PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
11585122-4	2001	Furthermore, fluprostenol, a specific FP receptor agonist, increased MMP-1 production and induced a synergistic enhancement of IL-1beta-induced MMP-1 production in HGF, similar to PGF2alpha.	fluprostenol	13-25	matrix metallopeptidase 1	Homo sapiens	69-74
11996904-15	2002	Finally, we tested the effect of RGS-2 overexpression on PTH- and fluprostenol-induced interleukin (IL)-6 promoter activity in MOB cells.	fluprostenol	66-78	regulator of G-protein signaling 2	Mus musculus	33-38
11996904-16	2002	PTH induces IL-6 through PKA activation, whereas fluprostenol induces IL-6 through PKC activation.	fluprostenol	49-61	interleukin 6	Mus musculus	70-74
11996904-17	2002	We found that RGS-2 overexpression significantly inhibited IL-6 promoter activity following fluprostenol treatment, but not following PTH treatment.	fluprostenol	92-104	regulator of G-protein signaling 2	Mus musculus	14-19
11996904-17	2002	We found that RGS-2 overexpression significantly inhibited IL-6 promoter activity following fluprostenol treatment, but not following PTH treatment.	fluprostenol	92-104	interleukin 6	Mus musculus	59-63
11832489-6	2002	In PGF(2alpha) or (+)-fluprostenol-treated cells, a dose-dependent increase in the expression of NOX1, a homolog of the catalytic subunit of the phagocyte NADPH oxidase gp91(phox), was demonstrated by Northern blot analysis.	fluprostenol	18-34	NADPH oxidase 1	Rattus norvegicus	97-101
11585122-4	2001	Furthermore, fluprostenol, a specific FP receptor agonist, increased MMP-1 production and induced a synergistic enhancement of IL-1beta-induced MMP-1 production in HGF, similar to PGF2alpha.	fluprostenol	13-25	interleukin 1 beta	Homo sapiens	127-135
11585122-4	2001	Furthermore, fluprostenol, a specific FP receptor agonist, increased MMP-1 production and induced a synergistic enhancement of IL-1beta-induced MMP-1 production in HGF, similar to PGF2alpha.	fluprostenol	13-25	matrix metallopeptidase 1	Homo sapiens	144-149
11585122-4	2001	Furthermore, fluprostenol, a specific FP receptor agonist, increased MMP-1 production and induced a synergistic enhancement of IL-1beta-induced MMP-1 production in HGF, similar to PGF2alpha.	fluprostenol	13-25	hepatocyte growth factor	Homo sapiens	164-167
11327082-7	2001	Fluprostenol, a selective FP receptor agonist, could mimic PGF2alpha-induced IL-6 production.	fluprostenol	0-12	interleukin 6	Homo sapiens	77-81
10567951-6	1999	Fluprostenol, a selective FP receptor agonist, could mimic PGF2 alpha-induced effect on ICAM-1 expression.	fluprostenol	0-12	intercellular adhesion molecule 1	Homo sapiens	88-94
8964835-3	1996	PGF2 alpha and fluprostenol activated PLC (determined by measuring the formation of inositol phosphates) and increased [Ca2+]i in a concentration-dependent manner.	fluprostenol	15-27	heparan sulfate proteoglycan 2	Homo sapiens	38-41
9870750-6	1998	The effects of PGE2 were unaffected by the EP1 antagonist, SC-51322, but reduced to 80% of control by the EP1/FP/TP antagonist, ONO-NT-012, which reduced the effects of fluprostenol to 32% of control.	fluprostenol	169-181	prostaglandin E receptor 1	Rattus norvegicus	106-115
9112374-10	1997	Fluprostenol, a specific agonist of PGF2alpha receptor, mimicked the actions of PGF2alpha consistent with a PGF2alpha receptor pathway.	fluprostenol	0-12	prostaglandin F receptor	Mus musculus	36-54
9112374-10	1997	Fluprostenol, a specific agonist of PGF2alpha receptor, mimicked the actions of PGF2alpha consistent with a PGF2alpha receptor pathway.	fluprostenol	0-12	prostaglandin F receptor	Mus musculus	108-126
8908208-7	1996	Fluprostenol (1 microM), a PGF2 alpha receptor agonist > 17-phenyl-trinor-PGE2 (1 microM), an EP1 receptor agonist stimulated [3H]thymidine incorporation, but an EP3 receptor agonist, ONO-AP-324 nor an EP4 (EP2) receptor agonist, 11-deoxy-PGE1 (1 microM) did not.	fluprostenol	0-12	prostaglandin F receptor	Mus musculus	27-46
