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EPHB2 — HGF

Text-mined interactions from Literome

Sipeki et al., Cell Signal 1999 (Carcinoma, Hepatocellular...) : Experiments performed with LY294002 indicated that phosphatidylinositol 3-kinase contributed to the HGF stimulated phosphorylation of Erk1/Erk2
Kim et al., J Surg Res 2000 : ( i ) Both hypoosmotic cell swelling and HGF phosphorylate p38, ERK 1 and 2, and SAPK/JNK, and ( ii ) HGF , but not hypoosmotic stress, activates NF-kappaB via p38 and ERK 1 and 2 phosphorylation
Sipeki et al., Cell Signal 2000 (MAP Kinase Signaling System) : Protein kinase C reduces the HGF induced phosphorylation of Erk1/Erk2 , and in this way it can limit the intensity of Erk1/Erk2 dependent gene-expression
Paumelle et al., Mol Biol Cell 2000 : Sequential activation of ERK and repression of JNK by scatter factor/hepatocyte growth factor in madin-darby canine kidney epithelial cells ... Together, these data demonstrate that in a sequential manner SF/HGF activates ERK and MKP2, which in turn dephosphorylates JNK
Kuba et al., Cancer Res 2000 (Carcinoma, Lewis Lung...) : NK4 inhibited HGF induced ERK1/2 ( p44/42 mitogen activated protein kinase ) activation, but allowed for bFGF- and VEGF induced ERK1/2 activation
Karihaloo et al., J Biol Chem 2001 : Examination of EGF stimulated cells demonstrated that extracellular regulated kinase 5 (ERK5) was activated in response to EGF but not HGF , and that activation of ERK5 was only 60 % inhibited by 50 microm PD98059
Osada et al., Cancer 2001 (Stomach Neoplasms) : In addition, U0126, which is a potent inhibitor for ERK phosphorylation, antagonized increase of cyclin D1, thus suggesting that EGF- or HGF mediated ERK phosphorylation might have played an essential role for cell growth
Liang et al., J Biol Chem 2001 : Conversely, HGF induced a sustained ( at least 12 h ) activation of ERK in the cells
Frasca et al., Oncogene 2001 (Thyroid Neoplasms) : The STI571 enhanced motile response can be correlated with an increase in the Met receptor tyrosine phosphorylation as well as ERK and Akt activation by HGF
Tsukada et al., J Biol Chem 2001 (Carcinoma, Hepatocellular...) : HGF induced strong activation of ERK in HepG2 cells ... Although the serum dependent proliferation of HepG2 cells was inhibited by the MEK inhibitor PD98059 in a dose dependent manner, 10 microM PD98059 reduced the HGF induced strong activation of ERK to a weak activation ; and as a result, the proliferation inhibited by HGF was completely restored
Liu et al., J Biol Chem 2002 (MAP Kinase Signaling System) : In addition, HGF induced association of paxillin and activated ERK , correlating with a gel retardation of paxillin that was prevented with the ERK inhibitor U0126
Takami et al., Am J Respir Cell Mol Biol 2002 : Further, we investigated the molecular mechanisms underlying the effects of HGF and IFN-gamma in BEAS-2B cells and found that the MEK1 inhibitor PD98059, but not the p38 M-associated protein kinase inhibitor SB203580, abrogates HGF induced ERK activation and proliferation in response to HGF and serum ... IFN-gamma does not interfere with the effects of HGF on either ERK activation or cyclin D1 induction ; however, it prevents the downregulation of p27 ( kip1 ) CDK inhibitor that takes place in response to a combination of HGF and serum
Baatar et al., Am J Pathol 2002 (Esophageal Diseases...) : In an ex vivo organ-culture system, exogenous HGF significantly increased ERK2 phosphorylation levels in esophageal mucosa
Yu et al., J Biol Chem 2002 : HGF stimulated ERK activation increases the Gab1/PI3K association, whereas EGF stimulated ERK activation results in a decrease in the tyrosine phosphorylation of Gab1 and a decreased association with the PI3K
Abiru et al., Hepatology 2002 (Carcinoma, Hepatocellular...) : Aspirin and NS-398, in contrast to PD98059, did not suppress ERK1/2 phosphorylation induced by HGF
Tanimura et al., J Biol Chem 2002 : HGF stimulation of the cells induces not only a rapid, marked, and sustained activation and rapid nuclear accumulation of ERK1/2 , but also a prolonged nuclear retention of the activated ERK1/2
Liu et al., FASEB J 2002 : HGF rapidly stimulated phosphatidylinositol 3'-kinase, ERK , p38 mitogen activated protein kinase, and protein kinase C activities
