PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 33478055-6 2021 Interestingly, these terpenoids inhibited the phosphorylation of c-Jun N-terminal kinase (JNK), which further inhibited the production of pro-inflammatory mediators, including prostaglandin E2, tumor necrosis factor, and interleukins (IL-6 and IL-1beta), with a potency greater than that of the well-known iNOS inhibitor NG-mono-methyl-L-arginine (L-NMMA). Dinoprostone 176-192 mitogen-activated protein kinase 8 Mus musculus 90-93 29262525-5 2017 Moreover, our data also showed that not only Abeta1-42 oligomers but also Abeta1-42 fibrils have the ability to involve in mediating the antagonistic effects of PGE2 and PGI2 on regulating the expression of TNF-alpha via a p38- and JNK/c-Jun-dependent, AP1-transactivating mechanism. Dinoprostone 161-165 mitogen-activated protein kinase 8 Mus musculus 232-235 33840687-5 2021 We have previously reported that prostaglandin (PG) E2 and PGF2alpha induce osteoprotegerin synthesis through p38 mitogen-activated protein kinase (MAPK), p44/p42 MAPK and stress-activated protein kinase/c-Jun N-terminal kinase (SAPK/JNK) in osteoblast-like MC3T3-E1 cells. Dinoprostone 48-54 mitogen-activated protein kinase 8 Mus musculus 229-237 33840687-9 2021 Acetaminophen markedly downregulated the phosphorylation of SAPK/JNK stimulated by PGE2 and PGF2alpha, but not those of p38 MAPK or p44/p42 MAPK. Dinoprostone 83-87 mitogen-activated protein kinase 8 Mus musculus 65-68 33840687-10 2021 SP600125, an inhibitor of SAPK/JNK, suppressed the levels of PGE2- and PGF2alpha-upregulated osteoprotegerin mRNA expression. Dinoprostone 61-65 mitogen-activated protein kinase 8 Mus musculus 31-34 33840687-11 2021 Taken together, these results strongly suggest that acetaminophen reduces the PGE2- and PGF2alpha-stimulated synthesis of osteoprotegerin in osteoblasts, and that the suppressive effect is exerted via attenuation of SAPK/JNK. Dinoprostone 78-82 mitogen-activated protein kinase 8 Mus musculus 216-224 29262525-3 2017 Specifically, PGE2 accumulation in astrocyte activated the p38 and JNK/c-Jun signaling pathways via phosphorylation, resulting in TNF-alpha expression. Dinoprostone 14-18 mitogen-activated protein kinase 8 Mus musculus 67-70 16644903-11 2006 injection of PGE2 (3 nmol/paw) induced a significant activation of MAPKs, namely, JNK and p38, an effect that was largely prevented by the selective EP3 receptor antagonist L826266 (10 nmol/paw). Dinoprostone 13-17 mitogen-activated protein kinase 8 Mus musculus 82-85 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 8 Mus musculus 185-188 25936351-8 2015 The increase in COX-2 expression and the release of PGE2 were inhibited by transduction with LV.shGPR91 and ERK1/2, JNK and COX-2 inhibitors. Dinoprostone 52-56 mitogen-activated protein kinase 8 Mus musculus 116-119 21298000-4 2011 METHODOLOGY/PRINCIPAL FINDINGS: In this study, we first demonstrated that prostaglandin E2 (PGE2), which is one of the lipid mediators derived from arachidonic acid and is known to suppress activation of microglia, reduced the aberrant MIP-1alpha production by SD-Mg to the same level as by WT-Mg. PGE2 also attenuated the activation of Akt and JNK. Dinoprostone 74-90 mitogen-activated protein kinase 8 Mus musculus 345-348 21298000-4 2011 METHODOLOGY/PRINCIPAL FINDINGS: In this study, we first demonstrated that prostaglandin E2 (PGE2), which is one of the lipid mediators derived from arachidonic acid and is known to suppress activation of microglia, reduced the aberrant MIP-1alpha production by SD-Mg to the same level as by WT-Mg. PGE2 also attenuated the activation of Akt and JNK. Dinoprostone 92-96 mitogen-activated protein kinase 8 Mus musculus 345-348 19837872-0 2009 Forkhead box O1/pancreatic and duodenal homeobox 1 intracellular translocation is regulated by c-Jun N-terminal kinase and involved in prostaglandin E2-induced pancreatic beta-cell dysfunction. Dinoprostone 135-151 mitogen-activated protein kinase 8 Mus musculus 95-118 