PMID-sentid	Pub_year	Sent_text	comp_official_name	comp_offset	protein_name	organism	prot_offset
23959544-6	2014	Phosphorylation levels of Ser(1177) and Thr(495) in eNOS were determined after exposure to amlodipine, S(-)-amlodipine, and Ro 31-8220.	Serine	26-29	nitric oxide synthase 3	Homo sapiens	52-56
23959544-6	2014	Phosphorylation levels of Ser(1177) and Thr(495) in eNOS were determined after exposure to amlodipine, S(-)-amlodipine, and Ro 31-8220.	Threonine	40-43	nitric oxide synthase 3	Homo sapiens	52-56
23959544-6	2014	Phosphorylation levels of Ser(1177) and Thr(495) in eNOS were determined after exposure to amlodipine, S(-)-amlodipine, and Ro 31-8220.	Amlodipine	91-101	nitric oxide synthase 3	Homo sapiens	52-56
23959544-6	2014	Phosphorylation levels of Ser(1177) and Thr(495) in eNOS were determined after exposure to amlodipine, S(-)-amlodipine, and Ro 31-8220.	Amlodipine	104-118	nitric oxide synthase 3	Homo sapiens	52-56
23959544-7	2014	RESULTS: FMD, NO, and eNOS levels significantly improved after treatment with amlodipine and S(-)-amlodipine.	Amlodipine	78-88	nitric oxide synthase 3	Homo sapiens	22-26
23959544-7	2014	RESULTS: FMD, NO, and eNOS levels significantly improved after treatment with amlodipine and S(-)-amlodipine.	Amlodipine	93-108	nitric oxide synthase 3	Homo sapiens	22-26
23959544-10	2014	Western blot assay showed that both amlodipine and Ro31-8220 induced Ser(1177) phosphorylation and weakened Thr(495) phosphorylation in eNOS.	Amlodipine	36-46	nitric oxide synthase 3	Homo sapiens	136-140
23959544-10	2014	Western blot assay showed that both amlodipine and Ro31-8220 induced Ser(1177) phosphorylation and weakened Thr(495) phosphorylation in eNOS.	ro31	51-55	nitric oxide synthase 3	Homo sapiens	136-140
23959544-10	2014	Western blot assay showed that both amlodipine and Ro31-8220 induced Ser(1177) phosphorylation and weakened Thr(495) phosphorylation in eNOS.	Threonine	108-111	nitric oxide synthase 3	Homo sapiens	136-140
23959544-15	2014	It affects eNOS phosphorylation at Ser(1177) and Thr(495) by the PKC pathway, further enhancing eNOS activation.	Serine	35-38	nitric oxide synthase 3	Homo sapiens	11-15
23959544-15	2014	It affects eNOS phosphorylation at Ser(1177) and Thr(495) by the PKC pathway, further enhancing eNOS activation.	Serine	35-38	nitric oxide synthase 3	Homo sapiens	96-100
23959544-15	2014	It affects eNOS phosphorylation at Ser(1177) and Thr(495) by the PKC pathway, further enhancing eNOS activation.	Threonine	49-52	nitric oxide synthase 3	Homo sapiens	96-100
24112082-0	2014	The smoking-associated oxidant hypothiocyanous acid induces endothelial nitric oxide synthase dysfunction.	hypothiocyanous acid	31-51	nitric oxide synthase 3	Homo sapiens	60-93
24112082-3	2014	We hypothesized that this thiol-specific oxidant may target the Zn(2+)-thiol cluster of eNOS (endothelial nitric oxide synthase), resulting in enzyme dysfunction and reduced formation of the critical signalling molecule NO .	Sulfhydryl Compounds	26-31	nitric oxide synthase 3	Homo sapiens	94-127
24112082-3	2014	We hypothesized that this thiol-specific oxidant may target the Zn(2+)-thiol cluster of eNOS (endothelial nitric oxide synthase), resulting in enzyme dysfunction and reduced formation of the critical signalling molecule NO .	zn(2+)-thiol	64-76	nitric oxide synthase 3	Homo sapiens	94-127
24745027-2	2014	EECs and IMCEs can exercise substantial control over the contractility of cardiomyocytes by releasing various factors such as nitric oxide (NO) via a constitutive endothelial NO-synthase (eNOS), endothelin-1, prostaglandins, angiotensin II, peptide growth factors, and neuregulin-1.	Nitric Oxide	126-138	nitric oxide synthase 3	Homo sapiens	188-192
25114926-2	2014	The purpose of this study was to investigate the expression of GABAB receptors, a subclass of receptors to the inhibitory neurotransmitter gamma-aminobutyric acid (GABA), in cultured human aortic endothelial cells (HAECs), and to explore if altering receptor activation modified [Ca2+]i and endothelial nitric oxide synthase (eNOS) translocation.	gamma-Aminobutyric Acid	63-67	nitric oxide synthase 3	Homo sapiens	291-324
24949428-0	2014	Progesterone attenuates experimental subarachnoid hemorrhage-induced vasospasm by upregulation of endothelial nitric oxide synthase via Akt signaling pathway.	Progesterone	0-12	nitric oxide synthase 3	Homo sapiens	98-131
24949428-9	2014	The SAH-induced suppression of eNOS protein and phospho-Akt were relieved by progesterone treatment.	Progesterone	77-89	nitric oxide synthase 3	Homo sapiens	31-35
24745027-2	2014	EECs and IMCEs can exercise substantial control over the contractility of cardiomyocytes by releasing various factors such as nitric oxide (NO) via a constitutive endothelial NO-synthase (eNOS), endothelin-1, prostaglandins, angiotensin II, peptide growth factors, and neuregulin-1.	Prostaglandins	209-223	nitric oxide synthase 3	Homo sapiens	188-192
24180383-7	2014	In addition, eNOS associations with cationic amino acid transporter-1 (CAT-1), argininosuccinate synthase (ASS), argininosuccinate lyase (ASL), and soluble guanylate cyclase (sGC) facilitate directed delivery of substrate (L-arginine) to eNOS and optimizing NO production and NO action on its target.	Arginine	223-233	nitric oxide synthase 3	Homo sapiens	13-17
24180387-0	2014	Tetrahydrobiopterin regulation of eNOS redox function.	sapropterin	0-19	nitric oxide synthase 3	Homo sapiens	34-38
24180387-3	2014	Evidence from humans and animals have demonstrated that decreased BH4 bioavailability, with subsequent uncoupling of eNOS, has significant effects on the pathogenesis of endothelial dysfunction, which is a hallmark of vascular injury in cardiovascular disorders, including hypertension, hyperlipidemia, and diabetes.	sapropterin	66-69	nitric oxide synthase 3	Homo sapiens	117-121
24200868-1	2014	Human endothelial nitric oxide synthase (eNOS) activity is important for maintaining blood pressure homeostasis and vascular integrity through nitric oxide (NO).The in vitro study aimed at investigating a role of p38alpha signaling in modulating NO production in human umbilical vein endothelial cell-12 (HUVEC-12).	Nitric Oxide	18-30	nitric oxide synthase 3	Homo sapiens	41-45
24180387-4	2014	In this review, we discuss the synthesis of BH4, its molecular mechanisms regulating eNOS coupling, the pathophysiologic roles of decreased BH4 bioavailability in cardiovascular diseases, and the potential therapeutic application of BH4 in clinics.	sapropterin	44-47	nitric oxide synthase 3	Homo sapiens	85-89
24959009-3	2014	Production of RMs mainly superoxides ( O2 (-)) has been found in a variety of predominating cellular enzyme systems including nicotinamide adenine dinucleotide phosphate oxidase, xanthine oxidase, cyclooxygenase, endothelial nitric oxide synthase (eNOS) and myeloperoxidase.	Superoxides	25-36	nitric oxide synthase 3	Homo sapiens	213-246
24959009-3	2014	Production of RMs mainly superoxides ( O2 (-)) has been found in a variety of predominating cellular enzyme systems including nicotinamide adenine dinucleotide phosphate oxidase, xanthine oxidase, cyclooxygenase, endothelial nitric oxide synthase (eNOS) and myeloperoxidase.	Superoxides	39-41	nitric oxide synthase 3	Homo sapiens	213-246
24804268-0	2014	Ang (1-7) protects islet endothelial cells from palmitate-induced apoptosis by AKT, eNOS, p38 MAPK, and JNK pathways.	Palmitates	48-57	nitric oxide synthase 3	Homo sapiens	84-88
24804268-7	2014	Palmitate decreased the phosphorylation of AKT and eNOS, and Ang (1-7) increased the phosphorylation of these kinases (P < 0.05), with a concomitant reduction in MS-1 cells apoptosis.	Palmitates	0-9	nitric oxide synthase 3	Homo sapiens	51-55
23875992-4	2014	Increased l-arginine uptake via hCAT-1 and NO synthesis by eNOS is associated with GDM.	Arginine	10-20	nitric oxide synthase 3	Homo sapiens	59-63
24706320-17	2014	Irritant agents in the breathing air and environment may cause increase in eNOS values at apical part of epithelium and may promote polyp formation by vasodilatation and increased glandular secretion due to increased nitric oxide values.	Nitric Oxide	217-229	nitric oxide synthase 3	Homo sapiens	75-79
24200868-2	2014	Consistent with the stimulation of lipopolysaccharide (LPS) or tumor necrosis factor (TNF)-alpha, the over-expression of p38alpha markedly down-regulated the eNOS promoter activity in HUVEC-12, which could be reversed by its negative mutant p38alpha (AF) or p38-specific inhibitor SB203580.	SB 203580	281-289	nitric oxide synthase 3	Homo sapiens	158-162
23875992-6	2014	GDM associates with NO-reduced adenosine uptake in placental endothelium, suggested to maintain and/or facilitate insulin vasodilation likely increasing hCAT-1 and eNOS expression and activity.	Adenosine	31-40	nitric oxide synthase 3	Homo sapiens	164-168
25460725-3	2014	Production of RMs mainly superoxide (O2(-)) has been found in a variety of predominating cellular enzyme systems including NAD(P)H oxidase, xanthine oxidase (XO), cyclooxygenase (COX), uncoupled endothelial nitric oxide synthase (eNOS) and myeloperoxidase (MPO).	Superoxides	25-35	nitric oxide synthase 3	Homo sapiens	195-228
24573998-0	2014	Endothelial nitric oxide (eNOS) gene G894T and VNTR polymorphisms are closely associated with the risk of ischemic stroke development for Asians: meta-analysis of epidemiological studies.	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	26-30
24868319-6	2014	The underlying mechanisms involve the inhibition of H2O2-induced activation of endothelial nitric oxide synthase (eNOS), adenosine monophosphate-activated protein kinase (AMPK), and Akt, as well as the redox sensitive transcription factor, NF-kappa B (NF- kappa B).	Hydrogen Peroxide	52-56	nitric oxide synthase 3	Homo sapiens	79-112
24300283-0	2014	Interactive effects of in vitro binge-like alcohol and ATP on umbilical endothelial nitric oxide synthase post-translational modifications and redox modulation.	Alcohols	43-50	nitric oxide synthase 3	Homo sapiens	72-105
24300283-0	2014	Interactive effects of in vitro binge-like alcohol and ATP on umbilical endothelial nitric oxide synthase post-translational modifications and redox modulation.	Adenosine Triphosphate	55-58	nitric oxide synthase 3	Homo sapiens	72-105
25460725-3	2014	Production of RMs mainly superoxide (O2(-)) has been found in a variety of predominating cellular enzyme systems including NAD(P)H oxidase, xanthine oxidase (XO), cyclooxygenase (COX), uncoupled endothelial nitric oxide synthase (eNOS) and myeloperoxidase (MPO).	Superoxides	37-39	nitric oxide synthase 3	Homo sapiens	195-228
24300283-2	2014	We herein investigated chronic in vitro binge-like alcohol effects on umbilical endothelial nitric oxide synthase (eNOS) multi-site phosphorylation and related redox switches under basal (unstimulated) and stimulated (with ATP) states.	Alcohols	51-58	nitric oxide synthase 3	Homo sapiens	80-113
24971375-3	2014	In this study, a treatment with NaHS profoundly increased the expression and the activity of endothelial nitric oxide synthase.	sodium bisulfide	32-36	nitric oxide synthase 3	Homo sapiens	93-126
25189395-1	2014	Endothelial nitric oxide synthase (eNOS or NOS3), an enzyme constitutively expressed especially in endothelial cells, is largely responsible for nitric oxide (NO) bioavailability at the endothelial level.	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	35-39
25093198-1	2014	Nitric oxide (NO), produced by endothelial nitric oxide synthase (eNOS), is a major antiatherogenic factor in the blood vessel.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	31-64
25093198-1	2014	Nitric oxide (NO), produced by endothelial nitric oxide synthase (eNOS), is a major antiatherogenic factor in the blood vessel.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	66-70
26104257-9	2014	CONCLUSIONS: These results indicate the relationship between reduced nitric oxide levels and eNOS gene polymorphism leading to its altered expression in preeclamptic women.	Nitric Oxide	69-81	nitric oxide synthase 3	Homo sapiens	93-97
25189395-1	2014	Endothelial nitric oxide synthase (eNOS or NOS3), an enzyme constitutively expressed especially in endothelial cells, is largely responsible for nitric oxide (NO) bioavailability at the endothelial level.	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	43-47
25189387-1	2014	Nitric oxide (NO) production is catalyzed by three distinct enzymes, namely, neuronal nitric oxide synthase (nNOS), inducible NOS (iNOS), and endothelial NOS (eNOS).	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	142-157
24379783-2	2013	In blood vessels, it is synthesized in a dynamic fashion by endothelial nitric oxide synthase (eNOS) and influences vascular function via two distinct mechanisms, the activation of soluble guanylyl cyclase (sGC)/cyclic guanosine monophosphate (cGMP)-dependent signaling and the S-nitrosylation of proteins with reactive thiols (S-nitrosylation).	Cyclic GMP	212-242	nitric oxide synthase 3	Homo sapiens	60-93
24376548-0	2013	Platelet content of nitric oxide synthase 3 phosphorylated at Serine 1177 is associated with the functional response of platelets to aspirin.	Serine	62-68	nitric oxide synthase 3	Homo sapiens	20-43
24376548-0	2013	Platelet content of nitric oxide synthase 3 phosphorylated at Serine 1177 is associated with the functional response of platelets to aspirin.	Aspirin	133-140	nitric oxide synthase 3	Homo sapiens	20-43
24376548-4	2013	Protein expression of nitric oxide synthase 3 (NOS3) was higher in ASA-sensitive than in ASA-resistant platelets but there were no differences in the platelet expression of nitric oxide synthase 2 (NOS2) isoform.	Aspirin	67-70	nitric oxide synthase 3	Homo sapiens	22-45
24376548-4	2013	Protein expression of nitric oxide synthase 3 (NOS3) was higher in ASA-sensitive than in ASA-resistant platelets but there were no differences in the platelet expression of nitric oxide synthase 2 (NOS2) isoform.	Aspirin	67-70	nitric oxide synthase 3	Homo sapiens	47-51
24376548-4	2013	Protein expression of nitric oxide synthase 3 (NOS3) was higher in ASA-sensitive than in ASA-resistant platelets but there were no differences in the platelet expression of nitric oxide synthase 2 (NOS2) isoform.	Aspirin	89-92	nitric oxide synthase 3	Homo sapiens	22-45
24376548-4	2013	Protein expression of nitric oxide synthase 3 (NOS3) was higher in ASA-sensitive than in ASA-resistant platelets but there were no differences in the platelet expression of nitric oxide synthase 2 (NOS2) isoform.	Aspirin	89-92	nitric oxide synthase 3	Homo sapiens	47-51
24376548-5	2013	The highest NOS3 expression in ASA-sensitive platelets was independent of the presence of T-to-C mutation at nucleotide position -786 (T(-786)   C) in the NOS3-coding gene.	Aspirin	31-34	nitric oxide synthase 3	Homo sapiens	12-16
24376548-6	2013	However, platelet content of phosphorylated NOS3 at Serine (Ser)(1177), an active form of NOS3, was higher in ASA-sensitive than in ASA-resistant platelets.	Serine	52-58	nitric oxide synthase 3	Homo sapiens	44-48
24376548-6	2013	However, platelet content of phosphorylated NOS3 at Serine (Ser)(1177), an active form of NOS3, was higher in ASA-sensitive than in ASA-resistant platelets.	Serine	52-58	nitric oxide synthase 3	Homo sapiens	90-94
24376548-6	2013	However, platelet content of phosphorylated NOS3 at Serine (Ser)(1177), an active form of NOS3, was higher in ASA-sensitive than in ASA-resistant platelets.	Serine	52-55	nitric oxide synthase 3	Homo sapiens	44-48
24376548-6	2013	However, platelet content of phosphorylated NOS3 at Serine (Ser)(1177), an active form of NOS3, was higher in ASA-sensitive than in ASA-resistant platelets.	Serine	52-55	nitric oxide synthase 3	Homo sapiens	90-94
24376548-6	2013	However, platelet content of phosphorylated NOS3 at Serine (Ser)(1177), an active form of NOS3, was higher in ASA-sensitive than in ASA-resistant platelets.	Aspirin	110-113	nitric oxide synthase 3	Homo sapiens	44-48
24376548-6	2013	However, platelet content of phosphorylated NOS3 at Serine (Ser)(1177), an active form of NOS3, was higher in ASA-sensitive than in ASA-resistant platelets.	Aspirin	110-113	nitric oxide synthase 3	Homo sapiens	90-94
24376548-6	2013	However, platelet content of phosphorylated NOS3 at Serine (Ser)(1177), an active form of NOS3, was higher in ASA-sensitive than in ASA-resistant platelets.	Aspirin	132-135	nitric oxide synthase 3	Homo sapiens	44-48
24376548-6	2013	However, platelet content of phosphorylated NOS3 at Serine (Ser)(1177), an active form of NOS3, was higher in ASA-sensitive than in ASA-resistant platelets.	Aspirin	132-135	nitric oxide synthase 3	Homo sapiens	90-94
24376548-7	2013	The level of platelet NOS3 Ser(1177) phosphorylation was positively associated with the closure time in the PFA-100 test.	Serine	27-30	nitric oxide synthase 3	Homo sapiens	22-26
24376548-7	2013	The level of platelet NOS3 Ser(1177) phosphorylation was positively associated with the closure time in the PFA-100 test.	Foscarnet	108-111	nitric oxide synthase 3	Homo sapiens	22-26
24376548-11	2013	CONCLUSIONS: Functional platelet responsiveness to ASA was associated with the platelet content of phosphorylated NOS3 at Ser(1177).	Aspirin	51-54	nitric oxide synthase 3	Homo sapiens	114-118
24376548-11	2013	CONCLUSIONS: Functional platelet responsiveness to ASA was associated with the platelet content of phosphorylated NOS3 at Ser(1177).	Serine	122-125	nitric oxide synthase 3	Homo sapiens	114-118
24144633-7	2013	In these tissues and cultured murine and human primary endothelial cells, MG increased eNOS monomerization and decreased BH4/total biopterin ratio, effects that were significantly mitigated by supplementation of BH4 or its precursor sepiapterin but not by L-NAME or tetrahydroneopterin, indicative of MG-triggered eNOS uncoupling.	Pyruvaldehyde	74-76	nitric oxide synthase 3	Homo sapiens	87-91
24144633-7	2013	In these tissues and cultured murine and human primary endothelial cells, MG increased eNOS monomerization and decreased BH4/total biopterin ratio, effects that were significantly mitigated by supplementation of BH4 or its precursor sepiapterin but not by L-NAME or tetrahydroneopterin, indicative of MG-triggered eNOS uncoupling.	Pyruvaldehyde	74-76	nitric oxide synthase 3	Homo sapiens	314-318
24144633-7	2013	In these tissues and cultured murine and human primary endothelial cells, MG increased eNOS monomerization and decreased BH4/total biopterin ratio, effects that were significantly mitigated by supplementation of BH4 or its precursor sepiapterin but not by L-NAME or tetrahydroneopterin, indicative of MG-triggered eNOS uncoupling.	sapropterin	212-215	nitric oxide synthase 3	Homo sapiens	87-91
24144633-7	2013	In these tissues and cultured murine and human primary endothelial cells, MG increased eNOS monomerization and decreased BH4/total biopterin ratio, effects that were significantly mitigated by supplementation of BH4 or its precursor sepiapterin but not by L-NAME or tetrahydroneopterin, indicative of MG-triggered eNOS uncoupling.	sapropterin	212-215	nitric oxide synthase 3	Homo sapiens	314-318
24379783-2	2013	In blood vessels, it is synthesized in a dynamic fashion by endothelial nitric oxide synthase (eNOS) and influences vascular function via two distinct mechanisms, the activation of soluble guanylyl cyclase (sGC)/cyclic guanosine monophosphate (cGMP)-dependent signaling and the S-nitrosylation of proteins with reactive thiols (S-nitrosylation).	Cyclic GMP	212-242	nitric oxide synthase 3	Homo sapiens	95-99
24379783-2	2013	In blood vessels, it is synthesized in a dynamic fashion by endothelial nitric oxide synthase (eNOS) and influences vascular function via two distinct mechanisms, the activation of soluble guanylyl cyclase (sGC)/cyclic guanosine monophosphate (cGMP)-dependent signaling and the S-nitrosylation of proteins with reactive thiols (S-nitrosylation).	Cyclic GMP	244-248	nitric oxide synthase 3	Homo sapiens	95-99
24379783-2	2013	In blood vessels, it is synthesized in a dynamic fashion by endothelial nitric oxide synthase (eNOS) and influences vascular function via two distinct mechanisms, the activation of soluble guanylyl cyclase (sGC)/cyclic guanosine monophosphate (cGMP)-dependent signaling and the S-nitrosylation of proteins with reactive thiols (S-nitrosylation).	Sulfhydryl Compounds	320-326	nitric oxide synthase 3	Homo sapiens	60-93
24379783-2	2013	In blood vessels, it is synthesized in a dynamic fashion by endothelial nitric oxide synthase (eNOS) and influences vascular function via two distinct mechanisms, the activation of soluble guanylyl cyclase (sGC)/cyclic guanosine monophosphate (cGMP)-dependent signaling and the S-nitrosylation of proteins with reactive thiols (S-nitrosylation).	Sulfhydryl Compounds	320-326	nitric oxide synthase 3	Homo sapiens	95-99
24152727-6	2013	These PCN-enhanced cellular responses were associated with increased protein levels of HIF1A and NOS3, but not FGFR1, VEGFR1, and VEGFR2.	PREGNENOLONE CARBONITRILE	6-9	nitric oxide synthase 3	Homo sapiens	97-101
24096875-6	2013	The inhibition of Lys(118) acetylation promoted the generation of NOS3-promoting prosurvival form of p53.	Lysine	18-21	nitric oxide synthase 3	Homo sapiens	66-70
23804534-5	2013	HDL-mediated phosphorylation of endothelial nitric oxide synthase (eNOS)-Ser(1177) , eNOS-Thr(495) , and PKC-ssII was evaluated.	Serine	73-76	nitric oxide synthase 3	Homo sapiens	32-65
24278136-1	2013	Endothelial nitric oxide synthase 3 (NOS3) catalyzes the production of nitric oxide from L-arginine in endothelial cells.	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	37-41
24278136-1	2013	Endothelial nitric oxide synthase 3 (NOS3) catalyzes the production of nitric oxide from L-arginine in endothelial cells.	Arginine	89-99	nitric oxide synthase 3	Homo sapiens	37-41
23811616-10	2013	These positive effects of chronic exercise seem to be closely related to the bioavailability of nitric oxide, including increased activity of endothelial nitric oxide synthase and antioxidant enzymes, and activation of matrix metalloproteinase 9.	Nitric Oxide	96-108	nitric oxide synthase 3	Homo sapiens	142-175
22555214-7	2013	Isosorbide-5-mononitrate up-regulated the expression of NADPH subunits and caused uncoupling of the endothelial nitric oxide synthase (eNOS) likely due to a down-regulation of the tetrahydrobiopterin-synthesizing enzyme GTP-cyclohydrolase-1 and to S-glutathionylation of eNOS.	isosorbide-5-mononitrate	0-24	nitric oxide synthase 3	Homo sapiens	100-133
23750556-0	2013	Up-regulation of endothelial nitric oxide synthase (eNOS), silent mating type information regulation 2 homologue 1 (SIRT1) and autophagy-related genes by repeated treatments with resveratrol in human umbilical vein endothelial cells.	Resveratrol	179-190	nitric oxide synthase 3	Homo sapiens	17-50
23750556-0	2013	Up-regulation of endothelial nitric oxide synthase (eNOS), silent mating type information regulation 2 homologue 1 (SIRT1) and autophagy-related genes by repeated treatments with resveratrol in human umbilical vein endothelial cells.	Resveratrol	179-190	nitric oxide synthase 3	Homo sapiens	52-56
23750556-1	2013	Resveratrol, a polyphenolic phytoalexin found in red wine and various plants, has been reported to up-regulate the expression of endothelial NO synthase (eNOS) in human umbilical vein endothelial cells (HUVEC).	Resveratrol	0-11	nitric oxide synthase 3	Homo sapiens	129-152
23750556-1	2013	Resveratrol, a polyphenolic phytoalexin found in red wine and various plants, has been reported to up-regulate the expression of endothelial NO synthase (eNOS) in human umbilical vein endothelial cells (HUVEC).	Resveratrol	0-11	nitric oxide synthase 3	Homo sapiens	154-158
23750556-1	2013	Resveratrol, a polyphenolic phytoalexin found in red wine and various plants, has been reported to up-regulate the expression of endothelial NO synthase (eNOS) in human umbilical vein endothelial cells (HUVEC).	polyphenolic phytoalexin	15-39	nitric oxide synthase 3	Homo sapiens	129-152
23750556-1	2013	Resveratrol, a polyphenolic phytoalexin found in red wine and various plants, has been reported to up-regulate the expression of endothelial NO synthase (eNOS) in human umbilical vein endothelial cells (HUVEC).	polyphenolic phytoalexin	15-39	nitric oxide synthase 3	Homo sapiens	154-158
23750556-4	2013	The expression levels of eNOS and silent mating type information regulation 2 homologue 1 (SIRT1) were up-regulated in HUVEC by repeated treatments with 1 muM-resveratrol for 6 d, but not with fenofibrate.	Resveratrol	159-170	nitric oxide synthase 3	Homo sapiens	25-29
23921313-2	2013	At the beginning of reperfusion, a transient release of NO is promptly scavenged by ROS to form the highly toxic peroxynitrite, which is responsible for a further increase of ROS through endothelial nitric oxide synthase uncoupling.	Reactive Oxygen Species	84-87	nitric oxide synthase 3	Homo sapiens	187-220
23921313-2	2013	At the beginning of reperfusion, a transient release of NO is promptly scavenged by ROS to form the highly toxic peroxynitrite, which is responsible for a further increase of ROS through endothelial nitric oxide synthase uncoupling.	Peroxynitrous Acid	113-126	nitric oxide synthase 3	Homo sapiens	187-220
23921313-2	2013	At the beginning of reperfusion, a transient release of NO is promptly scavenged by ROS to form the highly toxic peroxynitrite, which is responsible for a further increase of ROS through endothelial nitric oxide synthase uncoupling.	Reactive Oxygen Species	175-178	nitric oxide synthase 3	Homo sapiens	187-220
24055736-0	2013	Polymorphisms in the endothelial nitric oxide synthase gene in thalidomide embryopathy.	Thalidomide	63-74	nitric oxide synthase 3	Homo sapiens	21-54
24041741-7	2013	Combining the statin pretreatment with the eNOS inhibitor L-NNA as well as bypassing the HMG-CoA reductase (EC number: 1.1.1.34) by adding mevalonic acid or geranyl pyrophosphate restored the exocytotic effect of PMA.	Nitroarginine	58-63	nitric oxide synthase 3	Homo sapiens	43-47
23745825-1	2013	Complex regulatory processes alter the activity of endothelial nitric oxide synthase (eNOS) leading to nitric oxide (NO) production by endothelial cells under various physiological states.	Nitric Oxide	63-75	nitric oxide synthase 3	Homo sapiens	86-90
24096875-0	2013	p53"s choice of myocardial death or survival: Oxygen protects infarct myocardium by recruiting p53 on NOS3 promoter through regulation of p53-Lys(118) acetylation.	Oxygen	46-52	nitric oxide synthase 3	Homo sapiens	102-106
24096875-0	2013	p53"s choice of myocardial death or survival: Oxygen protects infarct myocardium by recruiting p53 on NOS3 promoter through regulation of p53-Lys(118) acetylation.	Lysine	142-145	nitric oxide synthase 3	Homo sapiens	102-106
24096875-4	2013	p53 exhibited a differential DNA-binding, namely, BAX-p53RE in the infarct heart or NOS3-p53RE in the oxygenated heart, which was regulated by oxygen-induced, post-translational modification of p53.	Oxygen	102-108	nitric oxide synthase 3	Homo sapiens	84-88
23738793-0	2013	Protocatechuic acid induces angiogenesis through PI3K-Akt-eNOS-VEGF signalling pathway.	protocatechuic acid	0-19	nitric oxide synthase 3	Homo sapiens	58-62
23954998-0	2013	Analysing calcium dependent and independent regulation of eNOS in endothelium triggered by extracellular signalling events.	Calcium	10-17	nitric oxide synthase 3	Homo sapiens	58-62
23954998-1	2013	The vascular endothelium, the intima of blood vessels, coordinately interacts with several biochemical factors expressing endothelial nitric oxide synthase (eNOS) to produce nitric oxide (NO), a potent endogenous vasodilator.	Nitric Oxide	134-146	nitric oxide synthase 3	Homo sapiens	157-161
23954998-3	2013	In response to signal transduction upstream by VEGF-A and shear stress, different signalling pathways mediated by kinases and intracellular calcium potentiates eNOS activation leading to nitric oxide release.	Calcium	140-147	nitric oxide synthase 3	Homo sapiens	160-164
23954998-3	2013	In response to signal transduction upstream by VEGF-A and shear stress, different signalling pathways mediated by kinases and intracellular calcium potentiates eNOS activation leading to nitric oxide release.	Nitric Oxide	187-199	nitric oxide synthase 3	Homo sapiens	160-164
23954998-5	2013	A transient response to eNOS activation was observed under VEGF-A and shear stress stimulus when mediated by calcium dependent cascades, whereas a sustained response was produced by calcium independent vascular signalling kinases.	Calcium	109-116	nitric oxide synthase 3	Homo sapiens	24-28
23940049-0	2013	Nox4 NADPH oxidase mediates peroxynitrite-dependent uncoupling of endothelial nitric-oxide synthase and fibronectin expression in response to angiotensin II: role of mitochondrial reactive oxygen species.	Peroxynitrous Acid	28-41	nitric oxide synthase 3	Homo sapiens	66-99
23940049-2	2013	Here, we demonstrate that, in MCs, Ang II induces endothelial nitric-oxide synthase (eNOS) uncoupling with enhanced generation of reactive oxygen species (ROS) and decreased production of NO.	Reactive Oxygen Species	130-153	nitric oxide synthase 3	Homo sapiens	50-83
23291092-0	2013	Propranolol given orally for proliferating infantile haemangiomas: analysis of efficacy and serological changes in vascular endothelial growth factor and endothelial nitric oxide synthase in 35 patients.	Propranolol	0-11	nitric oxide synthase 3	Homo sapiens	154-187
23965989-0	2013	A pivotal role for tryptophan 447 in enzymatic coupling of human endothelial nitric oxide synthase (eNOS): effects on tetrahydrobiopterin-dependent catalysis and eNOS dimerization.	Tryptophan	19-29	nitric oxide synthase 3	Homo sapiens	65-98
23965989-0	2013	A pivotal role for tryptophan 447 in enzymatic coupling of human endothelial nitric oxide synthase (eNOS): effects on tetrahydrobiopterin-dependent catalysis and eNOS dimerization.	Tryptophan	19-29	nitric oxide synthase 3	Homo sapiens	100-104
23965989-0	2013	A pivotal role for tryptophan 447 in enzymatic coupling of human endothelial nitric oxide synthase (eNOS): effects on tetrahydrobiopterin-dependent catalysis and eNOS dimerization.	sapropterin	118-137	nitric oxide synthase 3	Homo sapiens	65-98
23965989-0	2013	A pivotal role for tryptophan 447 in enzymatic coupling of human endothelial nitric oxide synthase (eNOS): effects on tetrahydrobiopterin-dependent catalysis and eNOS dimerization.	sapropterin	118-137	nitric oxide synthase 3	Homo sapiens	100-104
23965989-2	2013	Bioavailability of BH4 is a critical factor in regulating the balance between NO and superoxide production by endothelial NOS (eNOS coupling).	sapropterin	19-22	nitric oxide synthase 3	Homo sapiens	127-131
23965989-2	2013	Bioavailability of BH4 is a critical factor in regulating the balance between NO and superoxide production by endothelial NOS (eNOS coupling).	Superoxides	85-95	nitric oxide synthase 3	Homo sapiens	127-131
23965989-5	2013	We overexpressed human eNOS W447A and W447F mutants in novel cell lines with tetracycline-regulated expression of human GTP cyclohydrolase I, the rate-limiting enzyme in BH4 synthesis, to determine the importance of BH4 and Trp-447 in eNOS uncoupling.	Tetracycline	77-89	nitric oxide synthase 3	Homo sapiens	23-27
23965989-5	2013	We overexpressed human eNOS W447A and W447F mutants in novel cell lines with tetracycline-regulated expression of human GTP cyclohydrolase I, the rate-limiting enzyme in BH4 synthesis, to determine the importance of BH4 and Trp-447 in eNOS uncoupling.	Tetracycline	77-89	nitric oxide synthase 3	Homo sapiens	235-239
23965989-5	2013	We overexpressed human eNOS W447A and W447F mutants in novel cell lines with tetracycline-regulated expression of human GTP cyclohydrolase I, the rate-limiting enzyme in BH4 synthesis, to determine the importance of BH4 and Trp-447 in eNOS uncoupling.	sapropterin	170-173	nitric oxide synthase 3	Homo sapiens	23-27
23965989-7	2013	eNOS-derived superoxide production was significantly elevated in W447A and W447F versus wild-type eNOS, and this was sufficient to oxidize BH4 to 7,8-dihydrobiopterin.	Superoxides	13-23	nitric oxide synthase 3	Homo sapiens	0-4
23965989-7	2013	eNOS-derived superoxide production was significantly elevated in W447A and W447F versus wild-type eNOS, and this was sufficient to oxidize BH4 to 7,8-dihydrobiopterin.	Superoxides	13-23	nitric oxide synthase 3	Homo sapiens	98-102
23965989-7	2013	eNOS-derived superoxide production was significantly elevated in W447A and W447F versus wild-type eNOS, and this was sufficient to oxidize BH4 to 7,8-dihydrobiopterin.	sapropterin	139-142	nitric oxide synthase 3	Homo sapiens	0-4
23965989-7	2013	eNOS-derived superoxide production was significantly elevated in W447A and W447F versus wild-type eNOS, and this was sufficient to oxidize BH4 to 7,8-dihydrobiopterin.	sapropterin	139-142	nitric oxide synthase 3	Homo sapiens	98-102
23965989-7	2013	eNOS-derived superoxide production was significantly elevated in W447A and W447F versus wild-type eNOS, and this was sufficient to oxidize BH4 to 7,8-dihydrobiopterin.	7,8-dihydrobiopterin	146-166	nitric oxide synthase 3	Homo sapiens	0-4
23965989-9	2013	eNOS dimerization was attenuated in W447A eNOS cells and further reduced in BH4-deficient cells, as demonstrated using a novel split Renilla luciferase biosensor.	sapropterin	76-79	nitric oxide synthase 3	Homo sapiens	0-4
23965989-10	2013	Reduction of cellular BH4 levels resulted in a switch from an eNOS dimer to an eNOS monomer.	sapropterin	22-25	nitric oxide synthase 3	Homo sapiens	62-66
23965989-10	2013	Reduction of cellular BH4 levels resulted in a switch from an eNOS dimer to an eNOS monomer.	sapropterin	22-25	nitric oxide synthase 3	Homo sapiens	79-83
23965989-11	2013	These data reveal a key role for Trp-447 in determining NO versus superoxide production by eNOS, by effects on BH4-dependent catalysis, and by modulating eNOS dimer formation.	Tryptophan	33-36	nitric oxide synthase 3	Homo sapiens	91-95
23965989-11	2013	These data reveal a key role for Trp-447 in determining NO versus superoxide production by eNOS, by effects on BH4-dependent catalysis, and by modulating eNOS dimer formation.	Tryptophan	33-36	nitric oxide synthase 3	Homo sapiens	154-158
23965989-11	2013	These data reveal a key role for Trp-447 in determining NO versus superoxide production by eNOS, by effects on BH4-dependent catalysis, and by modulating eNOS dimer formation.	Superoxides	66-76	nitric oxide synthase 3	Homo sapiens	91-95
24283106-2	2013	Endothelial nitric oxide synthase (eNOS) intron 4a/b polymorphism has been shown to be related to plasma nitric oxide concentrations and coronary artery disease in various population studies.	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	35-39
23738793-11	2013	These data suggest that protocatechuic acid may be a candidate therapy for stroke recovery by promoting angiogenesis via a programmed PI3K/Akt/eNOS/VEGF signalling axis.	protocatechuic acid	24-43	nitric oxide synthase 3	Homo sapiens	143-147
23943785-6	2013	Acacetin inhibited Stat-1 (Tyr701) and Stat-3 (Tyr705) phosphorylation, and downregulated proangiogenic factors including VEGF, endothelial nitric oxide synthase (eNOS), inducible nitric oxide synthase (iNOS), matrix metalloproteinase-2 (MMP-2), and basic fibroblast growth factor (bFGF) in HUVEC.	acacetin	0-8	nitric oxide synthase 3	Homo sapiens	128-161
24078390-2	2013	This review focuses on the role of endothelial nitric oxide synthase (eNOS)-derived nitric oxide (NO) in regulating S-Nitrosation of adherens junction proteins.	Nitric Oxide	47-59	nitric oxide synthase 3	Homo sapiens	70-74
23947593-0	2013	Human metabolic transformation of quercetin blocks its capacity to decrease endothelial nitric oxide synthase (eNOS) expression and endothelin-1 secretion by human endothelial cells.	Quercetin	34-43	nitric oxide synthase 3	Homo sapiens	76-109
23359565-7	2013	RESULTS: It was found that Glu/Glu, Glu/Asp, and Asp/Asp genotype frequencies of the eNOS gene polymorphism were 35.2%, 59.2%, and 5.6% of the control group, and 32.9%, 65.1%, and 2.0% of the patient group, respectively (P > 0.05).	Glutamic Acid	27-30	nitric oxide synthase 3	Homo sapiens	85-89
23359565-7	2013	RESULTS: It was found that Glu/Glu, Glu/Asp, and Asp/Asp genotype frequencies of the eNOS gene polymorphism were 35.2%, 59.2%, and 5.6% of the control group, and 32.9%, 65.1%, and 2.0% of the patient group, respectively (P > 0.05).	Glutamic Acid	31-34	nitric oxide synthase 3	Homo sapiens	85-89
23359565-7	2013	RESULTS: It was found that Glu/Glu, Glu/Asp, and Asp/Asp genotype frequencies of the eNOS gene polymorphism were 35.2%, 59.2%, and 5.6% of the control group, and 32.9%, 65.1%, and 2.0% of the patient group, respectively (P > 0.05).	Glutamic Acid	31-34	nitric oxide synthase 3	Homo sapiens	85-89
23359565-7	2013	RESULTS: It was found that Glu/Glu, Glu/Asp, and Asp/Asp genotype frequencies of the eNOS gene polymorphism were 35.2%, 59.2%, and 5.6% of the control group, and 32.9%, 65.1%, and 2.0% of the patient group, respectively (P > 0.05).	Aspartic Acid	49-52	nitric oxide synthase 3	Homo sapiens	85-89
23359565-7	2013	RESULTS: It was found that Glu/Glu, Glu/Asp, and Asp/Asp genotype frequencies of the eNOS gene polymorphism were 35.2%, 59.2%, and 5.6% of the control group, and 32.9%, 65.1%, and 2.0% of the patient group, respectively (P > 0.05).	Aspartic Acid	49-52	nitric oxide synthase 3	Homo sapiens	85-89