8908208-7	1996	Fluprostenol (1 microM), a PGF2 alpha receptor agonist > 17-phenyl-trinor-PGE2 (1 microM), an EP1 receptor agonist stimulated [3H]thymidine incorporation, but an EP3 receptor agonist, ONO-AP-324 nor an EP4 (EP2) receptor agonist, 11-deoxy-PGE1 (1 microM) did not.	fluprostenol	0-12	prostaglandin E receptor 1 (subtype EP1)	Mus musculus	97-100
8908208-7	1996	Fluprostenol (1 microM), a PGF2 alpha receptor agonist > 17-phenyl-trinor-PGE2 (1 microM), an EP1 receptor agonist stimulated [3H]thymidine incorporation, but an EP3 receptor agonist, ONO-AP-324 nor an EP4 (EP2) receptor agonist, 11-deoxy-PGE1 (1 microM) did not.	fluprostenol	0-12	prostaglandin E receptor 3 (subtype EP3)	Mus musculus	165-168
8908208-7	1996	Fluprostenol (1 microM), a PGF2 alpha receptor agonist > 17-phenyl-trinor-PGE2 (1 microM), an EP1 receptor agonist stimulated [3H]thymidine incorporation, but an EP3 receptor agonist, ONO-AP-324 nor an EP4 (EP2) receptor agonist, 11-deoxy-PGE1 (1 microM) did not.	fluprostenol	0-12	prostaglandin E receptor 4 (subtype EP4)	Mus musculus	205-208
8908208-7	1996	Fluprostenol (1 microM), a PGF2 alpha receptor agonist > 17-phenyl-trinor-PGE2 (1 microM), an EP1 receptor agonist stimulated [3H]thymidine incorporation, but an EP3 receptor agonist, ONO-AP-324 nor an EP4 (EP2) receptor agonist, 11-deoxy-PGE1 (1 microM) did not.	fluprostenol	0-12	prostaglandin E receptor 2 (subtype EP2)	Mus musculus	210-223
8964835-2	1996	We measured the effects of PGF2 alpha and fluprostenol, a selective PGF2 alpha receptor (FP receptor) agonist, on phospholipase C(PLC) activation, on changes in the intracellular free calcium concentration ([Ca2+]i), and on protein tyrosine phosphorylation.	fluprostenol	42-54	heparan sulfate proteoglycan 2	Homo sapiens	130-133
8964835-4	1996	The apparent affinity of the FP receptor for fluprostenol was higher than that for PGF2 alpha when measuring PLC activation, but the receptor displayed similar affinities for both agonists when measuring increases in [Ca2+]i.	fluprostenol	45-57	heparan sulfate proteoglycan 2	Homo sapiens	109-112
8964835-9	1996	These data suggest that fluprostenol and oxytocin activate PLC-beta rather than PLC-gamma isoforms.	fluprostenol	24-36	heparan sulfate proteoglycan 2	Homo sapiens	59-62
8964835-9	1996	These data suggest that fluprostenol and oxytocin activate PLC-beta rather than PLC-gamma isoforms.	fluprostenol	24-36	heparan sulfate proteoglycan 2	Homo sapiens	80-83
8838244-3	1995	Expression of FPR mRNA was increased in Pyla, MN-7 and marrow cells with prolonged culture or dexamethasone treatment and decreased after treatment with fluprostenol, a selective FPR agonist.	fluprostenol	153-165	formyl peptide receptor 1	Mus musculus	14-17
8838244-3	1995	Expression of FPR mRNA was increased in Pyla, MN-7 and marrow cells with prolonged culture or dexamethasone treatment and decreased after treatment with fluprostenol, a selective FPR agonist.	fluprostenol	153-165	formyl peptide receptor 1	Mus musculus	179-182
32036038-7	2020	In contrast, treatment with fluprostenol, an FP receptor agonist, decreased the LPS + IFN-gamma-induced expression of M1 markers.	fluprostenol	28-40	interferon gamma	Mus musculus	86-95
7872059-4	1994	The prostaglandin F receptor (FP) selective agonist, fluprostenol, was the most potent agonist tested, significantly inhibiting incorporation of [3H]proline into both collagen and noncollagen protein at 10(-11) M, with more than 90% inhibition of collagen synthesis at 10(-8) M. The PGE2 analog, sulprostone, and PGD2 showed activity similar to that of PGE2.	fluprostenol	53-65	prostaglandin F receptor	Rattus norvegicus	4-28
