Gene interactions and pathways from curated databases and text-mining

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AKT2 — FGF2

Text-mined interactions from Literome

Ebner et al., J Neurosci Res 2000 : We demonstrate that PI3K and Akt ( Ser-473 phosphorylation ) are activated in response to platelet derived growth factor but not basic fibroblast growth factor-2 ( FGF2 ) and that distinct forms of PI3K are activated in early progenitors and later-maturation pro-oligodendroblasts as identified by their sensitivity to wortmannin ... Our results therefore demonstrate that PI3K-Akt signaling independently regulates proliferation and survival, that the form of PI3K is distinct in early progenitors and pro-oligodendroblasts, and that FGF2 does not activate this pathway in either primary glial cell population
Chaudhary et al., J Cell Biochem 2001 : The cell survival signal Akt is differentially activated by PDGF-BB, EGF, and FGF-2 in osteoblastic cells ... In this study we have investigated the signaling pathways activated by growth factors PDGF-BB, EGF, and FGF-2 and determined whether PDGF-BB, EGF, and FGF-2 activated Akt in human or mouse osteoblastic cells ... Taken together, our data for the first time revealed that the activation of ERK1/2 by PDGF-BB is mediated by PI 3-K, and secondly, Akt is activated by PDGF-BB and EGF but not by FGF-2 in human and mouse osteoblastic cells
Yanai et al., Invest Ophthalmol Vis Sci 2002 : Basic fibroblast growth factor , keratinocyte growth factor, nerve growth factor, and hepatocyte growth factor stimulated cell proliferation but did not induce Akt activation or protect the cells from SNP induced apoptosis ... Basic fibroblast growth factor , keratinocyte growth factor, nerve growth factor, and hepatocyte growth factor stimulated cell proliferation but did not induce Akt activation or protect the cells from SNP induced apoptosis
Sulpice et al., Blood 2002 (MAP Kinase Signaling System) : Surprisingly, PF-4 did not affect FGF2 induced Akt phosphorylation ... To exclude the possibility that PF-4 inhibited the binding of FGF2 to only one FGF receptor, preferentially activating the ERK pathway, we investigated the effect of PF-4 on FGF2 induced ERK and Akt phosphorylation, using mutant heparan sulfate-deficient Chinese hamster ovary cells transfected with the FGF-R1 cDNA
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
Salvarezza et al., J Neurochem 2003 : Also, bFGF activated AKT and ERKs in single P-neurons, and this activation was blocked by the same inhibitors
Varet et al., Cell Mol Life Sci 2003 (Neovascularization, Pathologic) : At the molecular level, fenofibrate markedly decreased basic fibroblast growth factor induced Akt activation and cyclooxygenase 2 gene expression
Lai et al., Oncogene 2004 (Carcinoma, Squamous Cell...) : Clonal lines of HSulf-1 expressing 012SCC attenuated the activation of ERK/mitogen activated protein kinase ( MAPK ) signaling mediated by fibroblast growth factor ( FGF-2 ) and both ERK/MAPK and Akt signaling mediated by hepatocyte growth factor (HGF)
Debiais et al., Exp Cell Res 2004 : FGF-2 increased PI3K activity but did not induce phosphorylation of Akt or the downstream effector p70 S6 kinase
Kokkinakis et al., J Neuropathol Exp Neurol 2004 (Cell Transformation, Neoplastic) : Western blot analyses demonstrated that MNU exposure caused progressive reduction of p21 protein levels, an increase of Rb phosphorylation, activation of AKT and CDK2, and upregulation of FGF receptors
Shi et al., Zhonghua Yi Xue Za Zhi 2004 (Breast Neoplasms) : SU5402 remarkably dose-dependently blocked the bFGF induced phosphorylation of ERK1/2, Akt and p38 ... 15 micromol/L LY294002 completely blocked the bFGF induced phosphorylation of Akt
