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EPHB2 — FGF1

Text-mined interactions from Literome

Corbit et al., Mol Cell Biol 1999 : In contrast, EGF induced ERK activation was inhibited by the phosphatidylinositol-3-kinase inhibitor wortmannin, which had no effect upon FGF induced ERK activation
Bryckaert et al., Oncogene 1999 : Thus, FGF2 induced cell survival is a progressive adaptive phenomenon involving ERK2 activation by excreted FGF1 and ERK2 dependent Bcl-x production
Wu et al., J Biol Chem 2000 : MAPK/ERK kinase inhibition diminished VEGF-, FGF- , and EGF promoted thymidine incorporation into DNA
Browaeys-Poly et al., Eur J Biochem 2000 : The Grb2 adaptor was recruited by the upstream Src homology 2/alpha-collagen related ( Shc ) effector, as the SH2-Shc domain prevented the GVBD and the ERK2 phosphorylation induced by FGF1
Bryckaert et al., Oncogene 2000 : Secreted FGF1 induced short-term activation of both FGFR1 and ERK2 , which were required for cell proliferation ... Secreted FGF1 induced long-term activation of FGFR1 and ERK2 , which was necessary to induce a constant and high level of Bcl-x production, and to induce cell survival in FGFI cells
Jones et al., J Cell Physiol 2001 : Additionally, inhibition of MKK1/2 by treatment with pharmacological inhibitors also blocks FGF mediated stimulation of ERK1/2 and blocks the G1 to S phase transition of myoblasts ... We conclude that FGF stimulated ERK1/2 signaling is required during the G1 phase of the cell cycle for commitment of myoblasts to DNA synthesis but is not required for mitosis once cells have entered the S-phase
Janulis et al., Mol Cell Biol 2001 : Conversely, the related kinase ERK5 is activated by EGF but not FGF
Hayashi et al., J Cell Sci 2001 : Pretreatment with BMP-2 also enhanced peak and sustained levels of FGF induced ERK1/2 phosphorylation in PC12 cells
Browaeys-Poly et al., Cell Signal 2001 (Breast Neoplasms...) : FGF1 induces ERK2 phosphorylation and G2/M transition
Le et al., J Cell Biol 2001 : FGF induced sustained activation of extracellular signal regulated kinase ( ERK ) in lens cells, an event necessary and sufficient to increase gap junctional coupling ... We also identify vitreous humor as an in vivo source of an FGF-like intercellular communication promoting activity and show that FGF induced ERK activation in the intact lens is higher in the equatorial region than in polar and core fibers
Sasaki et al., J Biol Chem 2001 : Forced expression of Sprouty2 and Sprouty4 inhibited FGF induced ERK activation but did not affect EGF- or PDBu induced ERK activation
Mehta et al., Oncogene 2001 (Prostatic Neoplasms) : In prostate DU145 cells, both FGF1 and FGF2 activated ERK1/2 potently and p38 moderately
Shinya et al., Development 2001 (MAP Kinase Signaling System) : Experiments with Fgf inhibitors reveal that ERK activation at this stage is totally dependent on Fgf signalling
Lovicu et al., Development 2001 : We show that FGF induced a dose dependent activation of extracellular regulated kinase 1/2 ( ERK1/2 ) as early as 15 minutes in culture, with a high ( differentiating ) dose of FGF stimulating a greater level of ERK phosphorylation than a lower ( proliferating ) dose
Pintucci et al., FASEB J 2002 : In addition, FGF-2 induced ERK activation mediates endothelial cell migration in response to wounding without a significant effect on proliferation
Hanafusa et al., Nat Cell Biol 2002 (MAP Kinase Signaling System) : A non phosphorylated Spry mutant can not bind Grb2 and acts as a dominant negative, inducing prolonged activation of ERK in response to FGF and promoting the FGF induced outgrowth of neurites in PC12 cells
Kovalenko et al., J Biol Chem 2003 : Sef inhibits fibroblast growth factor signaling by inhibiting FGFR1 tyrosine phosphorylation and subsequent ERK activation
Jackson et al., Mol Endocrinol 2003 (MAP Kinase Signaling System...) : FGF induction of rPRL transcription is independent of Ras, but mediated by a protein kinase C-delta (PKCdelta) dependent activation of MAPK ( ERK )
Zhang et al., Zhonghua Yi Xue Za Zhi 2003 (Neoplasms, Glandular and Epithelial...) : The intracellular PKC and ERK activity increased with aFGF in a dose dependent manner, Genistein suppressed the intracellular PKC and ERK activity also in a dose dependent manner
