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ANG — EPHB2

Text-mined interactions from Literome

Aoki et al., Biochem J 2000 (Cardiomegaly) : Dominant negative Ras inhibited both ERK activation and ANF up-regulation by Ang II, whereas constitutively active forms of Ras and MEK were sufficient to activate the ANF promoter
Mondorf et al., FEBS Lett 2000 : In mesangial cells angiotensin II (Ang II) has been shown to activate extracellular regulated kinases 1 and 2 ( ERK1/2 )
Bokemeyer et al., Kidney Int 2000 (Coronary Artery Disease...) : In addition, the same nanomolar concentrations of AG 1478 that were effective in EGF signaling blocked the Ang II-induced activation of ERK and PI3 kinase in a dose dependent manner
Matrougui et al., Hypertension 2000 : In unpressurized arteries, Ang II increased ERK1/2 activity by 26 %, and pressure ( 70 mm Hg ) itself increased ERK1/2 activity by 72 %
Matrougui et al., Arterioscler Thromb Vasc Biol 2001 : However, the mechanisms by which pressure and Ang II activate ERK1/2 in intact resistance arteries remain to be determined
Yoshizumi et al., Mol Pharmacol 2001 : Ang II-induced JNK activation was inhibited by 3,3',4',5,7-pentahydroxyflavone ( quercetin ), a major bioflavonoid in foods of plant origin, whereas ERK1/2 and p38 activation by Ang II were not affected by quercetin
Shah et al., Mol Pharmacol 2002 : Agonist activation of endogenous angiotensin II (Ang II) AT(1) receptors expressed in hepatic C9 cells markedly stimulated inositol phosphate production, phosphorylation of the proline-rich tyrosine kinase PyK-2, and ERK activation
Zhong et al., Sheng Li Xue Bao 2001 : Ang II increased VSMC DNA and protein synthesis, and promoted protein expression of PKC-zeta and ERK1/2
Wei et al., J Renin Angiotensin Aldosterone Syst 2000 : Ang II increased ERK and p38 activities in human cardiomyocytes
Sharma et al., Mol Cell Biochem 2002 : Angiotensin II (ANG II) and platelet derived growth factor ( PDGF ) stimulated the immunoreactive Erk2 and p38MAPK activities and their protein levels by 2-4 fold
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
Marsigliante et al., J Physiol 2003 : Ang II was not able to affect the intracellular Ca ( 2+ ) concentration in fura-2 loaded cells, but it stimulated the translocation from the cytosol to the plasma membrane of atypical protein kinase C-zeta (PKC-zeta) and -iota ( PKC- ) isoforms with subsequent phosphorylation of the extracellular signal regulated kinases 1 and 2 ( ERK1 and 2 )
Chiu et al., Am J Physiol Gastrointest Liver Physiol 2003 (MAP Kinase Signaling System) : ANG II stimulates PKC dependent ERK activation, DNA synthesis, and cell division in intestinal epithelial cells ... To investigate the effects of receptor mediated PKC activation on mitogenesis, we demonstrated that ANG II induced ERK activation, a response completely blocked by pretreatment with mitogen/extracellular signal regulated kinase inhibitors or specific PKC inhibitors
Suárez et al., Am J Physiol Endocrinol Metab 2003 (Hyperplasia) : ANG II increased ERK phosphorylation in a time- and concentration dependent way
Yoon et al., Biochem Biophys Res Commun 2003 : Ang1 induced MEK/ERK activation was abrogated when PLD was inhibited, suggesting that PLD mediates Ang1 induced MEK/ERK activation
Tallant et al., Hypertension 2003 : Ang- ( 1-7 ) ( 1 micromol/L ) reduced 100 nmol/L Ang II-stimulated ERK1 and ERK2 activation by 42.3+/-6.2 % and 41.2+/-4.2 %, respectively ( P < 0.01 )
Mukhin et al., J Biol Chem 2004 : Angiotensin II (Ang II) and 5-hydroxytryptamine ( 5-HT ) stimulated both ERK and NHE-1 activities, with activation of NHE-1 preceding that of ERK ... Inhibition of NHE-1 with pharmacological agents or by isotonic replacement of sodium in the perfusate with choline or tetramethylammonium greatly attenuated ERK activation by 5-HT or Ang II
Tournaire et al., EMBO Rep 2004 : We further show that NLLMAAS specifically suppresses both Ang1 induced ERK activity and migration in human umbilical endothelial cells