23977830-1	2013	S-Glutathionylation is a redox-regulated modification that uncouples endothelial nitric oxide synthase (eNOS), switching its function from nitric oxide (NO) synthesis to ( )O2(-) generation, and serves to regulate vascular function.	Nitric Oxide	81-93	nitric oxide synthase 3	Homo sapiens	104-108
23977830-1	2013	S-Glutathionylation is a redox-regulated modification that uncouples endothelial nitric oxide synthase (eNOS), switching its function from nitric oxide (NO) synthesis to ( )O2(-) generation, and serves to regulate vascular function.	Oxygen	173-175	nitric oxide synthase 3	Homo sapiens	104-108
23977830-2	2013	While in vitro or in vivo eNOS S-glutathionylation with modification of Cys689 and Cys908 of its reductase domain is triggered by high levels of glutathione disulfide (GSSG) or oxidative thiyl radical formation, it remains unclear how this process may be reversed.	Glutathione Disulfide	145-166	nitric oxide synthase 3	Homo sapiens	26-30
23977830-2	2013	While in vitro or in vivo eNOS S-glutathionylation with modification of Cys689 and Cys908 of its reductase domain is triggered by high levels of glutathione disulfide (GSSG) or oxidative thiyl radical formation, it remains unclear how this process may be reversed.	Glutathione Disulfide	168-172	nitric oxide synthase 3	Homo sapiens	26-30
23977830-2	2013	While in vitro or in vivo eNOS S-glutathionylation with modification of Cys689 and Cys908 of its reductase domain is triggered by high levels of glutathione disulfide (GSSG) or oxidative thiyl radical formation, it remains unclear how this process may be reversed.	thiyl radical	187-200	nitric oxide synthase 3	Homo sapiens	26-30
23977830-4	2013	We demonstrate that Grx1 in the presence of glutathione (GSH) (1 mM) reverses GSSG-mediated eNOS S-glutathionylation with restoration of NO synthase activity.	Glutathione	44-55	nitric oxide synthase 3	Homo sapiens	92-96
23977830-4	2013	We demonstrate that Grx1 in the presence of glutathione (GSH) (1 mM) reverses GSSG-mediated eNOS S-glutathionylation with restoration of NO synthase activity.	Glutathione	57-60	nitric oxide synthase 3	Homo sapiens	92-96
23977830-5	2013	Because Grx1 also catalyzes protein S-glutathionylation with an increased [GSSG]/[GSH] ratio, we measured its effect on eNOS S-glutathionylation when the [GSSG]/[GSH] ratio was >0.2, which can occur in cells and tissues under oxidative stress, and observed an increased level of eNOS S-glutathionylation with a marked decrease in eNOS activity without uncoupling.	Glutathione Disulfide	155-159	nitric oxide synthase 3	Homo sapiens	120-124
23977830-6	2013	This eNOS S-glutathionylation was reversed with a decrease in the [GSSG]/[GSH] ratio to <0.1.	Glutathione Disulfide	67-71	nitric oxide synthase 3	Homo sapiens	5-9
23977830-6	2013	This eNOS S-glutathionylation was reversed with a decrease in the [GSSG]/[GSH] ratio to <0.1.	Glutathione	74-77	nitric oxide synthase 3	Homo sapiens	5-9
24050620-0	2013	Methylglyoxal modulates endothelial nitric oxide synthase-associated functions in EA.hy926 endothelial cells.	Pyruvaldehyde	0-13	nitric oxide synthase 3	Homo sapiens	24-57
23947593-0	2013	Human metabolic transformation of quercetin blocks its capacity to decrease endothelial nitric oxide synthase (eNOS) expression and endothelin-1 secretion by human endothelial cells.	Quercetin	34-43	nitric oxide synthase 3	Homo sapiens	111-115
23947593-2	2013	This study examined the relative abilities of quercetin and its human metabolites to modulate the expression of eNOS and ET-1, which are involved in regulating endothelial homeostasis.	Quercetin	46-55	nitric oxide synthase 3	Homo sapiens	112-116
23947593-3	2013	Quercetin aglycone significantly reduced both eNOS protein and gene expression in HUVEC, mirroring the effects of the pro-inflammatory cytokine TNFalpha.	quercetin aglycone	0-18	nitric oxide synthase 3	Homo sapiens	46-50
23947593-4	2013	In the presence of TNFalpha the aglycone caused further reductions in eNOS, whereas the metabolites were without effect in either TNFalpha-stimulated or unstimulated cells.	CHEBI:166892	32-40	nitric oxide synthase 3	Homo sapiens	70-74
23947593-7	2013	These results suggest that metabolic transformation of quercetin prevents it from causing a potentially deleterious decrease in eNOS in endothelial cells.	Quercetin	55-64	nitric oxide synthase 3	Homo sapiens	128-132
23876348-4	2013	Moreover, we verified whether obese women carrying the C variant of T(-786)C polymorphism located in eNOS may have increased levels of nitrite after treatment compared to TT genotype.	Nitrites	135-142	nitric oxide synthase 3	Homo sapiens	101-105
23876348-0	2013	Simvastatin treatment increases nitrite levels in obese women: modulation by T(-786)C polymorphism of eNOS.	Simvastatin	0-11	nitric oxide synthase 3	Homo sapiens	102-106
23876348-0	2013	Simvastatin treatment increases nitrite levels in obese women: modulation by T(-786)C polymorphism of eNOS.	Nitrites	32-39	nitric oxide synthase 3	Homo sapiens	102-106
23774601-6	2013	Treatment with gamma interferon (IFN-gamma), l-arginine, and tetrahydrobiopterin enhanced expression of NOS2 and NOS3 isoforms, as well as NO production.	Arginine	45-55	nitric oxide synthase 3	Homo sapiens	113-117
23774601-6	2013	Treatment with gamma interferon (IFN-gamma), l-arginine, and tetrahydrobiopterin enhanced expression of NOS2 and NOS3 isoforms, as well as NO production.	sapropterin	61-80	nitric oxide synthase 3	Homo sapiens	113-117
23756085-1	2013	In testis, eNOS is responsible for synthesis of nitric oxide (NO) which is an essential gas message regulator in spermatogenesis, suggesting that eNOS gene plays a role in normal spermatogenesis and the genetic variants of eNOS gene may be potential genetic risk factors of spermatogenesis impairment.	Nitric Oxide	48-60	nitric oxide synthase 3	Homo sapiens	11-15
23825361-6	2013	Elevated plasma ADMA is associated with increased risk for cardiovascular disease, likely because of its attenuation of the vasoprotective effects of endothelial nitric oxide synthase.	N,N-dimethylarginine	16-20	nitric oxide synthase 3	Homo sapiens	150-183
22369111-6	2013	Accordingly, cells treated with KCN 6 muM showed higher levels of phospho-CREB, PGC1alpha mRNA, eNOS mRNA, and mtTFA mRNA.	kcn 6	32-37	nitric oxide synthase 3	Homo sapiens	96-100
23796957-0	2013	Folic acid modulates eNOS activity via effects on posttranslational modifications and protein-protein interactions.	Folic Acid	0-10	nitric oxide synthase 3	Homo sapiens	21-25
23796957-3	2013	Particular focus was placed on folic acid-induced changes in posttranslational modifications of endothelial nitric oxide synthase (eNOS).	Folic Acid	31-41	nitric oxide synthase 3	Homo sapiens	96-129
23796957-3	2013	Particular focus was placed on folic acid-induced changes in posttranslational modifications of endothelial nitric oxide synthase (eNOS).	Folic Acid	31-41	nitric oxide synthase 3	Homo sapiens	131-135
23796957-8	2013	Intracellular localisation of eNOS was investigated using sucrose gradient centrifugation and confocal microscopy.	Sucrose	58-65	nitric oxide synthase 3	Homo sapiens	30-34
23796957-9	2013	Folic acid promoted eNOS dephosphorylation at negative regulatory sites, and increased phosphorylation at positive regulatory sites.	Folic Acid	0-10	nitric oxide synthase 3	Homo sapiens	20-24
23796957-11	2013	Inhibition of PI3K/Akt revealed specific roles for this kinase pathway in folic acid-mediated eNOS phosphorylation.	Folic Acid	74-84	nitric oxide synthase 3	Homo sapiens	94-98
23796957-13	2013	Folic acid-mediated eNOS activation involves the modulation of eNOS phosphorylation status at multiple residues and positive changes in important protein-protein interactions.	Folic Acid	0-10	nitric oxide synthase 3	Homo sapiens	20-24
23796957-13	2013	Folic acid-mediated eNOS activation involves the modulation of eNOS phosphorylation status at multiple residues and positive changes in important protein-protein interactions.	Folic Acid	0-10	nitric oxide synthase 3	Homo sapiens	63-67
23756085-1	2013	In testis, eNOS is responsible for synthesis of nitric oxide (NO) which is an essential gas message regulator in spermatogenesis, suggesting that eNOS gene plays a role in normal spermatogenesis and the genetic variants of eNOS gene may be potential genetic risk factors of spermatogenesis impairment.	Nitric Oxide	48-60	nitric oxide synthase 3	Homo sapiens	146-150
23756085-1	2013	In testis, eNOS is responsible for synthesis of nitric oxide (NO) which is an essential gas message regulator in spermatogenesis, suggesting that eNOS gene plays a role in normal spermatogenesis and the genetic variants of eNOS gene may be potential genetic risk factors of spermatogenesis impairment.	Nitric Oxide	48-60	nitric oxide synthase 3	Homo sapiens	146-150
23583951-0	2013	Role of SIRT1 and FOXO factors in eNOS transcriptional activation by resveratrol.	Resveratrol	69-80	nitric oxide synthase 3	Homo sapiens	34-38
23583951-6	2013	Knockdown of the NAD(+)-dependent protein deacetylase sirtuin 1 (SIRT1) by siRNA prevented the upregulation of eNOS mRNA and protein by resveratrol.	Resveratrol	136-147	nitric oxide synthase 3	Homo sapiens	111-115
23583951-1	2013	Many of the cardiovascular protective effects of resveratrol are attributable to an enhanced production of nitric oxide (NO) by the endothelial NO synthase (eNOS).	Resveratrol	49-60	nitric oxide synthase 3	Homo sapiens	157-161
23583951-8	2013	siRNA-mediated knockdown of FOXO1 and FOXO3a abolished the effect of resveratrol on eNOS expression, indicating the involvement of these factors.	Resveratrol	69-80	nitric oxide synthase 3	Homo sapiens	84-88
23583951-1	2013	Many of the cardiovascular protective effects of resveratrol are attributable to an enhanced production of nitric oxide (NO) by the endothelial NO synthase (eNOS).	Nitric Oxide	107-119	nitric oxide synthase 3	Homo sapiens	157-161
23583951-11	2013	In electrophoretic mobility shift assay, the enhanced binding of nuclear proteins to the eNOS promoter regions by resveratrol could be blocked by antibodies against FOXO1 and FOXO3a.	Resveratrol	114-125	nitric oxide synthase 3	Homo sapiens	89-93
23583951-2	2013	Resveratrol has been shown to enhance eNOS gene expression as well as eNOS enzymatic activity.	Resveratrol	0-11	nitric oxide synthase 3	Homo sapiens	38-42
23583951-13	2013	The SIRT1/FOXO factor axis is involved in resveratrol-induced eNOS transcriptional activation.	Resveratrol	42-53	nitric oxide synthase 3	Homo sapiens	62-66
23583951-2	2013	Resveratrol has been shown to enhance eNOS gene expression as well as eNOS enzymatic activity.	Resveratrol	0-11	nitric oxide synthase 3	Homo sapiens	70-74
23583951-3	2013	The aim of the present study was to analyze the molecular mechanisms of eNOS transcriptional activation by resveratrol.	Resveratrol	107-118	nitric oxide synthase 3	Homo sapiens	72-76
23583951-4	2013	Treatment of human EA.hy 926 endothelial cells with resveratrol led to a concentration-dependent upregulation of eNOS expression.	Resveratrol	52-63	nitric oxide synthase 3	Homo sapiens	113-117
23583951-5	2013	In luciferase reporter gene assay, resveratrol enhanced the activity of human eNOS promoter fragments (3500, 1600, 633 and 263bp in length, respectively), indicating that the proximal promoter region is required for resveratrol-induced eNOS transcriptional activation.	Resveratrol	35-46	nitric oxide synthase 3	Homo sapiens	78-82
23583951-5	2013	In luciferase reporter gene assay, resveratrol enhanced the activity of human eNOS promoter fragments (3500, 1600, 633 and 263bp in length, respectively), indicating that the proximal promoter region is required for resveratrol-induced eNOS transcriptional activation.	Resveratrol	35-46	nitric oxide synthase 3	Homo sapiens	236-240
23583951-5	2013	In luciferase reporter gene assay, resveratrol enhanced the activity of human eNOS promoter fragments (3500, 1600, 633 and 263bp in length, respectively), indicating that the proximal promoter region is required for resveratrol-induced eNOS transcriptional activation.	Resveratrol	216-227	nitric oxide synthase 3	Homo sapiens	78-82
23583951-6	2013	Knockdown of the NAD(+)-dependent protein deacetylase sirtuin 1 (SIRT1) by siRNA prevented the upregulation of eNOS mRNA and protein by resveratrol.	NAD	17-23	nitric oxide synthase 3	Homo sapiens	111-115
23624269-6	2013	Furthermore, uric acid did not change the activity of arginase II, an enzyme degrading l-arginine, a substrate of eNOS, and intracellular level of calcium, a cofactor for eNOS activation.	Calcium	147-154	nitric oxide synthase 3	Homo sapiens	171-175
23624269-0	2013	Uric acid attenuates nitric oxide production by decreasing the interaction between endothelial nitric oxide synthase and calmodulin in human umbilical vein endothelial cells: a mechanism for uric acid-induced cardiovascular disease development.	Uric Acid	0-9	nitric oxide synthase 3	Homo sapiens	83-116
23624269-8	2013	In vitro and in cell coimmunoprecipitation studies, however, revealed that uric acid significantly decreased the interaction between eNOS and calmodulin (CaM), an eNOS activator, although it did not change the intracellular CaM level.	Uric Acid	75-84	nitric oxide synthase 3	Homo sapiens	133-137
23624269-0	2013	Uric acid attenuates nitric oxide production by decreasing the interaction between endothelial nitric oxide synthase and calmodulin in human umbilical vein endothelial cells: a mechanism for uric acid-induced cardiovascular disease development.	Nitric Oxide	21-33	nitric oxide synthase 3	Homo sapiens	83-116
23624269-0	2013	Uric acid attenuates nitric oxide production by decreasing the interaction between endothelial nitric oxide synthase and calmodulin in human umbilical vein endothelial cells: a mechanism for uric acid-induced cardiovascular disease development.	Uric Acid	191-200	nitric oxide synthase 3	Homo sapiens	83-116
23624269-3	2013	Using human umbilical vascular endothelial cells (HUVEC), we explored the molecular mechanism of uric acid on endothelial NO synthase (eNOS) activity and NO production.	Uric Acid	97-106	nitric oxide synthase 3	Homo sapiens	135-139
23624269-4	2013	Although high dose of uric acid (12mg/dl for 24h treatment) significantly decreased eNOS activity and NO production, it did not alter eNOS expression and phosphorylations at eNOS-Ser(1177), eNOS-Thr(495) and eNOS-Ser(114).	Uric Acid	22-31	nitric oxide synthase 3	Homo sapiens	84-88
23624269-8	2013	In vitro and in cell coimmunoprecipitation studies, however, revealed that uric acid significantly decreased the interaction between eNOS and calmodulin (CaM), an eNOS activator, although it did not change the intracellular CaM level.	Uric Acid	75-84	nitric oxide synthase 3	Homo sapiens	163-167
23624269-10	2013	Finally, uric acid attenuated ionomycin-induced increase in the interaction between eNOS and CaM.	Uric Acid	9-18	nitric oxide synthase 3	Homo sapiens	84-88
23624269-10	2013	Finally, uric acid attenuated ionomycin-induced increase in the interaction between eNOS and CaM.	Ionomycin	30-39	nitric oxide synthase 3	Homo sapiens	84-88
23624269-11	2013	This study suggests firstly that uric acid decreased eNOS activity and NO production through reducing the binding between eNOS and CaM in EC.	Uric Acid	33-42	nitric oxide synthase 3	Homo sapiens	53-57
23624269-11	2013	This study suggests firstly that uric acid decreased eNOS activity and NO production through reducing the binding between eNOS and CaM in EC.	Uric Acid	33-42	nitric oxide synthase 3	Homo sapiens	122-126
23922896-3	2013	Endothelial nitric oxide synthase which encoded by nitric oxide synthase 3 (NOS3), can generate nitric oxide in endothelial cells.	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	51-74
23922896-3	2013	Endothelial nitric oxide synthase which encoded by nitric oxide synthase 3 (NOS3), can generate nitric oxide in endothelial cells.	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	76-80
23806688-1	2013	n-3-Polyunsaturated fatty acids (PUFAs) protect against myocardial infarction, arteriosclerosis and high blood pressure by stimulating endothelial nitric oxide synthase (eNOS) to increase nitric oxide (NO) production.	Fatty Acids, Omega-3	0-31	nitric oxide synthase 3	Homo sapiens	135-168
23996753-6	2013	RESULTS: The expression of eNOS and NO secretion decreased obviously in HUVECs incubated with 600 micromol/L uric acid.	Uric Acid	109-118	nitric oxide synthase 3	Homo sapiens	27-31
23996753-9	2013	Expression of eNOS and secretion of NO were elevated in endothelial cells transfected with miR-155 inhibitor after incubation with high-concentration uric acid.	Uric Acid	150-159	nitric oxide synthase 3	Homo sapiens	14-18
23996753-10	2013	CONCLUSION: High-concentration uric acid can down-regulate eNOS expression via miR-155 to induce endothelial dysfunction.	Uric Acid	31-40	nitric oxide synthase 3	Homo sapiens	59-63
23806688-1	2013	n-3-Polyunsaturated fatty acids (PUFAs) protect against myocardial infarction, arteriosclerosis and high blood pressure by stimulating endothelial nitric oxide synthase (eNOS) to increase nitric oxide (NO) production.	Fatty Acids, Omega-3	33-38	nitric oxide synthase 3	Homo sapiens	135-168
23648561-4	2013	Rosuvastatin maintain the balance between oxidant generation and oxidant scavenging by reducing NADPH (nicotinamide adenine dinucleotide phosphate)-dependent production of reactive oxygen species, suppressing endothelial nitric oxide synthase (eNOS) uncoupling, inducing and upregulating antioxidant defense mechanism.	Rosuvastatin Calcium	0-12	nitric oxide synthase 3	Homo sapiens	209-242
23756809-0	2013	Far-infrared radiation acutely increases nitric oxide production by increasing Ca(2+) mobilization and Ca(2+)/calmodulin-dependent protein kinase II-mediated phosphorylation of endothelial nitric oxide synthase at serine 1179.	Nitric Oxide	41-53	nitric oxide synthase 3	Homo sapiens	177-210
23756809-0	2013	Far-infrared radiation acutely increases nitric oxide production by increasing Ca(2+) mobilization and Ca(2+)/calmodulin-dependent protein kinase II-mediated phosphorylation of endothelial nitric oxide synthase at serine 1179.	Serine	214-220	nitric oxide synthase 3	Homo sapiens	177-210
23648561-4	2013	Rosuvastatin maintain the balance between oxidant generation and oxidant scavenging by reducing NADPH (nicotinamide adenine dinucleotide phosphate)-dependent production of reactive oxygen species, suppressing endothelial nitric oxide synthase (eNOS) uncoupling, inducing and upregulating antioxidant defense mechanism.	NADP	96-101	nitric oxide synthase 3	Homo sapiens	209-242
23847616-1	2013	Nitric oxide (NO) generated through L-arginine metabolism by endothelial nitric oxide synthase (eNOS) is an important regulator of the vessel wall.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	61-94
23847616-1	2013	Nitric oxide (NO) generated through L-arginine metabolism by endothelial nitric oxide synthase (eNOS) is an important regulator of the vessel wall.	Arginine	36-46	nitric oxide synthase 3	Homo sapiens	61-94
23727078-3	2013	In this study, we show that activation of eNOS in response to a variety of other eNOS-activating agonists and the cytosolic calcium-elevating agent, thapsigargin also involves CsA-inhibitable S116 dephosphorylation.	Calcium	124-131	nitric oxide synthase 3	Homo sapiens	42-46
23847624-3	2013	In endothelial cells, NO is generated by endothelial nitric oxide synthase (eNOS) through the conversion of its substrate, l-arginine to l-citrulline.	Arginine	123-133	nitric oxide synthase 3	Homo sapiens	41-74
23847624-3	2013	In endothelial cells, NO is generated by endothelial nitric oxide synthase (eNOS) through the conversion of its substrate, l-arginine to l-citrulline.	Citrulline	137-149	nitric oxide synthase 3	Homo sapiens	41-74
23641912-3	2013	Significant OS difference was also observed in the endothelial nitric oxide synthase (eNOS)-786 T>C polymorphism.	Osmium	12-14	nitric oxide synthase 3	Homo sapiens	51-84
23641912-3	2013	Significant OS difference was also observed in the endothelial nitric oxide synthase (eNOS)-786 T>C polymorphism.	Osmium	12-14	nitric oxide synthase 3	Homo sapiens	86-90
23897679-10	2013	Furthermore, low levels of tetrahydrobiopterin (BH4) and L-arginine the rate limiting cofactor and substrate for endothelial nitric oxide synthase (eNOS), can cause the uncoupling of eNOS, resulting in decreased NO production and increased ROS production.	sapropterin	27-46	nitric oxide synthase 3	Homo sapiens	113-146
23897679-10	2013	Furthermore, low levels of tetrahydrobiopterin (BH4) and L-arginine the rate limiting cofactor and substrate for endothelial nitric oxide synthase (eNOS), can cause the uncoupling of eNOS, resulting in decreased NO production and increased ROS production.	sapropterin	48-51	nitric oxide synthase 3	Homo sapiens	113-146
23897679-10	2013	Furthermore, low levels of tetrahydrobiopterin (BH4) and L-arginine the rate limiting cofactor and substrate for endothelial nitric oxide synthase (eNOS), can cause the uncoupling of eNOS, resulting in decreased NO production and increased ROS production.	Arginine	57-67	nitric oxide synthase 3	Homo sapiens	113-146
23897679-10	2013	Furthermore, low levels of tetrahydrobiopterin (BH4) and L-arginine the rate limiting cofactor and substrate for endothelial nitric oxide synthase (eNOS), can cause the uncoupling of eNOS, resulting in decreased NO production and increased ROS production.	Reactive Oxygen Species	240-243	nitric oxide synthase 3	Homo sapiens	113-146
23670355-0	2013	Nicorandil inhibits hypoxia-induced apoptosis in human pulmonary artery endothelial cells through activation of mitoKATP and regulation of eNOS and the NF-kappaB pathway.	Nicorandil	0-10	nitric oxide synthase 3	Homo sapiens	139-143
23670355-9	2013	However, these protective effects of nicorandil were significantly inhibited by an antagonist of mitochondrial adenosine triphosphate-sensitive potassium (mitoKATP) channels, 5-hydroxydecanoate (5-HD, 500 microM), and by an eNOS inhibitor, NG-nitro-L-arginine methyl ester (L-NAME, 300 microM).	Nicorandil	37-47	nitric oxide synthase 3	Homo sapiens	224-228
23670355-10	2013	We further observed that nicorandil could upregulate the decreased protein expression of eNOS and IkappaBalpha, and downregulate the increased protein expression of NF-kappaB, induced by hypoxia.	Nicorandil	25-35	nitric oxide synthase 3	Homo sapiens	89-93
23670355-13	2013	Collectively, these findings suggest that nicorandil inhibits hypoxia-induced apoptosis of HPAECs through activation of mitoKATP channels and increased eNOS expression, which in turn inhibits the NF-kappaB pathway and the mitochondrial apoptotic pathway.	Nicorandil	42-52	nitric oxide synthase 3	Homo sapiens	152-156
23549379-3	2013	Uncoupling of eNOS exacerbated oxidative stress and enhanced nitric oxide (NO) depletion, and was associated with multiple secondary complications such as microthrombosis, neuronal apoptosis, and release of reactive oxygen species.	Nitric Oxide	61-73	nitric oxide synthase 3	Homo sapiens	14-18
23549379-3	2013	Uncoupling of eNOS exacerbated oxidative stress and enhanced nitric oxide (NO) depletion, and was associated with multiple secondary complications such as microthrombosis, neuronal apoptosis, and release of reactive oxygen species.	Reactive Oxygen Species	207-230	nitric oxide synthase 3	Homo sapiens	14-18
23549379-5	2013	Using a prechiasmatic injection model of SAH, we show here that eNOS knockout (KO) significantly alleviates vasospasm of the middle cerebral artery and reduces superoxide production.	Superoxides	160-170	nitric oxide synthase 3	Homo sapiens	64-68
23549379-9	2013	This work is consistent with our findings where, after SAH, increased oxidative stress can uncouple eNOS via Zn(2+) thiolate oxidation, or theoretically by depletion or oxidation of tetrahydrobiopterin, resulting in a paradoxical release of superoxide anion radical, further exacerbating oxidative stress and microvascular damage.	zn(2+) thiolate	109-124	nitric oxide synthase 3	Homo sapiens	100-104
23768697-12	2013	Western blot analysis further showed an earlier and greater S633 phosphorylation than that of S1177 in endothelial nitric oxide synthase after rosuvastatin treatment.	Rosuvastatin Calcium	143-155	nitric oxide synthase 3	Homo sapiens	103-136
23567873-8	2013	EGCG inhibited 7KC-induced monocytic adhesion to endothelial cells, and induced expression of eNOS and several genes involved in the CaMKKII pathway.	epigallocatechin gallate	0-4	nitric oxide synthase 3	Homo sapiens	94-98
23567873-9	2013	Stimulation of endothelial cells with EGCG produced intracellular ROS, whereas treatment with N-acetylcysteine (NAC) blocked EGCG-induced expression of eNOS and CaMKKII.	Acetylcysteine	94-110	nitric oxide synthase 3	Homo sapiens	152-156
23567873-9	2013	Stimulation of endothelial cells with EGCG produced intracellular ROS, whereas treatment with N-acetylcysteine (NAC) blocked EGCG-induced expression of eNOS and CaMKKII.	Acetylcysteine	112-115	nitric oxide synthase 3	Homo sapiens	152-156
23567873-9	2013	Stimulation of endothelial cells with EGCG produced intracellular ROS, whereas treatment with N-acetylcysteine (NAC) blocked EGCG-induced expression of eNOS and CaMKKII.	epigallocatechin gallate	125-129	nitric oxide synthase 3	Homo sapiens	152-156
23711612-4	2013	ADMA is an endogenous inhibitor of endothelial nitric oxide synthase.	N,N-dimethylarginine	0-4	nitric oxide synthase 3	Homo sapiens	35-68
23324897-0	2013	Atorvastatin improves erectile dysfunction in patients initially irresponsive to Sildenafil by the activation of endothelial nitric oxide synthase.	Atorvastatin	0-12	nitric oxide synthase 3	Homo sapiens	113-146
23604198-1	2013	PURPOSE: Nitric oxide (NO) synthesised by endothelial NO synthase (eNOS) is a potent regulator of internal haemodynamics.	Nitric Oxide	9-21	nitric oxide synthase 3	Homo sapiens	67-71
23742697-4	2013	Incubation of human umbilical vein endothelial cells (HUVECs-926) with NaHS (a H2 S donor) stimulated the phosphorylation of endothelial NO synthase (eNOS) and enhanced NO production.	sodium bisulfide	71-75	nitric oxide synthase 3	Homo sapiens	150-154
23742697-4	2013	Incubation of human umbilical vein endothelial cells (HUVECs-926) with NaHS (a H2 S donor) stimulated the phosphorylation of endothelial NO synthase (eNOS) and enhanced NO production.	Hydrogen	79-81	nitric oxide synthase 3	Homo sapiens	150-154
23742697-8	2013	LY294002 (Akt/PI3-K inhibitor) or SB203580 (p38 MAPK inhibitor) abolished the effects of H2 S on eNOS phosphorylation, NO production, cell proliferation and tube formation.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	0-8	nitric oxide synthase 3	Homo sapiens	97-101
23742697-8	2013	LY294002 (Akt/PI3-K inhibitor) or SB203580 (p38 MAPK inhibitor) abolished the effects of H2 S on eNOS phosphorylation, NO production, cell proliferation and tube formation.	SB 203580	34-42	nitric oxide synthase 3	Homo sapiens	97-101
23742697-8	2013	LY294002 (Akt/PI3-K inhibitor) or SB203580 (p38 MAPK inhibitor) abolished the effects of H2 S on eNOS phosphorylation, NO production, cell proliferation and tube formation.	Hydrogen Sulfide	89-93	nitric oxide synthase 3	Homo sapiens	97-101
23742697-9	2013	Blockade of NO production by eNOS-specific siRNA or nitro-L-arginine methyl ester (L-NAME) reversed, but eNOS overexpression potentiated, the proliferative effect of H2 S on ECs.	Hydrogen Sulfide	166-170	nitric oxide synthase 3	Homo sapiens	29-33
23742697-9	2013	Blockade of NO production by eNOS-specific siRNA or nitro-L-arginine methyl ester (L-NAME) reversed, but eNOS overexpression potentiated, the proliferative effect of H2 S on ECs.	Hydrogen Sulfide	166-170	nitric oxide synthase 3	Homo sapiens	105-109
23742697-10	2013	Our results suggest that H2 S stimulates the phosphorylation of eNOS through a p38 MAPK and Akt-dependent pathway, thus increasing NO production in ECs and vascular tissues and contributing to H2 S-induced angiogenesis.	Hydrogen Sulfide	25-29	nitric oxide synthase 3	Homo sapiens	64-68
23742697-10	2013	Our results suggest that H2 S stimulates the phosphorylation of eNOS through a p38 MAPK and Akt-dependent pathway, thus increasing NO production in ECs and vascular tissues and contributing to H2 S-induced angiogenesis.	Hydrogen Sulfide	193-197	nitric oxide synthase 3	Homo sapiens	64-68
23727078-0	2013	Calcineurin-mediated dephosphorylation of eNOS at serine 116 affects eNOS enzymatic activity indirectly by facilitating c-Src binding and tyrosine 83 phosphorylation.	Serine	50-56	nitric oxide synthase 3	Homo sapiens	42-46
23727078-0	2013	Calcineurin-mediated dephosphorylation of eNOS at serine 116 affects eNOS enzymatic activity indirectly by facilitating c-Src binding and tyrosine 83 phosphorylation.	Serine	50-56	nitric oxide synthase 3	Homo sapiens	69-73
23727078-0	2013	Calcineurin-mediated dephosphorylation of eNOS at serine 116 affects eNOS enzymatic activity indirectly by facilitating c-Src binding and tyrosine 83 phosphorylation.	Tyrosine	138-146	nitric oxide synthase 3	Homo sapiens	42-46
23727078-1	2013	It has been shown previously that phosphorylation of the endothelial nitric oxide synthase (eNOS) at serine 116 (S116) under basal conditions suppresses eNOS enzymatic activity in endothelial cells.	Serine	101-107	nitric oxide synthase 3	Homo sapiens	57-90
23727078-1	2013	It has been shown previously that phosphorylation of the endothelial nitric oxide synthase (eNOS) at serine 116 (S116) under basal conditions suppresses eNOS enzymatic activity in endothelial cells.	Serine	101-107	nitric oxide synthase 3	Homo sapiens	92-96
23727078-1	2013	It has been shown previously that phosphorylation of the endothelial nitric oxide synthase (eNOS) at serine 116 (S116) under basal conditions suppresses eNOS enzymatic activity in endothelial cells.	Serine	101-107	nitric oxide synthase 3	Homo sapiens	153-157
23727078-3	2013	In this study, we show that activation of eNOS in response to a variety of other eNOS-activating agonists and the cytosolic calcium-elevating agent, thapsigargin also involves CsA-inhibitable S116 dephosphorylation.	Thapsigargin	149-161	nitric oxide synthase 3	Homo sapiens	42-46
23727078-3	2013	In this study, we show that activation of eNOS in response to a variety of other eNOS-activating agonists and the cytosolic calcium-elevating agent, thapsigargin also involves CsA-inhibitable S116 dephosphorylation.	Thapsigargin	149-161	nitric oxide synthase 3	Homo sapiens	81-85
23727078-3	2013	In this study, we show that activation of eNOS in response to a variety of other eNOS-activating agonists and the cytosolic calcium-elevating agent, thapsigargin also involves CsA-inhibitable S116 dephosphorylation.	Cyclosporine	176-179	nitric oxide synthase 3	Homo sapiens	42-46
23727078-3	2013	In this study, we show that activation of eNOS in response to a variety of other eNOS-activating agonists and the cytosolic calcium-elevating agent, thapsigargin also involves CsA-inhibitable S116 dephosphorylation.	Cyclosporine	176-179	nitric oxide synthase 3	Homo sapiens	81-85
23727078-5	2013	Phospho-mimicking, however, does interfere with the interaction of eNOS with c-Src, an interaction which is known to activate eNOS by phosphorylation at tyrosine 83 (Y83).	Tyrosine	153-161	nitric oxide synthase 3	Homo sapiens	67-71
23727078-5	2013	Phospho-mimicking, however, does interfere with the interaction of eNOS with c-Src, an interaction which is known to activate eNOS by phosphorylation at tyrosine 83 (Y83).	Tyrosine	153-161	nitric oxide synthase 3	Homo sapiens	126-130
23727078-6	2013	Agonist-stimulated eNOS-Src complex formation, as well as agonist-stimulated Y83 phosphorylation, are blocked by calcineurin inhibition by CsA and by a cell-permeable calcineurin inhibitory peptide.	Cyclosporine	139-142	nitric oxide synthase 3	Homo sapiens	19-23
23357432-5	2013	Rapid activation of second messenger pathways by progesterone has been observed in vascular endothelial and smooth muscle cells, resulting in alterations in endothelial nitric oxide synthase (eNOS) activity and calcium influx, respectively.	Progesterone	49-61	nitric oxide synthase 3	Homo sapiens	157-190
23781221-3	2013	Increasing number of studies from recent years demonstrates that uncoupling of endothelial nitric oxide synthase (eNOS), whereby the enzyme eNOS produces detrimental amount of superoxide anion [Formula: see text] instead the vasoprotective nitric oxide (NO( )), plays a critical role in vascular dysfunction under various pathophysiological conditions and in aging.	Superoxides	176-192	nitric oxide synthase 3	Homo sapiens	79-112
23476046-8	2013	NOS3 methylation was negatively associated with PM10 (beta=-0.2, 95% CI -0.4 to -0.03), PM1 (beta=-0.8, 95% CI -1.4 to -0.1), zinc (beta=-0.9, 95% CI -1.4 to -0.3) and iron (beta=-0.7, 95% CI -1.4 to -0.01) exposures.	Iron	168-172	nitric oxide synthase 3	Homo sapiens	0-4
23476046-10	2013	Lower NOS3 (beta=-42.3; p<0.001) and EDN1 (beta=-14.5; p=0.05) were associated with higher ETP.	Ethionamide	94-97	nitric oxide synthase 3	Homo sapiens	6-10
23718875-1	2013	BACKGROUND: Our prior study revealed the loss in short-term L-Arginine (ARG) therapeutic efficacy after continuous exposure; resulting in tolerance development, mediated by endothelial nitric oxide synthase (eNOS) down-regulation, secondary to oxidative stress and induced glucose accumulation.	Arginine	60-70	nitric oxide synthase 3	Homo sapiens	173-206
23718875-1	2013	BACKGROUND: Our prior study revealed the loss in short-term L-Arginine (ARG) therapeutic efficacy after continuous exposure; resulting in tolerance development, mediated by endothelial nitric oxide synthase (eNOS) down-regulation, secondary to oxidative stress and induced glucose accumulation.	Arginine	72-75	nitric oxide synthase 3	Homo sapiens	173-206
23718875-1	2013	BACKGROUND: Our prior study revealed the loss in short-term L-Arginine (ARG) therapeutic efficacy after continuous exposure; resulting in tolerance development, mediated by endothelial nitric oxide synthase (eNOS) down-regulation, secondary to oxidative stress and induced glucose accumulation.	Glucose	273-280	nitric oxide synthase 3	Homo sapiens	173-206
23264539-2	2013	We performed immunohistochemical measurements of translocated eNOS activation as well as eNOS phosphorylation at Ser1177, Thr495, Ser 635, Ser114, and of the protein kinase B (Akt) in isolated right atrial trabeculae of patients undergoing cardiac bypass or valve surgery with (n = 12, 68.1 +- 2.5 yr) and without T2D (n = 12, 64.7 +- 2.7 yr).	Serine	113-116	nitric oxide synthase 3	Homo sapiens	89-93
23470294-5	2013	The serum levels of triglycerides and the risk of hypertriglyceridemia were shown to be influenced by the interactions between a single nucleotide polymorphism (SNP) in the NOS3 gene and physical activity level.	Triglycerides	20-33	nitric oxide synthase 3	Homo sapiens	173-177
23548909-7	2013	This ROS shifted endothelial NOS (eNOS) toward vesicle membranes and vesicles with a FC-rich domain trafficked toward perinuclear late endosomes/lysosomes, which resulted in the deterioration of eNOS Ser-1177 phosphorylation and NO production.	Reactive Oxygen Species	5-8	nitric oxide synthase 3	Homo sapiens	17-32
23548909-7	2013	This ROS shifted endothelial NOS (eNOS) toward vesicle membranes and vesicles with a FC-rich domain trafficked toward perinuclear late endosomes/lysosomes, which resulted in the deterioration of eNOS Ser-1177 phosphorylation and NO production.	Serine	200-203	nitric oxide synthase 3	Homo sapiens	17-32
23436331-1	2013	Nitric oxide (NO) release from endothelial NO synthase (eNOS) and/or neuronal NO synthase (nNOS) could be modulated by sympathetic nerve activity and contribute to increased blood flow after exercise.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	31-54
23436331-1	2013	Nitric oxide (NO) release from endothelial NO synthase (eNOS) and/or neuronal NO synthase (nNOS) could be modulated by sympathetic nerve activity and contribute to increased blood flow after exercise.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	56-60
23225320-8	2013	These findings indicated that histamine was able to synergistically augment bFGF-induced angiogenesis, and this action was linked to VEGF production through H1-receptor and the activation of endothelial nitric oxide synthase (eNOS), p38 MAPK, and IkappaBalpha in endothelial cells.	Histamine	30-39	nitric oxide synthase 3	Homo sapiens	191-224
22569406-7	2013	Since a high proportion of the vasa vasorum are removed in SSV using the CT, we suggest that preservation of the vasa vasorum and eNOS-derived NO contributes to the high patency for NT as compared with SSV grafts.	nt	182-184	nitric oxide synthase 3	Homo sapiens	130-134
23376231-8	2013	Suppression of RNS production by siRNA of eNOS or the antioxidant NAC reduced ICAM1 expression and prevented the stroma-mediated epithelial invasion.	Reactive Nitrogen Species	15-18	nitric oxide synthase 3	Homo sapiens	42-46
23463757-9	2013	The NOS3 894G/G genotype was associated with 15% lower VMCA (P=0.01).	vmca	55-59	nitric oxide synthase 3	Homo sapiens	4-8