8185669-9	1994	Pretreatment with a maximally effective concentration of PGF2 alpha, PGD2, or PGE2 rendered the cells refractory to the FP-receptor selective agonist fluprostenol, which further supports the hypothesis that Ca2+ transient signals in response to prostanoids in Swiss 3T3 cells are mediated by the FP-receptor.	fluprostenol	150-162	prostaglandin D2 synthase (brain)	Mus musculus	69-73
33486071-7	2021	Fluprostenol, a PGF2alpha receptor (FP) agonist (500 nM), suppressed 6-OHDA-induced cell death by decreasing the production of reactive oxygen species (ROS) and increasing the expression of the anti-oxidant genes.	fluprostenol	0-12	prostaglandin F receptor	Homo sapiens	16-34
33486071-10	2021	Furthermore, fluprostenol itself enhanced ERK phosphorylation and further elevated the 6-OHDA-induced phosphorylation of ERK.	fluprostenol	13-25	mitogen-activated protein kinase 1	Homo sapiens	42-45
33486071-10	2021	Furthermore, fluprostenol itself enhanced ERK phosphorylation and further elevated the 6-OHDA-induced phosphorylation of ERK.	fluprostenol	13-25	mitogen-activated protein kinase 1	Homo sapiens	121-124
29276208-7	2018	OVGP1 expression was significantly promoted by 10-6 M butaprost (a PTGER2 agonist) and decreased by 10-6 M fluprostenol (a PTGFR agonist).	fluprostenol	107-119	oviduct-specific glycoprotein	Bos taurus	0-5
29276208-7	2018	OVGP1 expression was significantly promoted by 10-6 M butaprost (a PTGER2 agonist) and decreased by 10-6 M fluprostenol (a PTGFR agonist).	fluprostenol	107-119	prostaglandin F receptor	Bos taurus	123-128
30340853-5	2018	Results of the present study indicated that the treatment with the PTGFR agonist, fluprostenol, resulted in an increase in abundance of proteins for PTGS-2, vascular endothelial growth factor (VEGF), connective tissue growth factor (CTGF), transforming growth factor beta 1 (TGF-beta1), and interleukin-8 (IL-8).	fluprostenol	82-94	prostaglandin F receptor	Bos taurus	67-72
30340853-5	2018	Results of the present study indicated that the treatment with the PTGFR agonist, fluprostenol, resulted in an increase in abundance of proteins for PTGS-2, vascular endothelial growth factor (VEGF), connective tissue growth factor (CTGF), transforming growth factor beta 1 (TGF-beta1), and interleukin-8 (IL-8).	fluprostenol	82-94	prostaglandin-endoperoxide synthase 2	Bos taurus	149-155
30340853-5	2018	Results of the present study indicated that the treatment with the PTGFR agonist, fluprostenol, resulted in an increase in abundance of proteins for PTGS-2, vascular endothelial growth factor (VEGF), connective tissue growth factor (CTGF), transforming growth factor beta 1 (TGF-beta1), and interleukin-8 (IL-8).	fluprostenol	82-94	vascular endothelial growth factor A	Bos taurus	157-191
30340853-5	2018	Results of the present study indicated that the treatment with the PTGFR agonist, fluprostenol, resulted in an increase in abundance of proteins for PTGS-2, vascular endothelial growth factor (VEGF), connective tissue growth factor (CTGF), transforming growth factor beta 1 (TGF-beta1), and interleukin-8 (IL-8).	fluprostenol	82-94	vascular endothelial growth factor A	Bos taurus	193-197
30340853-5	2018	Results of the present study indicated that the treatment with the PTGFR agonist, fluprostenol, resulted in an increase in abundance of proteins for PTGS-2, vascular endothelial growth factor (VEGF), connective tissue growth factor (CTGF), transforming growth factor beta 1 (TGF-beta1), and interleukin-8 (IL-8).	fluprostenol	82-94	cellular communication network factor 2	Bos taurus	200-231
30340853-5	2018	Results of the present study indicated that the treatment with the PTGFR agonist, fluprostenol, resulted in an increase in abundance of proteins for PTGS-2, vascular endothelial growth factor (VEGF), connective tissue growth factor (CTGF), transforming growth factor beta 1 (TGF-beta1), and interleukin-8 (IL-8).	fluprostenol	82-94	cellular communication network factor 2	Bos taurus	233-237
