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ANGPT2 — EPHB2

Text-mined interactions from Literome

Touyz et al., J Hypertens 1999 : Ang II significantly increased phosphorylation of ERK-1 and ERK-2, with maximum responses obtained at 5 min. PD98059 inhibited Ang II-stimulated ERK activity and abrogated agonist induced DNA and protein synthesis
Deguchi et al., Circ Res 1999 : In adult rat VSMCs, Ang II activates ERK and JNK, but weakly induces Egr-1, a transcription factor implicated in PDGF-B chain gene expression, compared with newborn VSMCs
Mondorf et al., FEBS Lett 2000 : Ang II induced activation of ERK1/2 via the AT(1) receptor, and this response was blocked by the PDGFR-selective tyrosine kinase inhibitor AG1295, but not by AG1478, an EGFR-selective tyrosine kinase inhibitor, indicating participation of the PDGFR, but not of the EGFR in Ang II-induced ERK1/2 activation
Touyz et al., Hypertension 2001 (Hypertension) : These data demonstrate that ( 1 ) Ang II-mediated activation of p38 and ERK1/2 is increased in SHR, ( 2 ) augmented growth responses are generated by ERK1/2 dependent, p38 MAP kinase independent pathways, and ( 3 ) p38 MAP kinase influences Ang II-induced collagen production in SHR but not in Wistar-Kyoto rats
Ding et al., Acta Pharmacol Sin 2000 : To investigate whether the effect of angiotensin (Ang) II or epidermal growth factor (EGF) on cardiac fibroblast proliferation involved in activation of extracellular signal regulated kinase ( ERK ) 1/2 or Ca ( 2+ ) -calmodulin dependent protein kinase ( CCDPK ) mediated by protein kinase C (PKC)-zeta
Matrougui et al., Arterioscler Thromb Vasc Biol 2001 : In mesenteric resistance arteries maintained at 70 mm Hg, Ang II ( 0.1 micromol/L ) induced contraction ( 29+/-1.4 % of phenylephrine, 10 micromol/L induced contraction ) and significantly increased ERK1/2 activity ... These results indicate that whereas pressure induced ERK1/2 activation requires an intact actin filament network, but not Rho-kinase, the activation of ERK1/2 and the contraction induced by Ang II require both Rho-kinase and an intact actin filament network in isolated, intact mesenteric resistance arteries
Yoshizumi et al., Mol Pharmacol 2001 : Our findings showed that Ang II stimulated rapid and significant activation of extracellular signal regulated kinase ( ERK ) 1/2, c-Jun N-terminal kinase (JNK), and p38 in RASMC
Sano et al., Circ Res 2001 : Ang II , as well as exogenous H ( 2 ) O ( 2 ), activated ERK , p38 MAPK, and JNK, which were significantly inhibited by N-acetylcysteine and DPI
Shah et al., Mol Endocrinol 2002 : However, the specific epidermal growth factor receptor (EGF-R) kinase inhibitor, AG1478, abolished Ang II-induced activation of ERK1/2 ... In COS-7 cells transiently expressing the rat AT1A-R, Ang II also caused ERK activation through EGF-R transactivation
Kagiyama et al., Circulation 2002 (Hypertension...) : Ang II requires EGFR to mediate ERK activation in VSMCs and the heart
Natarajan et al., Endocrine 2002 : In summary, in H295R cells, ANG II activated ERK and p38 MAPKs, ANG II-induced p38 MAPK was mediated by 12-LO activation, and ANG II-induced aldosterone synthesis was prevented by 12-LO- and p38 MAPK-specific inhibitors
Andresen et al., Hypertension 2003 (MAP Kinase Signaling System) : We conclude that transactivation of the EGFR is not primarily responsible for Ang II-mediated activation of ERK in PGSMCs
El Bekay et al., Blood 2003 (Calcium Signaling...) : Furthermore, Ang II induced a robust phosphorylation of p38MAPK, ERK1/2 , and JNK1/2 ( particularly JNK2 ), which was hindered by inhibitors of NADPH oxidase, tyrosine kinases, and ROS scavengers
Mukhin et al., J Biol Chem 2004 : EGF receptor blockade attenuated ERK activation , but not NHE-1 activation by 5-HT and Ang II , suggesting that the EGF receptor and NHE-1 work in parallel to stimulate ERK activity in RASM cells, converging distal to the EGF receptor but at or above the level of Ras in the Ras-MEK-ERK pathway