23478261-3	2013	Here, we show that the human eNOS 3" untranslated region (3" UTR) contains multiple, evolutionarily conserved pyrimidine (C and CU)-rich sequence elements that are both necessary and sufficient for mRNA stabilization.	pyrimidine	110-120	nitric oxide synthase 3	Homo sapiens	29-33
23478261-7	2013	Hypoxia disrupts hnRNP E1/eNOS 3"-UTR interactions via increased Akt-mediated serine phosphorylation (including serine 43) and increased nuclear localization of hnRNP E1.	Serine	78-84	nitric oxide synthase 3	Homo sapiens	26-30
23478261-7	2013	Hypoxia disrupts hnRNP E1/eNOS 3"-UTR interactions via increased Akt-mediated serine phosphorylation (including serine 43) and increased nuclear localization of hnRNP E1.	Serine	112-118	nitric oxide synthase 3	Homo sapiens	26-30
23463757-10	2013	ATbG-NOS3 haplotype homozygosity was associated with up to 64% higher nitrite/nitrate levels (P=0.003).	atbg	0-4	nitric oxide synthase 3	Homo sapiens	5-9
23463757-10	2013	ATbG-NOS3 haplotype homozygosity was associated with up to 64% higher nitrite/nitrate levels (P=0.003).	Nitrites	70-77	nitric oxide synthase 3	Homo sapiens	5-9
23463757-10	2013	ATbG-NOS3 haplotype homozygosity was associated with up to 64% higher nitrite/nitrate levels (P=0.003).	Nitrates	78-85	nitric oxide synthase 3	Homo sapiens	5-9
22996620-4	2013	An increase in aglycone isoflavones in ethanol extracts from fermented soy milk stimulated NO production and endothelial NO synthase (eNOS) activity in human umbilical vein endothelial cells.	aglycone isoflavones	15-35	nitric oxide synthase 3	Homo sapiens	134-138
23328840-12	2013	eNOS mRNA expression levels were assessed in a separate group of children and were significantly reduced in the OSAab group in comparison with the OSAn group.	osaab	112-117	nitric oxide synthase 3	Homo sapiens	0-4
23328840-12	2013	eNOS mRNA expression levels were assessed in a separate group of children and were significantly reduced in the OSAab group in comparison with the OSAn group.	osan	147-151	nitric oxide synthase 3	Homo sapiens	0-4
23395155-1	2013	Nitric oxide (NO) produced by the endothelial NO synthase (eNOS) is an antihypertensive, antithrombotic and anti-atherosclerotic molecule.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	34-57
23395155-1	2013	Nitric oxide (NO) produced by the endothelial NO synthase (eNOS) is an antihypertensive, antithrombotic and anti-atherosclerotic molecule.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	59-63
23395155-4	2013	NADPH oxidase-mediated oxidative stress leads to oxidation of tetrahydrobiopterin (BH4), the essential cofactor of eNOS.	sapropterin	62-81	nitric oxide synthase 3	Homo sapiens	115-119
23395155-4	2013	NADPH oxidase-mediated oxidative stress leads to oxidation of tetrahydrobiopterin (BH4), the essential cofactor of eNOS.	sapropterin	83-86	nitric oxide synthase 3	Homo sapiens	115-119
23395155-5	2013	In BH4 deficiency, oxygen reduction uncouples from NO synthesis, thereby converting eNOS to a superoxide-producing enzyme.	Oxygen	19-25	nitric oxide synthase 3	Homo sapiens	84-88
23395155-5	2013	In BH4 deficiency, oxygen reduction uncouples from NO synthesis, thereby converting eNOS to a superoxide-producing enzyme.	Superoxides	94-104	nitric oxide synthase 3	Homo sapiens	84-88
23395155-8	2013	Angiotensin-converting enzyme inhibitors, AT1 receptor blockers, statins, nebivolol and resveratrol have been shown to reverse eNOS uncoupling and to stimulate eNOS activity concurrently.	Nebivolol	74-83	nitric oxide synthase 3	Homo sapiens	127-131
23395155-8	2013	Angiotensin-converting enzyme inhibitors, AT1 receptor blockers, statins, nebivolol and resveratrol have been shown to reverse eNOS uncoupling and to stimulate eNOS activity concurrently.	Nebivolol	74-83	nitric oxide synthase 3	Homo sapiens	160-164
23395155-8	2013	Angiotensin-converting enzyme inhibitors, AT1 receptor blockers, statins, nebivolol and resveratrol have been shown to reverse eNOS uncoupling and to stimulate eNOS activity concurrently.	Resveratrol	88-99	nitric oxide synthase 3	Homo sapiens	127-131
23395155-8	2013	Angiotensin-converting enzyme inhibitors, AT1 receptor blockers, statins, nebivolol and resveratrol have been shown to reverse eNOS uncoupling and to stimulate eNOS activity concurrently.	Resveratrol	88-99	nitric oxide synthase 3	Homo sapiens	160-164
23269619-6	2013	Hypertension, diabetes, smoking, total cholesterol, triglycerides, LDLc, HDLc and TT genotype of the eNOS gene were independent risk factors for the development of PCAD.	Cholesterol	39-50	nitric oxide synthase 3	Homo sapiens	101-105
23269619-6	2013	Hypertension, diabetes, smoking, total cholesterol, triglycerides, LDLc, HDLc and TT genotype of the eNOS gene were independent risk factors for the development of PCAD.	Triglycerides	52-65	nitric oxide synthase 3	Homo sapiens	101-105
22064666-11	2013	Our findings show evidence that eNOS polymorphisms affect the responses of PED and clinical ED patients to sildenafil.	Sildenafil Citrate	107-117	nitric oxide synthase 3	Homo sapiens	32-36
23343509-7	2013	Palmitate-induced apoptosis stimulated cells to release NO and ROS, concomitant with upregulation of eNOS, which required activation of p38 MAPK and JNK.	Palmitates	0-9	nitric oxide synthase 3	Homo sapiens	101-105
23343509-11	2013	Our results support the notion that GLP1 receptor agonists restore eNOS-induced ROS production due to lipotoxicity and that such agonists protect against lipoapoptosis through PKA-PI3K/Akt-eNOS-p38 MAPK-JNK-dependent pathways via a GLP1 receptor-dependent mechanism.	ros	80-83	nitric oxide synthase 3	Homo sapiens	67-71
23455536-2	2013	Triiodothyronine was found to target endothelial nitric oxide synthase, which serves to enhance peripheral vascular relaxation by acting on vascular smooth muscle cells.	Triiodothyronine	0-16	nitric oxide synthase 3	Homo sapiens	37-70
23147264-2	2013	Controversial results regarding the association of eNOS gene variable number of tandem repeats (VNTR) polymorphism with IS have been reported by conventional PCR-polyacrylamide gel electrophoresis methods.	polyacrylamide	162-176	nitric oxide synthase 3	Homo sapiens	51-55
22064666-0	2013	Endothelial nitric oxide synthase genotypes and haplotypes modify the responses to sildenafil in patients with erectile dysfunction.	Sildenafil Citrate	83-93	nitric oxide synthase 3	Homo sapiens	0-33
22996620-4	2013	An increase in aglycone isoflavones in ethanol extracts from fermented soy milk stimulated NO production and endothelial NO synthase (eNOS) activity in human umbilical vein endothelial cells.	Ethanol	39-46	nitric oxide synthase 3	Homo sapiens	134-138
22996620-7	2013	Moreover, a small amount of O2- induced by water extracts from fermented soy milk at low concentration (1 mg mL-1) increased the content of calcium ions and activated eNOS, thereby promoting NO production and the coupling state of eNOS.	Superoxides	28-30	nitric oxide synthase 3	Homo sapiens	167-171
22996620-7	2013	Moreover, a small amount of O2- induced by water extracts from fermented soy milk at low concentration (1 mg mL-1) increased the content of calcium ions and activated eNOS, thereby promoting NO production and the coupling state of eNOS.	Superoxides	28-30	nitric oxide synthase 3	Homo sapiens	231-235
22996620-7	2013	Moreover, a small amount of O2- induced by water extracts from fermented soy milk at low concentration (1 mg mL-1) increased the content of calcium ions and activated eNOS, thereby promoting NO production and the coupling state of eNOS.	Water	43-48	nitric oxide synthase 3	Homo sapiens	167-171
22996620-7	2013	Moreover, a small amount of O2- induced by water extracts from fermented soy milk at low concentration (1 mg mL-1) increased the content of calcium ions and activated eNOS, thereby promoting NO production and the coupling state of eNOS.	Water	43-48	nitric oxide synthase 3	Homo sapiens	231-235
23202722-3	2013	TfR is regulated by both iron and nitric oxide (NO), the molecule produced by endothelial nitric oxide synthase (eNOS).	Nitric Oxide	34-46	nitric oxide synthase 3	Homo sapiens	78-111
23190749-5	2013	Furthermore, we investigated the biomodulation of insulin signaling by kakkalide along the insulin receptor substrate (IRS)-1/Akt/endothelial nitric oxide synthase (eNOS) pathway.	kakkalide	71-80	nitric oxide synthase 3	Homo sapiens	130-163
23255608-0	2013	Asymmetric dimethylarginine induces endothelial nitric-oxide synthase mitochondrial redistribution through the nitration-mediated activation of Akt1.	dimethylarginine	11-27	nitric oxide synthase 3	Homo sapiens	36-69
23255608-1	2013	We have recently demonstrated that asymmetric dimethylarginine (ADMA) induces the translocation of endothelial nitric-oxide synthase (eNOS) to the mitochondrion via a mechanism that requires protein nitration.	dimethylarginine	46-62	nitric oxide synthase 3	Homo sapiens	99-132
23255608-1	2013	We have recently demonstrated that asymmetric dimethylarginine (ADMA) induces the translocation of endothelial nitric-oxide synthase (eNOS) to the mitochondrion via a mechanism that requires protein nitration.	N,N-dimethylarginine	64-68	nitric oxide synthase 3	Homo sapiens	99-132
23202722-3	2013	TfR is regulated by both iron and nitric oxide (NO), the molecule produced by endothelial nitric oxide synthase (eNOS).	Iron	25-29	nitric oxide synthase 3	Homo sapiens	78-111
23255592-0	2013	Endothelial nitric-oxide synthase activation generates an inducible nitric-oxide synthase-like output of nitric oxide in inflamed endothelium.	Nitric Oxide	105-117	nitric oxide synthase 3	Homo sapiens	0-33
23030042-10	2013	As a result, we have developed aminopyridine compounds that are 3800-fold more selective for nNOS than eNOS, some of which show excellent neuroprotective effects in animal models.	Aminopyridines	31-44	nitric oxide synthase 3	Homo sapiens	103-107
23030042-12	2013	Initial crystal structures of nNOS and eNOS bound to selective dipeptide inhibitors showed that a single amino acid difference (Asp in nNOS and Asn in eNOS) results in much tighter binding to nNOS.	Dipeptides	63-72	nitric oxide synthase 3	Homo sapiens	39-43
23030042-12	2013	Initial crystal structures of nNOS and eNOS bound to selective dipeptide inhibitors showed that a single amino acid difference (Asp in nNOS and Asn in eNOS) results in much tighter binding to nNOS.	Dipeptides	63-72	nitric oxide synthase 3	Homo sapiens	151-155
23030042-12	2013	Initial crystal structures of nNOS and eNOS bound to selective dipeptide inhibitors showed that a single amino acid difference (Asp in nNOS and Asn in eNOS) results in much tighter binding to nNOS.	Aspartic Acid	128-131	nitric oxide synthase 3	Homo sapiens	39-43
23030042-12	2013	Initial crystal structures of nNOS and eNOS bound to selective dipeptide inhibitors showed that a single amino acid difference (Asp in nNOS and Asn in eNOS) results in much tighter binding to nNOS.	Aspartic Acid	128-131	nitric oxide synthase 3	Homo sapiens	151-155
23030042-12	2013	Initial crystal structures of nNOS and eNOS bound to selective dipeptide inhibitors showed that a single amino acid difference (Asp in nNOS and Asn in eNOS) results in much tighter binding to nNOS.	Asparagine	144-147	nitric oxide synthase 3	Homo sapiens	39-43
23030042-12	2013	Initial crystal structures of nNOS and eNOS bound to selective dipeptide inhibitors showed that a single amino acid difference (Asp in nNOS and Asn in eNOS) results in much tighter binding to nNOS.	Asparagine	144-147	nitric oxide synthase 3	Homo sapiens	151-155
23512673-1	2013	The endothelial nitric oxide synthase (eNOS) plays an important homeostatic role in the cardiovascular system (CVS) by maintaining appropriate blood pressure through production of nitric oxide.	Nitric Oxide	16-28	nitric oxide synthase 3	Homo sapiens	39-43
23341020-12	2013	Endothelial nitric oxide synthase (eNOS) phosphorylation via the cAMP/PKA and AMPK pathways and consequent activation of the soluble guanylyl cyclase/cyclic guanosine monophosphate pathway might play an important role in cilostazol-induced vasodilation of the retinal arterioles.	Cyclic AMP	65-69	nitric oxide synthase 3	Homo sapiens	0-33
23341020-12	2013	Endothelial nitric oxide synthase (eNOS) phosphorylation via the cAMP/PKA and AMPK pathways and consequent activation of the soluble guanylyl cyclase/cyclic guanosine monophosphate pathway might play an important role in cilostazol-induced vasodilation of the retinal arterioles.	Cyclic GMP	150-180	nitric oxide synthase 3	Homo sapiens	0-33
23341020-12	2013	Endothelial nitric oxide synthase (eNOS) phosphorylation via the cAMP/PKA and AMPK pathways and consequent activation of the soluble guanylyl cyclase/cyclic guanosine monophosphate pathway might play an important role in cilostazol-induced vasodilation of the retinal arterioles.	Cilostazol	221-231	nitric oxide synthase 3	Homo sapiens	0-33
22861189-7	2013	The supplementation with hydrogen peroxide (H(2)O(2)) increased NOS-3 activity and cell death in 4TO-NOS cells.	Hydrogen Peroxide	25-42	nitric oxide synthase 3	Homo sapiens	64-69
22861189-7	2013	The supplementation with hydrogen peroxide (H(2)O(2)) increased NOS-3 activity and cell death in 4TO-NOS cells.	Hydrogen Peroxide	44-53	nitric oxide synthase 3	Homo sapiens	64-69
23255592-3	2013	In inflamed HLMVEC (pretreated with interleukin-1beta and interferon-gamma), we found enhanced binding of eNOS to calcium-calmodulin at basal Ca(2+) levels, thereby increasing its basal activity that was dependent on extracellular l-Arg.	Arginine	231-236	nitric oxide synthase 3	Homo sapiens	106-110
23255592-7	2013	BK induced Ca(2+)-dependent eNOS phosphorylation at Ser(1177), Thr(495), and Ser(114) in cytokine-treated HLMVEC, but these modifications were not dependent on JNK1/2 activation and were not responsible for prolonged NO output.	Serine	52-55	nitric oxide synthase 3	Homo sapiens	28-32
22706620-0	2013	eNOS and BDKRB2 genotypes affect the antihypertensive responses to enalapril.	Enalapril	67-76	nitric oxide synthase 3	Homo sapiens	0-4
23457905-5	2013	Agarose gel electrophoresis was used to identify eNOS gene polymorphisms.	Sepharose	0-7	nitric oxide synthase 3	Homo sapiens	49-53
22052036-2	2013	There is evidence that such changes relate to nitric oxide (NO) bioavailability, an endothelial compound produced by the action of endothelial NO synthase (eNOS), and is regulated by sirtuin-1 (Sirt1), a NAD(+)-dependent protein deacetylase.	Nitric Oxide	46-58	nitric oxide synthase 3	Homo sapiens	156-160
23213194-0	2013	Aldosterone modulates endothelial permeability and endothelial nitric oxide synthase activity by rearrangement of the actin cytoskeleton.	Aldosterone	0-11	nitric oxide synthase 3	Homo sapiens	51-84
23213194-7	2013	Moreover, Aldo-induced cytoskeletal rearrangement led to rapid dephosphorylation of protein kinase B and subsequent deactivation of endothelial nitric oxide synthase.	Aldosterone	10-14	nitric oxide synthase 3	Homo sapiens	132-165
22706620-2	2013	It is possible that functional polymorphisms in endothelial nitric oxide synthase (eNOS) and bradykinin receptor B2 (BDKRB2) genes may affect the antihypertensive response to enalapril.	Enalapril	175-184	nitric oxide synthase 3	Homo sapiens	48-81
22706620-2	2013	It is possible that functional polymorphisms in endothelial nitric oxide synthase (eNOS) and bradykinin receptor B2 (BDKRB2) genes may affect the antihypertensive response to enalapril.	Enalapril	175-184	nitric oxide synthase 3	Homo sapiens	83-87
22706620-12	2013	However, we found significant gene-gene interactions: the CC genotype for the BDKRB2 C(-58)T polymorphism was associated with response to enalapril depending on eNOS T(-786)C genotypes.	Enalapril	138-147	nitric oxide synthase 3	Homo sapiens	161-165
22706620-13	2013	CONCLUSIONS: These findings suggest that eNOS T(-786)C and BDKRB2 C(-58)T polymorphisms may synergically affect the antihypertensive response to enalapril.	Enalapril	145-154	nitric oxide synthase 3	Homo sapiens	41-45
23671992-3	2013	20-HETE exerted oxidative stress and pro-inflammation effect through nicotinamide adenine dinucleotide phosphate (NADPH) oxidase system and nuclear factor-kappaB (NF-kappaB) pathway; it took part in the modulation of vascular dilation and constriction by mediating dissociation of endothelial nitric oxide synthase (eNOS) and inducing angiotensin converting enzyme in EC; it also promoted the proliferation of EC and angiogenesis.	20-hydroxy-5,8,11,14-eicosatetraenoic acid	0-7	nitric oxide synthase 3	Homo sapiens	281-314
23176758-1	2013	OBJECTIVES: The aim of our study was to investigate whether the endothelial nitric oxide synthase (eNOS) gene polymorphisms -786T>C, 4a4b, and 894G>T that affect nitric oxide (NO) generation confer a risk for primary ovarian insufficiency (POI) in Korean women.	Nitric Oxide	76-88	nitric oxide synthase 3	Homo sapiens	99-103
23104077-1	2013	(-)-Epigallocatechin-3-O-gallate (EGCg) has been shown to induce endothelium-dependent nitric oxide (NO)-mediated relaxation via the redox-sensitive Src/PI3-kinase/Akt-dependent phosphorylation of endothelial NO synthase (eNOS).	epigallocatechin gallate	0-32	nitric oxide synthase 3	Homo sapiens	222-226
23104077-1	2013	(-)-Epigallocatechin-3-O-gallate (EGCg) has been shown to induce endothelium-dependent nitric oxide (NO)-mediated relaxation via the redox-sensitive Src/PI3-kinase/Akt-dependent phosphorylation of endothelial NO synthase (eNOS).	epigallocatechin gallate	34-38	nitric oxide synthase 3	Homo sapiens	222-226
23104077-1	2013	(-)-Epigallocatechin-3-O-gallate (EGCg) has been shown to induce endothelium-dependent nitric oxide (NO)-mediated relaxation via the redox-sensitive Src/PI3-kinase/Akt-dependent phosphorylation of endothelial NO synthase (eNOS).	Nitric Oxide	87-99	nitric oxide synthase 3	Homo sapiens	222-226
23104077-2	2013	Although the presence of 8 hydroxyl functions, mainly on B and D rings, is essential for the EGCg-induced activation of eNOS, the relative role of each individual hydroxyl function still remains unclear.	epigallocatechin gallate	93-97	nitric oxide synthase 3	Homo sapiens	120-124
23104077-3	2013	This study examined the effect of selective replacement of hydroxyl functions by methoxy moieties on either the B or D ring on the EGCg-induced phosphorylation of Akt and eNOS, formation of reactive oxygen species (ROS) and NO in cultured coronary artery endothelial cells, and endothelium-dependent relaxation of coronary artery rings.	epigallocatechin gallate	131-135	nitric oxide synthase 3	Homo sapiens	171-175
23104077-5	2013	In contrast, the single methylation at position 3"" and the double methylation at both positions 3" and 4" reduced markedly the phosphorylation of Akt and eNOS, the formation of ROS and NO in endothelial cells and the relaxation of artery rings.	Reactive Oxygen Species	178-181	nitric oxide synthase 3	Homo sapiens	155-159
23104077-6	2013	These findings suggest that the hydroxyl group at the 3"" position of the gallate ring is essential and, also, to some extent, the two hydroxyl groups at positions 3" and 4", for the EGCg-induced redox-sensitive activation of eNOS leading to the subsequent NO-mediated vascular relaxation.	Gallic acid	74-81	nitric oxide synthase 3	Homo sapiens	226-230
23104077-6	2013	These findings suggest that the hydroxyl group at the 3"" position of the gallate ring is essential and, also, to some extent, the two hydroxyl groups at positions 3" and 4", for the EGCg-induced redox-sensitive activation of eNOS leading to the subsequent NO-mediated vascular relaxation.	epigallocatechin gallate	183-187	nitric oxide synthase 3	Homo sapiens	226-230
23072587-2	2013	3,5,3"-triiodothyronine (T(3)), the active form of TH, induces the activation of endothelial nitric oxide synthase via PI3K/AKT non-genomic signaling.	Triiodothyronine	0-23	nitric oxide synthase 3	Homo sapiens	81-114
23072587-2	2013	3,5,3"-triiodothyronine (T(3)), the active form of TH, induces the activation of endothelial nitric oxide synthase via PI3K/AKT non-genomic signaling.	Triiodothyronine	25-29	nitric oxide synthase 3	Homo sapiens	81-114
23099643-8	2013	Western blot and immunohistochemistry analysis showed that both NOX4 and endothelial nitric oxide synthase (eNOS) are expressed in smooth muscle layer of DFA.	Diphenylamine	154-157	nitric oxide synthase 3	Homo sapiens	73-106
23148920-0	2013	Hydrogen sulfide increases nitric oxide production with calcium-dependent activation of endothelial nitric oxide synthase in endothelial cells.	Hydrogen Sulfide	0-16	nitric oxide synthase 3	Homo sapiens	88-121
23148920-0	2013	Hydrogen sulfide increases nitric oxide production with calcium-dependent activation of endothelial nitric oxide synthase in endothelial cells.	Nitric Oxide	27-39	nitric oxide synthase 3	Homo sapiens	88-121
23148920-0	2013	Hydrogen sulfide increases nitric oxide production with calcium-dependent activation of endothelial nitric oxide synthase in endothelial cells.	Calcium	56-63	nitric oxide synthase 3	Homo sapiens	88-121
23148920-4	2013	We investigated whether H(2)S directly regulates endothelial NO synthase (eNOS) activity and NO production in endothelial cells.	Hydrogen Sulfide	24-29	nitric oxide synthase 3	Homo sapiens	74-78
23148920-8	2013	NaHS significantly increased intracellular calcium concentrations, and this effect was attenuated by dantrolene or xestospongin C. NaHS induced phosphorylation of eNOS at the activating phosphoserine residue 1179.	sodium bisulfide	0-4	nitric oxide synthase 3	Homo sapiens	163-167
23148920-8	2013	NaHS significantly increased intracellular calcium concentrations, and this effect was attenuated by dantrolene or xestospongin C. NaHS induced phosphorylation of eNOS at the activating phosphoserine residue 1179.	Calcium	43-50	nitric oxide synthase 3	Homo sapiens	163-167
23148920-8	2013	NaHS significantly increased intracellular calcium concentrations, and this effect was attenuated by dantrolene or xestospongin C. NaHS induced phosphorylation of eNOS at the activating phosphoserine residue 1179.	Dantrolene	101-111	nitric oxide synthase 3	Homo sapiens	163-167
23246837-0	2013	Effect of long-term piceatannol treatment on eNOS levels in cultured endothelial cells.	3,3',4,5'-tetrahydroxystilbene	20-31	nitric oxide synthase 3	Homo sapiens	45-49
23246837-3	2013	It was suggested that endothelial NO synthase (eNOS) might be involved in piceatannol-induced acute vasorelaxation.	3,3',4,5'-tetrahydroxystilbene	74-85	nitric oxide synthase 3	Homo sapiens	22-45
23246837-3	2013	It was suggested that endothelial NO synthase (eNOS) might be involved in piceatannol-induced acute vasorelaxation.	3,3',4,5'-tetrahydroxystilbene	74-85	nitric oxide synthase 3	Homo sapiens	47-51
23246837-4	2013	Here, we investigated the expression of eNOS in EA.hy926 human umbilical vein cells after long-term treatment with piceatannol, and compared this effect with that of resveratrol, an analog of piceatannol.	3,3',4,5'-tetrahydroxystilbene	115-126	nitric oxide synthase 3	Homo sapiens	40-44
23246837-5	2013	Long-term treatment with piceatannol up-regulated eNOS mRNA expression and increased eNOS protein expression in a dose-dependent manner.	3,3',4,5'-tetrahydroxystilbene	25-36	nitric oxide synthase 3	Homo sapiens	50-54
23246837-5	2013	Long-term treatment with piceatannol up-regulated eNOS mRNA expression and increased eNOS protein expression in a dose-dependent manner.	3,3',4,5'-tetrahydroxystilbene	25-36	nitric oxide synthase 3	Homo sapiens	85-89
23246837-6	2013	Moreover, piceatannol increased the levels of phosphorylated eNOS.	3,3',4,5'-tetrahydroxystilbene	10-21	nitric oxide synthase 3	Homo sapiens	61-65
23246837-7	2013	Treatment with resveratrol also increased eNOS expression, but to a lesser degree than piceatannol.	Resveratrol	15-26	nitric oxide synthase 3	Homo sapiens	42-46
23246837-8	2013	These findings indicate that piceatannol may improve vascular function by up-regulating eNOS expression.	3,3',4,5'-tetrahydroxystilbene	29-40	nitric oxide synthase 3	Homo sapiens	88-92
23139420-0	2013	Integrated redox sensor and effector functions for tetrahydrobiopterin- and glutathionylation-dependent endothelial nitric-oxide synthase uncoupling.	sapropterin	51-70	nitric oxide synthase 3	Homo sapiens	104-137
23139420-1	2013	Endothelial nitric-oxide synthase (eNOS) is a critical regulator of vascular homeostasis by generation of NO that is dependent on the cofactor tetrahydrobiopterin (BH4).	sapropterin	143-162	nitric oxide synthase 3	Homo sapiens	0-33
23139420-1	2013	Endothelial nitric-oxide synthase (eNOS) is a critical regulator of vascular homeostasis by generation of NO that is dependent on the cofactor tetrahydrobiopterin (BH4).	sapropterin	164-167	nitric oxide synthase 3	Homo sapiens	0-33
23148920-8	2013	NaHS significantly increased intracellular calcium concentrations, and this effect was attenuated by dantrolene or xestospongin C. NaHS induced phosphorylation of eNOS at the activating phosphoserine residue 1179.	xestospongin C	115-127	nitric oxide synthase 3	Homo sapiens	163-167
23148920-8	2013	NaHS significantly increased intracellular calcium concentrations, and this effect was attenuated by dantrolene or xestospongin C. NaHS induced phosphorylation of eNOS at the activating phosphoserine residue 1179.	sodium bisulfide	131-135	nitric oxide synthase 3	Homo sapiens	163-167
23148920-8	2013	NaHS significantly increased intracellular calcium concentrations, and this effect was attenuated by dantrolene or xestospongin C. NaHS induced phosphorylation of eNOS at the activating phosphoserine residue 1179.	Phosphoserine	186-199	nitric oxide synthase 3	Homo sapiens	163-167
23148920-9	2013	The NaHS-induced eNOS phosphorylation and NO production were not affected by a PI3K/Akt inhibitor (wortmannin).	sodium bisulfide	4-8	nitric oxide synthase 3	Homo sapiens	17-21
23148920-10	2013	The data of this study suggest that H(2)S directly acts on endothelial cells to induce eNOS activation and NO production by releasing calcium from the intracellular store in endoplasmic reticulum, which may explain one of mechanisms of its vasodilator function.	Hydrogen Sulfide	36-41	nitric oxide synthase 3	Homo sapiens	87-91
23148920-10	2013	The data of this study suggest that H(2)S directly acts on endothelial cells to induce eNOS activation and NO production by releasing calcium from the intracellular store in endoplasmic reticulum, which may explain one of mechanisms of its vasodilator function.	Calcium	134-141	nitric oxide synthase 3	Homo sapiens	87-91
23069892-0	2013	Effects of endothelial nitric oxide synthase tagSNPs haplotypes on nitrite levels in black subjects.	Nitrites	67-74	nitric oxide synthase 3	Homo sapiens	11-44
23069892-1	2013	Haplotypes formed by clinically relevant polymorphisms in the endothelial nitric oxide synthase (eNOS) gene have been associated with variations in endogenous nitric oxide (NO) formation in white and black subjects.	Nitric Oxide	74-86	nitric oxide synthase 3	Homo sapiens	97-101
23069892-5	2013	These findings suggest that these tagSNPs of the eNOS gene and haplotypes are associated with low levels of nitric oxide production in blacks, and could be used as a marker of cardiovascular risk.	Nitric Oxide	108-120	nitric oxide synthase 3	Homo sapiens	49-53
23099643-8	2013	Western blot and immunohistochemistry analysis showed that both NOX4 and endothelial nitric oxide synthase (eNOS) are expressed in smooth muscle layer of DFA.	Diphenylamine	154-157	nitric oxide synthase 3	Homo sapiens	108-112
23099643-10	2013	From the pharmacological data, as a mechanism for HVC(DFA), we suggest hypoxic inhibition of eNOS in myocytes.	Diphenylamine	54-57	nitric oxide synthase 3	Homo sapiens	93-97
24350275-3	2013	The effect of ropivacaine on endothelial nitric oxide synthase (eNOS) phosphorylation in human umbilical vein endothelial cells was examined by western blotting.	Ropivacaine	14-25	nitric oxide synthase 3	Homo sapiens	29-62
23644848-1	2013	OBJECTIVE: Nitric oxide is produced by endothelial nitric oxide synthase, and its production can be influenced by polymorphisms of the endothelial nitric oxide synthase gene.	Nitric Oxide	11-23	nitric oxide synthase 3	Homo sapiens	39-72
23164986-3	2013	This review will focus on the eNOS substrate (L-arginine), its cofactor (tetrahydrobiopterin), and mechanisms related to the uncoupling of eNOS activity.	Arginine	46-56	nitric oxide synthase 3	Homo sapiens	30-34
23164986-4	2013	RECENT FINDINGS: The global arginine bioavailability ratio has been proposed as a biomarker reflective of L-arginine availability, arginase activity, and citrulline cycling, as all of these processes impact eNOS activity.	Arginine	28-36	nitric oxide synthase 3	Homo sapiens	207-211
23164986-6	2013	Identification of transporters for biopterin species as well as signals that regulate endogenous arginine production have provided insight for alternative strategies to raise endothelial tetrahydrobiopterin levels while reducing dihydrobiopterin and alter eNOS activity.	Biopterin	35-44	nitric oxide synthase 3	Homo sapiens	256-260
23164986-6	2013	Identification of transporters for biopterin species as well as signals that regulate endogenous arginine production have provided insight for alternative strategies to raise endothelial tetrahydrobiopterin levels while reducing dihydrobiopterin and alter eNOS activity.	Arginine	97-105	nitric oxide synthase 3	Homo sapiens	256-260
23517789-6	2013	CONCLUSIONS: Our results support the idea that, the eNOS E298D polymorphism, which is not associated with hypertension, may increase the risk of hypertension when associated with high serum total-cholesterol levels.	Cholesterol	196-207	nitric oxide synthase 3	Homo sapiens	52-56
23204109-5	2013	Unexpectedly, we observed 1.7-fold higher basal endothelial nitric oxide synthase (eNOS) phosphorylation at serine 1177 in patients with diabetes mellitus (P=0.007) without a difference in total eNOS expression.	Serine	108-114	nitric oxide synthase 3	Homo sapiens	48-81
23448493-7	2013	Moreover levels of asymmetrical dimethyl-L-arginine (ADMA), an endogenous inhibitor of endothelial nitric oxide synthase (eNOS), are elevated in obesity.	N,N-dimethylarginine	32-51	nitric oxide synthase 3	Homo sapiens	87-120
23448493-7	2013	Moreover levels of asymmetrical dimethyl-L-arginine (ADMA), an endogenous inhibitor of endothelial nitric oxide synthase (eNOS), are elevated in obesity.	N,N-dimethylarginine	53-57	nitric oxide synthase 3	Homo sapiens	87-120
23594558-1	2013	BACKGROUND: Endothelial nitric oxide synthase (eNOS) as well as nitric oxide play an important role in the regulation of cardiovascular function.	Nitric Oxide	24-36	nitric oxide synthase 3	Homo sapiens	47-51
23644848-1	2013	OBJECTIVE: Nitric oxide is produced by endothelial nitric oxide synthase, and its production can be influenced by polymorphisms of the endothelial nitric oxide synthase gene.	Nitric Oxide	11-23	nitric oxide synthase 3	Homo sapiens	135-168
23644848-2	2013	Because candidate genes responsible for susceptibility to ankylosing spondylitis are mostly unknown and available data suggest that there may be problems related to the nitric oxide pathway, such as endothelial dysfunction and increased asymmetric dimethylarginine, this study aimed to assess the association of common endothelial nitric oxide synthase gene polymorphisms with ankylosing spondylitis.	Nitric Oxide	169-181	nitric oxide synthase 3	Homo sapiens	319-352
23276910-2	2013	In this study we examined the association between AMD risk and polymorphisms of genes encoding enzymes involved in the generation and removal of iron-mediated oxidation: NQO1 (609C> T, rs1800566), NOS3 (894G>T, rs1799983) and NFE2L2 (28312647A>G, rs6726395).	Iron	145-149	nitric oxide synthase 3	Homo sapiens	200-204
23543259-0	2013	Effect of eNOS polymorphisms on salbutamol evoked endothelium dependent vasodilation in South Indian healthy subjects.	Albuterol	32-42	nitric oxide synthase 3	Homo sapiens	10-14
24605586-3	2013	Two single nucleotide polymorphisms--MMP9 (C(-1562) --> T) and NOS3 (Glu298 --> Asp)--rs3918242 and rs1799983--were shown to represent the main independent effects with the highest predictive potential (77.1% as indicated by binary logistic regression and 74.6% testing accuracy shown by Multifactorial Dimensionality Reduction).	Aspartic Acid	86-89	nitric oxide synthase 3	Homo sapiens	66-70
24605586-4	2013	MMP9 (C(-1562 --> T) and NOS3 (Glu298 --> Asp) potentially may be used to create predictive algorithm for determination of predisposition to arterial hypertension in children.	Aspartic Acid	48-51	nitric oxide synthase 3	Homo sapiens	28-32
23400313-1	2013	Nitric oxide (NO) is highly reactive, produced in endothelial cells by endothelial NO synthase (eNOS) and has been implicated in sickle cell pathophysiology.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	96-100
24092346-10	2013	Enzymatic sources of ROS in PH that have been identified include the NAPDPH oxidases 1, 2, and 4, xanthine oxidase, uncoupled eNOS, and complex III of the mitochondrial electron transport chain.	ros	21-24	nitric oxide synthase 3	Homo sapiens	126-130
23543259-2	2013	Endothelial nitric oxide synthase (eNOS) gene polymorphism may influence the response to salbutamol in healthy subjects.	Albuterol	89-99	nitric oxide synthase 3	Homo sapiens	0-33
23543259-2	2013	Endothelial nitric oxide synthase (eNOS) gene polymorphism may influence the response to salbutamol in healthy subjects.	Albuterol	89-99	nitric oxide synthase 3	Homo sapiens	35-39
23457308-0	2013	Ceramide mediates inhibition of the Akt/eNOS pathway by high levels of glucose in human vascular endothelial cells.	Ceramides	0-8	nitric oxide synthase 3	Homo sapiens	40-44
23258079-8	2013	In addition, cells transfected with the reporter gene driven by the eNOS promoter fragment starting from position -740 exhibited a pitavastatin-induced increase of luciferase activity, which was not observed in cells transfected with the reporter gene driven by the fragment starting from -727.	pitavastatin	131-143	nitric oxide synthase 3	Homo sapiens	68-72
23457308-0	2013	Ceramide mediates inhibition of the Akt/eNOS pathway by high levels of glucose in human vascular endothelial cells.	Glucose	71-78	nitric oxide synthase 3	Homo sapiens	40-44
23457308-1	2013	OBJECTIVE: To investigate how ceramide mediates the effects of high-glucose-induced inhibition of the Akt/endothelial nitric oxide synthase (eNOS) signalling pathway in human vascular endothelial cells (HUVECs).	Ceramides	30-38	nitric oxide synthase 3	Homo sapiens	106-139
23457308-1	2013	OBJECTIVE: To investigate how ceramide mediates the effects of high-glucose-induced inhibition of the Akt/endothelial nitric oxide synthase (eNOS) signalling pathway in human vascular endothelial cells (HUVECs).	Ceramides	30-38	nitric oxide synthase 3	Homo sapiens	141-145
23457308-1	2013	OBJECTIVE: To investigate how ceramide mediates the effects of high-glucose-induced inhibition of the Akt/endothelial nitric oxide synthase (eNOS) signalling pathway in human vascular endothelial cells (HUVECs).	Glucose	68-75	nitric oxide synthase 3	Homo sapiens	106-139
23457308-1	2013	OBJECTIVE: To investigate how ceramide mediates the effects of high-glucose-induced inhibition of the Akt/endothelial nitric oxide synthase (eNOS) signalling pathway in human vascular endothelial cells (HUVECs).	Glucose	68-75	nitric oxide synthase 3	Homo sapiens	141-145
23457308-6	2013	We also show that exposure of HUVECs to high-glucose conditions inhibits the insulin-mediated activation of Akt/eNOS signalling and the subsequent NO generation in a dose-dependent manner (p<0.05).	Glucose	45-52	nitric oxide synthase 3	Homo sapiens	112-116
23457308-7	2013	Preventing de novo ceramide synthesis attenuated the antagonistic effects of high-glucose levels on the Akt/eNOS signalling pathway (p<0.05); conversely, inducing ceramide build-up augmented the inhibitory effects of high-glucose levels on the Akt/eNOS signalling pathway (p<0.05).	Ceramides	19-27	nitric oxide synthase 3	Homo sapiens	108-112
23457308-7	2013	Preventing de novo ceramide synthesis attenuated the antagonistic effects of high-glucose levels on the Akt/eNOS signalling pathway (p<0.05); conversely, inducing ceramide build-up augmented the inhibitory effects of high-glucose levels on the Akt/eNOS signalling pathway (p<0.05).	Ceramides	19-27	nitric oxide synthase 3	Homo sapiens	251-255
23457308-7	2013	Preventing de novo ceramide synthesis attenuated the antagonistic effects of high-glucose levels on the Akt/eNOS signalling pathway (p<0.05); conversely, inducing ceramide build-up augmented the inhibitory effects of high-glucose levels on the Akt/eNOS signalling pathway (p<0.05).	Glucose	82-89	nitric oxide synthase 3	Homo sapiens	108-112
23457308-8	2013	CONCLUSION: Ceramide is both necessary and sufficient for mediating the inhibition of the Akt/eNOS signalling pathway by high-glucose levels in endothelial cells.	Ceramides	12-20	nitric oxide synthase 3	Homo sapiens	94-98
23457308-8	2013	CONCLUSION: Ceramide is both necessary and sufficient for mediating the inhibition of the Akt/eNOS signalling pathway by high-glucose levels in endothelial cells.	Glucose	126-133	nitric oxide synthase 3	Homo sapiens	94-98
23734045-10	2013	DHT treatment (compared with placebo) induced i) a significant decrease in acetylcholine-induced aortic relaxations, with no change in calcitonin gene related peptide- or sodium nitroprusside-induced relaxations, as well as 5-hydroxytryptamine-induced contractions; ii) no change in eNOS expression/phosphorylation in lungs or in plasma ADMA levels; and iii) a twofold increase in aortic AR expression.	Dihydrotestosterone	0-3	nitric oxide synthase 3	Homo sapiens	283-287