30340853-5	2018	Results of the present study indicated that the treatment with the PTGFR agonist, fluprostenol, resulted in an increase in abundance of proteins for PTGS-2, vascular endothelial growth factor (VEGF), connective tissue growth factor (CTGF), transforming growth factor beta 1 (TGF-beta1), and interleukin-8 (IL-8).	fluprostenol	82-94	transforming growth factor beta 1	Bos taurus	240-273
30340853-5	2018	Results of the present study indicated that the treatment with the PTGFR agonist, fluprostenol, resulted in an increase in abundance of proteins for PTGS-2, vascular endothelial growth factor (VEGF), connective tissue growth factor (CTGF), transforming growth factor beta 1 (TGF-beta1), and interleukin-8 (IL-8).	fluprostenol	82-94	transforming growth factor beta 1	Bos taurus	275-284
30340853-5	2018	Results of the present study indicated that the treatment with the PTGFR agonist, fluprostenol, resulted in an increase in abundance of proteins for PTGS-2, vascular endothelial growth factor (VEGF), connective tissue growth factor (CTGF), transforming growth factor beta 1 (TGF-beta1), and interleukin-8 (IL-8).	fluprostenol	82-94	C-X-C motif chemokine ligand 8	Bos taurus	291-304
30340853-5	2018	Results of the present study indicated that the treatment with the PTGFR agonist, fluprostenol, resulted in an increase in abundance of proteins for PTGS-2, vascular endothelial growth factor (VEGF), connective tissue growth factor (CTGF), transforming growth factor beta 1 (TGF-beta1), and interleukin-8 (IL-8).	fluprostenol	82-94	C-X-C motif chemokine ligand 8	Bos taurus	306-310
30340853-6	2018	The increased abundances of these proteins were suppressed by the treatment with the PTGFR antagonist, AL8810.Furthermore, fluprostenol treatment also induced PKC phosphorylation.	fluprostenol	123-135	prostaglandin F receptor	Bos taurus	85-90
30340853-8	2018	Additionally, treatment with the PKC inhibitor, chelerythrine, reduced the fluprostenol-induced increase in the relative abundance of VEGF, CTGF, TGF-beta1, and IL-8 mRNA in bEECs.	fluprostenol	75-87	vascular endothelial growth factor A	Bos taurus	134-138
30340853-8	2018	Additionally, treatment with the PKC inhibitor, chelerythrine, reduced the fluprostenol-induced increase in the relative abundance of VEGF, CTGF, TGF-beta1, and IL-8 mRNA in bEECs.	fluprostenol	75-87	cellular communication network factor 2	Bos taurus	140-144
30340853-8	2018	Additionally, treatment with the PKC inhibitor, chelerythrine, reduced the fluprostenol-induced increase in the relative abundance of VEGF, CTGF, TGF-beta1, and IL-8 mRNA in bEECs.	fluprostenol	75-87	transforming growth factor beta 1	Bos taurus	146-155
30340853-8	2018	Additionally, treatment with the PKC inhibitor, chelerythrine, reduced the fluprostenol-induced increase in the relative abundance of VEGF, CTGF, TGF-beta1, and IL-8 mRNA in bEECs.	fluprostenol	75-87	C-X-C motif chemokine ligand 8	Bos taurus	161-165
28298246-6	2017	However, caspase-3 protein expression was reduced following treatment of explants with fluprostenol (10-9-10-5 M, P<0.05).	fluprostenol	87-99	caspase 3	Bos taurus	9-18
24576038-0	2014	The prostaglandin f2alpha analog fluprostenol attenuates the fibrotic effects of connective tissue growth factor on human trabecular meshwork cells.	fluprostenol	33-45	cellular communication network factor 2	Homo sapiens	81-112
24576038-3	2014	Here we studied whether treatment with the prostaglandin F2alpha analog fluprostenol modulates the CTGF-mediated increase of the TM extracellular matrix.	fluprostenol	72-84	cellular communication network factor 2	Homo sapiens	99-103
24576038-8	2014	Treatment with fluprostenol or combined fluprostenol/CTGF induced the activity of matrix metalloproteinase 2 (MMP2) in TM cells, whereas treatment with CTGF alone had no effects on MMP2 activity.	fluprostenol	40-52	matrix metallopeptidase 2	Homo sapiens	110-114
24576038-7	2014	The effects of CTGF were blocked by 1-h pretreatment with fluprostenol in a dose-dependent manner.	fluprostenol	58-70	cellular communication network factor 2	Homo sapiens	15-19