Ishida et al., Circ Res 2003 : PD98059 or introduction of kinase-inactive MEK1/MKK1, but not SB202190 or kinase-inactive p38 MAP kinase, inhibited Ang II-induced Mnk1 activation and eIF4E phosphorylation, suggesting that ERK , but not p38 MAP kinase, is required for Ang II-induced Mnk1-eIF4E activation
Hong et al., J Biomed Sci 2004 : Furthermore, E ( 2 ) and antioxidants, such as N-acetyl cysteine and diphenylene iodonium, decreased Ang-II induced cell proliferation, ET-1 promoter activity, ET-1 mRNA, ERK phosphorylation, and activator protein-1 mediated reporter activity
Xie et al., J Cell Physiol 2004 : Ang II activated ERK1/2 within 5 min of treatment, not JNKs. IL-1beta activated ERK1/2 and JNKs within 15 min of treatment
Li et al., Circulation 2004 (MAP Kinase Signaling System) : In WT aortae, Ang II increased NADPH dependent O2- production ( 2.5+/-0.5-fold ; P < 0.05 ), impaired relaxation to acetylcholine ( maximum 60+/-6 % versus 80+/-3 % ; P < 0.05 ), and increased ERK1/2 , p38MAPK, and JNK phosphorylation ( P < 0.05 )
Gorin et al., Biochem J 2004 (Hypertrophy...) : These results demonstrate that Ang II stimulates ERK1/ERK2 by AA and Nox4 derived reactive oxygen species, suggesting that these molecules act as downstream signal transducers of Ang II in the signalling pathway linking the Ang II receptor AT1 to ERK1/ERK2 activation
Touyz et al., J Hypertens 2004 : Ang II and ET-1 increased MAPK phosphorylation ( P < 0.01 ). Pre-treatment with Tiron and Tempol, *O2 scavengers, attenuated agonist stimulated phosphorylation of p38MAPK, c-Jun N-terminal kinases (JNK) and ERK5 , but not of ERK1/2 ( extracellular signal regulated kinases ). Apocynin and diphenylene iodinium ( DPI ), NAD ( P ) H oxidase inhibitors, decreased Ang II-induced responses 60-70 %. ET-1 mediated MAPK phosphorylation was unaffected by apocynin but was reduced ( > 50 % ) by thenoyltrifluoroacetone ( TIFT ) and carboxyl cyanide-m-chlorophenylhydrazone ( CCCP ), mitochondrial inhibitors
de Boer et al., J Mol Med (Berl) 2004 (Disease Models, Animal...) : Ang II induced LV remodeling and fibrosis are dependent on both ERK and Smad2 activation
Slice et al., J Biol Chem 2005 : Inhibition of ERK activation by U0126 or PD98059 significantly decreased EGF dependent COX-2 expression, but did not affect Ang II-dependent COX-2 expression
Andresen et al., American journal of physiology. Renal physiology 2005 (Hypertension, Renal) : ANG II activation of phospholipase D ( PLD ) is required for ERK and NAD ( P ) H oxidase activation, both of which are involved in hypertension
Zheng et al., Biol Reprod 2005 (MAP Kinase Signaling System) : ANG II rapidly induced positive staining for phosphorylated ERK1/2, appearing in cytosol after 1-5 min of ANG II treatment, accumulating in nuclei after 10 min, and disappearing at 15 min. ANG II increased ( P < 0.05 ) phosphorylated ERK1/2 protein levels
Touyz et al., Can J Physiol Pharmacol 2005 : Ang II significantly increased phosphorylation of p38MAP kinase, JNK, and ERK1/2 ( two- to threefold above control, p < 0.05 )
Ohsawa et al., Fundam Clin Pharmacol 2005 : Ang II stimulated activation of ERK1/2 and the activation was inhibited by CV-11974, an AT1 antagonist, and saralasin, an AT1/AT2 antagonist, but not by PD123,319, an AT2 antagonist in the CRGF
Smith et al., Endocrinology 2006 (MAP Kinase Signaling System) : Stimulation of Ishikawa cells and human endometrial biopsy explants with 100 nm iloprost ( a PGI analog ) rapidly activated ERK1/2 signaling and induced the expression of proangiogenic genes, basic fibroblast growth factor, angiopoietin-1 , and angiopoietin-2, in an epidermal growth factor receptor (EGFR) dependent manner ... Stimulation of Ishikawa cells and human endometrial biopsy explants with 100 nm iloprost ( a PGI analog ) rapidly activated ERK1/2 signaling and induced the expression of proangiogenic genes, basic fibroblast growth factor, angiopoietin-1, and angiopoietin-2 , in an epidermal growth factor receptor (EGFR) dependent manner