24385682-0	2013	Berberine protects against palmitate-induced endothelial dysfunction: involvements of upregulation of AMPK and eNOS and downregulation of NOX4.	Berberine	0-9	nitric oxide synthase 3	Homo sapiens	111-115
24385682-0	2013	Berberine protects against palmitate-induced endothelial dysfunction: involvements of upregulation of AMPK and eNOS and downregulation of NOX4.	Palmitates	27-36	nitric oxide synthase 3	Homo sapiens	111-115
24008236-0	2013	Endothelial nitric oxide synthase phosphorylation at Threonine 495 and mitochondrial reactive oxygen species formation in response to a high H2O2 concentration.	Threonine	53-62	nitric oxide synthase 3	Homo sapiens	0-33
24008236-0	2013	Endothelial nitric oxide synthase phosphorylation at Threonine 495 and mitochondrial reactive oxygen species formation in response to a high H2O2 concentration.	Reactive Oxygen Species	85-108	nitric oxide synthase 3	Homo sapiens	0-33
24008236-0	2013	Endothelial nitric oxide synthase phosphorylation at Threonine 495 and mitochondrial reactive oxygen species formation in response to a high H2O2 concentration.	Hydrogen Peroxide	141-145	nitric oxide synthase 3	Homo sapiens	0-33
24008236-2	2013	We investigated cellular pathways involved in endothelial nitric oxide synthase (eNOS) phosphorylation at Threonine 495 (Thr(495)) in human umbilical vein endothelial cells (HUVECs) exposed to H2O2.	Threonine	106-115	nitric oxide synthase 3	Homo sapiens	46-79
24008236-2	2013	We investigated cellular pathways involved in endothelial nitric oxide synthase (eNOS) phosphorylation at Threonine 495 (Thr(495)) in human umbilical vein endothelial cells (HUVECs) exposed to H2O2.	Threonine	106-109	nitric oxide synthase 3	Homo sapiens	46-79
24008236-2	2013	We investigated cellular pathways involved in endothelial nitric oxide synthase (eNOS) phosphorylation at Threonine 495 (Thr(495)) in human umbilical vein endothelial cells (HUVECs) exposed to H2O2.	Hydrogen Peroxide	193-197	nitric oxide synthase 3	Homo sapiens	46-79
24385682-9	2013	The expressions of eNOS were significantly increased, while NOX4 protein expression was decreased in berberine-treated HUVECs.	Berberine	101-110	nitric oxide synthase 3	Homo sapiens	19-23
22691914-1	2013	Polymorphisms in the endothelial nitric oxide synthase (eNOS) gene reduce shear stress-induced nitric oxide production.	Nitric Oxide	33-45	nitric oxide synthase 3	Homo sapiens	56-60
24385682-11	2013	Therefore, berberine ameliorates palmitate-induced endothelial dysfunction by upregulating eNOS expression and downregulating expression of NOX4.	Berberine	11-20	nitric oxide synthase 3	Homo sapiens	91-95
24385682-11	2013	Therefore, berberine ameliorates palmitate-induced endothelial dysfunction by upregulating eNOS expression and downregulating expression of NOX4.	Palmitates	33-42	nitric oxide synthase 3	Homo sapiens	91-95
23122700-1	2013	Placental vascular tone is critically influenced by nitric oxide (NO) derived from endothelial NO synthase (eNOS) activity.	Nitric Oxide	52-64	nitric oxide synthase 3	Homo sapiens	108-112
23122700-3	2013	Arginase-2 competes with eNOS for l-arginine and counteracts the NOS-dependent relaxation in umbilical vessels from normal pregnancies.	Arginine	34-44	nitric oxide synthase 3	Homo sapiens	25-29
23122700-11	2013	In IUGR-derived endothelium there was a generalized reduction in the in vitro eNOS activation (Ser(1177)-P-eNOS/eNOS), and therefore a decreased eNOS/arginase activity ratio.	Serine	95-98	nitric oxide synthase 3	Homo sapiens	78-82
23122700-11	2013	In IUGR-derived endothelium there was a generalized reduction in the in vitro eNOS activation (Ser(1177)-P-eNOS/eNOS), and therefore a decreased eNOS/arginase activity ratio.	Serine	95-98	nitric oxide synthase 3	Homo sapiens	107-111
23122700-11	2013	In IUGR-derived endothelium there was a generalized reduction in the in vitro eNOS activation (Ser(1177)-P-eNOS/eNOS), and therefore a decreased eNOS/arginase activity ratio.	Serine	95-98	nitric oxide synthase 3	Homo sapiens	107-111
23122700-11	2013	In IUGR-derived endothelium there was a generalized reduction in the in vitro eNOS activation (Ser(1177)-P-eNOS/eNOS), and therefore a decreased eNOS/arginase activity ratio.	Serine	95-98	nitric oxide synthase 3	Homo sapiens	107-111
23085930-2	2012	Genetic polymorphisms of eNOS gene have been suggested to play a role in nitric oxide (NO) abnormalities which may contribute to the development and progression of DR.	Nitric Oxide	73-85	nitric oxide synthase 3	Homo sapiens	25-29
23178275-8	2012	The phosphorylation of endothelial nitric oxide synthase (eNOS) and generation of nitric oxide (NO) were stimulated by CAL treatment in HUVECs and inhibited by treatment with L-NAME.	NG-Nitroarginine Methyl Ester	175-181	nitric oxide synthase 3	Homo sapiens	23-56
23063542-0	2012	Mechanism of reversal of high glucose-induced endothelial nitric oxide synthase uncoupling by tanshinone IIA in human endothelial cell line EA.hy926.	Glucose	30-37	nitric oxide synthase 3	Homo sapiens	46-79
23164599-0	2013	Derivation of endothelial cells from human embryonic stem cells in fully defined medium enables identification of lysophosphatidic acid and platelet activating factor as regulators of eNOS localization.	lysophosphatidic acid	114-135	nitric oxide synthase 3	Homo sapiens	184-188
23164599-6	2013	Further investigation revealed that that the serum-associated lipids, lysophosphatidic acid (LPA) and platelet activating factor (PAF), were the key molecules that affected eNOS localisation in hESC-ECs cultures.	lysophosphatidic acid	70-91	nitric oxide synthase 3	Homo sapiens	173-177
23164599-6	2013	Further investigation revealed that that the serum-associated lipids, lysophosphatidic acid (LPA) and platelet activating factor (PAF), were the key molecules that affected eNOS localisation in hESC-ECs cultures.	lysophosphatidic acid	93-96	nitric oxide synthase 3	Homo sapiens	173-177
22987726-2	2012	NO is synthesized from the amino acid L-arginine by nitric oxide synthases (NOS1, NOS2, and NOS3), which are encoded by separate genes and display different tissue distributions.	Arginine	38-48	nitric oxide synthase 3	Homo sapiens	92-96
22884597-2	2012	This less favorable outcome can be in part ascribed to impaired endothelium-derived nitric oxide (eNOS) production.	Nitric Oxide	84-96	nitric oxide synthase 3	Homo sapiens	98-102
22884597-11	2012	Nitric oxide-mediated vasomotor dynamics were consistent with reduced eNOS production.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	70-74
23230319-0	2012	Letter by Tsikas regarding article, "dietary nitrate ameliorates pulmonary hypertension: cytoprotective role for endothelial nitric oxide synthase and xanthine oxidoreductase".	Nitrates	45-52	nitric oxide synthase 3	Homo sapiens	113-146
23154675-4	2012	By genetic engineering of the nitric oxide synthase protein eNOS and insertion of light-oxygen-voltage (LOV) domains, we have created a photoactive version of the protein.	Nitric Oxide	30-42	nitric oxide synthase 3	Homo sapiens	60-64
23390838-7	2012	The Asp genome carriers with the NOS3 GLU298ASP GP were also shown to have significantly less re-PCI in contrast to the Glu/Glu genotype.	Glutamic Acid	120-123	nitric oxide synthase 3	Homo sapiens	33-37
23390838-7	2012	The Asp genome carriers with the NOS3 GLU298ASP GP were also shown to have significantly less re-PCI in contrast to the Glu/Glu genotype.	Glutamic Acid	124-127	nitric oxide synthase 3	Homo sapiens	33-37
23108655-0	2012	Fenofibrate improves vascular endothelial function by reducing oxidative stress while increasing endothelial nitric oxide synthase in healthy normolipidemic older adults.	Fenofibrate	0-11	nitric oxide synthase 3	Homo sapiens	97-130
23108655-9	2012	In vascular endothelial cells sampled from peripheral veins of the subjects, endothelial nitric oxide synthase protein expression was unchanged with placebo and after 2 days of fenofibrate, but was increased after 7 days of fenofibrate (0.54 +- 0.03 versus 2 days: 0.52 +- 0.04 and 7 days: 0.76 +- 0.11 intensity/human umbilical vein endothelial cell control; P<0.05, 7 days).	Fenofibrate	177-188	nitric oxide synthase 3	Homo sapiens	77-110
23108655-9	2012	In vascular endothelial cells sampled from peripheral veins of the subjects, endothelial nitric oxide synthase protein expression was unchanged with placebo and after 2 days of fenofibrate, but was increased after 7 days of fenofibrate (0.54 +- 0.03 versus 2 days: 0.52 +- 0.04 and 7 days: 0.76 +- 0.11 intensity/human umbilical vein endothelial cell control; P<0.05, 7 days).	Fenofibrate	224-235	nitric oxide synthase 3	Homo sapiens	77-110
23108655-10	2012	Short-term treatment with fenofibrate improves vascular endothelial function in healthy normolipidemic middle-aged and older adults by reducing oxidative stress and induces an increase in endothelial nitric oxide synthase.	Fenofibrate	26-37	nitric oxide synthase 3	Homo sapiens	188-221
23108656-1	2012	Nitric oxide generated by endothelial nitric oxide synthase (eNOS) plays an important role in maintaining cardiovascular homeostasis.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	26-59
23108656-1	2012	Nitric oxide generated by endothelial nitric oxide synthase (eNOS) plays an important role in maintaining cardiovascular homeostasis.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	61-65
23108656-10	2012	Moreover, we observed that simvastatin attenuated tumor necrosis factor-alpha-induced upregulation of miR-155 and ameliorated the effects of tumor necrosis factor-alpha on eNOS expression and endothelium-dependent vasodilation.	Simvastatin	27-38	nitric oxide synthase 3	Homo sapiens	172-176
22987726-4	2012	The results revealed a transient induction of NOS3 (known as the constitutively expressed endothelial nitric oxide synthase; eNOS) during the time course of the RA treatment.	Radium	161-163	nitric oxide synthase 3	Homo sapiens	46-50
22987726-4	2012	The results revealed a transient induction of NOS3 (known as the constitutively expressed endothelial nitric oxide synthase; eNOS) during the time course of the RA treatment.	Radium	161-163	nitric oxide synthase 3	Homo sapiens	90-123
22987726-6	2012	The subsequent analysis of cytosine methylation and histone H3 acetylation of the human NOS3 5" regulatory sequences indicated that epigenetic modifications, especially upstream of the proximal promoter (-734 to -989, relative to exon 2 TSS at +1), were also taking place.	Cytosine	27-35	nitric oxide synthase 3	Homo sapiens	88-92
23007404-5	2012	Using immunoprecipitation, ESI-MS/MS-based peptide sequencing and enzymatic assay we further demonstrate that human RBCs contain an endothelial NOS (eNOS) that converts L-(3)H-arginine to L-(3)H-citrulline in a Ca(2+)/calmodulin-dependent fashion.	l-(3)h-arginine	169-184	nitric oxide synthase 3	Homo sapiens	132-147
22899172-6	2012	Treatment with Apigenin (50 muM) counteracted the TNFalpha-induced expression of eNOS and MMP-9 and the TNFalpha- triggered activation of Akt, p38MAPK and JNK signalling suggesting that multiple signalling pathways are involved in mediating the protective effects of Apigenin on endothelial function.	Apigenin	15-23	nitric oxide synthase 3	Homo sapiens	81-85
23007404-5	2012	Using immunoprecipitation, ESI-MS/MS-based peptide sequencing and enzymatic assay we further demonstrate that human RBCs contain an endothelial NOS (eNOS) that converts L-(3)H-arginine to L-(3)H-citrulline in a Ca(2+)/calmodulin-dependent fashion.	l-(3)h-arginine	169-184	nitric oxide synthase 3	Homo sapiens	149-153
23007404-5	2012	Using immunoprecipitation, ESI-MS/MS-based peptide sequencing and enzymatic assay we further demonstrate that human RBCs contain an endothelial NOS (eNOS) that converts L-(3)H-arginine to L-(3)H-citrulline in a Ca(2+)/calmodulin-dependent fashion.	l-(3)h-citrulline	188-205	nitric oxide synthase 3	Homo sapiens	132-147
23007404-5	2012	Using immunoprecipitation, ESI-MS/MS-based peptide sequencing and enzymatic assay we further demonstrate that human RBCs contain an endothelial NOS (eNOS) that converts L-(3)H-arginine to L-(3)H-citrulline in a Ca(2+)/calmodulin-dependent fashion.	l-(3)h-citrulline	188-205	nitric oxide synthase 3	Homo sapiens	149-153
23011059-9	2012	Reduced arginine availability stemming from reduced de novo production and elevated arginase activity have been reported in various conditions of acute and chronic stress, which are often characterized by increased NOS2 and reduced NOS3 activity.	Arginine	8-16	nitric oxide synthase 3	Homo sapiens	232-236
23011059-11	2012	Therapeutic applications to influence (de novo) arginine and NO metabolism aim at increasing substrate availability or at influencing the metabolic fate of specific pathways related to NO bioavailability and prevention of NOS3 uncoupling.	Arginine	48-56	nitric oxide synthase 3	Homo sapiens	222-226
22810051-0	2012	Genetic variation in MDR1, LPL and eNOS genes and the response to atorvastatin treatment in ischemic stroke.	Atorvastatin	66-78	nitric oxide synthase 3	Homo sapiens	35-39
21895549-1	2012	The present review first summarizes the complex chain of events, in endothelial and vascular smooth muscle cells, that leads to endothelium-dependent relaxations (vasodilatations) due to the generation of nitric oxide (NO) by endothelial nitric oxide synthase (eNOS) and how therapeutic interventions may improve the bioavailability of NO and thus prevent/cure endothelial dysfunction.	Nitric Oxide	205-217	nitric oxide synthase 3	Homo sapiens	226-259
23328297-4	2012	The eNOS activities were detected by NOS assay kit, p-eNOS (ser-1177) level and total eNOS protein level by Western blot and eNOS mRNA level by real-time reverse transcription-polymerase chain reaction (RT-PCR).	Serine	60-63	nitric oxide synthase 3	Homo sapiens	4-8
23328297-7	2012	Compared with the control group, the levels of eNOS phosphorylation at ser-1177, mRNA and total protein were significantly elevated in the 5000 pmol/L GLP-1(9-36) group.	Serine	71-74	nitric oxide synthase 3	Homo sapiens	47-51
23124382-5	2012	We also found that NaHS activated the nitric oxide (NO)-producing Akt/endothelial nitric oxide synthase (eNOS) signaling pathway in response to OSS, whereas NaHS had no effect on IkappaB, a well-known molecule regulating pro-inflammatory signaling pathways.	sodium bisulfide	19-23	nitric oxide synthase 3	Homo sapiens	70-103
23124382-5	2012	We also found that NaHS activated the nitric oxide (NO)-producing Akt/endothelial nitric oxide synthase (eNOS) signaling pathway in response to OSS, whereas NaHS had no effect on IkappaB, a well-known molecule regulating pro-inflammatory signaling pathways.	Nitric Oxide	38-50	nitric oxide synthase 3	Homo sapiens	70-103
23124382-5	2012	We also found that NaHS activated the nitric oxide (NO)-producing Akt/endothelial nitric oxide synthase (eNOS) signaling pathway in response to OSS, whereas NaHS had no effect on IkappaB, a well-known molecule regulating pro-inflammatory signaling pathways.	OSS	144-147	nitric oxide synthase 3	Homo sapiens	70-103
22766265-0	2012	Cigarette smoke and LDL cooperate in reducing nitric oxide bioavailability in endothelial cells via effects on both eNOS and NADPH oxidase.	Nitric Oxide	46-58	nitric oxide synthase 3	Homo sapiens	116-120
22750393-9	2012	In contrast, beta-carotene increased the expression of CaMKKII, PI3K, PZK1, LKB1, eNOS, PON-1, and reduced the expression of ICAM-1 and MCP-1.	beta Carotene	13-26	nitric oxide synthase 3	Homo sapiens	82-86
22750393-10	2012	beta-carotene also induced phospho-AMP-activated protein kinase (p-AMPK), phospho-eNOS and PON-1 proteins.	beta Carotene	0-13	nitric oxide synthase 3	Homo sapiens	82-86
22750393-11	2012	Importantly, beta-carotene upregulated the IL-1beta-mediated decrease of CaMKKII, PZK1, LKB1, eNOS and PON-1.	beta Carotene	13-26	nitric oxide synthase 3	Homo sapiens	94-98
22750393-14	2012	These findings indicate that beta-carotene regulates the expression of PON-1, eNOS and adhesion molecules via CaMKK pathway activation.	beta Carotene	29-42	nitric oxide synthase 3	Homo sapiens	78-82
22771630-3	2012	Our recent studies revealed that andrographolide possesses potent antiplatelet activity by activating the endothelial nitric oxide synthase (eNOS)-NO-cyclic GMP pathway.	andrographolide	33-48	nitric oxide synthase 3	Homo sapiens	106-139
23122309-8	2012	NOS3 gene plays a role in regulating vascular tone and blood vessel diameter, which may be altered by the low-oxygen environment of Tibet.	Oxygen	110-116	nitric oxide synthase 3	Homo sapiens	0-4
22948895-0	2012	Polymorphisms in endothelial nitric oxide synthase (eNOS) and vascular endothelial growth factor (VEGF) predict sunitinib-induced hypertension.	Sunitinib	112-121	nitric oxide synthase 3	Homo sapiens	17-50
22948895-0	2012	Polymorphisms in endothelial nitric oxide synthase (eNOS) and vascular endothelial growth factor (VEGF) predict sunitinib-induced hypertension.	Sunitinib	112-121	nitric oxide synthase 3	Homo sapiens	52-56
22948895-7	2012	Genetic polymorphisms in VEGFA and eNOS independently predict rise in BP and/or development of severe hypertension in sunitinib-treated patients.	Sunitinib	118-127	nitric oxide synthase 3	Homo sapiens	35-39
22824620-0	2012	Sodium arsenite-induced abnormalities in expressions of Caveolin-1, eNOS, IKKbeta, and COX-2 in SV-40 immortalized human uroepithelial cells and in urothelial carcinomas.	sodium arsenite	0-15	nitric oxide synthase 3	Homo sapiens	68-72
22798153-12	2012	The contribution of the Hcy-derived methylation modifications to Ddah2 and eNOS gene expression seems to be tissue-specific and independent of the Ddah2/ADMA/eNOS pathway.	Homocysteine	24-27	nitric oxide synthase 3	Homo sapiens	75-79
22402736-6	2012	Endothelial nitric oxide synthase (eNOS) activation was measured by conversion of L-arginine to L-citrulline in endothelial cells incubated with HDL from 49 subjects.	Arginine	82-92	nitric oxide synthase 3	Homo sapiens	0-33
22402736-6	2012	Endothelial nitric oxide synthase (eNOS) activation was measured by conversion of L-arginine to L-citrulline in endothelial cells incubated with HDL from 49 subjects.	Citrulline	96-108	nitric oxide synthase 3	Homo sapiens	0-33
22877939-8	2012	In conclusion, increased expression of eNOS in glandular and luminal epithelium of the endometrium in women with recurrent miscarriages and unexplained infertility suggests a detrimental effect of excess nitric oxide in endometrial receptivity and implantation.	Nitric Oxide	204-216	nitric oxide synthase 3	Homo sapiens	39-43
22824620-3	2012	The aim of this study was to determine the effect of sodium arsenite on Caveolin-1 and downstream signaling molecules (eNOS, IKKbeta and COX-2) expression in human urothelial cells (SV-HUC-1).	sodium arsenite	53-68	nitric oxide synthase 3	Homo sapiens	119-123
22824620-5	2012	Immunocytochemical staining and Western blotting results revealed increased expression of Caveolin-1, IKKbeta, and COX-2 but decreased eNOS in SV-HUC-1 cells treated with low concentration of arsenite.	arsenite	192-200	nitric oxide synthase 3	Homo sapiens	135-139
22824620-6	2012	Additionally, MEK inhibitor (U0126) significantly attenuated arsenite-induced expression of Caveolin-1, IKKbeta and COX-2 while reducing eNOS expression.	U 0126	29-34	nitric oxide synthase 3	Homo sapiens	137-141
22824620-6	2012	Additionally, MEK inhibitor (U0126) significantly attenuated arsenite-induced expression of Caveolin-1, IKKbeta and COX-2 while reducing eNOS expression.	arsenite	61-69	nitric oxide synthase 3	Homo sapiens	137-141
22902249-0	2012	Cissus quadrangularis ethanol extract upregulates superoxide dismutase, glutathione peroxidase and endothelial nitric oxide synthase expression in hydrogen peroxide-injured human ECV304 cells.	Ethanol	22-29	nitric oxide synthase 3	Homo sapiens	99-132
22902249-0	2012	Cissus quadrangularis ethanol extract upregulates superoxide dismutase, glutathione peroxidase and endothelial nitric oxide synthase expression in hydrogen peroxide-injured human ECV304 cells.	Hydrogen Peroxide	147-164	nitric oxide synthase 3	Homo sapiens	99-132
22902249-8	2012	The protein expression of superoxide dismutase (Cu/Zn-SOD, Mn-SOD), glutathione peroxidase (GPx) and endothelial nitric oxide synthase (eNOS) increased in the cells treated with CQE, quercetin or resveratrol prior to H(2)O(2) exposure, as compared with control.	N-{4-[2-(1-cyclopropylpiperidin-4-yl)-4-(3-{[(2,5-difluorophenyl)sulfonyl]amino}-2-fluorophenyl)-1,3-thiazol-5-yl]pyridin-2-yl}acetamide	178-181	nitric oxide synthase 3	Homo sapiens	101-134
22902249-8	2012	The protein expression of superoxide dismutase (Cu/Zn-SOD, Mn-SOD), glutathione peroxidase (GPx) and endothelial nitric oxide synthase (eNOS) increased in the cells treated with CQE, quercetin or resveratrol prior to H(2)O(2) exposure, as compared with control.	Quercetin	183-192	nitric oxide synthase 3	Homo sapiens	101-134
23157875-1	2012	BACKGROUND: The present study was conducted to investigate the possible outcome of interaction between endothelial nitric oxide (NOS3) G894T and cholesteryl ester transfer TaqIB variants on the risk of coronary artery disease (CAD) and type 2 diabetes mellitus (T2DM).	Nitric Oxide	115-127	nitric oxide synthase 3	Homo sapiens	129-133
22856383-5	2012	Pathways proposed to underlie resveratrol-mediated cardioprotection include reduction of oxidative stress and activation of endothelial nitric oxide synthase.	Resveratrol	30-41	nitric oxide synthase 3	Homo sapiens	124-157
22683691-4	2012	However, the proportion of eNOS which was phosphorylated at serine 1117 and threonine 495 residues was decreased.	Serine	60-66	nitric oxide synthase 3	Homo sapiens	27-31
22683691-4	2012	However, the proportion of eNOS which was phosphorylated at serine 1117 and threonine 495 residues was decreased.	Threonine	76-85	nitric oxide synthase 3	Homo sapiens	27-31
22759779-1	2012	OBJECTIVES: To explore the association among Arg(972) insulin receptor substrate-1 (IRS-1), hypertension, insulin resistance, and plasma levels of endothelial nitric oxide synthase (eNOS) and endothelin-1 (ET-1).	Arginine	45-48	nitric oxide synthase 3	Homo sapiens	147-180
22333037-9	2012	Endothelial nitric oxide synthase may produce both superoxide anion (( )O(2)(-)) and nitric oxide (NO) leading to peroxynitrite (( )ONOO(-)) generation.	Superoxides	51-67	nitric oxide synthase 3	Homo sapiens	0-33
22333037-9	2012	Endothelial nitric oxide synthase may produce both superoxide anion (( )O(2)(-)) and nitric oxide (NO) leading to peroxynitrite (( )ONOO(-)) generation.	Peroxynitrous Acid	114-127	nitric oxide synthase 3	Homo sapiens	0-33
22966886-2	2012	In the present study, the association between eNOS gene polymorphisms and response to inhaled corticosteroids (ICS) and long-lasting beta(2)-agonists (LABAs) was investigated.	Iron-Sulfur-Molybdenum Cluster With Interstitial Carbon	111-114	nitric oxide synthase 3	Homo sapiens	46-50
23012797-3	2012	Angiotensin II stimulates the production of reactive oxygen species by the activation of NADPH oxidase and increases Rho-associated kinase activity that decreases the stability of endothelial nitric oxide synthase (eNOS) mRNA and phosphorylation of eNOS, leading to inactivation of NO bioavailability.	Reactive Oxygen Species	44-67	nitric oxide synthase 3	Homo sapiens	180-213
22716077-1	2012	In a brief overview, in NO-sGC-cGMP signaling in a blood vessel, l-arginine is converted in the endothelium monolayer by the endothelial nitric oxide synthase (eNOS) to NO which diffuses into both the vessel lumen and the vessel wall, thereby activating soluble guanylate cyclase (sGC).	Cyclic GMP	31-35	nitric oxide synthase 3	Homo sapiens	125-158
22771325-1	2012	Our previous study has demonstrated that testosterone rapidly activates endothelial nitric oxide synthase (eNOS), enhancing nitric oxide (NO) release from endothelial cells (ECs) via the phosphatidylinositol 3-kinase/Akt (PI3-kinase/Akt) pathway.	Testosterone	41-53	nitric oxide synthase 3	Homo sapiens	72-105
22404217-4	2012	Importantly, activation of PPARgamma plays a distinctive role in regulating the physiology and expression of endothelial nitric oxide synthase (eNOS) in the endothelium, resulting in enhanced generation of vascular nitric oxide.	Nitric Oxide	121-133	nitric oxide synthase 3	Homo sapiens	144-148
22339730-4	2012	We found that cilostazol treatment significantly increased colony formation by human early EPCs (endothelial progenitor cells) through a mechanism involving the activation of cAMP/PKA (protein kinase A), PI3K (phosphoinositide 3-kinase)/Akt/eNOS (endothelial NO synthase) and ERK (extracellular-signal-regulated kinase)/p38 MAPK (mitogen-activated protein kinase) signalling pathways.	Cilostazol	14-24	nitric oxide synthase 3	Homo sapiens	241-245
22339730-5	2012	Cilostazol also enhanced proliferation, chemotaxis, NO production and vascular tube formation in HUVECs (human umbilical vein endothelial cells) through activation of multiple signalling pathways downstream of PI3K/Akt/eNOS.	Cilostazol	0-10	nitric oxide synthase 3	Homo sapiens	219-223
22336756-0	2012	Endothelial nitric oxide synthase enhancer for protection of endothelial function from asymmetric dimethylarginine-induced injury in human internal thoracic artery.	dimethylarginine	98-114	nitric oxide synthase 3	Homo sapiens	0-33
22336756-2	2012	We hypothesized that novel endothelial nitric oxide synthase enhancer AVE3085 might improve the endothelial function altered by asymmetric dimethylarginine in the human internal thoracic artery.	dimethylarginine	139-155	nitric oxide synthase 3	Homo sapiens	27-60
22336756-8	2012	CONCLUSIONS: AVE3085 may restore endothelium-dependent relaxation reduced by asymmetric dimethylarginine through upregulation of endothelial nitric oxide synthase expression and inhibition of production of superoxide anion in human internal thoracic artery.	2,2-difluorobenzo(1,3)dioxole-5-carboxylic acid indan-2-ylamide	13-20	nitric oxide synthase 3	Homo sapiens	129-162
22336756-8	2012	CONCLUSIONS: AVE3085 may restore endothelium-dependent relaxation reduced by asymmetric dimethylarginine through upregulation of endothelial nitric oxide synthase expression and inhibition of production of superoxide anion in human internal thoracic artery.	dimethylarginine	88-104	nitric oxide synthase 3	Homo sapiens	129-162
22728282-6	2012	In studies using human coronary artery endothelial cells, GJ enhanced phosphorylation of endothelial NOS (eNOS) at Ser(1177) with increased cytosolic translocation of eNOS, and subsequently increased NO production.	Serine	115-118	nitric oxide synthase 3	Homo sapiens	89-104
22929836-7	2012	Nitric oxide (NO) synthase which comes in three isoforms, as inducible-, neuronal- and endothelial-NOS, or iNOS, nNOS or eNOS, respectively, catalyzes the conversion of L- arginine to L-citrulline, using NADPH to produce NO.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	121-125
22929836-7	2012	Nitric oxide (NO) synthase which comes in three isoforms, as inducible-, neuronal- and endothelial-NOS, or iNOS, nNOS or eNOS, respectively, catalyzes the conversion of L- arginine to L-citrulline, using NADPH to produce NO.	Arginine	169-180	nitric oxide synthase 3	Homo sapiens	121-125
22929836-7	2012	Nitric oxide (NO) synthase which comes in three isoforms, as inducible-, neuronal- and endothelial-NOS, or iNOS, nNOS or eNOS, respectively, catalyzes the conversion of L- arginine to L-citrulline, using NADPH to produce NO.	Citrulline	184-196	nitric oxide synthase 3	Homo sapiens	121-125
22929836-7	2012	Nitric oxide (NO) synthase which comes in three isoforms, as inducible-, neuronal- and endothelial-NOS, or iNOS, nNOS or eNOS, respectively, catalyzes the conversion of L- arginine to L-citrulline, using NADPH to produce NO.	NADP	204-209	nitric oxide synthase 3	Homo sapiens	121-125
22929836-9	2012	Under oxidative stress conditions, eNOS for example can switch from producing NO to O2 - in a process called uncoupling, which is believed to be caused by oxidation of heme or the co-factor, tetrahydrobiopterin (BH4).	Oxygen	84-86	nitric oxide synthase 3	Homo sapiens	35-39
22929836-9	2012	Under oxidative stress conditions, eNOS for example can switch from producing NO to O2 - in a process called uncoupling, which is believed to be caused by oxidation of heme or the co-factor, tetrahydrobiopterin (BH4).	Heme	168-172	nitric oxide synthase 3	Homo sapiens	35-39
22929836-9	2012	Under oxidative stress conditions, eNOS for example can switch from producing NO to O2 - in a process called uncoupling, which is believed to be caused by oxidation of heme or the co-factor, tetrahydrobiopterin (BH4).	sapropterin	191-210	nitric oxide synthase 3	Homo sapiens	35-39
22929836-9	2012	Under oxidative stress conditions, eNOS for example can switch from producing NO to O2 - in a process called uncoupling, which is believed to be caused by oxidation of heme or the co-factor, tetrahydrobiopterin (BH4).	sapropterin	212-215	nitric oxide synthase 3	Homo sapiens	35-39
22716077-1	2012	In a brief overview, in NO-sGC-cGMP signaling in a blood vessel, l-arginine is converted in the endothelium monolayer by the endothelial nitric oxide synthase (eNOS) to NO which diffuses into both the vessel lumen and the vessel wall, thereby activating soluble guanylate cyclase (sGC).	Arginine	65-75	nitric oxide synthase 3	Homo sapiens	125-158
22635074-5	2012	In a second set of experiments, we demonstrated that the increased expression of myocardial phosphorylated-Akt and endothelial nitric oxide synthase induced by intrathecal morphine was blocked by prior administration of hexamethonium.	Morphine	172-180	nitric oxide synthase 3	Homo sapiens	115-148
22635074-5	2012	In a second set of experiments, we demonstrated that the increased expression of myocardial phosphorylated-Akt and endothelial nitric oxide synthase induced by intrathecal morphine was blocked by prior administration of hexamethonium.	Hexamethonium	220-233	nitric oxide synthase 3	Homo sapiens	115-148
22683631-6	2012	Additionally, Celastrol inhibits the phosphorylation of VEGFR2, endothelial nitric oxide synthase (eNOS), and Akt to attenuate cell functions.	celastrol	14-23	nitric oxide synthase 3	Homo sapiens	64-97
22507035-11	2012	Western blot analysis revealed that high glucose downregulated the phosphorylation of AMPK and endothelial nitric oxide synthase, which could be reversed with TO treatment.	Glucose	41-48	nitric oxide synthase 3	Homo sapiens	95-128
22799578-5	2012	RESULTS: Rosuvastatin treatment of human umbilical vein endothelial cells (ECs) enhanced the enzymatic activity of endothelial nitric oxide synthase (eNOS) and the expression of 78 S-nitrosoproteins.	Rosuvastatin Calcium	9-21	nitric oxide synthase 3	Homo sapiens	115-148
22283728-2	2012	WHAT THIS STUDY ADDS:   The key finding from this study is that angiotensin II receptor blockers (ARBs) differentially enhanced nitric oxide (NO) release in a manner influenced by certain genetic variants of eNOS.	Nitric Oxide	128-140	nitric oxide synthase 3	Homo sapiens	208-212
22283728-7	2012	NO release was stimulated with calcium ionophore (1 microm) and its maximal concentration was correlated with eNOS variants.	Calcium	31-38	nitric oxide synthase 3	Homo sapiens	110-114
22283728-11	2012	Olmesartan increased maximal NO release by 30%, which was significantly greater (P < 0.01, n= 4-5 in all eNOS variants) than increases observed with other ARBs.	olmesartan	0-10	nitric oxide synthase 3	Homo sapiens	108-112
22517552-0	2012	Dehydroepiandrosterone prevents the aggregation of platelets obtained from postmenopausal women with type 2 diabetes mellitus through the activation of the PKC/eNOS/NO pathway.	Dehydroepiandrosterone	0-22	nitric oxide synthase 3	Homo sapiens	160-164
22669896-0	2012	Phytoestrogen genistein up-regulates endothelial nitric oxide synthase expression via activation of cAMP response element-binding protein in human aortic endothelial cells.	Cyclic AMP	100-104	nitric oxide synthase 3	Homo sapiens	37-70
22669896-5	2012	However, chemical inhibition of protein kinase A (PKA) or adenoviral transfer of the specific endogenous PKA inhibitor gene completely abolished PKA activity and genistein-stimulated eNOS expression and NO production.	Genistein	162-171	nitric oxide synthase 3	Homo sapiens	183-187
22586583-0	2012	Uncoupling endothelial nitric oxide synthase is ameliorated by green tea in experimental diabetes by re-establishing tetrahydrobiopterin levels.	sapropterin	117-136	nitric oxide synthase 3	Homo sapiens	11-44
22517552-4	2012	In light of these precedents and considering that DHEA is able to increase the production of NO in cultured endothelial cells, we suggest that DHEA prevents the aggregation of platelet from postmenopausal women with T2D through the activation of PKC/eNOS/NO/cGMP pathway.	Dehydroepiandrosterone	50-54	nitric oxide synthase 3	Homo sapiens	250-254
22517552-4	2012	In light of these precedents and considering that DHEA is able to increase the production of NO in cultured endothelial cells, we suggest that DHEA prevents the aggregation of platelet from postmenopausal women with T2D through the activation of PKC/eNOS/NO/cGMP pathway.	Dehydroepiandrosterone	143-147	nitric oxide synthase 3	Homo sapiens	250-254
22517552-7	2012	DHEA 1) prevented platelet aggregation by 40% compared to control, 2) increased NO production by 63%, 3) increased p-eNOS (phosphorylated endothelial nitric oxide synthase) levels, and 4) increased cGMP production.	Dehydroepiandrosterone	0-4	nitric oxide synthase 3	Homo sapiens	117-121
22517552-7	2012	DHEA 1) prevented platelet aggregation by 40% compared to control, 2) increased NO production by 63%, 3) increased p-eNOS (phosphorylated endothelial nitric oxide synthase) levels, and 4) increased cGMP production.	Dehydroepiandrosterone	0-4	nitric oxide synthase 3	Homo sapiens	138-171
22517552-10	2012	This effect is mediated by the activation of the PKCdelta/eNOS/NO/cGMP pathway.	Cyclic GMP	66-70	nitric oxide synthase 3	Homo sapiens	58-62
22518022-0	2012	Arginine attenuates methylglyoxal- and high glucose-induced endothelial dysfunction and oxidative stress by an endothelial nitric-oxide synthase-independent mechanism.	Arginine	0-8	nitric oxide synthase 3	Homo sapiens	111-144
22113731-8	2012	GSH levels were found to be inversely related to NOS activity and protein expression, and might be explained by a possible post-translational regulation by glutathionylation of eNOS protein.	Glutathione	0-3	nitric oxide synthase 3	Homo sapiens	177-181
22518022-0	2012	Arginine attenuates methylglyoxal- and high glucose-induced endothelial dysfunction and oxidative stress by an endothelial nitric-oxide synthase-independent mechanism.	Glucose	44-51	nitric oxide synthase 3	Homo sapiens	111-144
22518022-2	2012	We tested the hypothesis that L-arginine, and its inactive isomer D-arginine, can efficiently scavenge MG, administered exogenously or produced endogenously from high glucose, and attenuate its harmful effects including endothelial dysfunction and oxidative stress by an endothelial nitric-oxide synthase (eNOS)-independent mechanism.	Arginine	30-40	nitric oxide synthase 3	Homo sapiens	271-304
26105457-7	2012	OBJECTIVES: The aim of this study was to determine the maternal serum concentrations of endothelial nitric oxide synthase (eNOS) and its endogenous inhibitor, asymmetric dimethylarginine (ADMA) in pregnancies complicated by severe preeclampsia in comparison with healthy normotensive pregnant women.	dimethylarginine	170-186	nitric oxide synthase 3	Homo sapiens	88-121
22689471-2	2012	Many FV and their juices contain flavonoids, some of which increase endothelial nitric oxide synthase (eNOS) activity.	Flavonoids	33-43	nitric oxide synthase 3	Homo sapiens	68-101
22689471-2	2012	Many FV and their juices contain flavonoids, some of which increase endothelial nitric oxide synthase (eNOS) activity.	Flavonoids	33-43	nitric oxide synthase 3	Homo sapiens	103-107
22689471-3	2012	A single nucleotide polymorphism in the eNOS gene, where thymine (T) replaces guanine (G) at position 894 predicting substitution of glutamate for aspartate at codon 298 (Glu298Asp), has been associated with increased CVD risk due to effects on nitric oxide synthesis and subsequently vascular reactivity.	Thymine	57-64	nitric oxide synthase 3	Homo sapiens	40-44
22689471-3	2012	A single nucleotide polymorphism in the eNOS gene, where thymine (T) replaces guanine (G) at position 894 predicting substitution of glutamate for aspartate at codon 298 (Glu298Asp), has been associated with increased CVD risk due to effects on nitric oxide synthesis and subsequently vascular reactivity.	Guanine	78-85	nitric oxide synthase 3	Homo sapiens	40-44
22689471-3	2012	A single nucleotide polymorphism in the eNOS gene, where thymine (T) replaces guanine (G) at position 894 predicting substitution of glutamate for aspartate at codon 298 (Glu298Asp), has been associated with increased CVD risk due to effects on nitric oxide synthesis and subsequently vascular reactivity.	Nitric Oxide	245-257	nitric oxide synthase 3	Homo sapiens	40-44
