Gene interactions and pathways from curated databases and text-mining

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EPHB2 — GRAP2

Text-mined interactions from Literome

Chen et al., Cell Mol Biol Incl Cyto Enzymol 2000 : Pre-treatment of the cells with PD98059, a selective ERK pathway inhibitor, and SB203580, a p38 MAPK inhibitor , blocked the induction of HO-1 by the NO donor in a dose dependent manner
Ding et al., Int J Cancer 2001 (Pancreatic Neoplasms) : These findings suggest that both ERK and cellular protein tyrosine kinase activation are involved in 12 ( S ) -HETE induced pancreatic cancer cell proliferation but P38 and JNK/SAPK are not involved in this mitogenic effect
Steven Zatechka et al., Exp Eye Res 2002 : MEK inhibitor restrained the activations of ERK, SAPK/JNK ( under bFGF stimulated condition ) and p38 ( under galactose stimulated condition ) while p38 inhibitor suppressed ERK but stimulated SAPK/JNK
Sharma et al., J Biol Chem 2003 (MAP Kinase Signaling System) : These findings demonstrate that both p38 and ERK1/2 coordinate the dynamics of wound healing : while growth factor stimulated p38 induces epithelial migration, ERK1/2 activation induces proliferation
Kilic et al., Stroke 2005 (Brain Ischemia...) : In a mouse model of focal cerebral ischemia, tPA induces eNOS inhibition, ERK-2 activation, and p38 inhibition , possibly as part of a more complex signaling response exacerbating brain injury
Li et al., J Biol Chem 2005 (Arteriosclerosis...) : However, MKK3/p38 signaling was specifically involved in TNF-alpha induction, and Erk1/2 signaling was required for IL-6
Daoud et al., J Physiol 2005 : Furthermore, ERK1/2 and p38 are rapidly activated upon addition of FBS, but the activation of p38 is delayed compared to that of ERK1/2
Andrysík et al., Toxicol Appl Pharmacol 2006 : In contrast, the PAHs stimulating cell proliferation in WB-F344 cell line had no effect on activation of ERK1/2, p38 or JNKs. Synthetic inhibitors of ERK1/2 activation ( U0126 ) or p38 kinase activity ( SB203580 ) prevented both apoptosis and induction of p53 phosphorylation by DBalP
Lee et al., Free radical research 2005 : Pretreatment with the p38 MAP kinase inhibitor, SB203580 and the ERK1/2 inhibitor , PD98059, prevented t-BHP induced increases in p65 translocation, NF-kappaB luciferase activity, and phospho-IKKalpha/beta
Dai et al., J Immunol 2005 : Gal-9 induced phosphorylation of the MAPK p38 and ERK1/2 in DCs, and an inhibitor of p38 signaling, but not inhibitors of signaling by either ERK1/2 or PI3K, blocked Gal-9 induced up-regulation of costimulatory molecule expression and IL-12 production
Kobayashi et al., Exp Dermatol 2005 : We show ( i ) UV induced up-regulation of TNF-alpha mRNA and protein expression in keratinocytes ; ( ii ) cells treated with KTI before UV irradiation showed a significantly lower accumulation of TNF-alpha protein in a dose dependent manner and a reduced UV-induced up-regulation of TNF-alpha mRNA expression ; ( iii ) KTI inhibited the induction of TNF-alpha target molecules interleukin-1beta (IL-1beta) and IL-6 proteins ; ( iv ) UV irradiation transiently activated c-Jun N-terminal kinase (JNK) and Akt signaling but only weakly activated extracellular signal regulated kinase ( ERK ) and p38 ; ( v ) KTI specifically inhibited UV-induced activation of ERK , JNK, and p38, but not Akt ; ( vi ) treatment of cells with SP600125, a pharmacological inhibitor of JNK, predominantly suppressed UV-induced up-regulation of TNF-alpha expression ; and ( vii ) KTI did not enhance suppression of UV-induced JNK phosphorylation by SP600125
Yu et al., Toxicol Appl Pharmacol 2006 (MAP Kinase Signaling System) : In addition, atRA treatment caused a strong and sustained activation of c-Jun N-terminal kinase (JNK) and p38 kinase ( p38 ) , as well as an early but transient activation of extracellular signal regulated kinase ( ERK )
Øvrevik et al., Toxicology 2006 : The p38 inhibitor SB202190 increased the silica induced ERK1/2 phosphorylation suggesting that p38 activity may attenuate activation of ERK1/2
Guest et al., Antioxid Redox Signal 2006 (Mechanotransduction, Cellular) : Strain rapidly activated both ERK1/2 ( MAPK ) and p38 ( MAPK ), with peak activation at 5 min. Strain induced a twofold increase in MCP-1 mRNA, which was attenuated by PD 98059, a specific ERK1/2 ( MAPK ) inhibitor, and SB 203580, a specific p38 ( MAPK ) inhibitor
Pillinger et al., J Biol Chem 2007 (Helicobacter Infections...) : MEK inhibitors UO126 and PD98059 inhibited both CagA independent and -dependent MMP-1 secretion, whereas p38 inhibition enhanced MMP-1 secretion and ERK activation, suggesting p38 negative regulation of MMP-1 and ERK