Pulver-Kaste et al., Am J Physiol Heart Circ Physiol 2006 (Calcium Signaling) : TG and ANG II induced phosphorylation of ERK , which was sensitive to 2-APB and was selectively required for CRE binding protein phosphorylation
Flannery et al., Nephron. Experimental nephrology 2006 : In contrast, ANG2 had no effect on ERK phosphorylation in stably transfected HEK293 cells
Li et al., Am J Physiol Heart Circ Physiol 2007 (MAP Kinase Signaling System) : In addition, ANG II also enhanced the ERK1/2 phosphorylation that was restored to control levels by DPI
Ding et al., Am J Physiol Heart Circ Physiol 2007 (Disease Models, Animal...) : These findings suggest that ANG II infusion induces the production of superoxide and spontaneous tone and that both are dependent on ERK-MAPK activation
Niu et al., Cancer Res 2007 (Breast Neoplasms...) : Consistent with the important roles of AKT and mitogen activated protein kinase in the HER2 signaling pathway, AKT and ERK mitogen activated protein kinase ( MAPK ) kinase activity is necessary for Ang-2 up-regulation by HER2
Nazari et al., J Med Invest 2007 (MAP Kinase Signaling System) : The effect of Ang II on ERK1/2 phosphorylation was blocked by Ang II type 1 receptor antagonists, RNH6270 and PD98059 but not by SB203580 or Guanosine-5'-O- ( 2-ThioDiphosphate ), a G-protein inhibitor
Clark et al., Regul Pept 2007 : In summary, we found that Ang II stimulates the non-receptor tyrosine kinases Src and Pyk2 which mediate Ang II-induced ERK1/2 activation leading to stimulation of astrocyte growth
Li et al., Chin Med Sci J 2007 : In VSMC, Ang II stimulation increased the phosphorylation of ERK , which reached the peak around 60 minutes
Pham et al., J Cell Physiol 2008 : Ang II and EGF induced transient phosphorylation of ERK , p38 ( MAPK ) and CREB
Sampaio et al., Hypertension 2007 : Ang II significantly increased activation of c-Src, ERK1/2 , and NAD ( P ) H oxidase and reduced phosphorylation of SHP-2 ( P < 0.05 ) in human endothelial cells
Montezano et al., Arterioscler Thromb Vasc Biol 2008 : Aldo and Ang II costimulation induced c-Src dependent activation of NAD ( P ) H oxidase and c-Src independent activation of ERK1/2 ( P < 0.05 ), without effect on ERK5, p38MAPK, or JNK
Tabet et al., Circ Res 2008 (Hypertension) : Ang II stimulation increased activation of ERK1/2 , p38MAPK, and AKT, with enhanced effects in SHR. SHP-2 knockdown resulted in increased AKT phosphorylation, without effect on ERK1/2 or p38MAPK
Zhao et al., Mol Cell Biochem 2009 : Ang II rapidly induced phosphorylation of ERK5 at Thr218/Tyr220 residues in a time- and dose dependent manner
Nie et al., Mol Immunol 2009 : In conclusion, Ang II stimulates ERK1/2 phosphorylation via AT2 receptor in mouse DC, Ang- ( 1-7 ) enhances this effect
Calò et al., J Endocrinol Invest 2009 (Bartter Syndrome...) : Despite BS/GS 's higher plasma renin activity and aldosterone and unchanged level of AT1R, Ang II induced ERK1/2 phosphorylation was reduced vs both C and EH : 0.64 d.u.+/-0.08 vs 0.90+/-0.06 in C, p < 0.006, and vs 1.45+/-0.07 in EH, p < 0.001 ... As Bartter 's and Gitelman 's syndrome patients ( BS/GS ) have increased Ang II, and yet normo/hypotension, hyporesponsiveness to pressors and blunted Ang II signaling via type 1 receptors ( AT1R ), this study assesses BS/GS 's left ventricular ( LV ) mass and structure as well as Ang II induced ERK1/2 phosphorylation compared with essential hypertensive patients ( EH ) and normotensive healthy subjects ( C ) to gain insight into Ang II mediated processes
Chiou et al., Evidence-based complementary and alternative medicine : eCAM 2011 : Also, the CQC pretreatment markedly suppressed Ang-II induced phosphorylation of Akt and JNK rather than ERK1/2 , although it failed to affect p38 phosphorylation
Zhao et al., J Cell Biochem 2010 (Hypertrophy) : These data provide evidence that PKCepsilon dependent ERK5 phosphorylation and nucleocytoplasmic traffic mediates Ang II-induced MEF2C activation and cardiomyocyte hypertrophy