Taher et al., Biochem Biophys Res Commun 2002 (Arteriosclerosis...) : Stimulation with HGF led to activation of Met as well as to activation of PI3-K, PKB/Akt, MEK, and the MAP kinases Erk1 and -2
Fleigel et al., Otolaryngol Head Neck Surg 2002 (Carcinoma, Squamous Cell...) : HGF/SF induced phosphorylation of FAK and Erk was observed in both detached and attached SCCHN cells
Bessho et al., American journal of physiology. Renal physiology 2003 (Glomerulonephritis) : When PDGF and HGF were simultaneously added, HGF inhibited the prolonged activation of ERK , which suggests that early inactivation of PDGF induced ERK may be involved in the inhibitory effect of HGF on mesangial cell proliferation
Maejima et al., Atherosclerosis 2003 : ERK1/2 and p38 MAPK were phosphorylated by HGF and a MEK inhibitor PD98059 and a p38 MAPK inhibitor SB203580 inhibited HGF stimulated HUVEC growth by 66 % and by 58 % ; however, HGF induced phosphorylation of ERK1/2 and p38 MAPK was not inhibited by L-NAME, indicating that NO is not an upstream activator of ERK1/2 and p38 MAPK
Liu et al., Exp Cell Res 2003 : Regulation of amyloid precursor protein expression and secretion via activation of ERK1/2 by hepatocyte growth factor in HEK293 cells transfected with APP751
Chan et al., J Biol Chem 2003 : Finally, the increased phosphorylation of Gab1 by Src selectively potentiated HGF induced activation of ERK and AKT
Okano et al., Biochem Biophys Res Commun 2003 : The activation of AKT, p70 ( s6k ), and ERK1/2 induced by HGF was abolished by pre-treatment with LY294002, a phosphoinositide 3-OH kinase (PI3K) inhibitor, and U0126, a mitogen activated protein kinase/ERK kinase ( MEK ) inhibitor, respectively
Ma et al., Circ Res 2003 : Neither SB203580 nor LY294002 inhibited HGF induced ERK1/2 activation
Lee et al., Clin Exp Metastasis 2003 (MAP Kinase Signaling System...) : Pretreatment of PD98059 decreased HGF mediated phosphorylation of extracellular receptor kinase (ERK) , uPA secretion and expression of matrix metalloproteinases ( MMP-2 and MMP-9 ) in a dose dependent manner ... In contrast, SB203580 pretreatment increased HGF stimulated ERK phosphorylation, uPA secretion and expression of MMPs. SB203580 also reversed the inhibition of HGF mediated ERK activation and uPA secretion in the PD98059 pretreated cells ... These results suggest that ERK activation by HGF might play important roles in the metastasis of pancreatic cancer and the p38 MAPK pathway also involved in the HGF mediated uPA secretion and metastasis by regulation of ERK pathway
Ishibe et al., Mol Cell 2003 : In the present study we demonstrate that HGF stimulates the localization of ERK to sites of cell-matrix interactions and that this is mediated by the tyrosine phosphorylation dependent association of inactive ERK and the focal adhesion complex protein paxillin
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)
Taniguchi et al., Mol Reprod Dev 2004 (MAP Kinase Signaling System) : Here, we showed that HGF activated the distinct phosphorylation of Raf-1, MEK1/2, and ERK1/2 , but did not induce phosphorylation of Akt ... U0126, a MEK1/2 inhibitor, completely abrogated the phosphorylation of ERK1/2 and the cell proliferation in response to HGF ... In contrast, H-89, a protein kinase A inhibitor, further enhanced the HGF induced phosphorylation of ERK1/2 and cell proliferation
Yao et al., J Hepatol 2004 : We also observed activation of ERK1/2 , p38 MAPK, Akt and NF-kappaB signaling pathways by HGF in WB-F344 cells
Halevy et al., Exp Cell Res 2004 (MAP Kinase Signaling System) : In contrast, MAPK/ERK phosphorylation was higher in response to HGF and lasted longer, relative to IGF-I
Goda et al., J Gene Med 2004 (Cryptorchidism) : Adenovirus mediated HGF gene transfer induced overexpression of HGF in some seminiferous epithelial cells and interstitial cells, increased the phosphorylation of ERK and Akt, and decreased numbers of apoptotic cells of germ cells
Karihaloo et al., Mol Cell Biol 2004 : Embryonic IMCD cells expressing predominantly Gpc3 proliferated and migrated in response to HGF but activated ERK only transiently and failed to form tubules ... Overexpressing Gpc-4 but not Gpc-3 or Gpc-1 led to sustained HGF stimulated ERK activation and rescued the tubulogenic response in these cells