24576038-8	2014	Treatment with fluprostenol or combined fluprostenol/CTGF induced the activity of matrix metalloproteinase 2 (MMP2) in TM cells, whereas treatment with CTGF alone had no effects on MMP2 activity.	fluprostenol	15-27	matrix metallopeptidase 2	Homo sapiens	82-108
24576038-9	2014	CONCLUSIONS: Fluprostenol blocks the fibrotic effects of CTGF on human TM cells and increases the activity of MMP2.	fluprostenol	13-25	cellular communication network factor 2	Homo sapiens	57-61
24576038-9	2014	CONCLUSIONS: Fluprostenol blocks the fibrotic effects of CTGF on human TM cells and increases the activity of MMP2.	fluprostenol	13-25	matrix metallopeptidase 2	Homo sapiens	110-114
24576038-8	2014	Treatment with fluprostenol or combined fluprostenol/CTGF induced the activity of matrix metalloproteinase 2 (MMP2) in TM cells, whereas treatment with CTGF alone had no effects on MMP2 activity.	fluprostenol	15-27	matrix metallopeptidase 2	Homo sapiens	110-114
24576038-8	2014	Treatment with fluprostenol or combined fluprostenol/CTGF induced the activity of matrix metalloproteinase 2 (MMP2) in TM cells, whereas treatment with CTGF alone had no effects on MMP2 activity.	fluprostenol	40-52	matrix metallopeptidase 2	Homo sapiens	82-108
20720498-5	2010	The concentration-response curves of PGF2alpha (endogenous agonist of prostaglandin F receptor) and fluprostenol (prostaglandin F receptor selective agonist) were determined in normal and preeclamptic veins either in the absence or presence of BAY u3405 (thromboxane A2 receptor selective antagonist).	fluprostenol	100-112	prostaglandin F receptor	Homo sapiens	114-138
21668646-3	2011	COX-2 expression was enhanced with a peak at 1 h for the mRNA level and at 3 h for the protein level after the addition of Fluprostenol, an FP receptor agonist.	fluprostenol	123-135	cytochrome c oxidase II, mitochondrial	Mus musculus	0-5
21668646-4	2011	The Fluprostenol-derived elevation of COX-2 expression was suppressed by the co-treatment with an FP receptor antagonist, AL8810, with a mitogen-activated protein kinase (MEK; ERK kinase) inhibitor, PD98059.	fluprostenol	4-16	cytochrome c oxidase II, mitochondrial	Mus musculus	38-43
21668646-4	2011	The Fluprostenol-derived elevation of COX-2 expression was suppressed by the co-treatment with an FP receptor antagonist, AL8810, with a mitogen-activated protein kinase (MEK; ERK kinase) inhibitor, PD98059.	fluprostenol	4-16	midkine	Mus musculus	137-169
21668646-4	2011	The Fluprostenol-derived elevation of COX-2 expression was suppressed by the co-treatment with an FP receptor antagonist, AL8810, with a mitogen-activated protein kinase (MEK; ERK kinase) inhibitor, PD98059.	fluprostenol	4-16	midkine	Mus musculus	171-174
21668646-4	2011	The Fluprostenol-derived elevation of COX-2 expression was suppressed by the co-treatment with an FP receptor antagonist, AL8810, with a mitogen-activated protein kinase (MEK; ERK kinase) inhibitor, PD98059.	fluprostenol	4-16	mitogen-activated protein kinase 1	Mus musculus	176-179
21668646-5	2011	ERK was phosphorylated within 10 min after the addition of Fluprostenol, and its phosphorylation was inhibited by the co-treatment with AL8810 or PD98059.	fluprostenol	59-71	mitogen-activated protein kinase 1	Mus musculus	0-3
20124327-6	2010	Compared to age-matched controls, fluprostenol induced phosphorylation of ERK(1/2) (310%, 286%, and 554%), p38-MAPK (unchanged, 48%, and 148%), and JNK (78%, 88%, and 95%) in 6-, 30- and 36-mo aortas, respectively.	fluprostenol	34-46	mitogen activated protein kinase 3	Rattus norvegicus	74-81
20124327-6	2010	Compared to age-matched controls, fluprostenol induced phosphorylation of ERK(1/2) (310%, 286%, and 554%), p38-MAPK (unchanged, 48%, and 148%), and JNK (78%, 88%, and 95%) in 6-, 30- and 36-mo aortas, respectively.	fluprostenol	34-46	mitogen activated protein kinase 14	Rattus norvegicus	107-115