Montezano et al., Circ Res 2010 (Inflammation) : Nox5 activation by Ang II and ET-1 induces ROS generation and ERK1/2 phosphorylation
Marsh et al., Amino Acids 2011 (Diabetes Mellitus, Type 2...) : ANG II and PE significantly increased levels of ANP and a-actin and phosphorylation of p38 and ERK in the non-diabetic but not in the diabetic group ; phosphorylation of Akt was unchanged irrespective of group or treatment
Zhang et al., PloS one 2010 (MAP Kinase Signaling System) : These results suggest that Ang- ( 1-7 ) inhibits Ang II-induced SMC proliferation and migration, at least in part, through negative modulation of Ang II induced ERK1/2 activity
Wu et al., Zhongguo Ying Yong Sheng Li Xue Za Zhi 2007 (MAP Kinase Signaling System) : ( 3 ) Ang II significantly activated ERK1/2 , JNK and P38, only JNK activation was inhibited by Que and DPI but not ERK1/2 and P38 activation
Sun et al., Hypertens Res 2011 : In contrast, coexpression of the beta-2-adrenergic receptor or the pharmacologically non activated Ang II type 2 receptor ( AT(2) ) pretreated with the AT(2)-specific antagonist, PD123319, did not affect ERK1/2 phosphorylation through AT(1)
Yang et al., Mol Cell Biochem 2011 (MAP Kinase Signaling System) : These in vitro results indicate that Ang II induces ERK1/2 activation, contributing to the downregulation of CAT as well as promoting oxidative stress and adventitial fibroblast phenotypic differentiation in an AT1R mediated manner
Hua et al., American journal of physiology. Renal physiology 2012 : In these studies, we determined that ANG II induces phosphorylation of ETS-1 via activation of the type 1 ANG II receptor and that Erk1/2 and Akt/PKB phosphorylation are required for these effects
Shimizu et al., Life Sci 2012 (Arteriosclerosis) : The effect of indoxyl sulfate and Ang II on phosphorylation of ERK and epidermal growth factor receptor (EGFR), and migration were determined using VSMCs
Morales et al., Int J Biochem Cell Biol 2012 (Fibrosis) : The increase in pro-fibrotic factors levels was paralleled by enhanced p38MAPK and ERK1/2 phosphorylation in response to Ang-II ... Furthermore, we showed that the Ang-II dependent p38MAPK activation, but not the ERK1/2 phosphorylation, was necessary for the NOX derived ROS
Chao et al., PloS one 2013 : Furthermore, Ang II stimulated ERK and Akt phosphorylation in NSCs. Pretreatment of MEK inhibitor, but not PI3K inhibitor, inhibited Ang II-induced ERK phosphorylation as well as cell proliferation
Ishida et al., Circ Res 1998 : To determine whether c-Src is required for ERK1/2 activation by Ang II , we studied the effects of Src family-selective tyrosine kinase inhibitors on ERK1/2 activation and also studied Ang II-mediated signal events in Src-deficient and Src overexpressing VSMCs ... Basal ERK1/2 activity was lower, and activation of ERK1/2 by Ang II was significantly decreased in Src-/- mVSMCs compared with wild-type mVSMCs, whereas ERK1/2 protein expression and ERK1/2 activation by phorbol 12-myristate 13-acetate were similar ... ERK1/2 activation by Ang II was significantly increased in rVSMCs that overexpressed c-Src, whereas ERK1/2 activation by Ang II was significantly inhibited in rVSMCs that overexpressed dominant negative c-Src compared with control rVSMCs
Li et al., EMBO J 1998 : Induction of Ras ( N17 ) blocked EGF- but not Ang II- or phorbol ester ( TPA ) -dependent ERK activation ... In PKC depleted cells, Ang II increased Ras-GTP level and activated Raf and ERK in a Ras dependent manner
Murasawa et al., Hypertension 1998 : Intracellular Ca2+ chelation by BAPTA-AM or TMB-8 abolished Ang II induced ERK activation, whereas treatment with EGTA or nifedipine did not affect it
Maloney et al., Am J Physiol 1999 : ANG II-induced activations of Fyn, Raf-1, and ERK were augmented in cells pretreated with BAPTA-AM, but ANG II-induced expression of the dual-specificity phosphatase mitogen activated protein kinase phosphatase-1 was blocked by BAPTA-AM pretreatment