Thompson et al., Mol Cell Neurosci 2004 (MAP Kinase Signaling System) : Preventing Akt activation with the phosphatidylinositol-3 (PI-3) kinase inhibitor LY294002 blocked the HGF survival response, and inhibition of ERK activation with the MEK inhibitors PD98059 or U0126 reduced the HGF survival response and the neurite growth promoting effects of HGF
Wang et al., J Biol Chem 2005 : SSB-1 also enhanced HGF induced Erk phosphorylation
Wang et al., J Hepatol 2005 : However, HGF increased phosphorylated p90-RSK and ERK to 18- and 3-fold normal, respectively
Tjin et al., Blood 2006 (Lymphoma, B-Cell...) : In MET positive DLBCL cells, HGF induces MEK dependent activation of ERK and PI3K dependent phosphorylation of PKB, GSK3, and FOXO3a
Fleischer et al., Int J Oncol 2006 (Carcinoma, Hepatocellular...) : Furthermore, the hepatocyte growth factor and epidermal growth factor induced Mcl-1 expression in an Akt- and ERK dependent manner
Bigelow et al., Oncogene 2006 (Breast Neoplasms...) : HGF treatment in both cell lines induced rapid, sustained activation of Met, ERK and AKT ... Pretreatment of cells with concentrations of EGCG as low as 0.3 microM inhibited HGF induced Met phosphorylation and downstream activation of AKT and ERK ... ( - ) -Epigallocatechin ( EGC ), however, completely repressed HGF induced AKT and ERK phosphorylation at concentrations of 10 and 20 microM, but was incapable of blocking Met activation
Lee et al., Chem Biol Interact 2006 (Carcinoma, Hepatocellular...) : In addition, Western blotting and immunoprecipitation were performed to confirm luteolin suppressed the phosphorylation of c-Met, the membrane receptor of HGF, as well as ERK1/2 and Akt, but not JNK1/2, which is activated by HGF
Osada et al., J Gastroenterol Hepatol 2006 (Carcinoma, Hepatocellular...) : In contrast, HGF did not induce phosphorylation of ERK and JNK
Rush et al., Exp Cell Res 2007 (MAP Kinase Signaling System) : Stimulation of HBMECs by HGF led to rapid activation of ERK1/2 , phosphorylation of Raf-1 at Ser ( 338 ) and Tyr ( 340/341 ) and MEK1/2 at Ser ( 222 )
Yang et al., J Cell Physiol 2007 (Carcinoma, Hepatocellular...) : This involves cell density dependent differences in HGF induced ERK activation
Koike et al., Mol Pharmacol 2007 : These results are consistent with the conclusion that the HGF dependent phosphorylation of ERK1/2 is the endogenous signal that sequesters CAR in the cytoplasm of mouse primary hepatocytes
Park et al., Biochem Biophys Res Commun 2007 : Hepatocyte growth factor at S phase induces G2 delay through sustained ERK activation ... Taken together, HGF treatment of HeLa cells at S phase induces G2 delay partially through sustained activation of ERK signaling
Zhang et al., Chin Med J (Engl) 2007 (Colorectal Neoplasms...) : Hepatocyte growth factor induced phosphorylation of c-Met, ERK1/2 and AKT in a dose dependent manner
Na et al., Biochem Pharmacol 2007 (Hyperpigmentation...) : However ISCK03 did not inhibit hepatocyte growth factor (HGF) induced phosphorylation of p44/42 ERK proteins
Song et al., Hepatology 2007 : HGF rapidly induced c-Jun and small heterodimer partner mRNA and protein expression and increased phosphorylation of ERK1/2 , JNK, and c-Jun
He et al., Colloids Surf B Biointerfaces 2008 : HGF stimulated both ERK1/2 and Akt activities in cortical neurons
Lee et al., Toxicol Appl Pharmacol 2008 (Breast Neoplasms...) : The effect of apigenin on HGF induced signaling activation involving invasive growth was evaluated by immunoblotting analysis, it shows that apigenin blocks the HGF induced Akt phosphorylation but not Met, ERK , and JNK phosphorylation
Kondo et al., J Biol Chem 2008 (Carcinoma, Hepatocellular...) : Coupling of Grb2 to Gab1 mediates hepatocyte growth factor induced high intensity ERK signal required for inhibition of HepG2 hepatoma cell proliferation ... Knockdown of Gab1 using siRNA suppressed the HGF induced strong activation of ERK and inhibition of HepG2 cell proliferation
Esaki et al., Am J Physiol Heart Circ Physiol 2008 (Cardiomyopathies) : Among the mediators downstream of c-Met, the activation of extracellular signal regulated kinase ( ERK ) was reduced by doxorubicin, but the activity was restored by HGF ... These beneficial effects appear to be related to HGF induced ERK activation and upregulation of c-Met, GATA-4, and sarcomeric proteins
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
