Gene interactions and pathways from curated databases and text-mining

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ANGPT2 — MAPK14

Pathways - manually collected, often from reviews:

Text-mined interactions from Literome

Gendron et al., Mol Endocrinol 1999 : These results support the observation that inhibition of p21ras did not impair the effect of Ang II on its ability to stimulate MAPK activity
Morrell et al., Am J Physiol 1999 : In addition, ANG II led to rapid activation of mitogen activated protein kinase ( MAPK ), and ANG II-stimulated DNA synthesis was inhibited by the specific inhibitor of MAPK PD-98059
Parmentier et al., Hypertension 2001 : Ang II also activates ras/mitogen activated protein ( MAP ) kinase in VSMCs ; this activation is mediated by 20-hydroxyeicosatetraenoic acid ( HETE ) and 12 ( S ) -HETE, which are metabolites of arachidonic acid generated by cytochrome P450 4A and lipoxygenase, respectively, produced on activation of cPLA(2)
Everett et al., Am J Physiol Heart Circ Physiol 2001 : ANG II activated mitogen activated protein kinase , ( MAPK ) within 10 min of treatment, and blockade of MAPK activation with PD-98059 ( 1 -- 20 nM ) inhibited eEF-2 dephosphorylation
Kyaw et al., Hypertens Res 2001 (MAP Kinase Signaling System) : The present findings showed that Ang II stimulated rapid and significant activation of ERK 1/2, JNK and p38 MAPK in cultured rat aortic smooth muscle cells ( 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
Fan et al., Am J Physiol Gastrointest Liver Physiol 2002 : We conclude that ANG II causes contraction of rat IAS smooth muscle by the activation of AT(1) receptors at the SMC and involves multiple intracellular pathways, influx of Ca ( 2+ ), and activation of PKC, Rho kinase, and MAPK ( 44/42 )
Silfani et al., Arch Biochem Biophys 2002 : Also, using Western analysis, Ang II increased the phosphorylation of MAPK and cPLA(2) which were blocked by the MAPK kinase inhibitor PD98059 ( 10 microM/L )
Krikun et al., Am J Pathol 2002 (Uterine Hemorrhage) : To further examine the effects of progestin, hypoxia, and reactive oxygen species ( ROS ) on the regulation of Ang-1 and Ang-2 as well as the activation of MAPK , SAPK/JNK, and p38 by the relevant cell types, we conducted in vitro studies with cultured human endometrial stromal cells ( HESCs ) and human endometrial endothelial cells ( HEECs )
Espiritu et al., American journal of physiology. Renal physiology 2002 (Acidosis) : Regulation of renal Na-HCO cotransporter ( NBC1 ) activity by cholinergic agonists, ANG II , and acute acidosis ( CO ( 2 ) ) requires both Src family kinase (SFK) and classic MAPK pathway activation
Reddy et al., American journal of physiology. Renal physiology 2002 (Diabetic Nephropathies...) : ANG II and 12 ( S ) -HETE led to activation of p38 ( MAPK ) and its target transcription factor cAMP-responsive element binding protein ( CREB ) ... ANG II- and 12 ( S ) -HETE induced CREB activation and [ ( 3 ) H ] leucine incorporation were blocked by the p38 ( MAPK ) inhibitor SB-202190
Natarajan et al., Endocrine 2002 : However, both ANG II and 12-HETE led to significant dose dependent increases in p38 MAPK activity with peak effects at 5 min
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
Ishida et al., FEBS Lett 1992 : In cultured vascular smooth muscle cells ( VSMC ) angiotensin II (ang II) induces tyrosine and serine/threonine phosphorylation and activation of two mitogen activated protein ( MAP ) kinases
Han et al., American journal of physiology. Renal physiology 2004 : Indeed, ANG II increased p44/42 MAPK activity
Zheng et al., J Cardiovasc Pharmacol 2004 (Cardiomegaly) : EGCG pretreatment did not exert any significant changes in Ang II-stimulated activation of extracellular signal regulated kinase ( ERK ) and p38 MAPK
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 )
