PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
35410635-0	2022	p38-Dependent c-Jun Degradation Contributes to Reduced PGE2 Production in Sodium Orthovanadate-Treated Macrophages.	Dinoprostone	55-59	jun proto-oncogene	Mus musculus	14-19	
35410635-9	2022	Therefore, our results suggest that the hyperphosphorylation of p38 by SO contributes to c-Jun degradation, which is linked to the suppression of PGE2 secretion in inflammatory responses; and thus, finding drugs to increase p38 activity could be a novel strategy for the development of anti-inflammatory drugs.	Dinoprostone	146-150	jun proto-oncogene	Mus musculus	89-94	
29262525-4	2017	In contrast, the administration of PGI2 attenuated the effects of PGE2 in stimulating the production of TNF-alpha by inhibiting the activity of TNF-alpha promoter and the binding activity of AP1 on the promoter of TNF-alpha.	Dinoprostone	66-70	jun proto-oncogene	Mus musculus	191-194	
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	jun proto-oncogene	Mus musculus	236-241	
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	jun proto-oncogene	Mus musculus	71-76	
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	jun proto-oncogene	Mus musculus	253-256	
18567804-7	2008	Similarly, in vivo, we found that WT mice treated with PGE2 and untreated cyclooxygenase-2-overexpressing transgenic mice had higher levels of cell proliferation and expression of cyclin D1 and VEGF, as well as higher levels of activated EGFR, nuclear factor-kappa B, AP-1, and CREB, than vehicle-treated WT mice.	Dinoprostone	55-59	jun proto-oncogene	Mus musculus	268-272	
23411023-5	2013	MATERIALS AND METHODS: The anti-inflammatory mechanism of Ac-ME on the AP-1 activation pathway, which plays a critical role in the production of prostaglandin (PG)E2 in RAW264.7 cells and peritoneal macrophages and in induction of acute gastritis caused by HCl/EtOH, was investigated using immunoblotting, immunoprecipitation analyses, and reporter gene activity assays.	Dinoprostone	145-165	jun proto-oncogene	Mus musculus	71-75	
22406106-6	2012	This compound also inhibited the production of prostaglandin (PG)E(2) at the transcriptional level by suppression of Syk/NF-kappaB, IKKe/IRF-3, and p38/AP-1 pathways in lipopolysaccharide (LPS)-activated RAW264.7 cells and peritoneal macrophages.	Dinoprostone	47-69	jun proto-oncogene	Mus musculus	152-156	
18567804-6	2008	In addition, these inhibitors attenuated the PGE2-induced proliferation, nuclear factor-kappa B, activator protein-1 (AP-1), and CREB binding to the promoter regions of the cyclin D1 and vascular endothelial growth factor (VEGF) genes and expression of cyclin D1 and VEGF in primary mouse keratinocytes.	Dinoprostone	45-49	jun proto-oncogene	Mus musculus	97-116	
12209884-8	2002	These results demonstrated that PGE(2) is an important mediator in TPA-induced proliferation, and MAPK phosphorylation was located at the upstream of COX-2, c-Jun, and ODC gene expressions in TPA-induced responses.	Dinoprostone	32-38	jun proto-oncogene	Mus musculus	157-162	
18567804-6	2008	In addition, these inhibitors attenuated the PGE2-induced proliferation, nuclear factor-kappa B, activator protein-1 (AP-1), and CREB binding to the promoter regions of the cyclin D1 and vascular endothelial growth factor (VEGF) genes and expression of cyclin D1 and VEGF in primary mouse keratinocytes.	Dinoprostone	45-49	jun proto-oncogene	Mus musculus	118-122	
10799905-8	2000	PGE2 also stimulated activation of AP-1, a heterodimer of c-Jun and c-Fos, because the prostanoid increased specific binding of nuclear proteins to the AP-1 consensus sequence and stimulated AP-1-promoted luciferase activity.	Dinoprostone	0-4	jun proto-oncogene	Mus musculus	58-63	
10799905-9	2000	PGE2-stimulated expression of CD14 was inhibited by antisense c-fos and c-jun oligonucleotides, but not by their sense oligonucleotides.	Dinoprostone	0-4	jun proto-oncogene	Mus musculus	72-77	
10666498-0	2000	Prostaglandin E(2) (PGE(2)) induces the c-fos and c-jun expressions via the EP(1) subtype of PGE receptor in mouse osteoblastic MC3T3-E1 cells.	Dinoprostone	0-18	jun proto-oncogene	Mus musculus	50-55	
10666498-5	2000	Since MC3T3-E1 cells do not express the EP(3) subtype, these results suggest that PGE(2) induces c-fos and c-jun mRNA expressions through the EP(1) subtype of its receptor.	Dinoprostone	82-88	jun proto-oncogene	Mus musculus	107-112