Araki et al., J Biol Chem 2003 : Compared with wild type cells, ERK activation was decreased in Y542F- or Y580F infected cells in response to fibroblast growth factor and PDGF but not the epidermal growth factor
Wu et al., Biol Chem 2003 : Indeed, we show that the central portion of FRS2 constitutively associates with ERK1/2 , whereas the FRS2 carboxy-terminal region serves as substrate for ERK2 phosphorylation in response to EGF and FGF stimulation
Loeb et al., Neuron 1992 : The association of both ERK1 protein and ERK-like kinase activity with gp140prototrk is maximal by 5 min of NGF treatment, persists for approximately 1 hr, and subsequently declines by 18 hr. Treatment with either basic fibroblast growth factor , epidermal growth factor, or orthovanadate also leads to association of ERK1 with gp140prototrk without tyrosine phosphorylation of the latter
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)
Upadhyay et al., Am J Respir Cell Mol Biol 2004 (MAP Kinase Signaling System...) : Also, FGF-10 and H2O2 each induced negligible ERK1/2 phosphorylation in Ras dominant negative ( N17 ) cells
Thottassery et al., Cancer Res 2004 (Breast Neoplasms) : We found that either FGF-1 or HRGbeta1 but not EGF substantially reduced the inhibitory effects of U0126 on growth and ERK1/2 activation, including the combined inhibitory effects of U0126 and ICI 182780 ... FGF-1 and HRGbeta1 also reduced the inhibition of ERK1/2 phosphorylation by the MEK inhibitors PD98059 and PD184161 ... Despite a short lived activation of Ras and Raf-1 by all three of the growth factors, both FGF-1 and HRGbeta1, unlike EGF, induced a prolonged activation of MEK and ERK1/2 in these cells ... Thus, activation of FGF-1- and HRGbeta1-specific signaling causes MEK dependent prolonged activation of ERK1/2 , which is incompletely susceptible to known MEK inhibitors
Yang et al., J Biol Chem 2004 : By inhibiting FGFR1 tyrosine phosphorylation and/or Ras downstream events, Sef inhibits FGF mediated ERK activation and cell proliferation as well as PC12 cell differentiation
Kovalenko et al., Cell Signal 2006 : We also showed that SefECTM associated with FGFR1, and inhibited FGF induced ERK activation in HEK293T cells
Smith et al., FEBS Lett 2006 (MAP Kinase Signaling System) : Negative feedback predominates over cross-regulation to control ERK MAPK activity in response to FGF signalling in embryos ... We conclude that MKP-3/Pyst1 expression is mediated by ERK activation and that negative feedback control predominates in limiting the extent of FGF induced ERK activity
Rong et al., Cell Signal 2007 : By repressing events upstream and/or downstream Ras, Sef inhibits FGF induced ERK activation and cell proliferation
Nadeau et al., J Cell Biochem 2007 : Spry2 inhibits FGF dependent ERK activation and thus Spry acts as a feedback inhibitor of FGF mediated proliferation
Newell et al., FASEB J 2006 : FGF-1 induced robust phosphorylation of ERK1/2 in early differentiation and inhibition of ERK1/2 activity significantly reduced phPA differentiation
Li et al., Development 2007 : Dusp6 ( Mkp3 ) is a negative feedback regulator of FGF stimulated ERK signaling during mouse development
Vincent et al., Osteoarthritis Cartilage 2007 (Mechanotransduction, Cellular) : We have shown previously that cutting or loading articular cartilage resulted in a fibroblast growth factor-2 (FGF-2) dependent activation of the extracellularly regulated kinase (ERK) , and induction of a number of chondrocyte regulatory proteins including tissue inhibitor of metalloproteinase-1 and matrix metalloproteinases 1 and 3 ... Chondrocytes encapsulated in alginate were able to accumulate pericellular perlecan and FGF-2 in culture, and deliver an FGF dependent activation of ERK when loaded
Iyengar et al., Differentiation 2007 (MAP Kinase Signaling System) : Here, we show that FGF induced a dose dependent sustained activation of ERK1/2 , with both a high ( fiber differentiating ) dose of FGF and vitreous, stimulating and maintaining a prolonged ( up to 18 hr ) ERK1/2 phosphorylation profile
Ding et al., J Cell Physiol 2007 : Furthermore, we demonstrate that TGF-beta1 signaling can modulate EGF and FGF induced ERK-MAP kinase activation by controlling Spry2 expression and function