20124327-6	2010	Compared to age-matched controls, fluprostenol induced phosphorylation of ERK(1/2) (310%, 286%, and 554%), p38-MAPK (unchanged, 48%, and 148%), and JNK (78%, 88%, and 95%) in 6-, 30- and 36-mo aortas, respectively.	fluprostenol	34-46	mitogen-activated protein kinase 8	Rattus norvegicus	148-151
17760827-7	2007	RESULTS: Prostaglandin E2-, prostaglandin F2alpha- and fluprostenol-induced egr1 mRNA levels peaked at 0.5 h and returned to baseline by 4 h. Prostaglandin F2alpha and fluprostenol more potently induced egr1 compared with prostaglandin E2.	fluprostenol	55-67	early growth response 1	Homo sapiens	76-80
18703533-4	2008	FPR stimulation with fluprostenol increased contractility by approximately 100% above basal and increased phosphorylation of both MLC-2 (by approximately 30%) and MYPT-2 (by approximately 50%).	fluprostenol	21-33	myosin light chain 2	Rattus norvegicus	130-135
18160324-3	2008	Fluprostenol-induced hypertrophy was associated with increased ROS, mTOR translocation from the nucleus to the cytoplasm, along with Akt, mTOR, GSK-3beta, PTEN and ERK1/2 but not JNK phosphorylation.	fluprostenol	0-12	mechanistic target of rapamycin kinase	Homo sapiens	68-72
18160324-3	2008	Fluprostenol-induced hypertrophy was associated with increased ROS, mTOR translocation from the nucleus to the cytoplasm, along with Akt, mTOR, GSK-3beta, PTEN and ERK1/2 but not JNK phosphorylation.	fluprostenol	0-12	AKT serine/threonine kinase 1	Homo sapiens	133-136
18160324-3	2008	Fluprostenol-induced hypertrophy was associated with increased ROS, mTOR translocation from the nucleus to the cytoplasm, along with Akt, mTOR, GSK-3beta, PTEN and ERK1/2 but not JNK phosphorylation.	fluprostenol	0-12	mechanistic target of rapamycin kinase	Homo sapiens	138-142
18160324-3	2008	Fluprostenol-induced hypertrophy was associated with increased ROS, mTOR translocation from the nucleus to the cytoplasm, along with Akt, mTOR, GSK-3beta, PTEN and ERK1/2 but not JNK phosphorylation.	fluprostenol	0-12	glycogen synthase kinase 3 beta	Homo sapiens	144-153
18160324-3	2008	Fluprostenol-induced hypertrophy was associated with increased ROS, mTOR translocation from the nucleus to the cytoplasm, along with Akt, mTOR, GSK-3beta, PTEN and ERK1/2 but not JNK phosphorylation.	fluprostenol	0-12	phosphatase and tensin homolog	Homo sapiens	155-159
18160324-3	2008	Fluprostenol-induced hypertrophy was associated with increased ROS, mTOR translocation from the nucleus to the cytoplasm, along with Akt, mTOR, GSK-3beta, PTEN and ERK1/2 but not JNK phosphorylation.	fluprostenol	0-12	mitogen-activated protein kinase 3	Homo sapiens	164-170
18160324-3	2008	Fluprostenol-induced hypertrophy was associated with increased ROS, mTOR translocation from the nucleus to the cytoplasm, along with Akt, mTOR, GSK-3beta, PTEN and ERK1/2 but not JNK phosphorylation.	fluprostenol	0-12	mitogen-activated protein kinase 8	Homo sapiens	179-182
18160324-4	2008	Whereas inhibition of phosphatidylinositol 3-kinase (PI3K) by LY-294002 blocked fluprostenol-induced changes in total protein content, pre-treatment with rapamycin or with the MEK1/2 inhibitor U0126 did not.	fluprostenol	80-92	mitogen-activated protein kinase kinase 1	Homo sapiens	176-182
18160324-5	2008	Taken together, these findings suggest that fluprostenol-induced changes in A7r5 hypertrophy involve mTOR translocation and occur through PI3K-dependent mechanisms.	fluprostenol	44-56	mechanistic target of rapamycin kinase	Homo sapiens	101-105
17760827-9	2007	Protein kinase C inhibition significantly inhibited prostaglandin E2-, prostaglandin F2alpha- and fluprostenol-induced egr1 mRNA levels.	fluprostenol	98-110	early growth response 1	Homo sapiens	119-123
