PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 25936351-11 2015 Our data suggest that GPR91 modulates the succinate-induced release of VEGF through the MAPK/COX-2/PGE2 signaling pathway. Dinoprostone 99-103 mitogen-activated protein kinase 1 Mus musculus 88-92 26442583-8 2015 Treatment with PGE2 increased phospho-p44/42 ERK levels and also Cx43 phosphorylation at Ser(279)-Ser(282) sites. Dinoprostone 15-19 mitogen-activated protein kinase 1 Mus musculus 45-48 26442583-9 2015 Depletion of PGE2 from CM, and pre-treatment with a p44/42 ERK pathway-specific inhibitor, resulted in a complete inhibition of ERK-dependent Cx43 phosphorylation and attenuated the inhibition of hemichannels by CM and PGE2. Dinoprostone 13-17 mitogen-activated protein kinase 1 Mus musculus 128-131 26442583-9 2015 Depletion of PGE2 from CM, and pre-treatment with a p44/42 ERK pathway-specific inhibitor, resulted in a complete inhibition of ERK-dependent Cx43 phosphorylation and attenuated the inhibition of hemichannels by CM and PGE2. Dinoprostone 219-223 mitogen-activated protein kinase 1 Mus musculus 59-62 26442583-9 2015 Depletion of PGE2 from CM, and pre-treatment with a p44/42 ERK pathway-specific inhibitor, resulted in a complete inhibition of ERK-dependent Cx43 phosphorylation and attenuated the inhibition of hemichannels by CM and PGE2. Dinoprostone 219-223 mitogen-activated protein kinase 1 Mus musculus 128-131 26442583-12 2015 Together, results from this study suggest that extracellular PGE2 accumulated after continuous FFSS is responsible for activation of p44/42 ERK signaling and subsequently, direct Cx43 phosphorylation by activated ERK leads to hemichannel closure. Dinoprostone 61-65 mitogen-activated protein kinase 1 Mus musculus 140-143 26442583-12 2015 Together, results from this study suggest that extracellular PGE2 accumulated after continuous FFSS is responsible for activation of p44/42 ERK signaling and subsequently, direct Cx43 phosphorylation by activated ERK leads to hemichannel closure. Dinoprostone 61-65 mitogen-activated protein kinase 1 Mus musculus 213-216 22642975-11 2012 PGE2, PGI2, N-methyl-D-aspartate, and hypotension-induced pial artery dilation was blunted after FPI, partially protected by glucagon, and fully protected by glucagon+PAI-1DP, glucagon+JNK antagonist SP600125 or glucagon+ERK inhibitor U 0126. Dinoprostone 0-4 mitogen-activated protein kinase 1 Mus musculus 221-224 24842369-6 2014 In contradiction to previous in vitro studies that showed ERK activation by prostaglandin E2 (PGE2) engagement with prostaglandin receptor EP4, intravenous administration of EP4 agonist activated PKA, inhibited ERK, and suppressed migration of neutrophils. Dinoprostone 76-92 mitogen-activated protein kinase 1 Mus musculus 58-61 24842369-6 2014 In contradiction to previous in vitro studies that showed ERK activation by prostaglandin E2 (PGE2) engagement with prostaglandin receptor EP4, intravenous administration of EP4 agonist activated PKA, inhibited ERK, and suppressed migration of neutrophils. Dinoprostone 94-98 mitogen-activated protein kinase 1 Mus musculus 58-61 24842369-6 2014 In contradiction to previous in vitro studies that showed ERK activation by prostaglandin E2 (PGE2) engagement with prostaglandin receptor EP4, intravenous administration of EP4 agonist activated PKA, inhibited ERK, and suppressed migration of neutrophils. Dinoprostone 94-98 mitogen-activated protein kinase 1 Mus musculus 211-214 24376609-11 2013 CONCLUSIONS: These results suggest that BisGMA induced-PGE2 production may be via COX-2 expression, cPLA2 phosphorylation, and the phosphorylation of MAPK family. Dinoprostone 55-59 mitogen-activated protein kinase 1 Mus musculus 150-154 