PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
24378735-7	2014	These results indicate that CREB-dependent expression of COX-2 for the production of anti-adipogenic PGs is critical for the regulation of the early phase of adipogenesis.	Phosphatidylglycerols	101-104	cytochrome c oxidase II, mitochondrial	Mus musculus	57-62	
21577211-12	2011	The present study therefore suggests that lymphangiogenesis, together with recurrence of lymph flow after surgical induction of lymphedema, is upregulated by COX-2 possibly via generation of PGs.	Phosphatidylglycerols	191-194	cytochrome c oxidase II, mitochondrial	Mus musculus	158-163	
21668646-7	2011	An FP receptor antagonist and each inhibitor for MEK and COX-2 suppressed the PGF(2alpha) -derived induction of synthesis of these PGs.	Phosphatidylglycerols	131-134	cytochrome c oxidase II, mitochondrial	Mus musculus	57-62	
19749081-15	2009	Furthermore, for the first time, we demonstrated that the production of PGs depended in part on COX-2 in endocardial endothelium through the muscarinic M(3) receptor stimulation.	Phosphatidylglycerols	72-75	cytochrome c oxidase II, mitochondrial	Mus musculus	96-101	
17583568-10	2007	Additionally, K14.COX2 mice treated only with DMBA developed approximately 3.5 times more tumors than wild-type mice, suggesting that PGs have intrinsic tumor promoting activity.	Phosphatidylglycerols	134-137	cytochrome c oxidase II, mitochondrial	Mus musculus	18-22	
17187424-4	2007	In the present study, we demonstrate a protective role of COX-2 derived PGs in ConA-induced liver injury.	Phosphatidylglycerols	72-75	cytochrome c oxidase II, mitochondrial	Mus musculus	58-63	
11743745-7	2001	Microarray analyses indicated that increased injury associated with COX-2 deficiency coincided, most notably, with a profoundly impaired induction of heat shock proteins in COX-2(-/+) mice suggesting that PGs may act as critical endogenous stress signals following drug insult.	Phosphatidylglycerols	205-208	cytochrome c oxidase II, mitochondrial	Mus musculus	68-73	
15883739-7	2005	Corresponding with the induction of COX-2 protein expression, the latter three PGs induced PGE2 synthesis in a dose-dependent manner.	Phosphatidylglycerols	79-82	cytochrome c oxidase II, mitochondrial	Mus musculus	36-41	
11254702-7	2001	These findings, in conjunction with the known immunomodulatory capacities of PGs, suggest that COX-2 expression by the small intestine lamina propria is a basal state contributing to the hyporesponsiveness of the intestinal immune response.	Phosphatidylglycerols	77-80	cytochrome c oxidase II, mitochondrial	Mus musculus	95-100	
10828079-5	2000	We observed that AA and PGs induced COX-2, as well as COX-1, expression in cultured murine keratinocytes approximately 3 h after treatment.	Phosphatidylglycerols	24-27	cytochrome c oxidase II, mitochondrial	Mus musculus	36-41	
11028754-10	2000	Precise analyses of the expression of COX-2 may disclose fine modulation of cellular and organ functions by PGs.	Phosphatidylglycerols	108-111	cytochrome c oxidase II, mitochondrial	Mus musculus	38-43	
10773011-4	2000	Brief exposure to NMDA (5 min; 100 microM) elicited a time-dependent accumulation of PGs in the culture medium that preceded neuronal cell death and correlated with the induction of COX-2 mRNA.	Phosphatidylglycerols	85-88	cytochrome c oxidase II, mitochondrial	Mus musculus	182-187	
29676940-8	2018	Intriguingly, the highly expressed knockin COX-2 enzyme barely makes any PGs or thromboxane in neonatal P8 or adult mice, demonstrating that prostanoid biosynthesis requires native COX-1 and cannot be rescued by the knockin COX-2.	Phosphatidylglycerols	73-76	cytochrome c oxidase II, mitochondrial	Mus musculus	43-48