Shi et al., J Pathol 2005 (Breast Neoplasms) : The data show that HIF-1alpha expression is induced by bFGF in a dose- and time dependent fashion, while increased HIF-1alpha protein expression and transactivity of HIF-1 are due to the phosphorylation of Akt by bFGF, as indicated by application of the phosphatidylinositol 3-kinase (PI-3K) inhibitor LY294002
Mao et al., J Cell Biol 2005 : Gab2 suppression reduces bFGF dependent activation of AKT but not ERK, and constitutively active AKT, but not constitutively active MEK1, reverses the hypersensitization
Cao et al., Am J Physiol Cell Physiol 2006 : Thrombin also induced the expression of FGF-2 in a PI3K-Akt-Fra-1 dependent and mTOR independent manner, and neutralizing anti-FGF-2 antibodies inhibited thrombin stimulated VSMC DNA synthesis and motility
Maffucci et al., Cancer Res 2005 (Ovarian Neoplasms) : Here, we show that FGF-2 induces Akt phosphorylation in HUVEC resulting in antiapoptotic effect in serum deprived cells and increase in cellular motility ... Ins ( 1,3,4,5,6 ) P5 blocks FGF-2 mediated Akt phosphorylation and inhibits both survival and migration in HUVEC
Li et al., FASEB J 2006 (MAP Kinase Signaling System) : Importantly, APO modulated FGF-2 expression was independent of Akt/phosphoinositide 3-kinase signaling
Azadi et al., Brain Res 2007 (Disease Models, Animal...) : To shed light on the underlying mechanisms, we studied the effects of 9 days ( starting at postnatal day 2 ) in vitro CNTF+BDNF treatment on the endogenous production of CNTF, BDNF, fibroblast growth factor 2 (FGF2), or the activation of extracellular signal regulated kinase ( ERK ), Akt and cAMP-response-element binding protein ( CREB ) in retinal explants ... To shed light on the underlying mechanisms, we studied the effects of 9 days ( starting at postnatal day 2 ) in vitro CNTF+BDNF treatment on the endogenous production of CNTF, BDNF, fibroblast growth factor 2 (FGF2) , or the activation of extracellular signal regulated kinase ( ERK ), Akt and cAMP-response-element binding protein ( CREB ) in retinal explants
Takai et al., Mol Cell Endocrinol 2007 : The phosphorylation of Akt induced by FGF-2 was markedly attenuated by wortmannin and LY294002, inhibitors of phosphatidylinositol 3-kinase ( PI3-kinase ) in osteoblast-like MC3T3-E1 cells ... Furthermore, the FGF-2 induced Akt phosphorylation was not affected by PD98059, a MEK inhibitor, or SP600125, a SAPK/JNK inhibitor
Erdogan et al., Journal of thrombosis and haemostasis : JTH 2007 : Basic fibroblast growth factor induced Akt phosphorylation was also reduced by Api
Johnson-Farley et al., Brain Res 2007 : Co-treatment with maximal concentrations of either IGF-1 or BDNF enhanced FGF-2 stimulated Akt and ERK activation
Ito et al., J Lipid Res 2007 : When rat apoE/pcDNA3.his was transfected to transformed rat astrocyte GA-1 cells that otherwise do not synthesize apoE ( GA-1/25 ), FGF-1 did not influence apoE-mRNA, but did increase the apoE secretion and Akt phosphorylation that were suppressed by LY294002
Tassi et al., Am J Physiol Regul Integr Comp Physiol 2007 (Spinal Cord Injuries) : At the molecular level, FGF-BP enhanced FGF2 induced protein tyrosine phosphorylation and AKT/PKB activation
Kim et al., Growth Factors 2007 : FGF induced a transient activation of ERK, but not Akt , which was inhibited by an inhibitor of MEK, the upstream kinase of ERK, but not by inhibitors of PI3K/Akt ( LY294002 ), epidermal growth factor receptor ( EGFR, AG1478 ), and Src ( PP2 )
Black et al., Am J Physiol Cell Physiol 2008 : In addition, FGF-2 mediated increases in FGF-2 expression and PASMC proliferation were attenuated by inhibition of phosphatidylinositol 3-kinase, Akt , and NADPH oxidase