23416211-5 2013 Inhibitors of either protein kinase C (PKC), protein tyrosine kinase (PTK), or extracellular signal-regulated kinase (ERK) pathways abrogated MT-II-induced NF-kappaB activation and reduced COX-2 expression and PGE2 release, whereas the p38 mitogen-activated protein kinase (MAPK) inhibitor reduced MT-II-induced COX-2 expression and PGD2 production. Dinoprostone 210-214 mitogen-activated protein kinase 1 Mus musculus 79-116 23416211-5 2013 Inhibitors of either protein kinase C (PKC), protein tyrosine kinase (PTK), or extracellular signal-regulated kinase (ERK) pathways abrogated MT-II-induced NF-kappaB activation and reduced COX-2 expression and PGE2 release, whereas the p38 mitogen-activated protein kinase (MAPK) inhibitor reduced MT-II-induced COX-2 expression and PGD2 production. Dinoprostone 210-214 mitogen-activated protein kinase 1 Mus musculus 118-121 23525101-0 2013 The syndecan-4/protein kinase Calpha pathway mediates prostaglandin E2-induced extracellular regulated kinase (ERK) activation in endothelial cells and angiogenesis in vivo. Dinoprostone 54-70 mitogen-activated protein kinase 1 Mus musculus 79-109 23525101-0 2013 The syndecan-4/protein kinase Calpha pathway mediates prostaglandin E2-induced extracellular regulated kinase (ERK) activation in endothelial cells and angiogenesis in vivo. Dinoprostone 54-70 mitogen-activated protein kinase 1 Mus musculus 111-114 23525101-4 2013 We show that in the absence of proteoglycan syndecan-4 (Sdc4), PGE2-induced ERK activation is decreased significantly, as is endothelial cell migration and cord formation in a two-dimensional Matrigel assay. Dinoprostone 63-67 mitogen-activated protein kinase 1 Mus musculus 76-79 21396778-8 2011 Intravesical administration of prostaglandin E2 caused prompt phosphorylation of ERK in the L6 spinal cord, an effect blocked by ONO-8130. Dinoprostone 31-47 mitogen-activated protein kinase 1 Mus musculus 81-84 15123663-5 2004 The anti-proliferative effects of COX inhibition are rescued specifically by treatment with PGE(2) or the EP4 receptor-selective agonist PGE(1)-OH via phosphatidylinositol 3-kinase/extracellular signal-regulated kinase (ERK) activation, thus providing a functional link between PGE(2)-induced cell proliferation and EP4-mediated ERK signaling. Dinoprostone 92-98 mitogen-activated protein kinase 1 Mus musculus 220-223 20045950-7 2010 Therefore our data suggest that cafestol may be a novel ERK inhibitor with AP-1-targeted inhibitory activity against PGE(2) production in LPS-activated RAW264.7 cells. Dinoprostone 117-123 mitogen-activated protein kinase 1 Mus musculus 56-59 18295507-8 2008 In addition, the ERK/MAPK and IP(3) pathways were found to mediate PGE(2)-G-induced enhancement of LTP. Dinoprostone 67-73 mitogen-activated protein kinase 1 Mus musculus 17-20 18295507-8 2008 In addition, the ERK/MAPK and IP(3) pathways were found to mediate PGE(2)-G-induced enhancement of LTP. Dinoprostone 67-73 mitogen-activated protein kinase 1 Mus musculus 21-25 17310141-11 2007 However, inhibitors of PKA, PKC or ERK, but not p38 or JNK, also partially inhibited PGE(2)-induced mechanical allodynia. Dinoprostone 85-91 mitogen-activated protein kinase 1 Mus musculus 35-38 17310141-14 2007 Co-treatment with EP(3) or EP(4) receptor antagonists reduced PGE(2)-induced PKA and ERK, but not PKCalpha activation. Dinoprostone 62-68 mitogen-activated protein kinase 1 Mus musculus 85-88 19168156-6 2009 These results suggest that ivermectin suppresses NO and PGE(2) production, as well as iNOS and COX-2 expression, by inhibiting phosphorylation of mitogen-activated protein kinases (MAPK) (p38, ERK1/2, and JNK) in LPS-stimulated RAW 264.7 cells. Dinoprostone 56-62 