26105392-3	2012	There is an increase of nitric oxide (NO) serum levels in normal gestation due to an increment in the activity of the enzyme endothelial nitric oxide synthase (eNOS).	Nitric Oxide	24-36	nitric oxide synthase 3	Homo sapiens	125-158
26105290-10	2012	Nitric oxide is produced by the five-electron oxidation of L-arginine which is catalyzed by the enzyme eNOS.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	103-107
26105290-10	2012	Nitric oxide is produced by the five-electron oxidation of L-arginine which is catalyzed by the enzyme eNOS.	Arginine	59-69	nitric oxide synthase 3	Homo sapiens	103-107
26105457-7	2012	OBJECTIVES: The aim of this study was to determine the maternal serum concentrations of endothelial nitric oxide synthase (eNOS) and its endogenous inhibitor, asymmetric dimethylarginine (ADMA) in pregnancies complicated by severe preeclampsia in comparison with healthy normotensive pregnant women.	dimethylarginine	170-186	nitric oxide synthase 3	Homo sapiens	123-127
26105457-7	2012	OBJECTIVES: The aim of this study was to determine the maternal serum concentrations of endothelial nitric oxide synthase (eNOS) and its endogenous inhibitor, asymmetric dimethylarginine (ADMA) in pregnancies complicated by severe preeclampsia in comparison with healthy normotensive pregnant women.	N,N-dimethylarginine	188-192	nitric oxide synthase 3	Homo sapiens	88-121
22609206-3	2012	The endothelial nitric oxide synthase (eNOS)-inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME) reduced superoxide formation in platelets identifying "uncoupled" eNOS as a superoxide source.	NG-Nitroarginine Methyl Ester	55-89	nitric oxide synthase 3	Homo sapiens	4-37
22609206-3	2012	The endothelial nitric oxide synthase (eNOS)-inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME) reduced superoxide formation in platelets identifying "uncoupled" eNOS as a superoxide source.	NG-Nitroarginine Methyl Ester	91-97	nitric oxide synthase 3	Homo sapiens	4-37
22609206-3	2012	The endothelial nitric oxide synthase (eNOS)-inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME) reduced superoxide formation in platelets identifying "uncoupled" eNOS as a superoxide source.	Superoxides	107-117	nitric oxide synthase 3	Homo sapiens	4-37
22609206-3	2012	The endothelial nitric oxide synthase (eNOS)-inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME) reduced superoxide formation in platelets identifying "uncoupled" eNOS as a superoxide source.	Superoxides	175-185	nitric oxide synthase 3	Homo sapiens	4-37
22550140-1	2012	RATIONALE: We have previously demonstrated that the importance of endothelium-derived hyperpolarizing factor (EDHF) increases as the vessel size decreases and that endothelium-derived hydrogen peroxide (H(2)O(2)) is an EDHF in animals and humans, for which endothelial nitric oxide synthase (eNOS) is the major source.	Hydrogen Peroxide	184-201	nitric oxide synthase 3	Homo sapiens	257-290
22717632-4	2012	The production of NO and the activity of endothelial nitric oxide synthase (eNOS) were determined by the DAF-FM diacetate (DAF-FM DA).	4-amino-5-methylamino-2',7'-difluorofluorescein diacetate	105-121	nitric oxide synthase 3	Homo sapiens	41-74
21638020-0	2012	Effects of dietary L-arginine or N-carbamylglutamate supplementation during late gestation of sows on the miR-15b/16, miR-221/222, VEGFA and eNOS expression in umbilical vein.	Arginine	19-29	nitric oxide synthase 3	Homo sapiens	141-145
22717632-4	2012	The production of NO and the activity of endothelial nitric oxide synthase (eNOS) were determined by the DAF-FM diacetate (DAF-FM DA).	4-amino-5-methylamino-2',7'-difluorofluorescein diacetate	123-132	nitric oxide synthase 3	Homo sapiens	41-74
22682770-0	2012	Effect of dietary arginine and N-carbamoylglutamate supplementation on reproduction and gene expression of eNOS, VEGFA and PlGF1 in placenta in late pregnancy of sows.	Arginine	18-26	nitric oxide synthase 3	Homo sapiens	107-111
22682770-0	2012	Effect of dietary arginine and N-carbamoylglutamate supplementation on reproduction and gene expression of eNOS, VEGFA and PlGF1 in placenta in late pregnancy of sows.	N-carbamylglutamate	31-51	nitric oxide synthase 3	Homo sapiens	107-111
21638020-5	2012	Compared with the control diets, dietary Arg or NCG supplementation enhanced the reproductive performance of sows, significantly increased (P<0.05) plasma arginine and decreased plasma VEGF and eNOS (P<0.05).	Arginine	41-44	nitric oxide synthase 3	Homo sapiens	197-201
21638020-0	2012	Effects of dietary L-arginine or N-carbamylglutamate supplementation during late gestation of sows on the miR-15b/16, miR-221/222, VEGFA and eNOS expression in umbilical vein.	N-carbamylglutamate	33-52	nitric oxide synthase 3	Homo sapiens	141-145
21638020-8	2012	The expression of eNOS in both Arg-supplemented and NCG-supplemented group were lower (P<0.05) than in the control group.	Arginine	31-34	nitric oxide synthase 3	Homo sapiens	18-22
21638020-11	2012	In conclusion, this study demonstrated that dietary Arg or NCG supplementation may affect microRNAs (miR-15b, miR-222) targeting VEGFA and eNOS gene expressions in umbilical vein, so as to regulate the function and volume of the umbilical vein, provide more nutrients and oxygen from the maternal to the fetus tissue for fetal development and survival, and enhance the reproductive performance of sows.	Arginine	52-55	nitric oxide synthase 3	Homo sapiens	139-143
21638020-11	2012	In conclusion, this study demonstrated that dietary Arg or NCG supplementation may affect microRNAs (miR-15b, miR-222) targeting VEGFA and eNOS gene expressions in umbilical vein, so as to regulate the function and volume of the umbilical vein, provide more nutrients and oxygen from the maternal to the fetus tissue for fetal development and survival, and enhance the reproductive performance of sows.	Oxygen	272-278	nitric oxide synthase 3	Homo sapiens	139-143
22542797-3	2012	Enzymatic activity of eNOS and intracellular BH4 levels were assessed by means of an arginine-citrulline conversion assay and HPLC analysis, respectively.	Citrulline	94-104	nitric oxide synthase 3	Homo sapiens	22-26
22411126-3	2012	Neuronal NOS (nNOS) and endothelial NOS (eNOS) constitutively produce low levels of NO as a cell-signaling molecule in response to an increase in intracellular calcium concentration.	Calcium	160-167	nitric oxide synthase 3	Homo sapiens	24-39
22411126-3	2012	Neuronal NOS (nNOS) and endothelial NOS (eNOS) constitutively produce low levels of NO as a cell-signaling molecule in response to an increase in intracellular calcium concentration.	Calcium	160-167	nitric oxide synthase 3	Homo sapiens	41-45
22422158-1	2012	Endogenous nitric oxide (NO) is a molecule synthesized by endothelium nitric oxide synthase encoded by the ecNOS gene that plays an important role in regulating the systemic, cardiac and pulmonary circulation.	Nitric Oxide	11-23	nitric oxide synthase 3	Homo sapiens	107-112
22682929-1	2012	Nitric oxide (NO) is synthesized from l-arginine by endothelium nitric oxide synthase (NOS3) and plays important roles in many physiologic and pathologic processes.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	87-91
22682929-1	2012	Nitric oxide (NO) is synthesized from l-arginine by endothelium nitric oxide synthase (NOS3) and plays important roles in many physiologic and pathologic processes.	Arginine	38-48	nitric oxide synthase 3	Homo sapiens	87-91
22504554-9	2012	Western blot analysis demonstrated that the expression of phosphorylated endothelial nitric oxide synthase (eNOS) increased, whereas that of inducible nitric oxide synthase (iNOS) decreased following the 96-h steroid treatment of TNF-alpha-stimulated HCAECs.	Steroids	209-216	nitric oxide synthase 3	Homo sapiens	73-106
22542797-0	2012	Ascorbate stimulates endothelial nitric oxide synthase enzyme activity by rapid modulation of its phosphorylation status.	Ascorbic Acid	0-9	nitric oxide synthase 3	Homo sapiens	21-54
22542797-1	2012	Long-term exposure to ascorbate is known to enhance endothelial nitric oxide synthase (eNOS) activity by stabilizing the eNOS cofactor tetrahydrobiopterin (BH4).	Ascorbic Acid	22-31	nitric oxide synthase 3	Homo sapiens	52-85
22542797-1	2012	Long-term exposure to ascorbate is known to enhance endothelial nitric oxide synthase (eNOS) activity by stabilizing the eNOS cofactor tetrahydrobiopterin (BH4).	Ascorbic Acid	22-31	nitric oxide synthase 3	Homo sapiens	87-91
22564244-6	2012	We found that itraconazole inhibits angiogenesis markers such as VEGF, AAMP and e-NOS.	Itraconazole	14-26	nitric oxide synthase 3	Homo sapiens	80-85
21566204-7	2012	Results suggest that endothelial nitric oxide synthase-mediated formation of nitric oxide (NO) from L-NMMA in doses >3.2 micromol/min and continuous PE-induced alpha-adrenergic stimulation resulting in release of very small amounts of NO from L-NMMA contribute to the observed L-NMMA-induced increase in vein size.	omega-N-Methylarginine	100-106	nitric oxide synthase 3	Homo sapiens	21-54
21566204-7	2012	Results suggest that endothelial nitric oxide synthase-mediated formation of nitric oxide (NO) from L-NMMA in doses >3.2 micromol/min and continuous PE-induced alpha-adrenergic stimulation resulting in release of very small amounts of NO from L-NMMA contribute to the observed L-NMMA-induced increase in vein size.	omega-N-Methylarginine	246-252	nitric oxide synthase 3	Homo sapiens	21-54
21566204-7	2012	Results suggest that endothelial nitric oxide synthase-mediated formation of nitric oxide (NO) from L-NMMA in doses >3.2 micromol/min and continuous PE-induced alpha-adrenergic stimulation resulting in release of very small amounts of NO from L-NMMA contribute to the observed L-NMMA-induced increase in vein size.	omega-N-Methylarginine	246-252	nitric oxide synthase 3	Homo sapiens	21-54
22449386-7	2012	Phospholipase C (PLC)/nitric oxide synthase (NOS)/arginase pathway is involved in this effect, since carbachol stimulated nitric oxide production, increased NOS2 and NOS3 expressions, urea production, and arginase II expression (P<0.001).	Carbachol	101-110	nitric oxide synthase 3	Homo sapiens	166-170
22542797-1	2012	Long-term exposure to ascorbate is known to enhance endothelial nitric oxide synthase (eNOS) activity by stabilizing the eNOS cofactor tetrahydrobiopterin (BH4).	Ascorbic Acid	22-31	nitric oxide synthase 3	Homo sapiens	121-125
22542797-1	2012	Long-term exposure to ascorbate is known to enhance endothelial nitric oxide synthase (eNOS) activity by stabilizing the eNOS cofactor tetrahydrobiopterin (BH4).	sapropterin	135-154	nitric oxide synthase 3	Homo sapiens	52-85
22542797-4	2012	Over a period of 4h, ascorbate steadily increased eNOS activity, although endothelial BH4 levels remained unchanged compared to untreated control cells.	Ascorbic Acid	21-30	nitric oxide synthase 3	Homo sapiens	50-54
22542797-1	2012	Long-term exposure to ascorbate is known to enhance endothelial nitric oxide synthase (eNOS) activity by stabilizing the eNOS cofactor tetrahydrobiopterin (BH4).	sapropterin	135-154	nitric oxide synthase 3	Homo sapiens	87-91
22542797-5	2012	Immunoblot analyses revealed that as early as 5 min after treatment ascorbate dose-dependently increased phosphorylation at eNOS-Ser1177 and concomitantly decreased phosphorylation at eNOS-Thr495, a phosphorylation pattern indicative of increased eNOS activity.	Ascorbic Acid	68-77	nitric oxide synthase 3	Homo sapiens	124-128
22542797-1	2012	Long-term exposure to ascorbate is known to enhance endothelial nitric oxide synthase (eNOS) activity by stabilizing the eNOS cofactor tetrahydrobiopterin (BH4).	sapropterin	135-154	nitric oxide synthase 3	Homo sapiens	121-125
22542797-1	2012	Long-term exposure to ascorbate is known to enhance endothelial nitric oxide synthase (eNOS) activity by stabilizing the eNOS cofactor tetrahydrobiopterin (BH4).	sapropterin	156-159	nitric oxide synthase 3	Homo sapiens	52-85
22542797-5	2012	Immunoblot analyses revealed that as early as 5 min after treatment ascorbate dose-dependently increased phosphorylation at eNOS-Ser1177 and concomitantly decreased phosphorylation at eNOS-Thr495, a phosphorylation pattern indicative of increased eNOS activity.	Ascorbic Acid	68-77	nitric oxide synthase 3	Homo sapiens	184-188
22542797-1	2012	Long-term exposure to ascorbate is known to enhance endothelial nitric oxide synthase (eNOS) activity by stabilizing the eNOS cofactor tetrahydrobiopterin (BH4).	sapropterin	156-159	nitric oxide synthase 3	Homo sapiens	87-91
22542797-5	2012	Immunoblot analyses revealed that as early as 5 min after treatment ascorbate dose-dependently increased phosphorylation at eNOS-Ser1177 and concomitantly decreased phosphorylation at eNOS-Thr495, a phosphorylation pattern indicative of increased eNOS activity.	Ascorbic Acid	68-77	nitric oxide synthase 3	Homo sapiens	184-188
22542797-1	2012	Long-term exposure to ascorbate is known to enhance endothelial nitric oxide synthase (eNOS) activity by stabilizing the eNOS cofactor tetrahydrobiopterin (BH4).	sapropterin	156-159	nitric oxide synthase 3	Homo sapiens	121-125
22542797-2	2012	We investigated acute effects of ascorbate on eNOS function in primary (HUVEC) and immortalized human endothelial cells (EA.hy926), aiming to provide a molecular explanation for the rapid vasodilatation seen in vivo upon administration of ascorbate.	Ascorbic Acid	33-42	nitric oxide synthase 3	Homo sapiens	46-50
22542797-3	2012	Enzymatic activity of eNOS and intracellular BH4 levels were assessed by means of an arginine-citrulline conversion assay and HPLC analysis, respectively.	Arginine	85-93	nitric oxide synthase 3	Homo sapiens	22-26
22542797-7	2012	In this report, we unravel a novel mechanism for how ascorbate rapidly activates eNOS independent of its effects on BH4 stabilization.	Ascorbic Acid	53-62	nitric oxide synthase 3	Homo sapiens	81-85
22314268-7	2012	These effects of resveratrol were accompanied by activation of phosphoinositide 3 kinase (PI3-K)/Akt and Mitogen-Activated Protein Kinase (MAPK)/ERK signaling pathways that led to endothelial nitric oxide synthase upregulation and increased nitric oxide (NO) levels.	Resveratrol	17-28	nitric oxide synthase 3	Homo sapiens	180-213
22520393-4	2012	However, the same treatment of LPA-preactivated HUVECs produced elevated cell viability levels and an optimal vascular gene expression profile, including endothelial nitric oxide synthase overexpression, endothelin-1 repression, an anti-inflammatory genetic pattern, and upregulation of molecules involved in maintaining the endothelial barrier (vascular endothelial cadherin, claudin 5, tight junction protein 1, integrin beta4).	lysophosphatidic acid	31-34	nitric oxide synthase 3	Homo sapiens	154-187
22424734-11	2012	CONCLUSIONS: LPA causes endothelial dysfunction by a mechanism associated with decreased eNOS expression and increased oxidative stress in porcine coronary arteries and HCAECs.	lysophosphatidic acid	13-16	nitric oxide synthase 3	Homo sapiens	89-93
22450868-2	2012	We investigated whether endothelial nitric oxide synthase (eNOS) glutamate (Glu)298-aspartate (Asp) polymorphism may influence the vascular response to weight, as measured by BMI, in young, healthy individuals.	Glutamic Acid	65-74	nitric oxide synthase 3	Homo sapiens	24-57
22450868-2	2012	We investigated whether endothelial nitric oxide synthase (eNOS) glutamate (Glu)298-aspartate (Asp) polymorphism may influence the vascular response to weight, as measured by BMI, in young, healthy individuals.	Glutamic Acid	76-79	nitric oxide synthase 3	Homo sapiens	24-57
22450868-2	2012	We investigated whether endothelial nitric oxide synthase (eNOS) glutamate (Glu)298-aspartate (Asp) polymorphism may influence the vascular response to weight, as measured by BMI, in young, healthy individuals.	Aspartic Acid	84-93	nitric oxide synthase 3	Homo sapiens	24-57
22430140-1	2012	Endothelial argininosuccinate synthetase 1 (ASS1) regulates the provision of l-arginine to nitric oxide synthase 3 (NOS3).	Arginine	77-87	nitric oxide synthase 3	Homo sapiens	91-114
22326500-1	2012	AIMS: Nitric oxide (NO) is synthesized from L-arginine (L-Arg) by three different isoforms of NO synthase (NOS), i.e. the constitutive neuronal and endothelial NOS (nNOS and eNOS) and the inducible NOS (iNOS).	Nitric Oxide	6-18	nitric oxide synthase 3	Homo sapiens	174-178
22326500-1	2012	AIMS: Nitric oxide (NO) is synthesized from L-arginine (L-Arg) by three different isoforms of NO synthase (NOS), i.e. the constitutive neuronal and endothelial NOS (nNOS and eNOS) and the inducible NOS (iNOS).	Arginine	56-61	nitric oxide synthase 3	Homo sapiens	174-178
22652373-3	2012	Nitric oxide (NO) plays a relevant role in various events during atherogenesis, and in vitro data suggest that NO may modulate total homocysteine (tHcy) concentrations, whereas polymorphisms of the endothelial nitric oxide (NOS3) gene have been reported to be related to an increased risk of myocardial infarction (MI) and hyperhomocysteinemia, but the results have been controversial.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	224-228
22652373-4	2012	We hypothesized that the NOS3 synthase 4a4b VNTR polymorphism is a determinant of tHcy concentrations and tested this in 310 patients with MI and 250 controls.	thcy	82-86	nitric oxide synthase 3	Homo sapiens	25-29
22652373-8	2012	In patients with MI, plasma tHcy concentrations were significantly different among the NOS3 genotypes (13.5+-4.5, 18.5+-3.9, and 20.4+-2.1 mumol/L for 4b4b, 4a4b, and 4a4a genotypes, respectively; P<.001).	thcy	28-32	nitric oxide synthase 3	Homo sapiens	87-91
22326500-6	2012	KEY FINDINGS: In the GASH:Sal, cNOS activity increased in the mesencephalic areas studied while cNOS activity decreased in both the striatum and cerebral cortex after 10 sound-induced epileptic seizures.	sal	26-29	nitric oxide synthase 3	Homo sapiens	31-35
22430140-1	2012	Endothelial argininosuccinate synthetase 1 (ASS1) regulates the provision of l-arginine to nitric oxide synthase 3 (NOS3).	Arginine	77-87	nitric oxide synthase 3	Homo sapiens	116-120
22198555-2	2012	The modulation of eNOS during and/or following ischaemic injury often represents a futile compensatory mechanism due to a significant decrease in nitric oxide (NO) bioavailability coupled with dramatic increases in the levels of reactive oxygen species that further neutralise NO.	Nitric Oxide	146-158	nitric oxide synthase 3	Homo sapiens	18-22
22294688-1	2012	Endothelial cell nitric-oxide (NO) synthase (eNOS), the enzyme responsible for synthesis of NO in the vasculature, undergoes extensive post-translational modifications that modulate its activity.	nitric-	17-24	nitric oxide synthase 3	Homo sapiens	45-49
22469105-0	2012	Telmisartan-induced eNOS gene expression is partially independent of its PPAR-gamma agonist property.	Telmisartan	0-11	nitric oxide synthase 3	Homo sapiens	20-24
22469105-2	2012	Several studies have explored the PPAR-gamma-endothelial nitric oxide synthase (eNOS) pathway associated with improvement of endothelial function by telmisartan.	Telmisartan	149-160	nitric oxide synthase 3	Homo sapiens	34-78
22469105-2	2012	Several studies have explored the PPAR-gamma-endothelial nitric oxide synthase (eNOS) pathway associated with improvement of endothelial function by telmisartan.	Telmisartan	149-160	nitric oxide synthase 3	Homo sapiens	80-84
22469105-7	2012	Nonetheless, after the exposure to telmisartan, eNOS-Ser(1177) phosphorylation, associated with eNOS activity increment, reached its highest value while eNOS-Thr(495) phosphorylation, involved in the inhibition of eNOS activity, showed its lowest value.	Telmisartan	35-46	nitric oxide synthase 3	Homo sapiens	48-52
22469105-7	2012	Nonetheless, after the exposure to telmisartan, eNOS-Ser(1177) phosphorylation, associated with eNOS activity increment, reached its highest value while eNOS-Thr(495) phosphorylation, involved in the inhibition of eNOS activity, showed its lowest value.	Telmisartan	35-46	nitric oxide synthase 3	Homo sapiens	96-100
22469105-7	2012	Nonetheless, after the exposure to telmisartan, eNOS-Ser(1177) phosphorylation, associated with eNOS activity increment, reached its highest value while eNOS-Thr(495) phosphorylation, involved in the inhibition of eNOS activity, showed its lowest value.	Telmisartan	35-46	nitric oxide synthase 3	Homo sapiens	96-100
22469105-7	2012	Nonetheless, after the exposure to telmisartan, eNOS-Ser(1177) phosphorylation, associated with eNOS activity increment, reached its highest value while eNOS-Thr(495) phosphorylation, involved in the inhibition of eNOS activity, showed its lowest value.	Telmisartan	35-46	nitric oxide synthase 3	Homo sapiens	96-100
22469105-7	2012	Nonetheless, after the exposure to telmisartan, eNOS-Ser(1177) phosphorylation, associated with eNOS activity increment, reached its highest value while eNOS-Thr(495) phosphorylation, involved in the inhibition of eNOS activity, showed its lowest value.	Serine	53-56	nitric oxide synthase 3	Homo sapiens	48-52
22469105-7	2012	Nonetheless, after the exposure to telmisartan, eNOS-Ser(1177) phosphorylation, associated with eNOS activity increment, reached its highest value while eNOS-Thr(495) phosphorylation, involved in the inhibition of eNOS activity, showed its lowest value.	Serine	53-56	nitric oxide synthase 3	Homo sapiens	96-100
22469105-7	2012	Nonetheless, after the exposure to telmisartan, eNOS-Ser(1177) phosphorylation, associated with eNOS activity increment, reached its highest value while eNOS-Thr(495) phosphorylation, involved in the inhibition of eNOS activity, showed its lowest value.	Serine	53-56	nitric oxide synthase 3	Homo sapiens	96-100
22469105-7	2012	Nonetheless, after the exposure to telmisartan, eNOS-Ser(1177) phosphorylation, associated with eNOS activity increment, reached its highest value while eNOS-Thr(495) phosphorylation, involved in the inhibition of eNOS activity, showed its lowest value.	Serine	53-56	nitric oxide synthase 3	Homo sapiens	96-100
22469105-8	2012	CONCLUSION: The results suggest that telmisartan preserves eNOS activity via a mechanism that is partially independent of the PPARgamma-eNOS pathway in adipocytes.	Telmisartan	37-48	nitric oxide synthase 3	Homo sapiens	59-63
23153979-2	2012	This study determined the role of endothelial nitric oxide synthase (eNOS) Glu298Asp polymorphism and intergenotypic variation of plasma nitric oxide (NO) levels in coronary artery disease (CAD) patients with type 2 diabetes mellitus (DM).	Nitric Oxide	46-58	nitric oxide synthase 3	Homo sapiens	69-73
21093076-0	2012	Fluvastatin upregulates endothelial nitric oxide synthase activity via enhancement of its phosphorylation and expression and via an increase in tetrahydrobiopterin in vascular endothelial cells.	Fluvastatin	0-11	nitric oxide synthase 3	Homo sapiens	24-57
21093076-0	2012	Fluvastatin upregulates endothelial nitric oxide synthase activity via enhancement of its phosphorylation and expression and via an increase in tetrahydrobiopterin in vascular endothelial cells.	sapropterin	144-163	nitric oxide synthase 3	Homo sapiens	24-57
22198555-2	2012	The modulation of eNOS during and/or following ischaemic injury often represents a futile compensatory mechanism due to a significant decrease in nitric oxide (NO) bioavailability coupled with dramatic increases in the levels of reactive oxygen species that further neutralise NO.	Reactive Oxygen Species	229-252	nitric oxide synthase 3	Homo sapiens	18-22
24551766-3	2012	The mutated nitric oxide synthase 3 gene (NOS3), have a modifier effect on the severity of ADPKD by impairment of NOS3 activity and decreasing of renal vascular nitric oxide production and, subsequently, reduced kidney function.	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	42-46
24551766-3	2012	The mutated nitric oxide synthase 3 gene (NOS3), have a modifier effect on the severity of ADPKD by impairment of NOS3 activity and decreasing of renal vascular nitric oxide production and, subsequently, reduced kidney function.	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	114-118
22297680-8	2012	In cultured human endothelial cells, agonist-induced eNOS phosphorylation and nitric oxide production were decreased by ADMA at concentrations less than that of L-arginine in the media.	N,N-dimethylarginine	120-124	nitric oxide synthase 3	Homo sapiens	53-57
22323292-7	2012	Finally, Src FRET biosensor, eNOS small interfering RNA, and NO donor studies demonstrate NO-induced Src activation and Cav-1 phosphorylation at Tyr-14, resulting in increased eNOS/Cav-1 interaction and inhibition of eNOS activity.	Tyrosine	145-148	nitric oxide synthase 3	Homo sapiens	176-180
22286127-0	2012	dl-3n-Butylphthalide promotes angiogenesis via the extracellular signal-regulated kinase 1/2 and phosphatidylinositol 3-kinase/Akt-endothelial nitric oxide synthase signaling pathways.	3-n-butylphthalide	0-20	nitric oxide synthase 3	Homo sapiens	131-164
22323292-0	2012	Nitric oxide-dependent Src activation and resultant caveolin-1 phosphorylation promote eNOS/caveolin-1 binding and eNOS inhibition.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	87-91
22323292-7	2012	Finally, Src FRET biosensor, eNOS small interfering RNA, and NO donor studies demonstrate NO-induced Src activation and Cav-1 phosphorylation at Tyr-14, resulting in increased eNOS/Cav-1 interaction and inhibition of eNOS activity.	Tyrosine	145-148	nitric oxide synthase 3	Homo sapiens	176-180
22323292-0	2012	Nitric oxide-dependent Src activation and resultant caveolin-1 phosphorylation promote eNOS/caveolin-1 binding and eNOS inhibition.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	115-119
22323292-8	2012	Taken together, these data suggest that activation of eNOS promotes Src-dependent Cav-1-Tyr-14 phosphorylation and eNOS/Cav-1 binding, that is, eNOS feedback inhibition.	Tyrosine	88-91	nitric oxide synthase 3	Homo sapiens	54-58
22801313-2	2012	This study explored the role of PI3K/AKT signaling during genistein promoted eNOS activation.	Genistein	58-67	nitric oxide synthase 3	Homo sapiens	77-81
22323292-5	2012	The eNOS/Cav-1 interaction is blocked by eNOS inhibitor L-N(G)-nitroarginine methyl ester (hydrochloride) and Src kinase inhibitor 4-amino-5-(4-chlorophenyl)-7-(t-butyl) pyrazolo [3, 4-d] pyrimidine.	l-n(g)-nitroarginine methyl ester	56-89	nitric oxide synthase 3	Homo sapiens	4-8
22323292-5	2012	The eNOS/Cav-1 interaction is blocked by eNOS inhibitor L-N(G)-nitroarginine methyl ester (hydrochloride) and Src kinase inhibitor 4-amino-5-(4-chlorophenyl)-7-(t-butyl) pyrazolo [3, 4-d] pyrimidine.	l-n(g)-nitroarginine methyl ester	56-89	nitric oxide synthase 3	Homo sapiens	41-45
22323292-5	2012	The eNOS/Cav-1 interaction is blocked by eNOS inhibitor L-N(G)-nitroarginine methyl ester (hydrochloride) and Src kinase inhibitor 4-amino-5-(4-chlorophenyl)-7-(t-butyl) pyrazolo [3, 4-d] pyrimidine.	hydrochloride	91-104	nitric oxide synthase 3	Homo sapiens	4-8
22323292-5	2012	The eNOS/Cav-1 interaction is blocked by eNOS inhibitor L-N(G)-nitroarginine methyl ester (hydrochloride) and Src kinase inhibitor 4-amino-5-(4-chlorophenyl)-7-(t-butyl) pyrazolo [3, 4-d] pyrimidine.	hydrochloride	91-104	nitric oxide synthase 3	Homo sapiens	41-45
22323292-5	2012	The eNOS/Cav-1 interaction is blocked by eNOS inhibitor L-N(G)-nitroarginine methyl ester (hydrochloride) and Src kinase inhibitor 4-amino-5-(4-chlorophenyl)-7-(t-butyl) pyrazolo [3, 4-d] pyrimidine.	AG 1879	131-198	nitric oxide synthase 3	Homo sapiens	4-8
22792801-7	2012	They could enhance the NO content in cell culture supernatants, down-regulate the expression of Cav-1 and up-regulate the expression of eNOS at mRNA and protein levels, which was especially notable after treatment with serum containing TYTZF and simvastatin in large doses.	tytzf	236-241	nitric oxide synthase 3	Homo sapiens	136-140
22792801-7	2012	They could enhance the NO content in cell culture supernatants, down-regulate the expression of Cav-1 and up-regulate the expression of eNOS at mRNA and protein levels, which was especially notable after treatment with serum containing TYTZF and simvastatin in large doses.	Simvastatin	246-257	nitric oxide synthase 3	Homo sapiens	136-140
22801313-10	2012	CONCLUSION: Genistein could promote the activity of eNOS through increasing phosphorylation eNOS(Ser(1179)) level through PI3K/AKT pathway.	Genistein	12-21	nitric oxide synthase 3	Homo sapiens	52-56
22801313-10	2012	CONCLUSION: Genistein could promote the activity of eNOS through increasing phosphorylation eNOS(Ser(1179)) level through PI3K/AKT pathway.	Genistein	12-21	nitric oxide synthase 3	Homo sapiens	92-96
22801313-7	2012	The effect of genistein on phosphorylation eNOS(Ser(1179)) level was also observed in the presence of LY294002 or NSC154020 (PI3K and AKT inhibitors).	Genistein	14-23	nitric oxide synthase 3	Homo sapiens	43-47
22801313-10	2012	CONCLUSION: Genistein could promote the activity of eNOS through increasing phosphorylation eNOS(Ser(1179)) level through PI3K/AKT pathway.	Serine	97-100	nitric oxide synthase 3	Homo sapiens	52-56
22801313-10	2012	CONCLUSION: Genistein could promote the activity of eNOS through increasing phosphorylation eNOS(Ser(1179)) level through PI3K/AKT pathway.	Serine	97-100	nitric oxide synthase 3	Homo sapiens	92-96
22801313-7	2012	The effect of genistein on phosphorylation eNOS(Ser(1179)) level was also observed in the presence of LY294002 or NSC154020 (PI3K and AKT inhibitors).	Serine	48-51	nitric oxide synthase 3	Homo sapiens	43-47
22801313-7	2012	The effect of genistein on phosphorylation eNOS(Ser(1179)) level was also observed in the presence of LY294002 or NSC154020 (PI3K and AKT inhibitors).	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	102-110	nitric oxide synthase 3	Homo sapiens	43-47
22801313-8	2012	RESULTS: The concentration of NO and the expression level of phosphorylation eNOS(Ser(1179)) were significantly increased in ox-LDL + genistein treated cells than ox-LDL treated cells (all P < 0.05), and the peak effects were observed at 15 min, however, eNOS mRNA and non-phosphorylated eNOS protein expression were similar between the two groups (P > 0.05).	Serine	82-85	nitric oxide synthase 3	Homo sapiens	77-81
22801313-8	2012	RESULTS: The concentration of NO and the expression level of phosphorylation eNOS(Ser(1179)) were significantly increased in ox-LDL + genistein treated cells than ox-LDL treated cells (all P < 0.05), and the peak effects were observed at 15 min, however, eNOS mRNA and non-phosphorylated eNOS protein expression were similar between the two groups (P > 0.05).	Genistein	134-143	nitric oxide synthase 3	Homo sapiens	77-81
22801313-8	2012	RESULTS: The concentration of NO and the expression level of phosphorylation eNOS(Ser(1179)) were significantly increased in ox-LDL + genistein treated cells than ox-LDL treated cells (all P < 0.05), and the peak effects were observed at 15 min, however, eNOS mRNA and non-phosphorylated eNOS protein expression were similar between the two groups (P > 0.05).	Genistein	134-143	nitric oxide synthase 3	Homo sapiens	258-262
22801313-8	2012	RESULTS: The concentration of NO and the expression level of phosphorylation eNOS(Ser(1179)) were significantly increased in ox-LDL + genistein treated cells than ox-LDL treated cells (all P < 0.05), and the peak effects were observed at 15 min, however, eNOS mRNA and non-phosphorylated eNOS protein expression were similar between the two groups (P > 0.05).	Genistein	134-143	nitric oxide synthase 3	Homo sapiens	258-262
22801313-9	2012	Furthermore, the expression level of phosphorylation eNOS(Ser(1179)) was significantly lower in PIK3/AKT inhibitors LY294002 and NSC154020 treated cells compared with ox-LDL + genistein treated cells (all P < 0.05).	Serine	58-61	nitric oxide synthase 3	Homo sapiens	53-57
22801313-9	2012	Furthermore, the expression level of phosphorylation eNOS(Ser(1179)) was significantly lower in PIK3/AKT inhibitors LY294002 and NSC154020 treated cells compared with ox-LDL + genistein treated cells (all P < 0.05).	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	116-124	nitric oxide synthase 3	Homo sapiens	53-57
22801313-9	2012	Furthermore, the expression level of phosphorylation eNOS(Ser(1179)) was significantly lower in PIK3/AKT inhibitors LY294002 and NSC154020 treated cells compared with ox-LDL + genistein treated cells (all P < 0.05).	Genistein	176-185	nitric oxide synthase 3	Homo sapiens	53-57
22167522-1	2012	Endothelial nitric oxide synthase (eNOS) serves as a critical enzyme in maintaining vascular pressure by producing nitric oxide (NO); hence, it has a crucial role in the regulation of endothelial function.	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	35-39
22244921-3	2012	Pretreatment with U-73122 (a specific PLC inhibitor) or 2-APB (a specific IP3 receptor antagonist) attenuated this effect, suggesting that PLC/IP3 signaling cascade is involved in arsenite-induced elevation of [Ca2+]i. Cytotoxic concentrations of arsenite (5 and 10 muM) significantly enhanced endothelial nitric oxide synthase (eNOS) phosphorylation, nitric oxide (NO) production and apoptosis after 24-h exposure.	1-(6-((3-methoxyestra-1,3,5(10)-trien-17-yl)amino)hexyl)-1H-pyrrole-2,5-dione	18-25	nitric oxide synthase 3	Homo sapiens	294-327
22244921-3	2012	Pretreatment with U-73122 (a specific PLC inhibitor) or 2-APB (a specific IP3 receptor antagonist) attenuated this effect, suggesting that PLC/IP3 signaling cascade is involved in arsenite-induced elevation of [Ca2+]i. Cytotoxic concentrations of arsenite (5 and 10 muM) significantly enhanced endothelial nitric oxide synthase (eNOS) phosphorylation, nitric oxide (NO) production and apoptosis after 24-h exposure.	2-aminoethoxydiphenyl borate	56-61	nitric oxide synthase 3	Homo sapiens	294-327
22244921-3	2012	Pretreatment with U-73122 (a specific PLC inhibitor) or 2-APB (a specific IP3 receptor antagonist) attenuated this effect, suggesting that PLC/IP3 signaling cascade is involved in arsenite-induced elevation of [Ca2+]i. Cytotoxic concentrations of arsenite (5 and 10 muM) significantly enhanced endothelial nitric oxide synthase (eNOS) phosphorylation, nitric oxide (NO) production and apoptosis after 24-h exposure.	arsenite	180-188	nitric oxide synthase 3	Homo sapiens	294-327
22167522-3	2012	Uncoupling of eNOS, with subsequently less NO and more superoxide generation, is one of the major underlying causes of endothelial dysfunction found in atherosclerosis, diabetes, hypertension, cigarette smoking, hyperhomocysteinemia, and ischemia/reperfusion injury.	Superoxides	55-65	nitric oxide synthase 3	Homo sapiens	14-18
22245769-2	2012	We determined whether administration of tetrahydrobiopterin (BH(4)), a critical cofactor for endothelial nitric oxide synthase to produce nitric oxide, would increase vascular endothelial-dependent vasodilatory tone and decrease arterial stiffness in estrogen-deficient postmenopausal women.	sapropterin	40-59	nitric oxide synthase 3	Homo sapiens	93-126
22207730-8	2012	Pharmacological AMP kinase activation led to phosphorylation of endothelial nitric oxide synthase"s Ser633 activation site, reversing the adverse effects of low glucose.	Glucose	161-168	nitric oxide synthase 3	Homo sapiens	64-97
21791144-2	2012	Repeated treatment with resveratrol for 5 d resulted in an increase in endothelial NO synthase (eNOS) protein content and NO production in human umbilical vein endothelial cell (HUVEC) in a concentration-dependent manner.	Resveratrol	24-35	nitric oxide synthase 3	Homo sapiens	96-100
21791144-3	2012	A significant increase in functional eNOS protein content was observed with resveratrol, even at 50 nm.	Resveratrol	76-87	nitric oxide synthase 3	Homo sapiens	37-41
21791144-5	2012	Both eNOS protein and mRNA expression were promoted by 50 nm-resveratrol in a time-dependent manner.	Resveratrol	61-72	nitric oxide synthase 3	Homo sapiens	5-9
21791144-6	2012	Increased eNOS mRNA expression in response to resveratrol was not decreased by an oestrogen receptor (ER) antagonist ICI182780, a PPARalpha inhibitor MK886 or a sirtuin inhibitor Salermide.	Resveratrol	46-57	nitric oxide synthase 3	Homo sapiens	10-14
21791144-7	2012	However, a combination of ICI182780 and MK886 significantly inhibited resveratrol-induced eNOS mRNA expression.	Fulvestrant	26-35	nitric oxide synthase 3	Homo sapiens	90-94
21791144-7	2012	However, a combination of ICI182780 and MK886 significantly inhibited resveratrol-induced eNOS mRNA expression.	MK-886	40-45	nitric oxide synthase 3	Homo sapiens	90-94
21791144-7	2012	However, a combination of ICI182780 and MK886 significantly inhibited resveratrol-induced eNOS mRNA expression.	Resveratrol	70-81	nitric oxide synthase 3	Homo sapiens	90-94
21791144-9	2012	These results demonstrate that resveratrol within the physiological range increases eNOS mRNA and protein expression through ER and PPARalpha activation, thereby promoting NO production in endothelial cells.	Resveratrol	31-42	nitric oxide synthase 3	Homo sapiens	84-88
21791144-10	2012	eNOS induction might result from the accumulative effect of nanomolar concentrations of resveratrol.	Resveratrol	88-99	nitric oxide synthase 3	Homo sapiens	0-4
22017289-1	2012	BACKGROUND: Nitric oxide synthesized by endothelial nitric oxide synthase (eNOS) plays a key role in the regulation of endothelial function, and controversial results regarding the association of eNOS gene polymorphisms with diabetic complications have been reported.	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	40-73