17760827-10	2007	Finally, prostanoids maximally induced Egr1 protein at 1 h. CONCLUSION: egr1 is a primary response gene induced by prostaglandin E2, prostaglandin F2alpha and fluprostenol in OCCM cells through protein kinase C signaling, suggesting that Egr1 may be a key mediator of anabolic responses in cementoblasts.	fluprostenol	159-171	early growth response 1	Homo sapiens	39-43
17760827-10	2007	Finally, prostanoids maximally induced Egr1 protein at 1 h. CONCLUSION: egr1 is a primary response gene induced by prostaglandin E2, prostaglandin F2alpha and fluprostenol in OCCM cells through protein kinase C signaling, suggesting that Egr1 may be a key mediator of anabolic responses in cementoblasts.	fluprostenol	159-171	early growth response 1	Homo sapiens	72-76
17760827-7	2007	RESULTS: Prostaglandin E2-, prostaglandin F2alpha- and fluprostenol-induced egr1 mRNA levels peaked at 0.5 h and returned to baseline by 4 h. Prostaglandin F2alpha and fluprostenol more potently induced egr1 compared with prostaglandin E2.	fluprostenol	55-67	early growth response 1	Homo sapiens	203-207
17760827-10	2007	Finally, prostanoids maximally induced Egr1 protein at 1 h. CONCLUSION: egr1 is a primary response gene induced by prostaglandin E2, prostaglandin F2alpha and fluprostenol in OCCM cells through protein kinase C signaling, suggesting that Egr1 may be a key mediator of anabolic responses in cementoblasts.	fluprostenol	159-171	early growth response 1	Homo sapiens	238-242
17760827-7	2007	RESULTS: Prostaglandin E2-, prostaglandin F2alpha- and fluprostenol-induced egr1 mRNA levels peaked at 0.5 h and returned to baseline by 4 h. Prostaglandin F2alpha and fluprostenol more potently induced egr1 compared with prostaglandin E2.	fluprostenol	168-180	early growth response 1	Homo sapiens	76-80
16755666-10	2006	Fluprostenol, an FP receptor agonist, increased the accumulation of OPG in MG-63 but not in primary human osteoblasts or Saos-2.	fluprostenol	0-12	TNF receptor superfamily member 11b	Homo sapiens	68-71
17567965-5	2007	Sulprostone, misoprostol, and fluprostenol strongly enhanced DNA synthesis and inhibited glucagon-stimulated cAMP accumulation, indicating that they all activated EP3 receptors.	fluprostenol	30-42	prostaglandin E receptor 3	Rattus norvegicus	163-166
17567965-9	2007	Combining fluprostenol with misoprostol, but not with sulprostone, resulted in partially additive effects on DNA synthesis, suggesting that both EP3 and FP receptors are involved.	fluprostenol	10-22	prostaglandin E receptor 3	Rattus norvegicus	145-148
16881805-11	2006	Among the fluprostenol-induced genes was mitogen-activated protein (MAP) kinase phosphatase 1 (MKP1), a negative regulator of MAP kinase signaling.	fluprostenol	10-22	dual specificity phosphatase 1	Mus musculus	41-93
16881805-11	2006	Among the fluprostenol-induced genes was mitogen-activated protein (MAP) kinase phosphatase 1 (MKP1), a negative regulator of MAP kinase signaling.	fluprostenol	10-22	dual specificity phosphatase 1	Mus musculus	95-99
16881805-13	2006	The 0.001 to 1 microM fluprostenol and 0.01 to 1 microM PGF2 significantly induced MKP1 mRNA levels, which peaked at 1 hour of treatment and returned to baseline at 2 hours.	fluprostenol	22-34	dual specificity phosphatase 1	Mus musculus	83-87
15654655-1	2005	We have previously reported that prostaglandin F(2alpha) (PGF(2alpha)) and its selective agonist fluprostenol increase basic fibroblast growth factor (FGF-2) mRNA and protein production in osteoblastic Py1a cells.	fluprostenol	97-109	fibroblast growth factor 2	Homo sapiens	151-156
16505027-1	2006	PURPOSE: This study analyzes additional mechanisms behind the ocular hypotensive effect of prostaglandin F (PGF) receptor (FP receptor) agonists PGF2alpha and fluprostenol (fluprostenol-isopropyl ester [travoprost]), which reduce intraocular pressure (IOP) in patients with glaucoma probably by enhancing uveoscleral flow.	fluprostenol	159-171	prostaglandin F receptor	Homo sapiens	91-121
