Gene interactions and pathways from curated databases and text-mining

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EPHB2 — HRAS

Pathways - manually collected, often from reviews:

Text-mined interactions from Literome

Ikeda et al., Biochem Biophys Res Commun 1999 : In order to investigate the upstream pathway of strain induced ERK1/2 activation, we examined p21ras activation by cyclic strain and the effect of wortmannin and LY294002, phosphatidylinositol-3 kinase ( PI 3-kinase ) inhibitors on ERK1/2 phosphorylation
Page et al., Am J Respir Cell Mol Biol 1999 : We found that platelet derived growth factor ( PDGF ) treatment induced substantial activation of ERK2 that was blocked by expression of a dominant negative Ha-Ras ... Further, expression of a constitutively active Ha-Ras induced substantial ERK2 activity, consistent with the notion that Ras is required and sufficient for ERK activation
Shirokawa et al., Mol Endocrinol 2000 : As reported elsewhere, acute expression of H-Ras ( v12 ) also induces mitotic defects in PCCL3 cells through ERK ( extracellular ligand regulated kinase ) activation, suggesting that apoptosis may be secondary to DNA damage
Yashima et al., J Cell Physiol 2001 (MAP Kinase Signaling System) : Although dominant negative mutant of Ha-Ras substantially inhibited the basal activities of ERK and p38 MAPK, it exhibited marginal effect on VEGF induced activation of ERK and p38 MAPK in HUVECs and HAECs
Tsukada et al., J Biol Chem 2001 (Carcinoma, Hepatocellular...) : Expression of constitutively activated Ha-Ras , which induces strong activation of ERK , led to the proliferation inhibition of HepG2 cells, as was observed in HGF treated HepG2 cells
Katsanakis et al., Anticancer Res 2002 (Cell Transformation, Neoplastic...) : To examine the role of the transforming Ha-ras in controlling ERK signaling, transfection of an activated Ha-ras allele was tested in a squamous cell carcinoma cell line
Myou et al., J Immunol 2002 : We conclude that H-Ras mediated activation of ERK is critical for beta ( 2 ) -integrin adhesion and that Ras-protein functions as the common regulator for cytokine-, chemokine-, and G-protein coupled receptors in human eosinophils
Katsanakis et al., Mol Med 2002 (Cell Transformation, Neoplastic...) : The above finding was reproduced when transfecting human activated Ha-ras allele into PDV, thus demonstrating that Ha-ras enhances ERK1/2 signaling
Leevers et al., EMBO J 1992 : The 42 kDa kinase is the mitogen and extracellular-signal regulated kinase ERK2 , ( MAP2 kinase ), which is activated by phosphorylation on tyrosine and threonine in response to oncogenic p21ras , while the 46 kDa kinase is likely to be another member of the ERK family
Serù et al., J Neurochem 2004 (Neuroblastoma) : Hence, these data indicate that HaRas induced ERK1/2 signalling selectively activates NADPH oxidase system in neuroblastoma cells
Guo et al., Oncogene 2005 (Leukemia, Mast-Cell...) : Inhibition of either Erk or PI3 kinase blocked the capacity of both activated M-Ras and activated H-Ras to support proliferation and viability
David et al., J Immunol 2005 : In that pharmacological inhibitors of PI3K inhibited LPS induced activation of p21Ras , but not activation of ERK , we concluded that LPS induced activation of ERK occurs through a pathway that is not dependent on the activation of p21Ras
Raines et al., Biochem J 2006 : In contrast, exogenous expression of constitutively active mutants of Raf-1 and H-Ras only partially restored ERK1/2 activity, by 50 % and 10 % respectively
Wu et al., J Biol Chem 2010 (Skin Neoplasms) : The promoter of the Nol3 locus, encoding ARC, is activated by N-Ras and H-Ras in a MEK/ERK dependent manner
Wang et al., FASEB J 2011 : Dominant negative H-Ras or K-Ras reduced accumulation of H-Ras and K-Ras in focal adhesions induced by IL-1 and also blocked ERK activation and focal adhesion maturation
Poulikakos et al., Nature 2011 (MAP Kinase Signaling System...) : These data support the model that inhibition of ERK signalling by RAF inhibitors is dependent on levels of RAS-GTP too low to support RAF dimerization and identify a novel mechanism of acquired resistance in patients : expression of splicing isoforms of BRAF ( V600E ) that dimerize in a RAS independent manner
Eastman et al., Cell Signal 2012 : Autonomous ERK activation by uPAR requires H-Ras and Rac1
Nakanome et al., Oncogene 2013 (Cell Transformation, Neoplastic) : The Bach1-deficient cells showed diminished phosphorylation of MEK and ERK1/2 in response to H-Ras ( V12 ), which was consistent with the alterations in the gene expression profile, including phosphatase genes
Izquierdo et al., Eur J Immunol 1994 : The data demonstrate that phorbol ester and HM1R regulation of ERK2 was prevented by the PKC inhibitor, but that the inhibitor had no effect on ERK2 activation induced by expression of a constitutively active ras mutant p21v-Ha-ras
Burgering et al., Cell Growth Differ 1994 : In these cell lines, PDGF treatment resulted in activation of extracellular signal regulated kinase 2 ( ERK2 ), which could be blocked by the expression of a dominant negative mutant of p21ras ( p21ras ( asn17 ) ), indicating that these mutations in the PDGF receptor do not abolish p21ras mediated activation of ERK2
Burgering et al., Mol Cell Biol 1993 : However, a combined inhibition of both p21ras and calcium influx, but not PKC, resulted in a complete inhibition of EGF induced ERK2 phosphorylation ... In contrast, in Swiss 3T3 cells, inhibition of both p21ras activation and TPA-sensitive PKC, but not calcium influx, inhibited EGF induced ERK2 phosphorylation
Izquierdo et al., J Exp Med 1993 : In the human Jurkat T cell line, transient expression of constitutively active p21ras induces ERK2 activation, measured as an increase in the ability of an ERK2-tag reporter protein to phosphorylate myelin basic protein ... Taken together, these results demonstrate that the activation of p21ras is both necessary and sufficient to induce ERK2 activation in T cells
van Weering et al., Oncogene 1995 : This activation was strong and sustained for at least 2 h. Activation was abolished by the dominant negative p21rasasn17 mutant, showing that activation of ERK2 is mediated by p21ras
Nishiya et al., FEBS Lett 1997 (Glioma) : These results indicate that p21ras and MEK1 are required for IFN-gamma induced ERK1 and ERK2 activation
Foschi et al., EMBO J 1997 : However, the resulting secondary activation of p21ras at 30 min does not lead to ERK activation, correlating with intensive, ET-1 induced expression of MAP kinase phosphatase-1, but does result in increased p21ras associated phosphatidylinositol 3-kinase activity
Kashiwada et al., J Exp Med 1998 : Coexpression of the dominant negative H-Ras did not affect TRAF6 mediated ERK activity, suggesting that TRAF6 may activate ERK along a Ras independent pathway ... Transient expression of the dominant negative H-Ras significantly suppressed ERK activation by full-length CD40, but marginally suppressed ERK activation by CD40 delta 246, compatible with the possibility that TRAF6 is a major transducer of ERK activation by CD40 delta 246, whose activity is mediated by a Ras independent pathway