinositol 3 kinase (PI3-K) activity in anti-phosphotyrosine immunoprecipitates from cells expressing beta 763 as well as beta c, whereas it was only marginally increased from cells expressing beta 517 or beta 626
al-Shami et al., Blood 1997 : Although granulocyte-macrophage colony stimulating factor ( GM-CSF ) has been shown to activate PI3-kinase , the mechanisms by which this activation is mediated and regulated are incompletely understood ... 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
Kubota et al., Cell Growth Differ 1998 : Accordingly, activation of PDGF-R-, CSF-1R- , and EK-R expressing cells led to an increase in PI3-kinase activity