22280820-1	2012	We previously described a series of imidazole-based inhibitors substituted at N-1 with an arylethanone chain as interesting inhibitors of neuronal nitric oxide synthase (nNOS), endowed with good selectivity vs endothelial nitric oxide synthase (eNOS).	imidazole	36-45	nitric oxide synthase 3	Homo sapiens	210-243
22280820-1	2012	We previously described a series of imidazole-based inhibitors substituted at N-1 with an arylethanone chain as interesting inhibitors of neuronal nitric oxide synthase (nNOS), endowed with good selectivity vs endothelial nitric oxide synthase (eNOS).	imidazole	36-45	nitric oxide synthase 3	Homo sapiens	245-249
22280820-1	2012	We previously described a series of imidazole-based inhibitors substituted at N-1 with an arylethanone chain as interesting inhibitors of neuronal nitric oxide synthase (nNOS), endowed with good selectivity vs endothelial nitric oxide synthase (eNOS).	arylethanone	90-102	nitric oxide synthase 3	Homo sapiens	210-243
22280820-1	2012	We previously described a series of imidazole-based inhibitors substituted at N-1 with an arylethanone chain as interesting inhibitors of neuronal nitric oxide synthase (nNOS), endowed with good selectivity vs endothelial nitric oxide synthase (eNOS).	arylethanone	90-102	nitric oxide synthase 3	Homo sapiens	245-249
22017289-1	2012	BACKGROUND: Nitric oxide synthesized by endothelial nitric oxide synthase (eNOS) plays a key role in the regulation of endothelial function, and controversial results regarding the association of eNOS gene polymorphisms with diabetic complications have been reported.	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	75-79
22017289-1	2012	BACKGROUND: Nitric oxide synthesized by endothelial nitric oxide synthase (eNOS) plays a key role in the regulation of endothelial function, and controversial results regarding the association of eNOS gene polymorphisms with diabetic complications have been reported.	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	196-200
22156331-1	2012	BACKGROUND: Hyperglycemia, via peroxynitrite-mediated endothelial nitric oxide synthase (eNOS) enzymatic uncoupling, induced endothelial dysfunction.	Peroxynitrous Acid	31-44	nitric oxide synthase 3	Homo sapiens	54-87
21762184-10	2012	In vitro, alcohol (0.10% w/v) increased H(2)O(2) production, barrier dysfunction, eNOS, Nox1, and Nox4 expression in human umbilical vein endothelial cell (HUVEC) monolayers, effects also attenuated by rosiglitazone (10 muM).	Alcohols	10-17	nitric oxide synthase 3	Homo sapiens	82-86
21762184-12	2012	CONCLUSIONS: These results indicate that PPARgamma activation reduced expression of eNOS, Nox1, Nox4, the production of reactive species, and barrier dysfunction caused by chronic alcohol ingestion and suggest that PPARgamma represents a novel therapeutic target for strategies designed to reduce the risk of lung injury in patients with a history of chronic alcohol ingestion.	Alcohols	180-187	nitric oxide synthase 3	Homo sapiens	84-88
21762184-12	2012	CONCLUSIONS: These results indicate that PPARgamma activation reduced expression of eNOS, Nox1, Nox4, the production of reactive species, and barrier dysfunction caused by chronic alcohol ingestion and suggest that PPARgamma represents a novel therapeutic target for strategies designed to reduce the risk of lung injury in patients with a history of chronic alcohol ingestion.	Alcohols	359-366	nitric oxide synthase 3	Homo sapiens	84-88
22351865-0	2012	Decreased eNOS protein expression in involuting and propranolol-treated hemangiomas.	Propranolol	52-63	nitric oxide synthase 3	Homo sapiens	10-14
22095978-6	2012	Endothelial nitric oxide synthase inhibition with N(omega)-nitro-l-arginine methyl ester reduced subcutaneous vasodilation but had no effect on severely blunted visceral arteriolar responses.	NG-Nitroarginine Methyl Ester	50-88	nitric oxide synthase 3	Homo sapiens	0-33
22351865-1	2012	OBJECTIVE: To examine the location and degree of endothelial nitric oxide synthase (eNOS) protein expression in hemangioma growth, involution, and during propranolol therapy.	Propranolol	154-165	nitric oxide synthase 3	Homo sapiens	49-82
22351865-1	2012	OBJECTIVE: To examine the location and degree of endothelial nitric oxide synthase (eNOS) protein expression in hemangioma growth, involution, and during propranolol therapy.	Propranolol	154-165	nitric oxide synthase 3	Homo sapiens	84-88
22351865-11	2012	In a separate propranolol treatment group (n = 7), the eNOS protein level was significantly lower than in age-matched controls (n = 7; 0.08 [0.1] vs 0.45 [0.45]; P = .03).	Propranolol	14-25	nitric oxide synthase 3	Homo sapiens	55-59
21927815-1	2012	Human endothelial nitric oxide synthase (eNOS) is one isoform of the nitric oxide synthases that are responsible for nitric oxide synthesis from L-arginine.	Nitric Oxide	18-30	nitric oxide synthase 3	Homo sapiens	41-45
22351865-14	2012	Propranolol may suppress hemangioma growth by inhibiting expression of eNOS protein and subsequent production of nitric oxide.	Propranolol	0-11	nitric oxide synthase 3	Homo sapiens	71-75
21927815-1	2012	Human endothelial nitric oxide synthase (eNOS) is one isoform of the nitric oxide synthases that are responsible for nitric oxide synthesis from L-arginine.	Arginine	145-155	nitric oxide synthase 3	Homo sapiens	6-39
21927815-1	2012	Human endothelial nitric oxide synthase (eNOS) is one isoform of the nitric oxide synthases that are responsible for nitric oxide synthesis from L-arginine.	Arginine	145-155	nitric oxide synthase 3	Homo sapiens	41-45
22139440-6	2012	Furthermore, fisetin inhibited capillary-like tube formation on Matrigel (up to 85%, P < 0.001) as well as migration (up to 66%, P < 0.001), which were associated with decreased expression of endothelial nitric oxide synthase (eNOS) and VEGF in HUVEC.	fisetin	13-20	nitric oxide synthase 3	Homo sapiens	198-231
22063270-5	2012	Increases in cholesterol levels inversely correlated with neutral sphingomyelinase 2 (NSMase2) activity, endothelial nitric oxide synthase (eNOS) phospho-activation and NO-production.	Cholesterol	13-24	nitric oxide synthase 3	Homo sapiens	105-138
22139440-6	2012	Furthermore, fisetin inhibited capillary-like tube formation on Matrigel (up to 85%, P < 0.001) as well as migration (up to 66%, P < 0.001), which were associated with decreased expression of endothelial nitric oxide synthase (eNOS) and VEGF in HUVEC.	fisetin	13-20	nitric oxide synthase 3	Homo sapiens	233-237
21872972-8	2012	Although a multiplicative interaction was not observed, the protective effect of beta-carotene intake on breast cancer risk was observed predominantly in individuals with the TG:TG diplotype of NOS3 (OR = 0.68) but not observed with others diplotype.	beta Carotene	81-94	nitric oxide synthase 3	Homo sapiens	194-198
21872972-8	2012	Although a multiplicative interaction was not observed, the protective effect of beta-carotene intake on breast cancer risk was observed predominantly in individuals with the TG:TG diplotype of NOS3 (OR = 0.68) but not observed with others diplotype.	Thioguanine	175-177	nitric oxide synthase 3	Homo sapiens	194-198
21872972-9	2012	An inverse association between vitamin E intake and breast cancer risk was observed for individuals with the NOS3 786 TC + TT genotype and the NOS3 894 GG genotype.	Vitamin E	31-40	nitric oxide synthase 3	Homo sapiens	109-113
21872972-9	2012	An inverse association between vitamin E intake and breast cancer risk was observed for individuals with the NOS3 786 TC + TT genotype and the NOS3 894 GG genotype.	Vitamin E	31-40	nitric oxide synthase 3	Homo sapiens	143-147
21872972-9	2012	An inverse association between vitamin E intake and breast cancer risk was observed for individuals with the NOS3 786 TC + TT genotype and the NOS3 894 GG genotype.	Technetium	118-120	nitric oxide synthase 3	Homo sapiens	109-113
21872972-10	2012	In addition, folic acid had a protective effect in the NOS3 786 TT and NOS3 894 GT + TT genotype.	Folic Acid	13-23	nitric oxide synthase 3	Homo sapiens	55-59
21872972-10	2012	In addition, folic acid had a protective effect in the NOS3 786 TT and NOS3 894 GT + TT genotype.	Folic Acid	13-23	nitric oxide synthase 3	Homo sapiens	71-75
22219320-3	2012	In cultured ECs, IL-17 increased expression of eNOS, eNOS phosphorylation at Ser(1177), and NO production.	Serine	77-80	nitric oxide synthase 3	Homo sapiens	53-57
21797845-0	2012	Pyridoxine inhibits endothelial NOS uncoupling induced by oxidized low-density lipoprotein via the PKCalpha signalling pathway in human umbilical vein endothelial cells.	Pyridoxine	0-10	nitric oxide synthase 3	Homo sapiens	20-35
21797845-1	2012	BACKGROUND AND PURPOSE: One key mechanism for endothelial dysfunction is endothelial NOS (eNOS) uncoupling, whereby eNOS generates superoxide (O(2) ( -) ) rather than NO.	Superoxides	131-141	nitric oxide synthase 3	Homo sapiens	73-88
21797845-1	2012	BACKGROUND AND PURPOSE: One key mechanism for endothelial dysfunction is endothelial NOS (eNOS) uncoupling, whereby eNOS generates superoxide (O(2) ( -) ) rather than NO.	Superoxides	143-147	nitric oxide synthase 3	Homo sapiens	73-88
22120969-10	2012	GLP-1R antagonist exendin(9-39) or DPP-4 inhibitor sitagliptin, which abolished GLP-1(9-36) formation, at the concentration of 5000 pmol/L partially blocked the effects of GLP-1 on eNOS.	Sitagliptin Phosphate	51-62	nitric oxide synthase 3	Homo sapiens	181-185
22098722-5	2012	A novel contribution is the theory that endothelial nitric oxide synthase produces not only nitric oxide but also sulfate, and that sulfate production is stimulated by sunlight.	Sulfates	114-121	nitric oxide synthase 3	Homo sapiens	40-73
20926145-1	2012	BACKGROUND: The endothelial nitric oxide synthase (eNOS) inhibitor asymmetric dimethylarginine (ADMA) is a well-established risk factor for oxidative stress, vascular dysfunction, and congestive heart failure.	dimethylarginine	78-94	nitric oxide synthase 3	Homo sapiens	16-49
20926145-1	2012	BACKGROUND: The endothelial nitric oxide synthase (eNOS) inhibitor asymmetric dimethylarginine (ADMA) is a well-established risk factor for oxidative stress, vascular dysfunction, and congestive heart failure.	N,N-dimethylarginine	96-100	nitric oxide synthase 3	Homo sapiens	16-49
22120969-7	2012	Incubation of HUVECs with GLP-1 (500-5000 pmol/L) for 5 or 10 min increased eNOS phosphorylated at ser-1177.	Serine	99-102	nitric oxide synthase 3	Homo sapiens	76-80
22120969-9	2012	GLP-1R agonists exenatide and GLP-1(9-36) at the concentration of 5000 pmol/L increased the activity, phosphorylation and protein level of eNOS.	Exenatide	16-25	nitric oxide synthase 3	Homo sapiens	139-143
22155639-0	2012	Acetylation-dependent regulation of mitochondrial ALDH2 activation by SIRT3 mediates acute ethanol-induced eNOS activation.	Ethanol	91-98	nitric oxide synthase 3	Homo sapiens	107-111
22155639-1	2012	Moderate alcohol consumption has beneficial effects on endothelial nitric-oxide synthase (eNOS) activation, which can engender an array of anti-atherogenic actions.	Alcohols	9-16	nitric oxide synthase 3	Homo sapiens	55-88
22155639-1	2012	Moderate alcohol consumption has beneficial effects on endothelial nitric-oxide synthase (eNOS) activation, which can engender an array of anti-atherogenic actions.	Alcohols	9-16	nitric oxide synthase 3	Homo sapiens	90-94
22155639-2	2012	Here we show that in human aortic endothelial cells (HAECs), rapid activation of mitochondrial aldehyde dehydrogenase 2 (ALDH2) mediates ethanol-induced eNOS activation by preventing reactive oxygen species (ROS) accumulation.	Ethanol	137-144	nitric oxide synthase 3	Homo sapiens	153-157
22155639-2	2012	Here we show that in human aortic endothelial cells (HAECs), rapid activation of mitochondrial aldehyde dehydrogenase 2 (ALDH2) mediates ethanol-induced eNOS activation by preventing reactive oxygen species (ROS) accumulation.	Reactive Oxygen Species	183-206	nitric oxide synthase 3	Homo sapiens	153-157
22155639-2	2012	Here we show that in human aortic endothelial cells (HAECs), rapid activation of mitochondrial aldehyde dehydrogenase 2 (ALDH2) mediates ethanol-induced eNOS activation by preventing reactive oxygen species (ROS) accumulation.	Reactive Oxygen Species	208-211	nitric oxide synthase 3	Homo sapiens	153-157
22155639-4	2012	These data suggest that ethanol-induced eNOS activation in HAECs may be dependent on ALDH2 hyperacetylation by SIRT3 inactivation.	Ethanol	24-31	nitric oxide synthase 3	Homo sapiens	40-44
22950347-7	2012	Polyphenols activate and enhance endothelial nitric oxide synthase (eNOS) expression by several signaling pathways, increase glutathione (GSH), and inhibit ROS-producing enzymes such as NADPH and xanthine oxidases.	Polyphenols	0-11	nitric oxide synthase 3	Homo sapiens	33-66
21998134-1	2012	OBJECTIVE: Geranylgeranylacetone (GGA) induces expression of heat shock protein 90 (Hsp90), an adaptor molecule for assembly of endothelial nitric oxide synthase (eNOS) phosphorylation complex.	geranylgeranylacetone	11-32	nitric oxide synthase 3	Homo sapiens	128-161
21998134-1	2012	OBJECTIVE: Geranylgeranylacetone (GGA) induces expression of heat shock protein 90 (Hsp90), an adaptor molecule for assembly of endothelial nitric oxide synthase (eNOS) phosphorylation complex.	geranylgeranylacetone	11-32	nitric oxide synthase 3	Homo sapiens	163-167
21883939-8	2012	The present review discusses the importance of endothelial ROS in health and disease and focuses on the major ROS-generating systems in the endothelium, namely uncoupled endothelial nitric oxide synthase and NADPH oxidases.	Reactive Oxygen Species	110-113	nitric oxide synthase 3	Homo sapiens	170-203
22032308-11	2012	In contrast, NO production, eNOS phosphorylation and ATF3 expression were enhanced by tanshinone IIA.	tanshinone	86-96	nitric oxide synthase 3	Homo sapiens	28-32
22382311-2	2012	Historically, resveratrol has been identified as a phytoalexin, antioxidant, cyclooxygenase (COX) inhibitor, peroxisome proliferator-activated receptor (PPAR) activator, endothelial nitric oxide synthase (eNOS) inducer, silent mating type information regulation 2 homolog 1 (SIRT1) activator, and more.	Resveratrol	14-25	nitric oxide synthase 3	Homo sapiens	170-203
22466633-3	2012	It has previously been demonstrated that endothelium-derived hydrogen peroxide (H(2)O(2)) is an EDHF in animals and humans and that endothelial nitric oxide synthase (eNOS) plays diverse roles as a nitric oxide (NO) generating system in conduit arteries and as an EDHF/H(2)O(2) generating system in microvessels.	edhf	264-268	nitric oxide synthase 3	Homo sapiens	132-165
22466633-3	2012	It has previously been demonstrated that endothelium-derived hydrogen peroxide (H(2)O(2)) is an EDHF in animals and humans and that endothelial nitric oxide synthase (eNOS) plays diverse roles as a nitric oxide (NO) generating system in conduit arteries and as an EDHF/H(2)O(2) generating system in microvessels.	Water	269-274	nitric oxide synthase 3	Homo sapiens	132-165
22572461-0	2012	p38 Mitogen-activated protein kinase is required for glucosamine-induced endothelial nitric oxide synthase uncoupling and plasminogen-activator inhibitor expression.	Glucosamine	53-64	nitric oxide synthase 3	Homo sapiens	73-106
22572461-1	2012	BACKGROUND: Hexosamine biosynthetic pathway (HBP) is implicated in increased plasminogen activator inhibitor-1 (PAI-1), and endothelial nitric oxide synthase (eNOS) dysfunction in diabetes.	Hexosamines	12-22	nitric oxide synthase 3	Homo sapiens	124-157
22834122-1	2012	Streptozotocin-induced diabetes leads to the development of endothelial dysfunction, as evidenced by decreased expression of endothelial nitric oxide synthase (eNOS) and increased expression of endothelin-1 as specific markers of endothelial disorders.	Streptozocin	0-14	nitric oxide synthase 3	Homo sapiens	125-158
22834122-1	2012	Streptozotocin-induced diabetes leads to the development of endothelial dysfunction, as evidenced by decreased expression of endothelial nitric oxide synthase (eNOS) and increased expression of endothelin-1 as specific markers of endothelial disorders.	Streptozocin	0-14	nitric oxide synthase 3	Homo sapiens	160-164
22834122-3	2012	With respect to the degree of impact on the eNOS and endothelin-1 levels, the compounds studied can be rated as follows: sulodexide > meksidol.	glucuronyl glucosamine glycan sulfate	121-131	nitric oxide synthase 3	Homo sapiens	44-48
22112349-8	2012	These strategies include targeting NO synthesis by modulation of endothelial nitric oxide synthase (eNOS) coupling, such as folates and tetrahydrobiopterin.	Folic Acid	124-131	nitric oxide synthase 3	Homo sapiens	65-98
22834122-3	2012	With respect to the degree of impact on the eNOS and endothelin-1 levels, the compounds studied can be rated as follows: sulodexide > meksidol.	meksidol	137-145	nitric oxide synthase 3	Homo sapiens	44-48
22037549-5	2012	eNOS-suppressing miR-221 and miR-222 were increased and eNOS protein and eNOS activation (phosphorylation at serine1177) were lower in senescent HAEC.	serine1177	109-119	nitric oxide synthase 3	Homo sapiens	0-4
23109853-1	2012	l-Arginine (Arg) is oxidized to l-citrulline and nitric oxide (NO) by the action of endothelial nitric oxide synthase (NOS).	Arginine	0-10	nitric oxide synthase 3	Homo sapiens	84-117
22810094-1	2012	Cerebral hypoperfusion due to impaired bioavailability of nitric oxide (NO) synthesized by endothelial nitric oxide synthase and neuronal nitric oxide synthase leads to cognitive decline and neurodegeneration in Alzheimer"s disease (AD).	Nitric Oxide	58-70	nitric oxide synthase 3	Homo sapiens	91-124
23109853-1	2012	l-Arginine (Arg) is oxidized to l-citrulline and nitric oxide (NO) by the action of endothelial nitric oxide synthase (NOS).	Arginine	2-5	nitric oxide synthase 3	Homo sapiens	84-117
23109853-1	2012	l-Arginine (Arg) is oxidized to l-citrulline and nitric oxide (NO) by the action of endothelial nitric oxide synthase (NOS).	Citrulline	32-44	nitric oxide synthase 3	Homo sapiens	84-117
23109853-1	2012	l-Arginine (Arg) is oxidized to l-citrulline and nitric oxide (NO) by the action of endothelial nitric oxide synthase (NOS).	Nitric Oxide	49-61	nitric oxide synthase 3	Homo sapiens	84-117
21968328-5	2012	Intriguingly, a considerable number of studies demonstrated the potential modulatory role of statins on endothelial nitric oxide synthase (eNOS), a key enzyme involved in the regulation of cardiovascular function by generating endothelium-derived relaxing factor (often represented "nitric oxide").	Nitric Oxide	116-128	nitric oxide synthase 3	Homo sapiens	139-143
21968328-7	2012	The upregulation of eNOS by statins is mediated through inhibition of synthesis of isoprenoids and subsequent prevention of isoprenylation of small GTPase Rho, whereas statin-induced activation of eNOS is mediated through activation of phosphotidylinositol-3-kinase (PI3K)/protein kinase B (PKB/Akt) signals.	Terpenes	83-94	nitric oxide synthase 3	Homo sapiens	20-24
23284736-6	2012	In addition, the phosphorylation levels of both Akt kinase and endothelial NO synthases (eNOS) were markedly increased by FSS treatment, which was abolished by an Akt inhibitor triciribine.	triciribine	177-188	nitric oxide synthase 3	Homo sapiens	63-87
21854848-4	2012	The stabilization and nuclear activation of HIF-1alpha in the presence of cyanide were also observed, which resulted in an increase in vascular endothelial growth factor (VEGF), endothelial nitric oxide synthase (eNOS) and erythropoietin (EPO) protein levels reflecting an adaptive response.	Cyanides	74-81	nitric oxide synthase 3	Homo sapiens	178-211
23284736-6	2012	In addition, the phosphorylation levels of both Akt kinase and endothelial NO synthases (eNOS) were markedly increased by FSS treatment, which was abolished by an Akt inhibitor triciribine.	triciribine	177-188	nitric oxide synthase 3	Homo sapiens	89-93
23284736-8	2012	Finally, FSS elevated intracellular Ca(2+) levels in HUVECs, and the Ca(2+) chelator BAPTA-AM inhibited the FSS-stimulated eNOS phosphorylation.	1,2-bis(2-aminophenoxy)ethane N,N,N',N'-tetraacetic acid acetoxymethyl ester	85-93	nitric oxide synthase 3	Homo sapiens	123-127
23284736-9	2012	The present results show that this ancient herbal decoction benefits endothelial function through increased activity of Akt kinase and eNOS; this effect is causally via a rise of intracellular Ca(2+) and a reduction of ROS.	ros	219-222	nitric oxide synthase 3	Homo sapiens	135-139
22768143-0	2012	Lobe-specific calcium binding in calmodulin regulates endothelial nitric oxide synthase activation.	Calcium	14-21	nitric oxide synthase 3	Homo sapiens	54-87
22844486-1	2012	The release of the main vasodilator nitric oxide (NO) by the endothelial NO synthase (eNOS) is a hallmark of endothelial function.	Nitric Oxide	36-48	nitric oxide synthase 3	Homo sapiens	86-90
22808143-6	2012	After 24 h of exposure to simulated microgravity, HUVEC-C tube formation and migration were significantly promoted.This was reversed by co-incubation with the specific inhibitor of N-nitro-L-arginine methyl ester hydrochloride (eNOS).	L-NAME hydrochloride	181-226	nitric oxide synthase 3	Homo sapiens	228-232
22558392-1	2012	BACKGROUND: Asymmetric dimethylarginine (ADMA) is an endogenous inhibitor of endothelial nitric oxide synthase, which was associated with insulin resistance.	dimethylarginine	23-39	nitric oxide synthase 3	Homo sapiens	77-110
22558392-1	2012	BACKGROUND: Asymmetric dimethylarginine (ADMA) is an endogenous inhibitor of endothelial nitric oxide synthase, which was associated with insulin resistance.	N,N-dimethylarginine	41-45	nitric oxide synthase 3	Homo sapiens	77-110
22768143-3	2012	Citrulline formation and cytochrome c reduction assays revealed that in comparison with nNOS or iNOS, eNOS was less stringent in the requirement of calcium binding to each of four calcium-binding sites.	Citrulline	0-10	nitric oxide synthase 3	Homo sapiens	102-106
22768143-3	2012	Citrulline formation and cytochrome c reduction assays revealed that in comparison with nNOS or iNOS, eNOS was less stringent in the requirement of calcium binding to each of four calcium-binding sites.	Calcium	148-155	nitric oxide synthase 3	Homo sapiens	102-106
22768143-3	2012	Citrulline formation and cytochrome c reduction assays revealed that in comparison with nNOS or iNOS, eNOS was less stringent in the requirement of calcium binding to each of four calcium-binding sites.	Calcium	180-187	nitric oxide synthase 3	Homo sapiens	102-106
22768143-4	2012	However, lobe-specific disruption with double mutations in calcium-binding sites either at N- (B12Q) or at C-terminal (B34Q) lobes greatly diminished both eNOS oxygenase and reductase activities.	Calcium	59-66	nitric oxide synthase 3	Homo sapiens	155-159
22768143-5	2012	Gel mobility shift assay and flavin fluorescence measurement indicated that N- and C-lobes of CaM played distinct roles in regulating eNOS catalysis; the C-terminal EF-hands in its calcium-bound form was responsible for the binding of canonical CaM-binding domain, while N-terminal EF-hands in its calcium-bound form controlled the movement of FMN domain.	Calcium	181-188	nitric oxide synthase 3	Homo sapiens	134-138
22768143-7	2012	CONCLUSIONS: Our results clearly demonstrate that CaM controls eNOS electron transfer primarily through its lobe-specific calcium binding.	Calcium	122-129	nitric oxide synthase 3	Homo sapiens	63-67
22134029-0	2012	Intron 4 polymorphism of the endothelial nitric oxide synthase (eNOS) gene is associated with decreased NO production in a mercury-exposed population.	Mercury	123-130	nitric oxide synthase 3	Homo sapiens	29-62
22590587-6	2012	PRINCIPAL FINDINGS: In non-asthmatics, after correction for multiple comparisons, we found significant associations of Fe(NO) levels with three SNPs in NOS3 and NOS2 (P <= 0.002), and of EBC NO2-NO3 level with NOS2 (P = 0.002).	fe(no)	119-125	nitric oxide synthase 3	Homo sapiens	152-156
22590587-6	2012	PRINCIPAL FINDINGS: In non-asthmatics, after correction for multiple comparisons, we found significant associations of Fe(NO) levels with three SNPs in NOS3 and NOS2 (P <= 0.002), and of EBC NO2-NO3 level with NOS2 (P = 0.002).	NSC638702	190-193	nitric oxide synthase 3	Homo sapiens	152-156
22590587-6	2012	PRINCIPAL FINDINGS: In non-asthmatics, after correction for multiple comparisons, we found significant associations of Fe(NO) levels with three SNPs in NOS3 and NOS2 (P <= 0.002), and of EBC NO2-NO3 level with NOS2 (P = 0.002).	no2-no3	194-201	nitric oxide synthase 3	Homo sapiens	152-156
22590587-7	2012	In asthmatics, a single significant association was detected between Fe(NO) levels and one SNP in NOS3 (P = 0.004).	fe(no)	69-75	nitric oxide synthase 3	Homo sapiens	98-102
22590587-8	2012	Moreover, there was significant heterogeneity of NOS3 SNP effect on Fe(NO) between asthmatics and non-asthmatics (P = 0.0002 to 0.005).	fe(no)	68-74	nitric oxide synthase 3	Homo sapiens	49-53
22134029-0	2012	Intron 4 polymorphism of the endothelial nitric oxide synthase (eNOS) gene is associated with decreased NO production in a mercury-exposed population.	Mercury	123-130	nitric oxide synthase 3	Homo sapiens	64-68
22134029-1	2012	Nitric oxide (NO), produced by endothelial nitric oxide synthase (eNOS), is a potent vasodilator and plays a prominent role in regulating the cardiovascular system.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	31-64
22134029-1	2012	Nitric oxide (NO), produced by endothelial nitric oxide synthase (eNOS), is a potent vasodilator and plays a prominent role in regulating the cardiovascular system.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	66-70
22134029-13	2012	Taken together, our results show that the 27 nt repeat polymorphism of the intron 4 in the eNOS gene increases susceptibility to cardiovascular diseases after MeHg exposure by modulating nitric oxide levels.	Nitric Oxide	187-199	nitric oxide synthase 3	Homo sapiens	91-95
22319601-11	2012	Pre-treatment with both wortmannin or geldanamycinin (inhibitors of eNOS phosphorylation and heath shock protein 90 recruitment, respectively) significantly reduced U-II-induced relaxation (0.1 nM-10 microM) in human corpus cavernosum strips.	Wortmannin	24-34	nitric oxide synthase 3	Homo sapiens	68-72
21940786-0	2011	Nectandrin B activates endothelial nitric-oxide synthase phosphorylation in endothelial cells: role of the AMP-activated protein kinase/estrogen receptor alpha/phosphatidylinositol 3-kinase/Akt pathway.	nectandrin-B	0-12	nitric oxide synthase 3	Homo sapiens	23-56
22319601-11	2012	Pre-treatment with both wortmannin or geldanamycinin (inhibitors of eNOS phosphorylation and heath shock protein 90 recruitment, respectively) significantly reduced U-II-induced relaxation (0.1 nM-10 microM) in human corpus cavernosum strips.	geldanamycinin	38-52	nitric oxide synthase 3	Homo sapiens	68-72
20832877-4	2011	Therefore, we hypothesized that atorvastatin could protect MSCs from H/SF injury through AMPK-eNOS pathway.	Atorvastatin	32-44	nitric oxide synthase 3	Homo sapiens	94-98
20832877-7	2011	Meanwhile, MSCs treated with atorvastatin increased phosphorylation of AMPK and eNOS.	Atorvastatin	29-41	nitric oxide synthase 3	Homo sapiens	80-84
20832877-8	2011	The uptrend was partially inhibited by compound C. CONCLUSIONS: Atorvastatin can activate AMPK and the phosphorylation of AMPK results in eNOS activated, which provides a novel explanation for the multi-effect of statins on cardiovascular system.	Atorvastatin	64-76	nitric oxide synthase 3	Homo sapiens	138-142
21801125-1	2011	CONTEXT: Presence of endothelial nitric oxide synthase (eNOS) gene polymorphism has been associated with cardiovascular disease (CVD) whereas exercise training (EX) promotes beneficial effects on CVD which is related to increased nitric oxide levels (NO).	Nitric Oxide	33-45	nitric oxide synthase 3	Homo sapiens	56-60
22052999-11	2011	Moreover, abrogation of ERbeta/eNOS function by 3beta-adiol emphasizes the significance of circulating or locally produced sex steroid hormones or their metabolites in PCa biology with relevant clinical/therapeutic implications.	3beta-adiol	48-59	nitric oxide synthase 3	Homo sapiens	31-35
22116695-10	2012	Ascorbate also regulates nitric oxide concentration by releasing nitric oxide from adducts and by acting through tetrahydrobiopterin (BH4) to stimulate endothelial nitric oxide synthase (eNOS).	Ascorbic Acid	0-9	nitric oxide synthase 3	Homo sapiens	152-185
22116695-10	2012	Ascorbate also regulates nitric oxide concentration by releasing nitric oxide from adducts and by acting through tetrahydrobiopterin (BH4) to stimulate endothelial nitric oxide synthase (eNOS).	sapropterin	113-132	nitric oxide synthase 3	Homo sapiens	152-185
22116695-10	2012	Ascorbate also regulates nitric oxide concentration by releasing nitric oxide from adducts and by acting through tetrahydrobiopterin (BH4) to stimulate endothelial nitric oxide synthase (eNOS).	sapropterin	134-137	nitric oxide synthase 3	Homo sapiens	152-185
22116698-10	2012	Folates interact with the endothelial enzyme NO synthase (eNOS) and, exert effects on the cofactor bioavailability of NO and thus, on peroxynitrite formation.	Folic Acid	0-7	nitric oxide synthase 3	Homo sapiens	58-62
22116698-10	2012	Folates interact with the endothelial enzyme NO synthase (eNOS) and, exert effects on the cofactor bioavailability of NO and thus, on peroxynitrite formation.	Peroxynitrous Acid	134-147	nitric oxide synthase 3	Homo sapiens	58-62
22194727-4	2011	H(2)S stimulated a twofold increase in NO production from endothelial nitric oxide synthase (eNOS), which was maximal 30 min after exposure to 25-150 muM H(2)S.	Hydrogen Sulfide	0-5	nitric oxide synthase 3	Homo sapiens	58-91
20662602-7	2011	Increased expressions of transforming growth factor beta-1, endothelial nitric oxide synthase and TUNEL in sciatic nerve from streptozotocin induced diabetes were reduced by Atorvastatin.	Streptozocin	126-140	nitric oxide synthase 3	Homo sapiens	60-93
20662602-7	2011	Increased expressions of transforming growth factor beta-1, endothelial nitric oxide synthase and TUNEL in sciatic nerve from streptozotocin induced diabetes were reduced by Atorvastatin.	Atorvastatin	174-186	nitric oxide synthase 3	Homo sapiens	60-93
20706876-1	2011	Endothelial nitric oxide synthase (eNOS)-derived nitric oxide (NO) is involved in numerous physiologic and pathophysiologic process including tumor angiogenesis and apoptosis.	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	35-39
21940786-2	2011	In this study, we investigated whether nectandrin B affects phosphorylation of endothelial nitric-oxide synthase (eNOS) in human endothelial cells.	nectandrin-B	39-51	nitric oxide synthase 3	Homo sapiens	79-112
21947555-5	2011	Stress hormones, such as glucocorticoids and pro-inflammatory cytokines, and endothelin-1 liberated in response to mental stress participate in endothelial dysfunction possibly via downregulation of endothelial nitric oxide synthase (eNOS) expression, eNOS inactivation, decreased nitric oxide (NO) actions, and increased NO degradation, together with vasoconstriction counteracting against NO-induced vasodilatation.	Nitric Oxide	211-223	nitric oxide synthase 3	Homo sapiens	234-238
20531373-0	2011	Endothelial nitric oxide synthase gene haplotypes affect nitrite levels in black subjects.	Nitrites	57-64	nitric oxide synthase 3	Homo sapiens	0-33
20531373-1	2011	Polymorphisms in the endothelial nitric oxide synthase (eNOS) gene have been associated with variations in nitric oxide (NO) formation and response to drugs in white subjects.	Nitric Oxide	33-45	nitric oxide synthase 3	Homo sapiens	56-60
21947555-5	2011	Stress hormones, such as glucocorticoids and pro-inflammatory cytokines, and endothelin-1 liberated in response to mental stress participate in endothelial dysfunction possibly via downregulation of endothelial nitric oxide synthase (eNOS) expression, eNOS inactivation, decreased nitric oxide (NO) actions, and increased NO degradation, together with vasoconstriction counteracting against NO-induced vasodilatation.	Nitric Oxide	211-223	nitric oxide synthase 3	Homo sapiens	252-256
21963997-6	2011	We also determined the effects of YC-1 on expression of endothelin-1 (ET-1) and phosphorylation status of endothelial nitric oxide synthase (eNOS) at Ser(1179) in human pulmonary artery endothelial cells (HPAECs) under hypoxia.	Serine	150-153	nitric oxide synthase 3	Homo sapiens	106-139
21980126-5	2011	3-Deazaneplanocin A was not sufficient to increase eNOS expression, but the combination of 3-deazaneplanocin A and the histone deacetylase inhibitor Trichostatin A augmented eNOS expression, indicating that the concomitant inhibition of silencing histone modification and enhancement of activating histone modification facilitates eNOS expression.	3-deazaneplanocin	91-110	nitric oxide synthase 3	Homo sapiens	174-178
21884717-0	2011	Puerarin activates endothelial nitric oxide synthase through estrogen receptor-dependent PI3-kinase and calcium-dependent AMP-activated protein kinase.	puerarin	0-8	nitric oxide synthase 3	Homo sapiens	19-52
21884717-1	2011	The cardioprotective properties of puerarin, a natural product, have been attributed to the endothelial nitric oxide synthase (eNOS)-mediated production of nitric oxide (NO) in EA.hy926 endothelial cells.	puerarin	35-43	nitric oxide synthase 3	Homo sapiens	92-125
21980126-5	2011	3-Deazaneplanocin A was not sufficient to increase eNOS expression, but the combination of 3-deazaneplanocin A and the histone deacetylase inhibitor Trichostatin A augmented eNOS expression, indicating that the concomitant inhibition of silencing histone modification and enhancement of activating histone modification facilitates eNOS expression.	3-deazaneplanocin	91-110	nitric oxide synthase 3	Homo sapiens	174-178
21980126-5	2011	3-Deazaneplanocin A was not sufficient to increase eNOS expression, but the combination of 3-deazaneplanocin A and the histone deacetylase inhibitor Trichostatin A augmented eNOS expression, indicating that the concomitant inhibition of silencing histone modification and enhancement of activating histone modification facilitates eNOS expression.	trichostatin A	149-163	nitric oxide synthase 3	Homo sapiens	174-178
21980126-5	2011	3-Deazaneplanocin A was not sufficient to increase eNOS expression, but the combination of 3-deazaneplanocin A and the histone deacetylase inhibitor Trichostatin A augmented eNOS expression, indicating that the concomitant inhibition of silencing histone modification and enhancement of activating histone modification facilitates eNOS expression.	trichostatin A	149-163	nitric oxide synthase 3	Homo sapiens	174-178
21986532-8	2011	Reduced (15)N(4)-ARG cellular uptake in CAT-1 siRNA transfected cells vs. control was accompanied by reduced eNOS activity, as determined by (15)N-nitrite, total nitrite and (15)N(3)-citrulline formation.	n(4)-arg	12-20	nitric oxide synthase 3	Homo sapiens	109-113
21986532-1	2011	We examined the relative contributory roles of extracellular vs. intracellular L-arginine (ARG) toward cellular activation of endothelial nitric oxide synthase (eNOS) in human endothelial cells.	Arginine	79-89	nitric oxide synthase 3	Homo sapiens	126-159
21986532-1	2011	We examined the relative contributory roles of extracellular vs. intracellular L-arginine (ARG) toward cellular activation of endothelial nitric oxide synthase (eNOS) in human endothelial cells.	Arginine	91-94	nitric oxide synthase 3	Homo sapiens	126-159
21986532-1	2011	We examined the relative contributory roles of extracellular vs. intracellular L-arginine (ARG) toward cellular activation of endothelial nitric oxide synthase (eNOS) in human endothelial cells.	Arginine	91-94	nitric oxide synthase 3	Homo sapiens	161-165
21986532-5	2011	eNOS activity was determined by nitrite/nitrate accumulation, either via a fluorometric assay or by(15)N-nitrite or estimated (15)N(3)-citrulline concentrations when (15)N(4)-ARG was used to challenge the cells.	Nitrites	32-39	nitric oxide synthase 3	Homo sapiens	0-4
21986532-5	2011	eNOS activity was determined by nitrite/nitrate accumulation, either via a fluorometric assay or by(15)N-nitrite or estimated (15)N(3)-citrulline concentrations when (15)N(4)-ARG was used to challenge the cells.	Nitrates	40-47	nitric oxide synthase 3	Homo sapiens	0-4
21986532-5	2011	eNOS activity was determined by nitrite/nitrate accumulation, either via a fluorometric assay or by(15)N-nitrite or estimated (15)N(3)-citrulline concentrations when (15)N(4)-ARG was used to challenge the cells.	n-nitrite	103-112	nitric oxide synthase 3	Homo sapiens	0-4
21986532-5	2011	eNOS activity was determined by nitrite/nitrate accumulation, either via a fluorometric assay or by(15)N-nitrite or estimated (15)N(3)-citrulline concentrations when (15)N(4)-ARG was used to challenge the cells.	(3)-citrulline	131-145	nitric oxide synthase 3	Homo sapiens	0-4
21986532-10	2011	It is likely that once transported inside the cell, ARG can no longer gain access to the membrane-bound eNOS.	Arginine	52-55	nitric oxide synthase 3	Homo sapiens	104-108