Ikeda et al., J Biol Chem 2005 (Cardiomegaly...) : Western blot analysis of the myocardium revealed that activation of extracellular signal regulated kinases ( ERK ) 1/2 and ERK5 by Ang II stimulation were lower in ARKO mice than those of WT mice
Pinzar et al., FEBS Lett 2005 : Angiotensin II (Ang II) induces a prominent and sustained nitration and activation of ERK1/2 in rat vascular smooth muscle cells, both mediated via AT1 receptor
Chan et al., Circ Res 2005 : These results suggest that NADPH oxidase derived O2*- underlies the activation of p38 MAPK or ERK1/2 by Ang II in the ventrolateral medulla
Flannery et al., Nephron. Experimental nephrology 2006 : The signaling pathways linked to ANG2 dependent ERK activation were determined in an immortalized mouse podocyte cell line by monitoring ANG2 stimulated phosphorylation of ERK1/2 ... ANG2 dependent ERK activation was inhibited by : ( 1 ) the type-1 ANG2-selective antagonist losartan ; ( 2 ) the type-2 ANG2-selective antagonist PD123319 ; ( 3 ) an inhibitor of MMP2/9 ; ( 4 ) the EGFR kinase inhibitor AG1478, and ( 5 ) the HB-EGF antagonists CRM197 and heparin ... ANG2 dependent ERK activation was mediated by both protein kinase C ( PKC ) - and calcium dependent mechanisms and was associated with tyrosine phosphorylation of EGFR ... In contrast, ANG2 had no effect on ERK phosphorylation in stably transfected HEK293 cells ... Both the MMP2/9 inhibitor and AG1478 attenuated ANG2 dependent phosphorylation of GFP-ERK2 in the co-culture system ... These data indicate that ERK activation is induced by ANG2 in podocytes by mechanisms involving ANG2 dependent release of HB-EGF which, in turn, may act in an autocrine and paracrine fashion to stimulate ERK activity
Su et al., Kidney Int 2006 : While incubation of proximal tubular cells with Ang- ( 1-7 ) alone did not significantly affect MAPK phosphorylation, Ang- ( 1-7 ) ( 10 ( -7 ) M ) completely inhibited Ang II-stimulated phosphorylation of p38, ERK 1/2, and JNK
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
Deng et al., Am J Physiol Cell Physiol 2007 (Neoplasms, Experimental...) : We also found that MEKK3 is required for angiopoietin-1 (Ang1) induced p38 and ERK5 activation
Giani et al., Exp Physiol 2008 : Accordingly, in the present study we examined whether ANG- ( 1-7 ) affects the ANG II-mediated activation of ERK1/2 and Rho kinase, STAT3 and STAT5a/b in rat heart in vivo ... The ANG II-mediated phosphorylation of ERK1/2 and Rho kinase was prevented in a dose dependent manner by ANG- ( 1-7 ) and disappeared in the presence of the Mas receptor antagonist d-Ala7-ANG- ( 1-7 )
Zimpelmann et al., American journal of physiology. Renal physiology 2009 (MAP Kinase Signaling System) : Ang- ( 1-7 ) increased phosphorylation of p38, ERK1/ERK2 , and JNK MAPKs, which was blocked by the Ang- ( 1-7 ) antagonist A-779
Liu et al., Regul Pept 2010 (Atrial Fibrillation...) : Compared with the paced group, Ang- ( 1-7 ) prevented the increase of ERK1/ERK2 mRNA expression ( P < 0.01 and P < 0.05, respectively ), and attenuated the interstitial fibrosis ( P < 0.01 )
Lopez Verrilli et al., J Neurochem 2012 : Ang- ( 1-7 ) through Mas receptors stimulated Akt and ERK1/2 activities in spontaneously hypertensive rat neurons
El-Hashim et al., Br J Pharmacol 2012 (Asthma...) : Additionally, Ang- ( 1-7 ) reduced the ovalbumin induced increase in the phosphorylation of ERK1/2 and I?B-a
Li et al., EMBO J 1998 : In summary, Ang II can activate ERK via two pathways ; the latent EGF receptor, Ras dependent pathway is equipotent to the Ras independent pathway, but is masked by PKC action
Yang et al., Biochem Pharmacol 1999 : On the other hand, an obligatory tyrosine phosphorylation step for activation of ERK was indicated by the use of protein tyrosine kinase inhibitors, which profoundly inhibited the activation of ERK by EGF, Ang II, and PMA