Lai et al., Beijing Da Xue Xue Bao 2004 : ANG II promoted podocyte apoptosis in a time- and dose dependent manner ; ANG II stimulated p38MAPK , but inhibited JNK ; SB202190 inhibited both ANG II-induced podocyte apoptosis and p38MAPK phosphorylation ; Inhibition of ERK by PD98059 had no effect on ANG II-induced cell apoptosis
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
Slice et al., J Biol Chem 2005 : Luciferase promoter assays showed that Ang II-dependent transcriptional activation of the COX-2 promoter was dependent on activation of small GTPases and p38 ( MAPK ) and on Ca2+ signaling via the cAMP-responsive element/activating transcription factor cis acting element
Li et al., J Pharmacol Exp Ther 2005 : These data indicate that Ang II-stimulated Akt activity is mediated by cPLA(2) dependent, p38 MAPK regulated PLD(2) activation and EGFR transactivation
Saito et al., Regul Pept 2005 : Ang II and H2O2 also activated p38MAPK , and they were blocked by pre-treatment with NAC
Chan et al., Circ Res 2005 : Functionally, Ang II-elicited pressor response in the RVLM was attenuated by DPI, tempol, or a p38 MAPK inhibitor, SB203580
Kang et al., J Mol Endocrinol 2006 (MAP Kinase Signaling System) : Furthermore, stimulation of the cells with Ang-II increased both phosphorylation of p38 MAPK and MAP kinase kinase 3/6 ( MKK3/6 )
Su et al., Kidney Int 2006 : Ang II ( 5 min, 10 ( -7 ) M ) stimulated phosphorylation of the three MAPK ( p38, extracellular signal related kinase ( ERK 1/2 ), and c-Jun N-terminal kinase (JNK) )
Guo et al., Peptides 2006 (MAP Kinase Signaling System) : These results also demonstrate that Ang II leads to MAPK phosphorylation and p38MAPK pathway induced NF-kappaB activation
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
Li et al., Am J Physiol Cell Physiol 2007 (MAP Kinase Signaling System) : ANG II-dependent activation of MAPK and the increase in endothelial NOS (eNOS) were prevented when PAECs were transfected with Ras DN cDNA or treated with FTI-277, a farnesyl transferase inhibitor
Pham et al., J Cell Physiol 2008 : Ang II and EGF induced transient phosphorylation of ERK, p38 ( MAPK ) and CREB ... The p38 ( MAPK ) selective inhibitor, SB202190, but not the MEK selective inhibitor, PD98059, or the EGFR kinase inhibitor, AG1478, inhibited Ang II-dependent COX-2 expression and CREB phosphorylation
Bao et al., J Cardiovasc Pharmacol 2007 (Hypertension...) : Ang II infusion increased the levels of phosphorylated p38 MAPK in the heart and aorta ... The results suggest that Ang II induced hypertension, organ damage, and ROS production are possibly mediated by p38 MAPK and inhibition of p38 MAPK may offer a therapeutic approach for cardiovascular disease
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
Zhang et al., Cardiovasc Res 2009 : In isolated VSMCs or aorta from wild-type mice, Ang II stimulation markedly increased the levels of O2 ( - ) and MAPK phosphorylation ... FeTPPS did not suppress the Ang II-induced increase of O2 ( - ) levels, but markedly inhibited Ang II-induced MAPK phosphorylation
Nie et al., Mol Immunol 2009 : It is well known that angiotensin- ( 1-7 ) ( Ang- ( 1-7 ) ) counterbalances vasoconstrictive and proliferative functions of angiotensin II (Ang II), some of those actions are via inhibition of Ang II induced activation of mitogen activated protein kinases ( MAPK )
Samuel et al., Diabetes 2010 (Diabetes Mellitus, Experimental...) : We also observed increased phosphorylated mitogen activated protein kinase activated protein kinase-2, 2 days after the treatment and increased expression of vascular endothelial growth factor ( VEGF ), Flk-1, angiopoietin-1 (Ang-1), Tie-2, and survivin, 4 days after treatment in the diabetic animals
Gao et al., Am J Physiol Heart Circ Physiol 2010 (Body Weight...) : The ANG II-induced inhibition of Kv4.3 mRNA expression was mediated by ANG II-AT(1)R-ROS-p38 MAPK signaling