Ito et al., J Lipid Res 2007 : SU5402, an inhibitor of FGF receptor, inhibited FGF-1 induced phosphorylation of MEK, ERK , and Akt, as well as all the apoE-HDL biogenesis related events in rat astrocytes
Kondo et al., Hum Pathol 2007 (Carcinoma...) : Serum or fibroblast growth factor-1 stimulation further activates ERK1/2 in heterozygous BRAF ( V600E ) -positive carcinoma cells as well as BRAF ( V600E ) mutation negative carcinoma cells
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 )
Kilkenny et al., Mol Endocrinol 2008 : Significant FGF-1 dependent activation of ERK1/2 was observed in betaTC3 cells, dispersed beta-cells, and beta-cells in intact islets
Francavilla et al., J Cell Sci 2007 : The results demonstrate that NCAM expression reduces FGF stimulated ERK1/2 activation, cell proliferation and cell-matrix adhesion, in both L and NIH-3T3 cells
Nagayasu et al., J Biochem 2008 : Phosphorylation of Akt, ERK and MEK were induced by FGF-1 in W/W cells but not in W/M cells
Crisostomo et al., Am J Physiol Cell Physiol 2008 : VEGF, FGF2 , and HGF expression was significantly reduced by NF kappa B inhibition ( 50 % decrease ) but not ERK or JNK inhibition
Yan et al., Mol Cell Biol 2008 : These observations place Rap1 centrally in the human angiogenic process and suggest that both the Rap1a and Rap1b proteins are required for angiogenesis and that Rap1 is a critical mediator of FGF induced ERK activation
Boswell et al., Exp Eye Res 2009 : We show that FGF stimulates ERK in DCDMLs via the canonical Ras/Raf1 pathway, and that the reason that neither basal nor growth factor stimulated GJIC is blocked by activation of ERK is because it is not mediated by Cx43
Lin et al., Cell Signal 2009 : Our data suggest that SH2B1beta enhances and prolongs FGF1 induced MEK-ERK1/2 and PI3K-AKT pathways
Nishida et al., J Biochem 2009 : FGF-1 induced phosphorylation of Src, and phosphorylation of MEK, ERK and Ark was inhibited by Src inhibitors in rat astrocytes
Darby et al., Br J Cancer 2009 (Prostatic Neoplasms) : In signalling studies, hSef inhibited FGF induced ERK phosphorylation, migration to the nucleus and activation of a reporter gene
Wang et al., Placenta 2009 : Under both normoxia and hypoxia, FGF2 rapidly induced ERK1/2 and AKT1 phosphorylation, while VEGF induced ERK1/2 , but not AKT1 phosphorylation
Haling et al., Mol Biol Cell 2010 (MAP Kinase Signaling System) : PEA-15 binding prevented ERK1/2 membrane recruitment and threonine phosphorylation of fibroblast receptor substrate 2alpha ( FRS2alpha ), a key link in fibroblast growth factor ( FGF ) receptor activation of ERK1/2
Miyoshi et al., Mol Cell Endocrinol 2010 : Notably, FGF-8 induced ERK and SAPK/JNK phosphorylation in granulosa cells, in which ERK activation was further enhanced by FSH and oocytes
Perera et al., Arthritis Res Ther 2010 (Inflammation) : ERK1/2 activation by mechanical forces induced SRY related protein-9 ( SOX-9 ), vascular endothelial cell growth factor ( VEGF ), and c-Myc mRNA expression and AC proliferation
Ge et al., J Biol Chem 2011 : In conclusion, FGF21 induces GLUT1 expression and glucose uptake through sequential activation of ERK1/2 and SRF/Elk-1, which in turn triggers the transcriptional activation of GLUT1 in adipocytes
Dai et al., Clinical lymphoma, myeloma & leukemia 2011 (MAP Kinase Signaling System...) : Overexpression of MPS-1 resulted in decreased fibroblast growth factor ( FGF2 ) receptor 3 and impaired endogenous MAPK/ErK signaling
Huynh et al., J Hepatol 2012 (Carcinoma, Hepatocellular...) : Dovitinib inhibited basal expression and FGF induced phosphorylation of FGFR-1, FRS2-a and ERK1/2
Su et al., Oncogene 2012 (Carcinoma, Pancreatic Ductal...) : Finally, Ncad ( -/+ ) tumor cells exhibited decreased FGF stimulated ERK1/2 activation consistent with N-cadherin 's ability to promote FGFR signaling
van Puijenbroek et al., Oncogene 1997 (Neuroectodermal Tumors, Primitive, Peripheral) : Analysis of the kinetics of ERK2 activation and downstream events revealed that Ret and FGF receptor activation led to sustained ERK2 activation and SRE transactivation, while PDGF treatment led to transient ERK2 activation and failed to induce SRE transactivation
Florio et al., Mol Endocrinol 1999 : However, in these cells, somatostatin robustly activates MAP kinase ( also called extracellular signal regulated kinase ; ERK ) and augments fibroblast growth factor stimulated ERK activity