mitogen-activated protein kinase 1 Mus musculus 181-185 17401137-5 2007 The EP4 agonist-induced endothelial cell migration was inhibited by ERK, but not PKA inhibitors, defining a functional link between PGE(2)-induced endothelial cell migration and EP4-mediated ERK signaling. Dinoprostone 132-138 mitogen-activated protein kinase 1 Mus musculus 68-71 17401137-5 2007 The EP4 agonist-induced endothelial cell migration was inhibited by ERK, but not PKA inhibitors, defining a functional link between PGE(2)-induced endothelial cell migration and EP4-mediated ERK signaling. Dinoprostone 132-138 mitogen-activated protein kinase 1 Mus musculus 191-194 16777358-5 2006 A blockade of p38 MAPK pathway abrogated Cd-induced COX-2 expression and PGE(2) production. Dinoprostone 73-79 mitogen-activated protein kinase 1 Mus musculus 18-22 15664007-11 2005 U0126, a specific inhibitor of the ERK pathway, completely blocked both TGF(beta)- and PGE2-induced cell proliferation whereas SB203580 and SP600125, which are selective inhibitors of, respectively, p38 and JNK pathways, had no effect. Dinoprostone 87-91 mitogen-activated protein kinase 1 Mus musculus 35-38 15664007-12 2005 Finally, the effect of PGE2 on activation of ERK was mimicked by phorbol esters and not by forskolin, and was associated with activation of protein kinase C. This latter effect and the stimulation of ERK induced by PGE2 were completely blocked by a specific inhibitor of PKC. Dinoprostone 23-27 mitogen-activated protein kinase 1 Mus musculus 45-48 15664007-12 2005 Finally, the effect of PGE2 on activation of ERK was mimicked by phorbol esters and not by forskolin, and was associated with activation of protein kinase C. This latter effect and the stimulation of ERK induced by PGE2 were completely blocked by a specific inhibitor of PKC. Dinoprostone 23-27 mitogen-activated protein kinase 1 Mus musculus 200-203 15664007-12 2005 Finally, the effect of PGE2 on activation of ERK was mimicked by phorbol esters and not by forskolin, and was associated with activation of protein kinase C. This latter effect and the stimulation of ERK induced by PGE2 were completely blocked by a specific inhibitor of PKC. Dinoprostone 215-219 mitogen-activated protein kinase 1 Mus musculus 45-48 15664007-12 2005 Finally, the effect of PGE2 on activation of ERK was mimicked by phorbol esters and not by forskolin, and was associated with activation of protein kinase C. This latter effect and the stimulation of ERK induced by PGE2 were completely blocked by a specific inhibitor of PKC. Dinoprostone 215-219 mitogen-activated protein kinase 1 Mus musculus 200-203 15212812-2 2004 In the present study, we further investigated the mechanism of PGE2 production by Cd focusing on the main mitogen-activated protein kinase (MAPK) subfamilies that mediate prostaglandin synthesis, extracellular signal-regulated kinase (ERK1/2 MAPK), c-jun-amino-terminal kinase (JNK MAPK) and p38 MAPK, and protein kinase C (PKC) which is activated by Cd in several kinds of cells. Dinoprostone 63-67 mitogen-activated protein kinase 1 Mus musculus 140-144 15212812-5 2004 PD98059 inhibited PGE2 production stimulated by PMA as well as Cd, indicating that activation of PKC by ERK1/2 MAPK was necessary for Cd-stimulated PGE2 production. Dinoprostone 148-152 mitogen-activated protein kinase 1 Mus musculus 111-115 15123663-5 2004 The anti-proliferative effects of COX inhibition are rescued specifically by treatment with PGE(2) or the EP4 receptor-selective agonist PGE(1)-OH via phosphatidylinositol 3-kinase/extracellular signal-regulated kinase (ERK) activation, thus providing a functional link between PGE(2)-induced cell proliferation and EP4-mediated ERK signaling. Dinoprostone 