16105741-6	2005	In addition, administration of fluprostenol, a more selective agonist at the PGF(2alpha) receptor, induced cardiac hypertrophy in rats.	fluprostenol	31-43	prostaglandin F receptor	Rattus norvegicus	77-97
16168411-12	2005	However, supplementing stretched, COX2-/- myoblasts with prostaglandin E2 or fluprostenol increased proliferation.	fluprostenol	77-89	cytochrome c oxidase II, mitochondrial	Mus musculus	34-38
15654655-2	2005	The present report extends our previous studies by showing that Py1a cells express FGF receptor-2 (FGFR2) and that treatment with PGF(2alpha) or fluprostenol decreases FGFR2 mRNA.	fluprostenol	145-157	fibroblast growth factor receptor 2	Homo sapiens	83-97
15654655-2	2005	The present report extends our previous studies by showing that Py1a cells express FGF receptor-2 (FGFR2) and that treatment with PGF(2alpha) or fluprostenol decreases FGFR2 mRNA.	fluprostenol	145-157	fibroblast growth factor receptor 2	Homo sapiens	99-104
15654655-2	2005	The present report extends our previous studies by showing that Py1a cells express FGF receptor-2 (FGFR2) and that treatment with PGF(2alpha) or fluprostenol decreases FGFR2 mRNA.	fluprostenol	145-157	fibroblast growth factor receptor 2	Homo sapiens	168-173
14733708-2	2003	Travoprost acid ([+]-fluprostenol) was the most FP-receptor-selective compound, exhibiting a high affinity (Ki = 35 +/- 5 nM) for the FP receptor, and minimal affinity for DP (Ki = 52,000 nM), EP1 (Ki = 9540 nM), EP3 (Ki = 3501 nM), EP4 (Ki = 41,000 nM), IP (Ki > 90,000 nM), and TP (Ki = 121,000 nM) receptors.	fluprostenol	0-15	prostaglandin E receptor 1	Homo sapiens	193-196
14733708-2	2003	Travoprost acid ([+]-fluprostenol) was the most FP-receptor-selective compound, exhibiting a high affinity (Ki = 35 +/- 5 nM) for the FP receptor, and minimal affinity for DP (Ki = 52,000 nM), EP1 (Ki = 9540 nM), EP3 (Ki = 3501 nM), EP4 (Ki = 41,000 nM), IP (Ki > 90,000 nM), and TP (Ki = 121,000 nM) receptors.	fluprostenol	0-15	prostaglandin E receptor 3	Homo sapiens	213-216
14733708-2	2003	Travoprost acid ([+]-fluprostenol) was the most FP-receptor-selective compound, exhibiting a high affinity (Ki = 35 +/- 5 nM) for the FP receptor, and minimal affinity for DP (Ki = 52,000 nM), EP1 (Ki = 9540 nM), EP3 (Ki = 3501 nM), EP4 (Ki = 41,000 nM), IP (Ki > 90,000 nM), and TP (Ki = 121,000 nM) receptors.	fluprostenol	0-15	prostaglandin E receptor 4	Homo sapiens	233-236
14733708-2	2003	Travoprost acid ([+]-fluprostenol) was the most FP-receptor-selective compound, exhibiting a high affinity (Ki = 35 +/- 5 nM) for the FP receptor, and minimal affinity for DP (Ki = 52,000 nM), EP1 (Ki = 9540 nM), EP3 (Ki = 3501 nM), EP4 (Ki = 41,000 nM), IP (Ki > 90,000 nM), and TP (Ki = 121,000 nM) receptors.	fluprostenol	17-33	prostaglandin E receptor 1	Homo sapiens	193-196
14733708-2	2003	Travoprost acid ([+]-fluprostenol) was the most FP-receptor-selective compound, exhibiting a high affinity (Ki = 35 +/- 5 nM) for the FP receptor, and minimal affinity for DP (Ki = 52,000 nM), EP1 (Ki = 9540 nM), EP3 (Ki = 3501 nM), EP4 (Ki = 41,000 nM), IP (Ki > 90,000 nM), and TP (Ki = 121,000 nM) receptors.	fluprostenol	17-33	prostaglandin E receptor 3	Homo sapiens	213-216
14733708-2	2003	Travoprost acid ([+]-fluprostenol) was the most FP-receptor-selective compound, exhibiting a high affinity (Ki = 35 +/- 5 nM) for the FP receptor, and minimal affinity for DP (Ki = 52,000 nM), EP1 (Ki = 9540 nM), EP3 (Ki = 3501 nM), EP4 (Ki = 41,000 nM), IP (Ki > 90,000 nM), and TP (Ki = 121,000 nM) receptors.	fluprostenol	17-33	prostaglandin E receptor 4	Homo sapiens	233-236
12489107-6	2002	Erk activity and colony size were increased by cotreatment of JB6 cells with epidermal growth factor (EGF) and fluprostenol to a greater extent than with either treatment alone, whereas the cotreatment effect on colony number appeared to be simply additive.	fluprostenol	111-123	mitogen-activated protein kinase 1	Homo sapiens	0-3