Lu et al., Diabetes 2008 (Diabetes Mellitus, Type 2) : Because FGF2 stimulates the phosphatidylinositol 3-kinase (PI3K)-Akt pathway, we examined whether FGF2 transcription is regulated by Akt through a feedback mechanism ... In these cells, not only was Akt phosphorylation inhibited, but FGF2 transcription was also critically impaired
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 )
Ditlevsen et al., Neurochem Int 2008 : For comparison, we also evaluated the role of upstream signalling cascades on fibroblast growth factor 2 (FGF2) mediated phosphorylation of ERK, Akt , and CREB and found that FGF2 required the activity of both FGFR and Src-family kinases for phosphorylation of ERK, Akt, and CREB
Hayashi et al., Genes Cells 2008 : Here, we demonstrate that inhibition of the ERK pathway by the MEK inhibitor U0126 or PD98059 significantly potentiates EGF- and FGF induced Akt phosphorylation at both Thr308 and Ser473 ... We also show that hyperactivation of the ERK pathway greatly attenuates EGF- and FGF induced Akt phosphorylation
Vlotides et al., Endocrinology 2009 : Src inhibition with 4-amino-5- ( 4-chlorophenyl ) -7- ( t-butyl ) pyrazolo [ 3,4-d ] pyrimidine suppressed FGF-2 induced Akt and focal adhesion kinase, indicating effects downstream of FGF-2 induced Src activation
Palamakumbura et al., Oncogene 2009 (Prostatic Neoplasms) : FGF-2 stimulated DNA synthesis, ERK1/2, AKT and FRS2alpha activation were found all to be inhibited by LOX-PP in DU 145 cells
Maffucci et al., PloS one 2009 : Finally we show that PI3K dependent PLCgamma1 activation regulates FGF-2 mediated phosphorylation of Akt at its residue Ser473, determined by Western blotting analysis ... This occurs through protein kinase C (PKC)alpha activation since dowregulation of PKCalpha expression using specific siRNA or blockade of its activity using chemical inhibition affects the FGF-2 dependent Ser473 Akt phosphorylation
Wang et al., Invest Ophthalmol Vis Sci 2010 : Rat lens epithelial explants were used to compare the ability of vitreous, IGF-1, PDGF-A, EGF, and FGF-2 to stimulate the phosphorylation of ERK1/2 and Akt leading to fiber differentiation, in the presence or absence of selective receptor tyrosine kinase ( RTK ) inhibitors
Puhr et al., Endocr Relat Cancer 2010 (Carcinoma...) : In the presence of FGF-2 , neither STAT3, STAT1, nor Akt could be phosphorylated
Ramana et al., Mol Cancer Ther 2010 (Colonic Neoplasms) : More importantly, inhibition of AR prevented the EGF- and bFGF induced activation of phosphoinositide 3-kinase/AKT and reactive oxygen species generation in colon cancer cells
Dey et al., Cancer Res 2010 (Lung Neoplasms...) : Targeting fibroblast growth factor receptors blocks PI3K/AKT signaling, induces apoptosis, and impairs mammary tumor outgrowth and metastasis
Mailankot et al., Biochim Biophys Acta 2010 : Our data also show that KYN inhibits FGF2 induced Akt and ERK1/2 phosphorylation in mLEC, which are required for crystallin and MIP26 expression in the lens
Shiota et al., J Cell Mol Med 2012 : Moreover, depletion of extracellular FGF-2 by heparin prevented pravastatin induced phosphorylation of Akt and MAPK
Huang et al., Neurobiol Dis 2012 (Cerebral Hemorrhage, Traumatic) : Exogenous FGF2 increased activated FGFR, Akt , and Rac1 but reduced activated RhoA protein expression at 72 h after cICH ( p < 0.05, compared to vehicle ), which was reversed by FGFR and PI3K inhibition
Tsai et al., Biochem Pharmacol 2012 : While FGF did not enhance the phosphorylation of AKT in the CTR1 ( +/+ ) cells, both PDGF and EGF increased pAKT in the CTR1 ( +/+ ) but not CTR1 ( -/- ) cells
Sun et al., Biomaterials 2013 (MAP Kinase Signaling System) : The effects of luminescent ruthenium ( II ) polypyridyl functionalized selenium nanoparticles on bFGF induced angiogenesis and AKT/ERK signaling
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