92-98 mitogen-activated protein kinase 1 Mus musculus 329-332 11740948-6 2001 The further potentiation of bradykinin-induced prostaglandin E(2) release by combined preconditioning with fresh culture medium and genistein may be due to the activation of the MAPK/ERK-c phospholipase A(2) pathway by preconditioning with genistein. Dinoprostone 47-65 mitogen-activated protein kinase 1 Mus musculus 178-182 11740948-6 2001 The further potentiation of bradykinin-induced prostaglandin E(2) release by combined preconditioning with fresh culture medium and genistein may be due to the activation of the MAPK/ERK-c phospholipase A(2) pathway by preconditioning with genistein. Dinoprostone 47-65 mitogen-activated protein kinase 1 Mus musculus 183-186 35588334-6 2022 Mechanistically, PGE2/EP4 signals enhanced HSC autophagy through the Erk pathway. Dinoprostone 17-21 mitogen-activated protein kinase 1 Mus musculus 69-72 10217536-7 1999 This PGE2 release was blocked by inhibitors of tyrosine kinase (genistein), protein kinase C (PKC) (Ro 31-8220, Go 6976 or LY 379196), mitogen-activated protein kinase kinase (MEK) (PD 098059) or p38 mitogen-activated protein kinase (MAPK) (SB 203580). Dinoprostone 5-9 mitogen-activated protein kinase 1 Mus musculus 234-238 31545273-3 2019 The aim of this study was to investigate whether BA exerts anti-inflammatory effect against Carr-induced paw edema in mice, and how BA could mediate the expression of inflammation-associated MAPK-COX-2-PGE2 signal pathway. Dinoprostone 200-206 mitogen-activated protein kinase 1 Mus musculus 191-195 26255103-6 2016 Furthermore, LTD4 plus PGE2, through cysteinyl leukotriene receptor 1 (CysLT1R) and E-prostanoid receptor (EP) 3, enhanced extracellular signal-regulated kinase (Erk) and c-fos phosphorylation, inflammatory gene expression, macrophage inflammatory protein 1beta secretion, COX-2 upregulation, and PGD2 generation in mast cells. Dinoprostone 23-27 mitogen-activated protein kinase 1 Mus musculus 123-160 28918839-13 2017 PGE2-mediated phospho-ERK and COX-2 upregulation was suppressed by PRR silencing. Dinoprostone 0-4 mitogen-activated protein kinase 1 Mus musculus 22-25 30713782-0 2019 Mannan-binding lectin suppresses growth of hepatocellular carcinoma by regulating hepatic stellate cell activation via the ERK/COX-2/PGE2 pathway. Dinoprostone 133-137 mitogen-activated protein kinase 1 Mus musculus 123-126 30713782-6 2019 Mechanistic studies revealed that MBL could interact directly with HSCs and inhibit HCC-induced HSCs activation via downregulating the extracellular signal-regulated kinase (ERK)/COX-2/PGE2 signaling pathway. Dinoprostone 185-189 mitogen-activated protein kinase 1 Mus musculus 135-172 30713782-6 2019 Mechanistic studies revealed that MBL could interact directly with HSCs and inhibit HCC-induced HSCs activation via downregulating the extracellular signal-regulated kinase (ERK)/COX-2/PGE2 signaling pathway. Dinoprostone 185-189 mitogen-activated protein kinase 1 Mus musculus 174-177 26255103-6 2016 Furthermore, LTD4 plus PGE2, through cysteinyl leukotriene receptor 1 (CysLT1R) and E-prostanoid receptor (EP) 3, enhanced extracellular signal-regulated kinase (Erk) and c-fos phosphorylation, inflammatory gene expression, macrophage inflammatory protein 1beta secretion, COX-2 upregulation, and PGD2 generation in mast cells. Dinoprostone 23-27 mitogen-activated protein kinase 1 Mus musculus 162-165 26255103-9 2016 CONCLUSIONS: Our results unravel a unique LTD4-PGE2 interaction affecting mast cells through CysLT1R and EP3 involving Gi, protein kinase G, and Erk and contributing to vascular inflammation in vivo. Dinoprostone 47-51 mitogen-activated protein kinase 1 Mus musculus 145-148