Peng et al., Toxicology 2007 (Glioma) : Treatment of PD98059 ( ERK-specific inhibitor ), SB203580 ( p38 MAPK inhibitor ) and SP600125 ( JNK inhibitor ) decreases the elevation of NGF and p75 mRNA induced by ( Ac ) ( 5 ) GP, indicating possible transcription regulation via MAPKs
Kim et al., Chem Biol Interact 2008 : PD98059 ( ERK inhibitor ) and SB203580 ( p38 MAPK inhibitor ) down-regulated the COX-2 expression induced by TPA
Mao et al., Biochem Pharmacol 2008 : Similar to SFLLRN, the TFRRR-peptide caused phosphorylation of Akt and Erk in a P2Y ( 12 ) receptor dependent manner, and p-38 MAP kinase activation in a P2Y ( 12 ) -independent manner
Xue et al., J Cell Mol Med 2009 : APC dose-dependently stimulated phosphorylated ( P ) -ERK2 and inhibited P-p38
Daoud et al., Placenta 2008 : Furthermore, we showed that transient activation of ERK1/2 by FBS is independent of SFK and that PP2 induces rapid activation of p38
Li et al., J Nutr Biochem 2009 : These data indicate that GTPs down-regulate gene expression of Cav-1 time- and dose- dependently via activating ERK1/2 and inhibiting p38MAPK signaling
Luo et al., J Mol Neurosci 2009 (Reperfusion Injury) : At the same time, PD98059 ( ERK MAPK inhibitor ) and SB203580 ( P38 MAPK inhibitor ) also prevented the up-regulation of PGC-1alpha in OGD neurons and MK801 can inhibit the expression of P38 and ERK MAPK
Mori et al., Mol Cancer Res 2009 (Pancreatic Neoplasms) : In conclusion, overexpression of KLF5 in human pancreatic cancer cells is not mediated by KRAS/Raf/MAPK/Erk signaling, but involves the IL-1beta/IL-1R system, p38 , and the transcription factor HIF-1alpha
Sambade et al., Radiother Oncol 2009 (Breast Neoplasms...) : In SUM102 cells, an EGFR+ basal breast cancer cell line, exposure to ionizing radiation elicited strong activation of ERK1/2 and JNK, which was blocked by lapatinib, and weak/no activation of p38 , AKT or STAT3
Xu et al., Mol Cell 2010 (MAP Kinase Signaling System) : Conversely, depletion of p38alpha MAP kinase activity suppresses EGF receptor signaling and downstream Erk MAP kinase signaling, as well as autocrine EGF receptor dependent proliferation
Kunchithapautham et al., J Biol Chem 2011 : TER reduction could be attenuated by inhibiting Ras, Erk and Src activation, or blocking VDCC or VEGF-R2 activation, but not by inhibiting P38
Babykutty et al., Mol Carcinog 2012 (Colonic Neoplasms...) : It also caused activation of caspase mediated apoptosis through the inhibition of ERK1/2 and activation of p38 and JNK1/2
Wang et al., Molecular pain 2011 : The activation of spinal ERK , p38 and CaMKII, alongside nNOS, is involved in chronic morphine induced CGRP up-regulation in both the DRG and SCDH
Wu et al., J Biomed Sci 2011 (Hyperpigmentation...) : Cpc exerted dual antimelanogenic mechanisms by upregulation of MAPK/ERK dependent degradation of MITF and downregulation of p38 MAPK regulated CREB activation to modulate melanin formation
Dai et al., J Biol Chem 2012 (Carcinoma, Hepatocellular...) : Both p38 MAPK promoted glucose regulated protein 78 (GRP78) expression and sustained high basal activation of PI3K/Akt and MEK/ERK are involved in the cytoprotective function of p190Met ( NC )
Somvanshi et al., Int J Cardiol 2013 (Cardiomegaly) : SST enhances ß2AR agonist formoterol mediated effects on PKA, CREB and ERK1/2 phosphorylations whereas it inhibits isoproterenol mediated ERK1/2 and p38 signaling in concentration dependent manner
Maza et al., Microbes Infect 2012 : Moreover, P. brasiliensis yeasts induced activation of p38 mitogen activated protein kinase ( MAPK ), c-Jun NH ( 2 ) -terminal kinase ( JNK ) and extracellular signal regulated kinase ( ERK ) 1/2 in A549 cells, and IL-8 and IL-6 secretion promoted by this fungus was dependent on activation of p38 MAPK and ERK 1/2
Shin et al., Neurochem Res 2012 (Brain Ischemia) : Resveratrol increased expression of SIRT1 and phosphorylation of Akt and p38 but inhibited the increase in phosphorylation of ERK1/2
Rajapurohitam et al., Cell Signal 2012 (Cardiomegaly...) : The hypertrophic response to leptin was also associated with increased p38 and ERK1/2 MAPK phosphorylation and increased p38, but not ERK1/2 , translocation into nuclei
Huang et al., Diabetes 2012 (Diabetes Mellitus, Type 2) : The expression of p38, JNK, and Erk was comparable in all groups of mice, but the phosphorylation of p38 and JNK was increased in 3M and further increased in 9M diabetic mice, whereas the phosphorylation of Erk was substantially reduced in 9M diabetic mice
Foley et al., J Biol Chem 2012 (MAP Kinase Signaling System) : Pam3Cys, a specific TLR2 agonist, stimulated phosphorylation of JNK, ERK, and p38 , but only JNK and ERK inhibition blocked Pam3Cys stimulated chemotaxis
Souza-Fonseca-Guimaraes et al., J Biol Chem 2013 (MAP Kinase Signaling System) : IFN-? and GM-CSF production requires NF-?B and STAT3 activation as well as Erk dependent mechanisms for IFN-? and p38 signaling for GM-CSF