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FGF2 — PI3

Text-mined interactions from Literome

Donowitz et al., Ann N Y Acad Sci 2000 : PI 3-kinase was also involved in FGF stimulation of NHE3 expressed in fibroblasts
Hadari et al., Proc Natl Acad Sci U S A 2001 : Experiments with FRS2 alpha-deficient fibroblasts demonstrate that FRS2 alpha plays a critical role in FGF induced mitogen activated protein ( MAP ) kinase stimulation, phosphatidylinositol-3 (PI-3) kinase activation, chemotactic response, and cell proliferation
Zeng et al., J Biol Chem 2002 : 5 ( S ) -HETE induced the expression of basic fibroblast growth factor 2 ( bFGF-2 ) in a Jak-2- and PI3-kinase dependent manner ... Together these results suggest that 5 ( S ) -HETE stimulates HMVEC growth via Jak-2- and PI3-kinase dependent induction of expression of bFGF-2
Mochizuki et al., Oncogene 2002 : No increase in FGF-2 induced PI3-kinase activity was observed in proteins immunoprecipitated by anti-phosphotyrosine antibody ... Although stable expression of deleted mutant p85alpha regulatory subunit, which lacks association with p110 catalytic subunit, in IBE cells showed no dominant negative effect, transient expression of dominant negative Ras inhibited FGF-2 mediated PI3-kinase activation ... These results suggest that only activated Ras contributed the FGF-2 mediated PI3-kinase activation ... Taken together, activation of PI3-kinase by FGF-2 is Ras dependent and results in down-regulation of uPA production
Lee et al., Invest Ophthalmol Vis Sci 2003 : FGF-2 at 10 ng/mL markedly stimulated PI 3-kinase enzyme activity, and stimulation with FGF-2 also caused activation of Akt
Lee et al., Invest Ophthalmol Vis Sci 2003 : Results in an earlier study showed that FGF-2 activates phosphatidylinositol (PI) 3-kinase to stimulate the cell cycle machinery
Chandrasekher et al., Invest Ophthalmol Vis Sci 2003 : The presence of FGF-2 in proliferating rabbit lens epithelial cells enhanced the IGF-1-, but not the PDGF mediated PI-3K activation, suggesting a possible integration of FGF-2 signals with IGF-1
Qi et al., Angiogenesis 1999 : Activation of PI3-kinase was strictly required for FGF-2- and VEGF-A ( 165 ) -induced migration and DNA synthesis of BCE cells
Lee et al., J Biol Chem 2004 (Inflammation) : This early and rapid activation of PI 3-kinase greatly enhanced FGF-2 production in CECs ; pretreatment with LY294002 hampered the induction activity of IL-1 beta
Shi et al., Zhonghua Yi Xue Za Zhi 2004 (Breast Neoplasms) : [ Activation of HIF-1 by bFGF in breast cancer : role of PI-3K and MEK1/ERK pathways ]
Mannell et al., J Vasc Res 2008 : The inhibitory effect of SHP-2 knock-down on vessel growth was mediated by increased endothelial apoptosis ( annexin V staining, p < 0.05, n = 9 ), which was associated with reduced FGF-2 induced phosphorylation of phosphatidylinositol 3-kinase (PI3-K) , Akt and extracellular regulated kinase 1/2 ( ERK1/2 ) and involved diminished ERK1/2 phosphorylation after PI3-K inhibition ( n = 3 )
Luo et al., Biochem Pharmacol 2008 : Results showed that bFGF significantly increased mRNA expression of FGF receptor (FGFR)1 and FGFR2 at 10 min and increased expression of phosphorylated extracellular signal regulated kinase ( pERK1/pERK2 ) but not phosphorylated p38 mitogen activated protein kinase ( MAPK ) or phosphorylated phosphatidylinositol 3-kinase (PI3K) within 30 min
Kanazawa et al., PloS one 2010 (MAP Kinase Signaling System) : bFGF activated RhoA, Rac1, PI3-kinase , and JNK in cultured fibroblasts
Lee et al., Invest Ophthalmol Vis Sci 2012 : The induction of FGF-2 by IL-1ß was completely blocked by inhibitors to NF-?B activation ( sulfasalazine ) or PI 3-kinase ( LY294002 ), and both inhibitors greatly blocked cell proliferation of CECs
Kinehara et al., PloS one 2013 : Our study suggested complicated cross-talk in hPS cells that FGF-2 induced the phosphorylation of phosphatidylinositol-3 kinase (PI3K)/AKT , mitogen activated protein kinase/ERK-1/2 kinase ( MEK ), PKC/ERK-1/2 kinase, and PKC/GSK-3ß