Rabkin et al., J Heart Valve Dis 2009 : Alternatively, peroxynitrite may be involved in the pathway by which Ang II activates p38 MAPK
Freeman et al., Arch Biochem Biophys 2010 : In this study, Ang II increased phosphorylation of the EGFR and MAPK in cultured VSMC and these effects were attenuated by the cPLA(2) inhibitor arachidonyl trifluoromethyl ketone ( AACOCF ( 3 ) ), and restored by addition of ArAc
Hitomi et al., Am J Hypertens 2011 (Hypertrophy...) : To clarify the role of angiotensin II (Ang II) in insulin induced arteriosclerosis, we examined the effects of Ang II on insulin induced mitogen activated protein ( MAP ) kinase activation and cellular hypertrophy in rat vascular smooth muscle cells ( VSMCs )
Paravicini et al., Journal of the American Society of Hypertension : JASH 2012 (Disease Models, Animal...) : We examined effects of stretch and Ang II on activation of p38MAPK in vascular smooth muscle cells ( VSMC ) from WKY and SHR
Yu et al., Molecules (Basel, Switzerland) 2012 (MAP Kinase Signaling System) : The results showed that Ang II ( 10 ( -7 ) M ) stimulated the cardiac fibroblast proliferation which was inhibited by NAC ( an antioxidant ), SB203580 ( a p38MAPK inhibitor ) or enalaprilat ; Ang II caused an burst of intracellular ROS level within thirty minutes, an increase in p-p38MAPK ( 3.6-fold of that in the control group ), as well as an elevation of TGF-ß ( 1 ) meantime ; NAC, an antioxidant, and enalaprilat treatment attenuated cardiac fibroblast proliferation induced by Ang II and decreased ROS and p-p38MAPK protein levels in rat cardiac fibroblast ; SB203580 lowered TGF-ß ( 1 ) protein expression in rats ' CFb in a dose dependent manner
Ptasinska-Wnuk et al., TheScientificWorldJournal 2012 : The growth-inhibitory effect of ang II is possibly mediated by the p44/42 MAPK ... The p38 MAPK appears to mediate the inhibitory effects of both ang II and ang 5-8 upon cell survival
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 ... These results strongly suggest that the fibrotic response to Ang-II is mediated by the AT-1 receptor and requires the p38MAPK phosphorylation, NOX induced ROS, and TGF-ß1 expression increase mediated by Ang-II in skeletal muscle cells
Clark et al., International journal of hypertension 2013 : Previously, we showed that Ang II and Ang III induced mitogen activated protein ( MAP ) kinases ERK1/2 and stress activated protein kinase/Jun-terminal kinases ( SAPK/JNK ) phosphorylation in cultured rat astrocytes
Sadoshima et al., Circ Res 1995 (Cardiomegaly) : Rapamycin did not inhibit Ang II-induced activation of tyrosine kinase, mitogen activated protein kinase , RSK, and protein kinase C
Eguchi et al., J Biol Chem 1996 : The calmodulin inhibitor, calmidazolium, and the tyrosine kinase inhibitor, genistein, completely blocked MAPK activation by Ang II as well as by the Ca2+ ionophore A23187
Huang et al., J Biol Chem 1996 : Here, we have investigated the effects of Ang II on neuronal mitogen activated protein ( MAP ) kinases , potential targets for PP2A
Graves et al., J Biol Chem 1997 : In contrast, the Ang II-dependent activation of mitogen activated protein kinase and p90 ( RSK ) was not inhibited but was enhanced by BAPTA-AM
Dulin et al., Proc Natl Acad Sci U S A 1998 : Ang II stimulated transient dose dependent phosphorylation of MAPK with a maximum at 1 microM ( 10 min )
Muthalif et al., Proc Natl Acad Sci U S A 1998 : The present study was conducted to determine the contribution of AA and its metabolites as possible mediators of CaMKII induced MAPK activation by NE, Ang II , and epidermal growth factor (EGF) in vascular smooth muscle cells
Tsutsumi et al., Circ Res 1998 (Cardiomyopathy, Dilated...) : Mitogen activated protein kinase ( MAPK ) activation by Ang II was significantly decreased in fibroblast compartment from the failing hearts, and pretreatment with AT2-R antagonist caused an additional significant increase in Ang II-induced MAPK activity ( 36 % )