21986532-5	2011	eNOS activity was determined by nitrite/nitrate accumulation, either via a fluorometric assay or by(15)N-nitrite or estimated (15)N(3)-citrulline concentrations when (15)N(4)-ARG was used to challenge the cells.	(4)-arg	171-178	nitric oxide synthase 3	Homo sapiens	0-4
21836066-0	2011	C1q/TNF-related proteins, a family of novel adipokines, induce vascular relaxation through the adiponectin receptor-1/AMPK/eNOS/nitric oxide signaling pathway.	Nitric Oxide	128-140	nitric oxide synthase 3	Homo sapiens	123-127
21175585-11	2011	The mechanism of tianeptine"s action involved GS and cNOS stabilization and iNOS suppression.	tianeptine	17-27	nitric oxide synthase 3	Homo sapiens	53-57
21839088-3	2011	Our previous data with human umbilical vein (HUVEC) and EA.hy.926 endothelial cells demonstrated that eNOS can obtain its substrate from the conversion of l-citrulline to l-arginine and from protein breakdown.	Citrulline	155-167	nitric oxide synthase 3	Homo sapiens	102-106
21720712-9	2011	L-NAME treatment of LnCap cells resulted in a reduction in VEGF, iNOS and eNOS expression.	NG-Nitroarginine Methyl Ester	0-6	nitric oxide synthase 3	Homo sapiens	74-78
21839088-0	2011	Relative contribution of different l-arginine sources to the substrate supply of endothelial nitric oxide synthase.	Arginine	35-45	nitric oxide synthase 3	Homo sapiens	81-114
21213109-5	2011	We show that the promoter activity of prostacyclin synthase (PTGIS), the mRNA expression of PTGIS and endothelial nitric oxide synthase (eNOS), and the production of PGI2 and NO are significantly induced by fluvastatin.	Fluvastatin	207-218	nitric oxide synthase 3	Homo sapiens	102-135
21839088-3	2011	Our previous data with human umbilical vein (HUVEC) and EA.hy.926 endothelial cells demonstrated that eNOS can obtain its substrate from the conversion of l-citrulline to l-arginine and from protein breakdown.	Arginine	171-181	nitric oxide synthase 3	Homo sapiens	102-106
21839088-4	2011	In the present study, we determined the quantitative contribution of proteasomal and lysosomal protein degradation and investigated to what extent extracellular peptides and l-citrulline can provide substrate to eNOS.	Citrulline	174-186	nitric oxide synthase 3	Homo sapiens	212-216
21839088-8	2011	eNOS activity was fully restored by supplementing either l-citrulline or l-arginine-containing dipeptides.	Citrulline	57-69	nitric oxide synthase 3	Homo sapiens	0-4
21839088-8	2011	eNOS activity was fully restored by supplementing either l-citrulline or l-arginine-containing dipeptides.	Arginine	73-83	nitric oxide synthase 3	Homo sapiens	0-4
21839088-8	2011	eNOS activity was fully restored by supplementing either l-citrulline or l-arginine-containing dipeptides.	Dipeptides	95-105	nitric oxide synthase 3	Homo sapiens	0-4
21839088-9	2011	Histidine prevented the restoration of eNOS activity by the dipeptide, suggesting that a transporter accepting both, peptides and histidine, mediates the uptake of the extracellular peptide.	Histidine	0-9	nitric oxide synthase 3	Homo sapiens	39-43
21839088-9	2011	Histidine prevented the restoration of eNOS activity by the dipeptide, suggesting that a transporter accepting both, peptides and histidine, mediates the uptake of the extracellular peptide.	Dipeptides	60-69	nitric oxide synthase 3	Homo sapiens	39-43
21839088-9	2011	Histidine prevented the restoration of eNOS activity by the dipeptide, suggesting that a transporter accepting both, peptides and histidine, mediates the uptake of the extracellular peptide.	Peptides	117-125	nitric oxide synthase 3	Homo sapiens	39-43
21839088-9	2011	Histidine prevented the restoration of eNOS activity by the dipeptide, suggesting that a transporter accepting both, peptides and histidine, mediates the uptake of the extracellular peptide.	Histidine	130-139	nitric oxide synthase 3	Homo sapiens	39-43
21839088-11	2011	Our study thus demonstrates that l-citrulline and l-arginine-containing peptides derived from either intracellular protein breakdown or from the extracellular space seem to be good substrate sources for eNOS.	Citrulline	33-45	nitric oxide synthase 3	Homo sapiens	203-207
21729921-7	2011	Propofol ameliorated Ang II-induced NADPH oxidase expression and activation (P<0.01), lipid peroxidation (P<0.05), and superoxide anion generation (P<0.05), whereas restoring NOSIII phosphorylation and activity (P<0.01) were down-regulated by Ang II.	Propofol	0-8	nitric oxide synthase 3	Homo sapiens	184-190
21611796-2	2011	This study was to investigate the role of signal transducer and activator of transcription 3 (STAT3) in the regulation of eNOS expression and vascular EC proliferation by the intronic 27-nucleotide (nt) miRNA derived from the 27-base pair repeats in intron 4 of eNOS gene.	27-nucleotide	184-197	nitric oxide synthase 3	Homo sapiens	122-126
21611796-2	2011	This study was to investigate the role of signal transducer and activator of transcription 3 (STAT3) in the regulation of eNOS expression and vascular EC proliferation by the intronic 27-nucleotide (nt) miRNA derived from the 27-base pair repeats in intron 4 of eNOS gene.	27-nucleotide	184-197	nitric oxide synthase 3	Homo sapiens	262-266
21705677-6	2011	Further experiments demonstrated that FTY720 triggered nitric oxide release from cardiac myocytes is through pertussis toxin-sensitive phosphatidylinositol 3-kinase/Akt/endothelial nitric oxide synthase signaling.	Nitric Oxide	55-67	nitric oxide synthase 3	Homo sapiens	169-202
21807618-2	2011	Since tetrahydrobiopterin (BH(4)) is an essential cofactor for endothelial nitric oxide synthase (NOS3), decreased bioavailability of the substrate l-arginine and/or BH(4) may contribute to decreased NO production with hypercholesterolaemia.	sapropterin	6-25	nitric oxide synthase 3	Homo sapiens	63-96
21585521-6	2011	LPS inhibited eNOS mRNA and protein expression, which was reversed by atorvastatin and, to a lesser extent, by melatonin.	Atorvastatin	70-82	nitric oxide synthase 3	Homo sapiens	14-18
21585521-6	2011	LPS inhibited eNOS mRNA and protein expression, which was reversed by atorvastatin and, to a lesser extent, by melatonin.	Melatonin	111-120	nitric oxide synthase 3	Homo sapiens	14-18
21585521-7	2011	Together, melatonin + atorvastatin induced higher eNOS protein expression than either compound alone.	Melatonin	10-19	nitric oxide synthase 3	Homo sapiens	50-54
21585521-7	2011	Together, melatonin + atorvastatin induced higher eNOS protein expression than either compound alone.	Atorvastatin	22-34	nitric oxide synthase 3	Homo sapiens	50-54
21839593-5	2011	The aim of this study was to investigate the effects of non-alcoholic wine fractions from five different wines on the synthesis of nitric oxide (NO) via the expression and enzymatic activation of the endothelial nitric oxide synthase (eNOS) in human endothelial cells.	Nitric Oxide	131-143	nitric oxide synthase 3	Homo sapiens	200-233
21844127-5	2011	Significant differences in glucose-induced cell death and free 3NT-induced cell death were observed among the NOS3 genotypes.	Glucose	27-34	nitric oxide synthase 3	Homo sapiens	110-114
22031268-0	2011	Three polymorphisms of the eNOS gene and plasma levels of metabolites of nitric oxide in depressed Japanese patients: a preliminary report.	Nitric Oxide	73-85	nitric oxide synthase 3	Homo sapiens	27-31
21458460-3	2011	Experimental studies in humans and animals demonstrate that decreased BH(4)-bioavailability, with subsequent uncoupling of endothelial NOS (eNOS) plays an important role in the pathogenesis of endothelial dysfunction, hypertension, ischemia-reperfusion injury, and pathologic cardiac remodeling.	sapropterin	70-75	nitric oxide synthase 3	Homo sapiens	123-138
21807618-2	2011	Since tetrahydrobiopterin (BH(4)) is an essential cofactor for endothelial nitric oxide synthase (NOS3), decreased bioavailability of the substrate l-arginine and/or BH(4) may contribute to decreased NO production with hypercholesterolaemia.	sapropterin	6-25	nitric oxide synthase 3	Homo sapiens	98-102
21807618-2	2011	Since tetrahydrobiopterin (BH(4)) is an essential cofactor for endothelial nitric oxide synthase (NOS3), decreased bioavailability of the substrate l-arginine and/or BH(4) may contribute to decreased NO production with hypercholesterolaemia.	Arginine	148-158	nitric oxide synthase 3	Homo sapiens	63-96
21599719-1	2011	BACKGROUND: Pregnancy-induced utero-placental growth, angiogenic remodeling, and enhanced vasodilation are all partly regulated by estradiol-17beta-mediated activation of endothelial nitric oxide synthase (eNOS) and nitric oxide (NO) production.	Estradiol	131-147	nitric oxide synthase 3	Homo sapiens	171-204
21808054-6	2011	The stimulation of eNOS activity by BMPRII ligands was largely dependent on protein kinase A (PKA) activation, as demonstrated using the PKA inhibitors H89 and myristoylated PKI(6-22) amide.	Amides	184-189	nitric oxide synthase 3	Homo sapiens	19-23
21808054-7	2011	PAEC migration stimulated by BMP2 and BMP4 was inhibited by the NOS inhibitor l-nitroarginine methyl ester, providing functional evidence of eNOS activation.	NG-Nitroarginine Methyl Ester	78-106	nitric oxide synthase 3	Homo sapiens	141-145
21809851-1	2011	We report an efficient synthetic route to chiral pyrrolidine inhibitors of neuronal nitric oxide synthase (nNOS) and crystal structures of the inhibitors bound to nNOS and to endothelial NOS.	pyrrolidine	49-60	nitric oxide synthase 3	Homo sapiens	175-190
21757745-11	2011	PAF activated eNOS by increasing phosphorylation of Ser-1177 and inducing dephosphorylation of Thr-495, increasing NO production, and elevating permeability to FITC-dextran 70 in monolayers of cells expressing wild-type and cytosolic eNOS.	Serine	52-55	nitric oxide synthase 3	Homo sapiens	14-18
21757745-11	2011	PAF activated eNOS by increasing phosphorylation of Ser-1177 and inducing dephosphorylation of Thr-495, increasing NO production, and elevating permeability to FITC-dextran 70 in monolayers of cells expressing wild-type and cytosolic eNOS.	Threonine	95-98	nitric oxide synthase 3	Homo sapiens	14-18
21757745-11	2011	PAF activated eNOS by increasing phosphorylation of Ser-1177 and inducing dephosphorylation of Thr-495, increasing NO production, and elevating permeability to FITC-dextran 70 in monolayers of cells expressing wild-type and cytosolic eNOS.	fitc-dextran 70	160-175	nitric oxide synthase 3	Homo sapiens	14-18
21757745-13	2011	Interestingly, this occurred despite eNOS Ser-1177 phosphorylation and production of comparable amounts of NO.	Serine	42-45	nitric oxide synthase 3	Homo sapiens	37-41
22125674-1	2011	We compared the effects of genistein and daidzein on the expression of chemokines, cell adhesion molecules (CAMs), and endothelial nitric oxide synthase (eNOS) in tumor necrosis factor (TNF)-alpha-stimulated human umbilical vascular endothelial cells (HUVECs).	Genistein	27-36	nitric oxide synthase 3	Homo sapiens	119-152
22125674-1	2011	We compared the effects of genistein and daidzein on the expression of chemokines, cell adhesion molecules (CAMs), and endothelial nitric oxide synthase (eNOS) in tumor necrosis factor (TNF)-alpha-stimulated human umbilical vascular endothelial cells (HUVECs).	daidzein	41-49	nitric oxide synthase 3	Homo sapiens	119-152
22125674-6	2011	Pre-treatment with either genistein or daidzein elevated eNOS expression and nitric oxide production disturbed by TNF-alpha exposure.	Genistein	26-35	nitric oxide synthase 3	Homo sapiens	57-61
22125674-6	2011	Pre-treatment with either genistein or daidzein elevated eNOS expression and nitric oxide production disturbed by TNF-alpha exposure.	daidzein	39-47	nitric oxide synthase 3	Homo sapiens	57-61
21724868-0	2011	Suppression of eNOS-derived superoxide by caveolin-1: a biopterin-dependent mechanism.	Superoxides	28-38	nitric oxide synthase 3	Homo sapiens	15-19
21724868-0	2011	Suppression of eNOS-derived superoxide by caveolin-1: a biopterin-dependent mechanism.	Biopterin	56-65	nitric oxide synthase 3	Homo sapiens	15-19
21724868-1	2011	In the vasculature, nitric oxide (NO) is generated by endothelial NO synthase (eNOS) in a calcium/calmodulin-dependent reaction.	Nitric Oxide	20-32	nitric oxide synthase 3	Homo sapiens	79-83
21724868-2	2011	In the absence of the requisite eNOS cofactor tetrahydrobiopterin (BH(4)), NADPH oxidation is uncoupled from NO generation, leading to the production of superoxide.	sapropterin	46-65	nitric oxide synthase 3	Homo sapiens	32-36
21724868-2	2011	In the absence of the requisite eNOS cofactor tetrahydrobiopterin (BH(4)), NADPH oxidation is uncoupled from NO generation, leading to the production of superoxide.	NADP	75-80	nitric oxide synthase 3	Homo sapiens	32-36
21724868-2	2011	In the absence of the requisite eNOS cofactor tetrahydrobiopterin (BH(4)), NADPH oxidation is uncoupled from NO generation, leading to the production of superoxide.	Superoxides	153-163	nitric oxide synthase 3	Homo sapiens	32-36
21724868-3	2011	Although this phenomenon is apparent with purified enzyme, cellular studies suggest that formation of the BH(4) oxidation product, dihydrobiopterin, is the molecular trigger for eNOS uncoupling rather than BH(4) depletion alone.	7,8-dihydrobiopterin	131-147	nitric oxide synthase 3	Homo sapiens	178-182
21724868-4	2011	In the current study, we investigated the effects of both BH(4) depletion and oxidation on eNOS-derived superoxide production in endothelial cells in an attempt to elucidate the molecular mechanisms regulating eNOS oxidase activity.	sapropterin	58-63	nitric oxide synthase 3	Homo sapiens	91-95
21724868-4	2011	In the current study, we investigated the effects of both BH(4) depletion and oxidation on eNOS-derived superoxide production in endothelial cells in an attempt to elucidate the molecular mechanisms regulating eNOS oxidase activity.	Superoxides	104-114	nitric oxide synthase 3	Homo sapiens	91-95
21724868-6	2011	These findings suggest that the endothelium possesses regulatory mechanisms, which prevent eNOS oxidase activity from pterin-free eNOS.	Pterins	118-124	nitric oxide synthase 3	Homo sapiens	91-95
21724868-6	2011	These findings suggest that the endothelium possesses regulatory mechanisms, which prevent eNOS oxidase activity from pterin-free eNOS.	Pterins	118-124	nitric oxide synthase 3	Homo sapiens	130-134
21724868-7	2011	Using a combination of gene silencing and pharmacological approaches, we demonstrate that eNOS-caveolin-1 association is increased under conditions of reduced pterin bioavailability and that this sequestration serves to suppress eNOS uncoupling.	Pterins	159-165	nitric oxide synthase 3	Homo sapiens	90-94
21724868-9	2011	Moreover, when caveolin-1 silencing was combined with a pharmacological inhibitor of AKT, BH(4) depletion increased eNOS-derived superoxide to 165% of that observed with BH(4) oxidation.	Superoxides	129-139	nitric oxide synthase 3	Homo sapiens	116-120
22309020-6	2011	H2S contracts SMC through a reduction in nitric oxide (NO) availability by reacting with NO forming a nitrosothiol compound and through an inhibitory effect on endothelial nitric oxide synthase (eNOS) as well as a reduction in SMC cyclic AMP concentration.	Hydrogen Sulfide	0-3	nitric oxide synthase 3	Homo sapiens	160-193
21519233-9	2011	Serum nitric oxide level was found to be lower in carriers of the ecNOS 4a allele than in noncarriers (100.29+-27.32 vs. 152.73+-60.39 mumol/l, P=0.04).	Nitric Oxide	6-18	nitric oxide synthase 3	Homo sapiens	66-71
21956531-8	2011	Women without eNOS gene polymorphism at position -786T>C and Intron 4b/a showed a greater reduction of plasma cholesterol levels in response to ET.	Cholesterol	113-124	nitric oxide synthase 3	Homo sapiens	14-18
21198553-3	2011	Similar to all NOS isoforms, functional eNOS transfers electrons from nicotinamide adenine dinucleotide phosphate (NADPH), via the flavins flavin adenine dinucleotide and flavin mononucleotide in the carboxy-terminal reductase domain, to the heme in the amino-terminal oxygenase domain.	NADP	70-113	nitric oxide synthase 3	Homo sapiens	40-44
21198553-3	2011	Similar to all NOS isoforms, functional eNOS transfers electrons from nicotinamide adenine dinucleotide phosphate (NADPH), via the flavins flavin adenine dinucleotide and flavin mononucleotide in the carboxy-terminal reductase domain, to the heme in the amino-terminal oxygenase domain.	NADP	115-120	nitric oxide synthase 3	Homo sapiens	40-44
21198553-3	2011	Similar to all NOS isoforms, functional eNOS transfers electrons from nicotinamide adenine dinucleotide phosphate (NADPH), via the flavins flavin adenine dinucleotide and flavin mononucleotide in the carboxy-terminal reductase domain, to the heme in the amino-terminal oxygenase domain.	flavins flavin adenine dinucleotide	131-166	nitric oxide synthase 3	Homo sapiens	40-44
21198553-3	2011	Similar to all NOS isoforms, functional eNOS transfers electrons from nicotinamide adenine dinucleotide phosphate (NADPH), via the flavins flavin adenine dinucleotide and flavin mononucleotide in the carboxy-terminal reductase domain, to the heme in the amino-terminal oxygenase domain.	Flavin Mononucleotide	171-192	nitric oxide synthase 3	Homo sapiens	40-44
21198553-3	2011	Similar to all NOS isoforms, functional eNOS transfers electrons from nicotinamide adenine dinucleotide phosphate (NADPH), via the flavins flavin adenine dinucleotide and flavin mononucleotide in the carboxy-terminal reductase domain, to the heme in the amino-terminal oxygenase domain.	Heme	242-246	nitric oxide synthase 3	Homo sapiens	40-44
21198553-8	2011	NADPH-oxidase-derived superoxide avidly reacts with eNOS-derived NO to form peroxynitrite (ONOO(-)).	Superoxides	22-32	nitric oxide synthase 3	Homo sapiens	52-56
21198553-8	2011	NADPH-oxidase-derived superoxide avidly reacts with eNOS-derived NO to form peroxynitrite (ONOO(-)).	Peroxynitrous Acid	76-89	nitric oxide synthase 3	Homo sapiens	52-56
21198553-8	2011	NADPH-oxidase-derived superoxide avidly reacts with eNOS-derived NO to form peroxynitrite (ONOO(-)).	onoo	91-95	nitric oxide synthase 3	Homo sapiens	52-56
21198553-13	2011	These include the protein kinase C inhibitor midostaurin, the pentacyclic triterpenoids ursolic acid and betulinic acid, the eNOS enhancing compounds AVE9488 and AVE3085, and the polyphenolic phytoalexin trans-resveratrol.	4-fluoro-N-indan-2-yl-benzamide	150-157	nitric oxide synthase 3	Homo sapiens	125-129
21235458-2	2011	It is produced in intact endothelial cells by endothelial NO synthase (eNOS) as the key enzyme from L-arginine.	Arginine	100-110	nitric oxide synthase 3	Homo sapiens	71-75
21555345-0	2011	eNOS activation and NO function: pregnancy adaptive programming of capacitative entry responses alters nitric oxide (NO) output in vascular endothelium--new insights into eNOS regulation through adaptive cell signaling.	Nitric Oxide	103-115	nitric oxide synthase 3	Homo sapiens	0-4
21664268-9	2011	Vitamin C also plays a role in the function of endothelial nitric oxide synthase (eNOS) by recycling the eNOS cofactor, tetrahydrobiopterin, which is relevant to arterial elasticity and blood pressure regulation.	Ascorbic Acid	0-9	nitric oxide synthase 3	Homo sapiens	47-80
21664268-9	2011	Vitamin C also plays a role in the function of endothelial nitric oxide synthase (eNOS) by recycling the eNOS cofactor, tetrahydrobiopterin, which is relevant to arterial elasticity and blood pressure regulation.	sapropterin	120-139	nitric oxide synthase 3	Homo sapiens	47-80
21932180-5	2011	AGEs induced reactive oxygen species (ROS) generation and reduced endothelial nitric oxide synthase (eNOS) mRNA level in HUVEC, both of which were also completely blocked by the treatment with 10 pM GLP-1 and 0.5 muM sitagliptin, but not with GLP-1 or sitagliptin monotherapy.	Sitagliptin Phosphate	217-228	nitric oxide synthase 3	Homo sapiens	66-99
21642378-4	2011	Furthermore, new data are presented that provide novel insights into how disruption of the eNOS dimer prevents eNOS uncoupling and the production of superoxide under conditions of elevated oxidative stress and identifies a novel regulatory region we have termed the "flexible arm".	Superoxides	149-159	nitric oxide synthase 3	Homo sapiens	91-95
21642378-4	2011	Furthermore, new data are presented that provide novel insights into how disruption of the eNOS dimer prevents eNOS uncoupling and the production of superoxide under conditions of elevated oxidative stress and identifies a novel regulatory region we have termed the "flexible arm".	Superoxides	149-159	nitric oxide synthase 3	Homo sapiens	111-115
21555345-0	2011	eNOS activation and NO function: pregnancy adaptive programming of capacitative entry responses alters nitric oxide (NO) output in vascular endothelium--new insights into eNOS regulation through adaptive cell signaling.	Nitric Oxide	103-115	nitric oxide synthase 3	Homo sapiens	171-175
21741389-2	2011	Adenosine, histamine, salbutamol and thrombin cause activation of eNOS through widely different mechanisms.	Adenosine	0-9	nitric oxide synthase 3	Homo sapiens	66-70
21741389-2	2011	Adenosine, histamine, salbutamol and thrombin cause activation of eNOS through widely different mechanisms.	Albuterol	22-32	nitric oxide synthase 3	Homo sapiens	66-70
21741389-2	2011	Adenosine, histamine, salbutamol and thrombin cause activation of eNOS through widely different mechanisms.	Histamine	11-20	nitric oxide synthase 3	Homo sapiens	66-70
21741389-5	2011	Nevertheless, despite their divergent effects on intracellular Ca(2+) and on actin filament structure, we found by immunoprecipitation that adenosine, histamine, salbutamol and thrombin all caused an increase in association between eNOS and globular actin.	Adenosine	140-149	nitric oxide synthase 3	Homo sapiens	232-236
21761876-0	2011	Effect of black currant anthocyanins on the activation of endothelial nitric oxide synthase (eNOS) in vitro in human endothelial cells.	Anthocyanins	24-36	nitric oxide synthase 3	Homo sapiens	58-91
21741389-5	2011	Nevertheless, despite their divergent effects on intracellular Ca(2+) and on actin filament structure, we found by immunoprecipitation that adenosine, histamine, salbutamol and thrombin all caused an increase in association between eNOS and globular actin.	Histamine	151-160	nitric oxide synthase 3	Homo sapiens	232-236
21741389-5	2011	Nevertheless, despite their divergent effects on intracellular Ca(2+) and on actin filament structure, we found by immunoprecipitation that adenosine, histamine, salbutamol and thrombin all caused an increase in association between eNOS and globular actin.	Albuterol	162-172	nitric oxide synthase 3	Homo sapiens	232-236
21741389-8	2011	Agonist-induced phosphorylation of eNOS on serine 1177 was attenuated by Akt inhibition, whereas association of eNOS with actin was not.	Serine	43-49	nitric oxide synthase 3	Homo sapiens	35-39
21741389-10	2011	We conclude that association of globular actin with eNOS plays an essential and necessary role in agonist-induced eNOS activation, through enabling its phosphorylation by Akt at serine residue 1177.	Serine	178-184	nitric oxide synthase 3	Homo sapiens	52-56
21741389-10	2011	We conclude that association of globular actin with eNOS plays an essential and necessary role in agonist-induced eNOS activation, through enabling its phosphorylation by Akt at serine residue 1177.	Serine	178-184	nitric oxide synthase 3	Homo sapiens	114-118
21666221-4	2011	Spin trapping with 5,5-dimethyl-1-pyrroline N-oxide (DMPO) followed by immunoblotting using an anti-DMPO antibody demonstrated the formation of eNOS protein radicals, which were abolished by superoxide dismutase and L-NAME, indicating that protein radical formation was due to superoxide generation from the eNOS heme.	5,5-dimethyl-1-pyrroline-1-oxide	100-104	nitric oxide synthase 3	Homo sapiens	144-148
21666221-0	2011	Superoxide induces endothelial nitric-oxide synthase protein thiyl radical formation, a novel mechanism regulating eNOS function and coupling.	Superoxides	0-10	nitric oxide synthase 3	Homo sapiens	19-52
21666221-0	2011	Superoxide induces endothelial nitric-oxide synthase protein thiyl radical formation, a novel mechanism regulating eNOS function and coupling.	Superoxides	0-10	nitric oxide synthase 3	Homo sapiens	115-119
21666221-0	2011	Superoxide induces endothelial nitric-oxide synthase protein thiyl radical formation, a novel mechanism regulating eNOS function and coupling.	thiyl radical	61-74	nitric oxide synthase 3	Homo sapiens	19-52
21666221-0	2011	Superoxide induces endothelial nitric-oxide synthase protein thiyl radical formation, a novel mechanism regulating eNOS function and coupling.	thiyl radical	61-74	nitric oxide synthase 3	Homo sapiens	115-119
21666221-3	2011	We demonstrate endothelial NOS (eNOS) oxidant-induced protein thiyl radical formation from tetrahydrobiopterin-free enzyme or following exposure to exogenous superoxide using immunoblotting, immunostaining, and mass spectrometry.	thiyl radical	62-75	nitric oxide synthase 3	Homo sapiens	15-30
21666221-3	2011	We demonstrate endothelial NOS (eNOS) oxidant-induced protein thiyl radical formation from tetrahydrobiopterin-free enzyme or following exposure to exogenous superoxide using immunoblotting, immunostaining, and mass spectrometry.	thiyl radical	62-75	nitric oxide synthase 3	Homo sapiens	32-36
21666221-3	2011	We demonstrate endothelial NOS (eNOS) oxidant-induced protein thiyl radical formation from tetrahydrobiopterin-free enzyme or following exposure to exogenous superoxide using immunoblotting, immunostaining, and mass spectrometry.	sapropterin	91-110	nitric oxide synthase 3	Homo sapiens	15-30
21666221-3	2011	We demonstrate endothelial NOS (eNOS) oxidant-induced protein thiyl radical formation from tetrahydrobiopterin-free enzyme or following exposure to exogenous superoxide using immunoblotting, immunostaining, and mass spectrometry.	sapropterin	91-110	nitric oxide synthase 3	Homo sapiens	32-36
21666221-3	2011	We demonstrate endothelial NOS (eNOS) oxidant-induced protein thiyl radical formation from tetrahydrobiopterin-free enzyme or following exposure to exogenous superoxide using immunoblotting, immunostaining, and mass spectrometry.	Superoxides	158-168	nitric oxide synthase 3	Homo sapiens	15-30
21666221-3	2011	We demonstrate endothelial NOS (eNOS) oxidant-induced protein thiyl radical formation from tetrahydrobiopterin-free enzyme or following exposure to exogenous superoxide using immunoblotting, immunostaining, and mass spectrometry.	Superoxides	158-168	nitric oxide synthase 3	Homo sapiens	32-36
21666221-4	2011	Spin trapping with 5,5-dimethyl-1-pyrroline N-oxide (DMPO) followed by immunoblotting using an anti-DMPO antibody demonstrated the formation of eNOS protein radicals, which were abolished by superoxide dismutase and L-NAME, indicating that protein radical formation was due to superoxide generation from the eNOS heme.	5,5-dimethyl-1-pyrroline-1-oxide	19-51	nitric oxide synthase 3	Homo sapiens	144-148
21666221-4	2011	Spin trapping with 5,5-dimethyl-1-pyrroline N-oxide (DMPO) followed by immunoblotting using an anti-DMPO antibody demonstrated the formation of eNOS protein radicals, which were abolished by superoxide dismutase and L-NAME, indicating that protein radical formation was due to superoxide generation from the eNOS heme.	5,5-dimethyl-1-pyrroline-1-oxide	53-57	nitric oxide synthase 3	Homo sapiens	144-148
21666221-4	2011	Spin trapping with 5,5-dimethyl-1-pyrroline N-oxide (DMPO) followed by immunoblotting using an anti-DMPO antibody demonstrated the formation of eNOS protein radicals, which were abolished by superoxide dismutase and L-NAME, indicating that protein radical formation was due to superoxide generation from the eNOS heme.	5,5-dimethyl-1-pyrroline-1-oxide	100-104	nitric oxide synthase 3	Homo sapiens	308-312
21666221-4	2011	Spin trapping with 5,5-dimethyl-1-pyrroline N-oxide (DMPO) followed by immunoblotting using an anti-DMPO antibody demonstrated the formation of eNOS protein radicals, which were abolished by superoxide dismutase and L-NAME, indicating that protein radical formation was due to superoxide generation from the eNOS heme.	NG-Nitroarginine Methyl Ester	216-222	nitric oxide synthase 3	Homo sapiens	144-148
21666221-4	2011	Spin trapping with 5,5-dimethyl-1-pyrroline N-oxide (DMPO) followed by immunoblotting using an anti-DMPO antibody demonstrated the formation of eNOS protein radicals, which were abolished by superoxide dismutase and L-NAME, indicating that protein radical formation was due to superoxide generation from the eNOS heme.	Superoxides	191-201	nitric oxide synthase 3	Homo sapiens	144-148
21666221-4	2011	Spin trapping with 5,5-dimethyl-1-pyrroline N-oxide (DMPO) followed by immunoblotting using an anti-DMPO antibody demonstrated the formation of eNOS protein radicals, which were abolished by superoxide dismutase and L-NAME, indicating that protein radical formation was due to superoxide generation from the eNOS heme.	Superoxides	191-201	nitric oxide synthase 3	Homo sapiens	308-312
21666221-4	2011	Spin trapping with 5,5-dimethyl-1-pyrroline N-oxide (DMPO) followed by immunoblotting using an anti-DMPO antibody demonstrated the formation of eNOS protein radicals, which were abolished by superoxide dismutase and L-NAME, indicating that protein radical formation was due to superoxide generation from the eNOS heme.	Heme	313-317	nitric oxide synthase 3	Homo sapiens	144-148
21666221-5	2011	With tetrahydrobiopterin-reconstituted eNOS, eNOS protein radical formation was completely inhibited.	sapropterin	5-24	nitric oxide synthase 3	Homo sapiens	39-43
21666221-5	2011	With tetrahydrobiopterin-reconstituted eNOS, eNOS protein radical formation was completely inhibited.	sapropterin	5-24	nitric oxide synthase 3	Homo sapiens	45-49
21666221-7	2011	Mutagenesis of this key cysteine to alanine abolished eNOS thiyl radical formation and uncoupled eNOS, leading to increased superoxide generation.	Cysteine	24-32	nitric oxide synthase 3	Homo sapiens	54-58
21666221-7	2011	Mutagenesis of this key cysteine to alanine abolished eNOS thiyl radical formation and uncoupled eNOS, leading to increased superoxide generation.	Cysteine	24-32	nitric oxide synthase 3	Homo sapiens	97-101
21666221-7	2011	Mutagenesis of this key cysteine to alanine abolished eNOS thiyl radical formation and uncoupled eNOS, leading to increased superoxide generation.	Alanine	36-43	nitric oxide synthase 3	Homo sapiens	54-58
21666221-7	2011	Mutagenesis of this key cysteine to alanine abolished eNOS thiyl radical formation and uncoupled eNOS, leading to increased superoxide generation.	Alanine	36-43	nitric oxide synthase 3	Homo sapiens	97-101
21666221-7	2011	Mutagenesis of this key cysteine to alanine abolished eNOS thiyl radical formation and uncoupled eNOS, leading to increased superoxide generation.	thiyl	59-64	nitric oxide synthase 3	Homo sapiens	54-58
21666221-8	2011	Protein thiyl radical formation leads to oxidation or modification of cysteine with either disulfide bond formation or S-glutathionylation, which induces eNOS uncoupling.	thiyl radical	8-21	nitric oxide synthase 3	Homo sapiens	154-158
21666221-8	2011	Protein thiyl radical formation leads to oxidation or modification of cysteine with either disulfide bond formation or S-glutathionylation, which induces eNOS uncoupling.	Cysteine	70-78	nitric oxide synthase 3	Homo sapiens	154-158
21666221-8	2011	Protein thiyl radical formation leads to oxidation or modification of cysteine with either disulfide bond formation or S-glutathionylation, which induces eNOS uncoupling.	Disulfides	91-100	nitric oxide synthase 3	Homo sapiens	154-158
21666221-9	2011	Furthermore, in endothelial cells treated with menadione to trigger cellular superoxide generation, eNOS protein radical formation, as visualized with confocal microscopy, was increased, and these results were confirmed by immunoprecipitation with anti-eNOS antibody, followed by immunoblotting with an anti-DMPO antibody.	Vitamin K 3	47-56	nitric oxide synthase 3	Homo sapiens	100-104
21666221-9	2011	Furthermore, in endothelial cells treated with menadione to trigger cellular superoxide generation, eNOS protein radical formation, as visualized with confocal microscopy, was increased, and these results were confirmed by immunoprecipitation with anti-eNOS antibody, followed by immunoblotting with an anti-DMPO antibody.	Vitamin K 3	47-56	nitric oxide synthase 3	Homo sapiens	253-257
21666221-9	2011	Furthermore, in endothelial cells treated with menadione to trigger cellular superoxide generation, eNOS protein radical formation, as visualized with confocal microscopy, was increased, and these results were confirmed by immunoprecipitation with anti-eNOS antibody, followed by immunoblotting with an anti-DMPO antibody.	Superoxides	77-87	nitric oxide synthase 3	Homo sapiens	100-104
21666221-9	2011	Furthermore, in endothelial cells treated with menadione to trigger cellular superoxide generation, eNOS protein radical formation, as visualized with confocal microscopy, was increased, and these results were confirmed by immunoprecipitation with anti-eNOS antibody, followed by immunoblotting with an anti-DMPO antibody.	Superoxides	77-87	nitric oxide synthase 3	Homo sapiens	253-257
21666221-9	2011	Furthermore, in endothelial cells treated with menadione to trigger cellular superoxide generation, eNOS protein radical formation, as visualized with confocal microscopy, was increased, and these results were confirmed by immunoprecipitation with anti-eNOS antibody, followed by immunoblotting with an anti-DMPO antibody.	5,5-dimethyl-1-pyrroline-1-oxide	308-312	nitric oxide synthase 3	Homo sapiens	100-104
21666221-9	2011	Furthermore, in endothelial cells treated with menadione to trigger cellular superoxide generation, eNOS protein radical formation, as visualized with confocal microscopy, was increased, and these results were confirmed by immunoprecipitation with anti-eNOS antibody, followed by immunoblotting with an anti-DMPO antibody.	5,5-dimethyl-1-pyrroline-1-oxide	308-312	nitric oxide synthase 3	Homo sapiens	253-257
21666221-10	2011	Thus, eNOS protein radical formation provides the basis for a mechanism of superoxide-directed regulation of eNOS, involving thiol oxidation, defining a unique pathway for the redox regulation of cardiovascular function.	Superoxides	75-85	nitric oxide synthase 3	Homo sapiens	6-10
21666221-10	2011	Thus, eNOS protein radical formation provides the basis for a mechanism of superoxide-directed regulation of eNOS, involving thiol oxidation, defining a unique pathway for the redox regulation of cardiovascular function.	Superoxides	75-85	nitric oxide synthase 3	Homo sapiens	109-113
21666221-10	2011	Thus, eNOS protein radical formation provides the basis for a mechanism of superoxide-directed regulation of eNOS, involving thiol oxidation, defining a unique pathway for the redox regulation of cardiovascular function.	Sulfhydryl Compounds	125-130	nitric oxide synthase 3	Homo sapiens	6-10
21666221-10	2011	Thus, eNOS protein radical formation provides the basis for a mechanism of superoxide-directed regulation of eNOS, involving thiol oxidation, defining a unique pathway for the redox regulation of cardiovascular function.	Sulfhydryl Compounds	125-130	nitric oxide synthase 3	Homo sapiens	109-113
21897153-0	2011	Role of sepiapterin on endothelial nitric oxide synthase in acute kidney injury: an enigmatic story.	sepiapterin	8-19	nitric oxide synthase 3	Homo sapiens	23-56
21607713-0	2011	The 894G > T (Glu298Asp) variant in the endothelial NOS gene and MTHFR polymorphisms influence homocysteine levels in patients with cognitive decline.	Homocysteine	95-107	nitric oxide synthase 3	Homo sapiens	40-55
21607713-4	2011	In this study, we evaluated the relationships between plasma homocysteine levels and genetic risk factors for hyperhomocysteinemia, i.e., the presence of gene variants for methylenetetrahydrofolate reductase (MTHFR) and endothelial nitric oxide synthase (eNOS) in patients with cognitive impairment.	Homocysteine	61-73	nitric oxide synthase 3	Homo sapiens	220-253
21607713-4	2011	In this study, we evaluated the relationships between plasma homocysteine levels and genetic risk factors for hyperhomocysteinemia, i.e., the presence of gene variants for methylenetetrahydrofolate reductase (MTHFR) and endothelial nitric oxide synthase (eNOS) in patients with cognitive impairment.	Homocysteine	61-73	nitric oxide synthase 3	Homo sapiens	255-259
21607713-8	2011	In particular, the presence of eNOS TT894 genotype in patients with cognitive decline resulted significantly associated with increased plasma Hcy levels when compared with controls having the same genotype or patients having other eNOS genotypes (P = 0.02).	Homocysteine	142-145	nitric oxide synthase 3	Homo sapiens	31-35
21761876-11	2011	Assessment of individual anthocyanins also showed significant effects on p-Akt and p-eNOS.	Anthocyanins	25-37	nitric oxide synthase 3	Homo sapiens	83-89
21761876-0	2011	Effect of black currant anthocyanins on the activation of endothelial nitric oxide synthase (eNOS) in vitro in human endothelial cells.	Anthocyanins	24-36	nitric oxide synthase 3	Homo sapiens	93-97
21761876-5	2011	Vitamin C is also known to activate Akt and eNOS in in vitro models, and black currants are rich in vitamin C.	Ascorbic Acid	0-9	nitric oxide synthase 3	Homo sapiens	44-48
21761876-9	2011	Activation of Akt and eNOS was abolished by incubation with wortmannin, a PI3K inhibitor, supporting the involvement of PI3K/Akt.	Wortmannin	60-70	nitric oxide synthase 3	Homo sapiens	22-26