Makondo et al., Eur J Pharmacol 2008 : In addition, geldanamycin treatment did not enhance the HGF induced phosphorylation of Akt, ERK1/2 and p38MAPK
Motoki et al., J Cell Biochem 2008 : These results suggest that maleic acid indirectly induced HGF expression from human dermal fibroblasts through activation of ERK and JNK and that de novo protein synthesis is required for maleic acid induced upregulation of HGF mRNA
Lim et al., Cancer Lett 2008 (Hypopharyngeal Neoplasms...) : In addition, HGF induced the activation of Akt and Erk pathway as a downstreaming pathway of invasion
Rodland et al., J Biol Chem 2008 (MAP Kinase Signaling System) : In contrast, hepatocyte growth factor can stimulate ERK phosphorylation independent of the EGFR
Lee et al., Tumori 2008 (Carcinoma, Hepatocellular...) : Hepatocyte growth factor treatment induced the phosphorylation of ERK and p38 kinase in a dose dependent manner, resulting in an early peak of phosphorylation at 3 to 10 min, which then rapidly decreased to a near basal level
Tam et al., J Mol Biol 2009 : In MDA-MB435 cells, HB10 reduced HGF dependent Met phosphorylation by 70 %, and phosphorylation of downstream kinases AKT and ERK1/ERK2 by 74 % and 69 %, respectively
Laughlin et al., Differentiation 2009 (Melanoma, Experimental) : Decreased expression of c-Met, the receptor for hepatocyte growth factor, was also detected in the Hn1 depleted cells, however HGF dependent stimulation of phosphorylated-ERK was unaffected
Ushio et al., Mol Cancer Res 2009 (Carcinoma, Hepatocellular...) : Inhibition of the HGF induced high-intensity ERK activity had a modest effect on the Id1 down-regulation, and inhibition of the phosphatidylinositol 3-kinase pathway had no effect, showing that Id1 is regulated by ERK dependent and -independent pathways other than the phosphatidylinositol 3-kinase pathway
Zhou et al., Life Sci 2009 : ERK also was activated by HGF and rescued cells from apoptosis, although the cytoprotective effect was less marked than for PI3K/Akt
Duhon et al., Mol Carcinog 2010 (Prostatic Neoplasms) : EGCG added up to 4 h after the addition of HGF still blocked cell scattering and reduced the HGF induced phosphorylation of c-Met, Akt, and Erk , suggesting that EGCG could act both by preventing activation of c-Met by HGF and by attenuating the activity of pathways already induced by HGF
Raghavan et al., J Cell Sci 2010 : Comparing responses in 2D culture, microgels and macrogels demonstrated that HGF induced ERK signaling was driven by the dynamics of stimulation and not by whether cells were in a 2D or 3D environment, and that this ERK signaling was equally important for HGF induced cell scattering on 2D substrates and tubulogenesis in 3D
Togawa et al., Biochem Biophys Res Commun 2010 : Hepatocyte Growth Factor stimulated cell scattering requires ERK and Cdc42 dependent tight junction disassembly ... Erk activation by HGF is found to mediate the interaction of Par6 with GTP loaded Cdc42
Garner et al., Dev Biol 2011 : Although there is published evidence indicating a role for 2-O sulfation in HGF binding, primary epithelial cells isolated from Hs2st conditional deletions were able to activate Erk in the presence of HGF and there appeared to be only a slight reduction in HGF mediated c-Met phosphorylation in these cells compared to control
Lei et al., Arch Dermatol Res 2012 : HGF could promote the expressions of p-AKT1/2/3, p-ERK , p-GSK3ß, p-IKBa, and ß-catenin
Brusevold et al., J Oral Pathol Med 2012 (Carcinoma, Squamous Cell...) : In the E10 cell line, EGF and HGF induced phosphorylation of EGF receptor (EGFR) and Met, respectively, phosphorylation of ERK1/2 , p38 and Akt, and dose dependent activation of cell migration
Hu et al., Cell Signal 2013 (Carcinoma, Hepatocellular...) : Inhibitor studies revealed that ERK was required for HGF induced paxillin phosphorylation at Ser178, whereas PKC and Rac-1 may suppress HGF induced phosphorylation of ERK and paxillin ( at Ser178 ) and upregulate phosphorylation of paxillin at Tyr31 ... Based on shRNA technique, PKCa and d were responsible for suppressing HGF induced phosphorylation of ERK and paxillin ( at Ser178 ), whereas PKC e and ? were required for phosphorylation of paxillin at Tyr31 ... In conclusion, PKC is critical for mediating HGF induced fluctuant ERK-paxillin signaling during cell migration, probably via triggering endosomal degradation of c-Met