19837872-5 2009 JNK inhibition by the JNK-specific inhibitor SP600125 reversed PGE(2)-inhibited glucose-stimulated insulin secretion (GSIS). Dinoprostone 63-69 mitogen-activated protein kinase 8 Mus musculus 0-3 19837872-5 2009 JNK inhibition by the JNK-specific inhibitor SP600125 reversed PGE(2)-inhibited glucose-stimulated insulin secretion (GSIS). Dinoprostone 63-69 mitogen-activated protein kinase 8 Mus musculus 22-25 19837872-11 2009 Our results revealed that activation of the JNK is involved in PGE(2)-induced beta-cell dysfunction. Dinoprostone 63-69 mitogen-activated protein kinase 8 Mus musculus 44-47 19837872-12 2009 PGE(2)-mediated JNK1 activation, through dephosphorylation of Akt and FOXO1, leads to nuclear accumulation of FOXO1 and nucleocytoplasmic shuttling of PDX1, finally resulting in defective GSIS in pancreatic beta-cells. Dinoprostone 0-6 mitogen-activated protein kinase 8 Mus musculus 16-20 34381764-8 2021 To define the signaling pathway whereby PGE2 induces salivary gland dysfunction, primary parotid gland cells treated with PGE2 have increased c-Jun N-terminal Kinase (JNK) activation and cell proliferation and reduced amylase levels and store-operated calcium entry (SOCE). Dinoprostone 40-44 mitogen-activated protein kinase 8 Mus musculus 142-165 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 8 Mus musculus 207-210 34381764-8 2021 To define the signaling pathway whereby PGE2 induces salivary gland dysfunction, primary parotid gland cells treated with PGE2 have increased c-Jun N-terminal Kinase (JNK) activation and cell proliferation and reduced amylase levels and store-operated calcium entry (SOCE). Dinoprostone 40-44 mitogen-activated protein kinase 8 Mus musculus 167-170 34381764-8 2021 To define the signaling pathway whereby PGE2 induces salivary gland dysfunction, primary parotid gland cells treated with PGE2 have increased c-Jun N-terminal Kinase (JNK) activation and cell proliferation and reduced amylase levels and store-operated calcium entry (SOCE). Dinoprostone 122-126 mitogen-activated protein kinase 8 Mus musculus 142-165 34381764-8 2021 To define the signaling pathway whereby PGE2 induces salivary gland dysfunction, primary parotid gland cells treated with PGE2 have increased c-Jun N-terminal Kinase (JNK) activation and cell proliferation and reduced amylase levels and store-operated calcium entry (SOCE). Dinoprostone 122-126 mitogen-activated protein kinase 8 Mus musculus 167-170 34381764-9 2021 The in vivo effects of blocking PGE2 production were also examined and irradiated mice receiving indomethacin injections have reduced JNK activity at 8 days post-irradiation and reduced proliferation and increased amylase levels at day 30, as compared to irradiated mice without indomethacin. Dinoprostone 32-36 mitogen-activated protein kinase 8 Mus musculus 134-137 34381764-10 2021 Combined, these data suggest a mechanism whereby irradiation-induced PGE2 signaling to JNK blocks critical steps in saliva secretion manifested by a decrease in the quality (diminished amylase) and quantity (loss of calcium channel activity) of saliva, that can be restored with indomethacin. Dinoprostone 69-73 mitogen-activated protein kinase 8 Mus musculus 87-90 35379745-3 2022 Disruption of the PGE2-EP4-AKT signaling pathway resulted in IRE1alpha-induced activation of JNK, leading to accelerated death of SLPCs. Dinoprostone 18-22 mitogen-activated protein kinase 8 Mus musculus 93-96 35163786-9 2022 Silencing DUSP9 was found to facilitate the expression of proinflammatory cytokines and COX2 as well as PGE2 secretion in WISH cells, which could be attenuated by p38 inhibitor SB203580 or JNK inhibitor SP600125. Dinoprostone 104-108 mitogen-activated protein kinase 8 Mus musculus 189-192 35163786-11 2022 Collectively, miR-132-3p might participate in inflammation and PGE2 release via targeting DUSP9-dependent p38 and JNK signaling pathways to cause preterm birth. Dinoprostone 63-67 mitogen-activated protein kinase 8 Mus musculus 114-117