21761876-10	2011	Vitamin C alone significantly increased the p-Akt and p-eNOS (P < 0.05); however, removal of vitamin C from black currant did not significantly affect p-Akt and p-eNOS compared to black currant with vitamin C.	Ascorbic Acid	0-9	nitric oxide synthase 3	Homo sapiens	54-60
21527308-6	2011	Molecular studies were carried out to evaluate the expression profile of NOS isoforms in human lymphocytes and it was shown that H-DHPM decreases the increased iNOS in COPD along with reestablishing the normal levels of endothelial nitric oxide synthase (eNOS).	h-dhpm	129-135	nitric oxide synthase 3	Homo sapiens	220-253
21768538-7	2011	A complementary finding is that miR-92a inhibitor increased the mRNA and protein expression of KLF2, endothelial nitric oxide synthase, and thrombomodulin.	mir-92a	32-39	nitric oxide synthase 3	Homo sapiens	101-134
21131444-5	2011	Exposure to Cl(2) (250-400 ppm) significantly inhibited eNOS-dependent vasodilation (stimulated by acetycholine) at 24 to 48 hours after exposure without affecting constriction responses to phenylephrine or vasodilation responses to an NO donor, suggesting decreased NO formation.	Chlorine	12-17	nitric oxide synthase 3	Homo sapiens	56-60
21131444-5	2011	Exposure to Cl(2) (250-400 ppm) significantly inhibited eNOS-dependent vasodilation (stimulated by acetycholine) at 24 to 48 hours after exposure without affecting constriction responses to phenylephrine or vasodilation responses to an NO donor, suggesting decreased NO formation.	acetycholine	99-111	nitric oxide synthase 3	Homo sapiens	56-60
21616556-7	2011	Moreover, the avbeta3 antibody, the PI3-K inhibitor LY294002 and the eNOS inhibitor NMA suppressed the OPN-mediated increase in NO production and angiogenesis in EPCs.	nma	84-87	nitric oxide synthase 3	Homo sapiens	69-73
21747057-7	2011	Silencing Fis1 or Drp1 expression with siRNA blunted high glucose-induced alterations in mitochondrial networks, reactive oxygen species production, endothelial nitric oxide synthase activation, and cGMP production.	Glucose	58-65	nitric oxide synthase 3	Homo sapiens	149-182
21380725-1	2011	The present study has investigated the role of endothelial nitric oxide (eNOS) G894T polymorphism and its interaction with methylenetetrahydrofolate reductase (MTHFR) C677T and A1298C variants on the predisposition to diabetic nephropathy and its progression.	Nitric Oxide	59-71	nitric oxide synthase 3	Homo sapiens	73-77
21380725-6	2011	The presence of GT + TT genotypes of eNOS was significantly associated with increased risk of coronary artery disease in micro- and macro-albuminuric patients compared to normoalbuminuric patients.	gt + tt	16-23	nitric oxide synthase 3	Homo sapiens	37-41
21613201-5	2011	We also examined the effect of maternal ADRB2 and the endothelial nitric oxide synthase gene (NOS3) on ephedrine and phenylephrine requirements for treatment of maternal hypotension.	Ephedrine	103-112	nitric oxide synthase 3	Homo sapiens	94-98
21529755-0	2011	Placental endothelial nitric oxide synthase in multiple and single dose betamethasone exposed pregnancies.	Betamethasone	72-85	nitric oxide synthase 3	Homo sapiens	10-43
21613201-5	2011	We also examined the effect of maternal ADRB2 and the endothelial nitric oxide synthase gene (NOS3) on ephedrine and phenylephrine requirements for treatment of maternal hypotension.	Phenylephrine	117-130	nitric oxide synthase 3	Homo sapiens	94-98
21463621-0	2011	Amlodipine increases endothelial nitric oxide release by modulating binding of native eNOS protein complex to caveolin-1.	Amlodipine	0-10	nitric oxide synthase 3	Homo sapiens	86-90
21529755-1	2011	OBJECTIVE: To compare endothelial nitric oxide synthase expression and capillary density (CDS) in placentas exposed to single or multiple courses of betamethasone.	Betamethasone	149-162	nitric oxide synthase 3	Homo sapiens	22-55
21529755-5	2011	RESULTS: Mean and maximum capillary density were increased (P = .013 and .005) and the ratio of endothelial nitric oxide synthase to capillary density decreased (P = .016) in specimens exposed to 4 courses of betamethasone compared with 1 to 3 courses.	Betamethasone	209-222	nitric oxide synthase 3	Homo sapiens	96-129
21463621-2	2011	Because endothelial NO synthase (eNOS), the main source of NO in EC is known to be inhibited by caveolin-1 (Cav-1), the purpose of this study is to investigate the possibility that amlodipine can modulate eNOS interaction with Cav-1.	Amlodipine	181-191	nitric oxide synthase 3	Homo sapiens	205-209
21670344-0	2011	Endothelial nitric oxide synthase gene variants and primary open-angle glaucoma: interactions with hypertension, alcohol intake, and cigarette smoking.	Alcohols	113-120	nitric oxide synthase 3	Homo sapiens	0-33
21293034-12	2011	Increases in abundance of IFNT protein (the pregnancy recognition signal), NOS2, NOS3 and GCH1 for conversion of Arg to nitric oxide, and ODC1 for synthesis of polyamines are all important for growth and development of the ovine conceptus during pregnancy.	Arginine	113-116	nitric oxide synthase 3	Homo sapiens	81-85
21293034-12	2011	Increases in abundance of IFNT protein (the pregnancy recognition signal), NOS2, NOS3 and GCH1 for conversion of Arg to nitric oxide, and ODC1 for synthesis of polyamines are all important for growth and development of the ovine conceptus during pregnancy.	Nitric Oxide	120-132	nitric oxide synthase 3	Homo sapiens	81-85
21463621-0	2011	Amlodipine increases endothelial nitric oxide release by modulating binding of native eNOS protein complex to caveolin-1.	Nitric Oxide	33-45	nitric oxide synthase 3	Homo sapiens	86-90
21463621-5	2011	However, glutathione s-transferase (GST) pulldown assays reveal that amlodipine can prevent binding of native, acylated eNOS complexes to the active domain of Cav-1 in a concentration-dependent fashion, suggesting that amlodipine has an antagonistic effect on the native eNOS/Cav-1 signaling complex.	Amlodipine	69-79	nitric oxide synthase 3	Homo sapiens	120-124
21463621-5	2011	However, glutathione s-transferase (GST) pulldown assays reveal that amlodipine can prevent binding of native, acylated eNOS complexes to the active domain of Cav-1 in a concentration-dependent fashion, suggesting that amlodipine has an antagonistic effect on the native eNOS/Cav-1 signaling complex.	Amlodipine	219-229	nitric oxide synthase 3	Homo sapiens	120-124
21463621-2	2011	Because endothelial NO synthase (eNOS), the main source of NO in EC is known to be inhibited by caveolin-1 (Cav-1), the purpose of this study is to investigate the possibility that amlodipine can modulate eNOS interaction with Cav-1.	Amlodipine	181-191	nitric oxide synthase 3	Homo sapiens	33-37
21463621-6	2011	Moreover, experiments performed in a reconstituted cell line confirm that amlodipine"s effect on NO release is highly selective for the eNOS/Cav-1 interaction.	Amlodipine	74-84	nitric oxide synthase 3	Homo sapiens	136-140
21383022-0	2011	Protein kinase CbetaII-mediated phosphorylation of endothelial nitric oxide synthase threonine 495 mediates the endothelial dysfunction induced by FK506 (tacrolimus).	Threonine	85-94	nitric oxide synthase 3	Homo sapiens	51-84
21463621-7	2011	To our knowledge, these data are the first to demonstrate a direct effect of amlodipine on the eNOS/Cav-1 protein complex and support the concept of developing novel therapies specifically aimed at modulating the eNOS/Cav-1 interaction to improve endothelial function in cardiovascular diseases.	Amlodipine	77-87	nitric oxide synthase 3	Homo sapiens	95-99
21463621-7	2011	To our knowledge, these data are the first to demonstrate a direct effect of amlodipine on the eNOS/Cav-1 protein complex and support the concept of developing novel therapies specifically aimed at modulating the eNOS/Cav-1 interaction to improve endothelial function in cardiovascular diseases.	Amlodipine	77-87	nitric oxide synthase 3	Homo sapiens	213-217
21740847-10	2011	Metformin also increased phosphorylation of AMPK and eNOS, and reduced the expression of TGF-beta1, basic fibroblast growth factor (bFGF), and tumor necrosis factor (TNF)-alpha.	Metformin	0-9	nitric oxide synthase 3	Homo sapiens	53-57
21740847-11	2011	CONCLUSIONS: Metformin has beneficial effects on cardiomyocytes, and this effect involves activation of the AMPK-eNOS pathway.	Metformin	13-22	nitric oxide synthase 3	Homo sapiens	113-117
20559724-0	2011	Endothelial nitric oxide synthase gene intron 4 polymorphism predicts new onset diabetes mellitus after transplantation in kidney allograft recipients treated with cyclosporin A.	Cyclosporine	164-177	nitric oxide synthase 3	Homo sapiens	0-33
20559724-1	2011	BACKGROUND: Nitric oxide (NO), synthesized from LS: -arginine by the enzyme endothelial nitric oxide synthase (eNOS), is a potent vasodilator and has been implicated in mediating insulin-induced uptake and metabolism of glucose in skeletal muscle.	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	76-109
20559724-1	2011	BACKGROUND: Nitric oxide (NO), synthesized from LS: -arginine by the enzyme endothelial nitric oxide synthase (eNOS), is a potent vasodilator and has been implicated in mediating insulin-induced uptake and metabolism of glucose in skeletal muscle.	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	111-115
20559724-1	2011	BACKGROUND: Nitric oxide (NO), synthesized from LS: -arginine by the enzyme endothelial nitric oxide synthase (eNOS), is a potent vasodilator and has been implicated in mediating insulin-induced uptake and metabolism of glucose in skeletal muscle.	Arginine	53-61	nitric oxide synthase 3	Homo sapiens	76-109
20559724-1	2011	BACKGROUND: Nitric oxide (NO), synthesized from LS: -arginine by the enzyme endothelial nitric oxide synthase (eNOS), is a potent vasodilator and has been implicated in mediating insulin-induced uptake and metabolism of glucose in skeletal muscle.	Arginine	53-61	nitric oxide synthase 3	Homo sapiens	111-115
20559724-1	2011	BACKGROUND: Nitric oxide (NO), synthesized from LS: -arginine by the enzyme endothelial nitric oxide synthase (eNOS), is a potent vasodilator and has been implicated in mediating insulin-induced uptake and metabolism of glucose in skeletal muscle.	Glucose	220-227	nitric oxide synthase 3	Homo sapiens	76-109
20559724-1	2011	BACKGROUND: Nitric oxide (NO), synthesized from LS: -arginine by the enzyme endothelial nitric oxide synthase (eNOS), is a potent vasodilator and has been implicated in mediating insulin-induced uptake and metabolism of glucose in skeletal muscle.	Glucose	220-227	nitric oxide synthase 3	Homo sapiens	111-115
21383022-0	2011	Protein kinase CbetaII-mediated phosphorylation of endothelial nitric oxide synthase threonine 495 mediates the endothelial dysfunction induced by FK506 (tacrolimus).	Tacrolimus	147-152	nitric oxide synthase 3	Homo sapiens	51-84
21383022-0	2011	Protein kinase CbetaII-mediated phosphorylation of endothelial nitric oxide synthase threonine 495 mediates the endothelial dysfunction induced by FK506 (tacrolimus).	Tacrolimus	154-164	nitric oxide synthase 3	Homo sapiens	51-84
21383022-2	2011	We have previously shown that FK506 activates Ca(2+)/diacylglycerol-dependent conventional protein kinase C (cPKC), which phosphorylates endothelial nitric oxide synthase (eNOS) at one of its inhibitory sites, Thr495.	Tacrolimus	30-35	nitric oxide synthase 3	Homo sapiens	137-170
21383022-2	2011	We have previously shown that FK506 activates Ca(2+)/diacylglycerol-dependent conventional protein kinase C (cPKC), which phosphorylates endothelial nitric oxide synthase (eNOS) at one of its inhibitory sites, Thr495.	Diglycerides	53-67	nitric oxide synthase 3	Homo sapiens	137-170
21324713-6	2011	Western blot of phospho-eNOS (serine1177) and eNOS and was significantly induced by hypoxia but not after EPO treatment.	serine1177	30-40	nitric oxide synthase 3	Homo sapiens	24-28
21631225-3	2011	Endothelial nitric oxide synthase genes encode eNOS, which synthesizes NO from l-arginine.	Arginine	79-89	nitric oxide synthase 3	Homo sapiens	0-33
21631225-3	2011	Endothelial nitric oxide synthase genes encode eNOS, which synthesizes NO from l-arginine.	Arginine	79-89	nitric oxide synthase 3	Homo sapiens	47-51
21623570-0	2011	Ginkgolide B promotes proliferation and functional activities of bone marrow-derived endothelial progenitor cells: involvement of Akt/eNOS and MAPK/p38 signaling pathways.	ginkgolide B	0-12	nitric oxide synthase 3	Homo sapiens	134-138
21623570-8	2011	GB induced the phosphorylation of eNOS, Akt and p38, which in turn promoted cell proliferation and function.	ginkgolide B	0-2	nitric oxide synthase 3	Homo sapiens	34-38
21623570-9	2011	In conclusion, the present study demonstrates that GB, at a near medical applied dose, increases the number and functional activities of EPCs with involvement of Akt/endothelial nitric oxide synthase and mitogen-activated protein kinase (MAPK)/p38 signal pathways.	ginkgolide B	51-53	nitric oxide synthase 3	Homo sapiens	166-199
21261471-1	2011	Oxidative stress has been shown to convert endothelial nitric oxide synthase (eNOS) from an NO-producing enzyme to an enzyme that generates superoxide, a process termed NOS uncoupling.	Superoxides	140-150	nitric oxide synthase 3	Homo sapiens	43-76
21388435-8	2011	Immunoprecipitation of eNOS in human umbilical vein endothelial cells treated with 20-HETE revealed a decrease in basal and vascular endothelial growth factor-stimulated Hsp90 association with eNOS (P<0.05).	20-hydroxy-5,8,11,14-eicosatetraenoic acid	83-90	nitric oxide synthase 3	Homo sapiens	23-27
21388435-8	2011	Immunoprecipitation of eNOS in human umbilical vein endothelial cells treated with 20-HETE revealed a decrease in basal and vascular endothelial growth factor-stimulated Hsp90 association with eNOS (P<0.05).	20-hydroxy-5,8,11,14-eicosatetraenoic acid	83-90	nitric oxide synthase 3	Homo sapiens	193-197
21458418-7	2011	Triciribine, an Akt inhibitor, and wortmannin significantly inhibited RBP4-induced p-Akt and p-eNOS production.	triciribine	0-11	nitric oxide synthase 3	Homo sapiens	95-99
21623032-2	2011	A single nucleotide polymorphism G894T within exon 7 of endothelial nitric oxide synthase (eNOS-7) gene, resulting in a replacement of glutamic acid by aspartic acid, has been studied as a putative candidate gene for cardiovascular diseases.	Glutamic Acid	135-148	nitric oxide synthase 3	Homo sapiens	56-89
21623032-2	2011	A single nucleotide polymorphism G894T within exon 7 of endothelial nitric oxide synthase (eNOS-7) gene, resulting in a replacement of glutamic acid by aspartic acid, has been studied as a putative candidate gene for cardiovascular diseases.	Glutamic Acid	135-148	nitric oxide synthase 3	Homo sapiens	91-95
21623032-2	2011	A single nucleotide polymorphism G894T within exon 7 of endothelial nitric oxide synthase (eNOS-7) gene, resulting in a replacement of glutamic acid by aspartic acid, has been studied as a putative candidate gene for cardiovascular diseases.	Aspartic Acid	152-165	nitric oxide synthase 3	Homo sapiens	56-89
21623032-2	2011	A single nucleotide polymorphism G894T within exon 7 of endothelial nitric oxide synthase (eNOS-7) gene, resulting in a replacement of glutamic acid by aspartic acid, has been studied as a putative candidate gene for cardiovascular diseases.	Aspartic Acid	152-165	nitric oxide synthase 3	Homo sapiens	91-95
21332418-1	2011	Experimental studies suggest that nitric oxide produced by endothelial nitric oxide synthase (NOS3) plays a role in maintaining cerebral blood flow (CBF) after traumatic brain injury (TBI).	Nitric Oxide	34-46	nitric oxide synthase 3	Homo sapiens	59-92
21332418-1	2011	Experimental studies suggest that nitric oxide produced by endothelial nitric oxide synthase (NOS3) plays a role in maintaining cerebral blood flow (CBF) after traumatic brain injury (TBI).	Nitric Oxide	34-46	nitric oxide synthase 3	Homo sapiens	94-98
21513492-4	2011	Reactive oxygen species (ROS) are produced by various oxidase enzymes, including nicotinamide-adenine dinucleotide phosphate (NADPH) oxidase, xanthine oxidase, uncoupled endothelial NO synthase (eNOS), cyclooxygenase, glucose oxidase, and lipooxygenase, and mitochondrial electron transport.	Reactive Oxygen Species	0-23	nitric oxide synthase 3	Homo sapiens	195-199
21513492-4	2011	Reactive oxygen species (ROS) are produced by various oxidase enzymes, including nicotinamide-adenine dinucleotide phosphate (NADPH) oxidase, xanthine oxidase, uncoupled endothelial NO synthase (eNOS), cyclooxygenase, glucose oxidase, and lipooxygenase, and mitochondrial electron transport.	Reactive Oxygen Species	25-28	nitric oxide synthase 3	Homo sapiens	195-199
21458418-7	2011	Triciribine, an Akt inhibitor, and wortmannin significantly inhibited RBP4-induced p-Akt and p-eNOS production.	Wortmannin	35-45	nitric oxide synthase 3	Homo sapiens	95-99
21239633-4	2011	However, this is paralleled by changes in NO in response to ionomycin, suggesting this is solely due to higher levels of endothelial nitric oxide synthase (eNOS) protein in the follicular phase.	Ionomycin	60-69	nitric oxide synthase 3	Homo sapiens	121-154
21486801-13	2011	Reduced NOS3 substrate availability through upregulated arginase contributes to cutaneous microvascular dysfunction in hyperocholesterolaemic humans, which is corrected with atorvastatin therapy.	Atorvastatin	174-186	nitric oxide synthase 3	Homo sapiens	8-12
21297022-10	2011	These results indicate that secretoneurin acutely induces relaxation through the activation of endothelial nitric oxide synthase (eNOS) and cyclooxygenase, with nitric oxide playing the dominant role.	Nitric Oxide	107-119	nitric oxide synthase 3	Homo sapiens	130-134
20870316-1	2011	BACKGROUND & AIMS: Endothelial nitric oxide synthase (eNOS) gene variations have been linked to a higher risk for cardiovascular diseases (CVD) by unknown mechanisms.	Adenosine Monophosphate	12-15	nitric oxide synthase 3	Homo sapiens	58-62
21352809-8	2011	The phosphorylation of Akt, PI3K and eNOS were up-regulated by oxLDL, which was attenuated by LY294002.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	94-102	nitric oxide synthase 3	Homo sapiens	37-41
21352809-9	2011	Our results suggested that oxLDL at low concentration could promote in-vitro angiogenesis and activate nitric oxide synthesis through PI3K/Akt/eNOS pathway in HCAEC.	Nitric Oxide	103-115	nitric oxide synthase 3	Homo sapiens	143-147
20870316-1	2011	BACKGROUND & AIMS: Endothelial nitric oxide synthase (eNOS) gene variations have been linked to a higher risk for cardiovascular diseases (CVD) by unknown mechanisms.	Adenosine Monophosphate	12-15	nitric oxide synthase 3	Homo sapiens	23-56
21172428-1	2011	The homodimeric flavohemeprotein endothelial nitric oxide synthase (eNOS) oxidizes l-arginine to l-citrulline and nitric oxide (NO), which acutely vasodilates blood vessels and inhibits platelet aggregation.	Arginine	83-93	nitric oxide synthase 3	Homo sapiens	33-66
21338328-2	2011	It is formed from L-arginine by NOS isoforms (nNOS, iNOS and eNOS).	Arginine	18-28	nitric oxide synthase 3	Homo sapiens	61-65
21172428-1	2011	The homodimeric flavohemeprotein endothelial nitric oxide synthase (eNOS) oxidizes l-arginine to l-citrulline and nitric oxide (NO), which acutely vasodilates blood vessels and inhibits platelet aggregation.	Arginine	83-93	nitric oxide synthase 3	Homo sapiens	68-72
21172428-1	2011	The homodimeric flavohemeprotein endothelial nitric oxide synthase (eNOS) oxidizes l-arginine to l-citrulline and nitric oxide (NO), which acutely vasodilates blood vessels and inhibits platelet aggregation.	Citrulline	97-109	nitric oxide synthase 3	Homo sapiens	33-66
21172428-1	2011	The homodimeric flavohemeprotein endothelial nitric oxide synthase (eNOS) oxidizes l-arginine to l-citrulline and nitric oxide (NO), which acutely vasodilates blood vessels and inhibits platelet aggregation.	Citrulline	97-109	nitric oxide synthase 3	Homo sapiens	68-72
21172428-1	2011	The homodimeric flavohemeprotein endothelial nitric oxide synthase (eNOS) oxidizes l-arginine to l-citrulline and nitric oxide (NO), which acutely vasodilates blood vessels and inhibits platelet aggregation.	Nitric Oxide	45-57	nitric oxide synthase 3	Homo sapiens	68-72
21172428-4	2011	Uncoupled eNOS monomerizes and generates reactive oxygen species (ROS) rather than NO.	Reactive Oxygen Species	41-64	nitric oxide synthase 3	Homo sapiens	10-14
21172428-4	2011	Uncoupled eNOS monomerizes and generates reactive oxygen species (ROS) rather than NO.	Reactive Oxygen Species	66-69	nitric oxide synthase 3	Homo sapiens	10-14
21172428-6	2011	Therefore, modulating uncoupled eNOS, in particular eNOS-dependent ROS generation, is an attractive therapeutic approach to preventing and/or treating cardiopulmonary disorders, including protective effects during cardiothoracic surgery.	Reactive Oxygen Species	67-70	nitric oxide synthase 3	Homo sapiens	32-36
21172428-6	2011	Therefore, modulating uncoupled eNOS, in particular eNOS-dependent ROS generation, is an attractive therapeutic approach to preventing and/or treating cardiopulmonary disorders, including protective effects during cardiothoracic surgery.	Reactive Oxygen Species	67-70	nitric oxide synthase 3	Homo sapiens	52-56
21172428-8	2011	In addition, the related therapeutic possibilities such as supplementation with the eNOS substrate l-arginine, volatile NO, and direct NO donors as well as eNOS modulators such as the eNOS cofactor tetrahydrobiopterin and folic acid are discussed in detail.	Arginine	99-109	nitric oxide synthase 3	Homo sapiens	84-88
24250362-0	2011	Spironolactone inhibits NADPH oxidase-induced oxidative stress and enhances eNOS in human endothelial cells.	Spironolactone	0-14	nitric oxide synthase 3	Homo sapiens	76-80
21300668-0	2011	Equol-stimulated mitochondrial reactive oxygen species activate endothelial nitric oxide synthase and redox signaling in endothelial cells: roles for F-actin and GPR30.	Reactive Oxygen Species	31-54	nitric oxide synthase 3	Homo sapiens	64-97
24250362-11	2011	While aldosterone effectively inhibited endothelial nitric oxide (eNOS) protein expression, pretreatment with spiro markedly restored it to its normal level.	Aldosterone	6-17	nitric oxide synthase 3	Homo sapiens	66-70
24250362-11	2011	While aldosterone effectively inhibited endothelial nitric oxide (eNOS) protein expression, pretreatment with spiro markedly restored it to its normal level.	Nitric Oxide	52-64	nitric oxide synthase 3	Homo sapiens	66-70
20599230-9	2011	Cilnidipine increased the expression of endothelial nitric oxide synthase mRNA by 42.4% (P < .05) and enhanced phosphorylation level of endothelial nitric oxide synthase at Ser(1177) by 37.0% (P < .05).	Serine	176-179	nitric oxide synthase 3	Homo sapiens	139-172
20599230-10	2011	CONCLUSIONS: The new generation of calcium channel antagonist cilnidipine relaxes human arteries through calcium channel antagonism and increases production of nitric oxide by enhancement of endothelial nitric oxide synthase.	cilnidipine	62-73	nitric oxide synthase 3	Homo sapiens	191-224
20599230-0	2011	Dual actions of cilnidipine in human internal thoracic artery: inhibition of calcium channels and enhancement of endothelial nitric oxide synthase.	cilnidipine	16-27	nitric oxide synthase 3	Homo sapiens	113-146
20599230-5	2011	The expression level of endothelial nitric oxide synthase mRNA was assayed by quantitative real-time polymerase chain reaction, and the phosphorylation of endothelial nitric oxide synthase at Ser(1177) was determined by Western blotting analysis.	Serine	192-195	nitric oxide synthase 3	Homo sapiens	155-188
20599230-9	2011	Cilnidipine increased the expression of endothelial nitric oxide synthase mRNA by 42.4% (P < .05) and enhanced phosphorylation level of endothelial nitric oxide synthase at Ser(1177) by 37.0% (P < .05).	cilnidipine	0-11	nitric oxide synthase 3	Homo sapiens	40-73
21178821-2	2011	BH4 is a cofactor for endothelial NOS (eNOS).	sapropterin	0-3	nitric oxide synthase 3	Homo sapiens	22-37
20599230-9	2011	Cilnidipine increased the expression of endothelial nitric oxide synthase mRNA by 42.4% (P < .05) and enhanced phosphorylation level of endothelial nitric oxide synthase at Ser(1177) by 37.0% (P < .05).	cilnidipine	0-11	nitric oxide synthase 3	Homo sapiens	139-172
20580385-4	2011	Treatment of HGMEC with fenofibrate resulted in transient activation of adenosine monophosphate-activated protein kinase (AMPK), thereby inducing the phosphorylation of Akt and endothelial nitric oxide synthase, leading to nitric oxide production.	hgmec	13-18	nitric oxide synthase 3	Homo sapiens	177-210
20580385-4	2011	Treatment of HGMEC with fenofibrate resulted in transient activation of adenosine monophosphate-activated protein kinase (AMPK), thereby inducing the phosphorylation of Akt and endothelial nitric oxide synthase, leading to nitric oxide production.	Fenofibrate	24-35	nitric oxide synthase 3	Homo sapiens	177-210
21237248-0	2011	Molsidomine modulates the cNOS activity in an experimental model of cholinergic damage induced by 192-IgG saporin.	Molsidomine	0-11	nitric oxide synthase 3	Homo sapiens	26-30
21039601-2	2011	In the nitric oxide (NO) synthesis pathway, nitric oxide synthases (encoded by NOS1, NOS2A, and NOS3) and arginases (encoded by ARG1 and ARG2) compete for L-arginine.	Nitric Oxide	7-19	nitric oxide synthase 3	Homo sapiens	96-100
21039601-2	2011	In the nitric oxide (NO) synthesis pathway, nitric oxide synthases (encoded by NOS1, NOS2A, and NOS3) and arginases (encoded by ARG1 and ARG2) compete for L-arginine.	Arginine	155-165	nitric oxide synthase 3	Homo sapiens	96-100
21328466-2	2011	Data report that anandamide in a dose-and time-dependent manner increased NO and cGMP levels and stimulated endothelial nitric oxide synthase (eNOS) activity.	anandamide	17-27	nitric oxide synthase 3	Homo sapiens	108-141
21886581-1	2011	Endothelial nitric oxide synthase (NOS3) is one of the enzymes influencing nitric oxide (NO) function in the human brain.	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	35-39
21886581-4	2011	Methamphetamine (METH) use disorder is a known psychotic disorder, and we therefore conducted a gene-based case-control study between tagging single nucleotide polymorphisms (SNPs) (rs2070744, rs1799983) in NOS3 and METH-induced psychosis in Japanese subjects (183 with METH-induced psychosis and 267 controls).	Methamphetamine	0-15	nitric oxide synthase 3	Homo sapiens	207-211
21256614-1	2011	UNLABELLED: SUBJECT AND AIMS: Endothelial derived nitric oxide (eNOS) is involved in several functions playing important role in development of type 2 diabetes and insulin resistance.	Nitric Oxide	50-62	nitric oxide synthase 3	Homo sapiens	64-68
21273388-10	2011	nNO levels were higher in PCD subjects with the NOS3 thymidine 894 mutation, and this was associated with a higher ciliary beat frequency (p = 0.045).	Nitrous Oxide	0-3	nitric oxide synthase 3	Homo sapiens	48-52
21047628-0	2011	Role of glucocorticoid receptor in the inhibitory effect of medroxyprogesterone acetate on the estrogen-induced endothelial nitric oxide synthase phosphorylation in human umbilical vein endothelial cells.	Medroxyprogesterone Acetate	60-87	nitric oxide synthase 3	Homo sapiens	112-145
21047628-1	2011	We aimed to clarify which steroid receptor is involved in the inhibitory effect of medroxyprogesterone acetate (MPA) on estrogen-induced endothelial nitric oxide synthase (eNOS) phosphorylation in human umbilical vein endothelial cells (HUVEC).	Medroxyprogesterone Acetate	83-110	nitric oxide synthase 3	Homo sapiens	137-170
25961244-2	2011	Nitric oxide (NO), the product of eNOS, is a free radical involved in the physiology and pathophysiology of living organisms and in a variety of biological processes including the maintenance of vascular homeostasis.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	34-38
20661250-11	2011	CONCLUSIONS: Our findings suggest that the eNOS haplotype, C b Glu, is associated with hypertension in obese children and adolescents.	Glutamic Acid	63-66	nitric oxide synthase 3	Homo sapiens	43-47
21328466-2	2011	Data report that anandamide in a dose-and time-dependent manner increased NO and cGMP levels and stimulated endothelial nitric oxide synthase (eNOS) activity.	anandamide	17-27	nitric oxide synthase 3	Homo sapiens	143-147
21383590-3	2011	Our study demonstrated that acute nicotine treatment enhanced nitric oxide release, eNOS activation, and proangiogenic activity.	Nicotine	34-42	nitric oxide synthase 3	Homo sapiens	84-88
21328466-5	2011	Finally the anandamide effect on NO and cGMP levels, eNOS and AKT phosphorylation/activation were inhibited by SR141716, specific cannabinoid receptor 1 antagonist, supporting the involvement of anandamide binding to this receptor.	anandamide	12-22	nitric oxide synthase 3	Homo sapiens	53-57
21383590-5	2011	These findings seem to be related to eNOS gene expression and nitric oxide production, which may be involved in the pathophysiology of chronic nicotine addicts.	Nicotine	143-151	nitric oxide synthase 3	Homo sapiens	37-41
21328466-5	2011	Finally the anandamide effect on NO and cGMP levels, eNOS and AKT phosphorylation/activation were inhibited by SR141716, specific cannabinoid receptor 1 antagonist, supporting the involvement of anandamide binding to this receptor.	Rimonabant	111-119	nitric oxide synthase 3	Homo sapiens	53-57
21328466-6	2011	Overall data of this report indicate that low concentrations of anandamide, through PI3K/AKT pathway activation, stimulates eNOS activity and increases NO levels in human platelets.	anandamide	64-74	nitric oxide synthase 3	Homo sapiens	124-128
21108657-10	2011	The melatonin benefits correlated with the generation of nitric oxide (through constitutive e-NOS activation) and the prevention of oxidative stress and inflammatory cytokine release including tumor necrosis factor and adiponectin, respectively.	Melatonin	4-13	nitric oxide synthase 3	Homo sapiens	92-97
21108657-10	2011	The melatonin benefits correlated with the generation of nitric oxide (through constitutive e-NOS activation) and the prevention of oxidative stress and inflammatory cytokine release including tumor necrosis factor and adiponectin, respectively.	Nitric Oxide	57-69	nitric oxide synthase 3	Homo sapiens	92-97
21417768-9	2011	An Hsp90 inhibitor, 17-DMAG, was able to inhibit the eNOS and Hsp90 interaction, decrease the level of eNOS, and significantly inhibit cord formation to 38% of the level observed in the control.	17-(dimethylaminoethylamino)-17-demethoxygeldanamycin	20-27	nitric oxide synthase 3	Homo sapiens	53-57
21150639-2	2011	The mechanism may involve decreased production of nitric oxide via endothelial nitric oxide synthase (eNOS), impaired bioavailability of nitric oxide, and elevated plasma levels of asymmetric dimethylarginine (ADMA).	Nitric Oxide	50-62	nitric oxide synthase 3	Homo sapiens	67-100
21150639-2	2011	The mechanism may involve decreased production of nitric oxide via endothelial nitric oxide synthase (eNOS), impaired bioavailability of nitric oxide, and elevated plasma levels of asymmetric dimethylarginine (ADMA).	Nitric Oxide	50-62	nitric oxide synthase 3	Homo sapiens	102-106
21417768-9	2011	An Hsp90 inhibitor, 17-DMAG, was able to inhibit the eNOS and Hsp90 interaction, decrease the level of eNOS, and significantly inhibit cord formation to 38% of the level observed in the control.	17-(dimethylaminoethylamino)-17-demethoxygeldanamycin	20-27	nitric oxide synthase 3	Homo sapiens	103-107
20930716-6	2011	Carriers of the NOS3 Asp298 allele had higher %BF only in the presence of an adverse environment (low SES).	benzo(b)fluoranthene	47-49	nitric oxide synthase 3	Homo sapiens	16-20
21069449-1	2011	In an analysis of the possible association of endothelial constitutive nitric oxide synthase (ecNOS) gene polymorphism and plasma nitric oxide levels in patients with acute coronary syndrome, we investigated 106 patients with the syndrome and 100 healthy controls.	Nitric Oxide	71-83	nitric oxide synthase 3	Homo sapiens	94-99
21239969-4	2011	Endothelial nitric oxide synthase and caveolin-1 phosphorylation was measured in human umbilical vein endothelial cells treated with levobupivacaine alone and with the addition of LE.	Levobupivacaine	133-148	nitric oxide synthase 3	Homo sapiens	0-33
21239969-9	2011	Treatment with LE also inhibited the phosphorylation of endothelial nitric oxide synthase induced by levobupivacaine in human umbilical vein endothelial cells.	Leu-Glu	15-17	nitric oxide synthase 3	Homo sapiens	56-89
21239969-9	2011	Treatment with LE also inhibited the phosphorylation of endothelial nitric oxide synthase induced by levobupivacaine in human umbilical vein endothelial cells.	Levobupivacaine	101-116	nitric oxide synthase 3	Homo sapiens	56-89
21145922-0	2011	eNOS activation mediated by AMPK after stimulation of endothelial cells with histamine or thrombin is dependent on LKB1.	Histamine	77-86	nitric oxide synthase 3	Homo sapiens	0-4
21145922-2	2011	Previously, we have shown that under culture conditions that allow reduction of ATP-levels after stimulation, activation of AMPK contributes to eNOS phosphorylation and activation in endothelial cells after treatment with thrombin.	Adenosine Triphosphate	80-83	nitric oxide synthase 3	Homo sapiens	144-148
21145922-3	2011	In this paper we examined the signaling pathways mediating phosphorylation and activation of eNOS after stimulation of cultured human umbilical vein endothelial cells (HUVEC) with histamine and the role of LKB1-AMPK in the signaling.	Histamine	180-189	nitric oxide synthase 3	Homo sapiens	93-97
21145922-6	2011	Downregulation of AMPK with siRNA partially inhibited eNOS phosphorylation caused by histamine in cells maintained in medium 199.	Histamine	85-94	nitric oxide synthase 3	Homo sapiens	54-58
21145922-12	2011	Under conditions where intracellular ATP is lowered by histamine, AMPK is activated by both LKB1 and CaMKK and, in turn, mediates eNOS phosphorylation in an LKB1 dependent manner.	Adenosine Triphosphate	37-40	nitric oxide synthase 3	Homo sapiens	130-134
21145922-12	2011	Under conditions where intracellular ATP is lowered by histamine, AMPK is activated by both LKB1 and CaMKK and, in turn, mediates eNOS phosphorylation in an LKB1 dependent manner.	Histamine	55-64	nitric oxide synthase 3	Homo sapiens	130-134
21145922-14	2011	Under conditions where intracellular ATP is unchanged after histamine treatment, CaMKK alone activates AMPK and eNOS is phosphorylated and activated independent of AMPK.	Histamine	60-69	nitric oxide synthase 3	Homo sapiens	112-116
21111729-3	2011	Nitric oxide (NO) generated in the pulmonary vascular endothelium by endothelial nitric oxide synthase (eNOS) plays a pivotal role in perinatal circulatory adaptation.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	69-102
21258964-11	2011	Furthermore, atorvastatin suppressed Hcy-induced dysfunction of EPCs, increased NO production and eNOS expression, and down-regulated ROS accumulation and Nox4 activation.	Atorvastatin	13-25	nitric oxide synthase 3	Homo sapiens	98-102
21258964-11	2011	Furthermore, atorvastatin suppressed Hcy-induced dysfunction of EPCs, increased NO production and eNOS expression, and down-regulated ROS accumulation and Nox4 activation.	Homocysteine	37-40	nitric oxide synthase 3	Homo sapiens	98-102
21258964-13	2011	CONCLUSION: AMPK activation inhibits eNOS down-regulation and Nox4-derived ROS accumulation induced by Hcy in EPCs, and may contribute to the protective effects of atorvastatin on endothelial function.	Atorvastatin	164-176	nitric oxide synthase 3	Homo sapiens	37-41
21111729-3	2011	Nitric oxide (NO) generated in the pulmonary vascular endothelium by endothelial nitric oxide synthase (eNOS) plays a pivotal role in perinatal circulatory adaptation.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	104-108
21111729-4	2011	OBJECTIVE: To compare the expression of eNOS using IHC in postmortem lung tissue from newborns diagnosed clinically with PPHN and CDH.	pphn	121-125	nitric oxide synthase 3	Homo sapiens	40-44
21111729-10	2011	CONCLUSIONS: Upregulation of eNOS was seen both in infants with CDH and PPHN but was more marked in infants with CDH.	pphn	72-76	nitric oxide synthase 3	Homo sapiens	29-33
20563853-6	2011	Further experiments showed that morphine and EM-2 decreased endothelial nitric oxide synthase (eNOS) mRNA level and nitric oxide (NO) secretion in MCF-7 cells.	Morphine	32-40	nitric oxide synthase 3	Homo sapiens	60-93
21270322-1	2011	Caveolin 1 is required for the activation of endothelial nitric oxide synthase in response to 17beta-estradiol.	Estradiol	94-110	nitric oxide synthase 3	Homo sapiens	45-78
21106532-1	2011	Laminar shear stress (LSS) is known to increase endothelial nitric oxide (NO) production, which is essential for vascular health, through expression and activation of nitric oxide synthase 3 (NOS3).	Nitric Oxide	60-72	nitric oxide synthase 3	Homo sapiens	167-190
21375934-12	2011	However, activities of cNOS and iNOS in myocardium and the expression of eNOS mRNA were significantly decreased in H2S donor group (P<0.01), while the myocardial function significantly increased (P<0.05).	Hydrogen Sulfide	115-118	nitric oxide synthase 3	Homo sapiens	23-27
21375934-12	2011	However, activities of cNOS and iNOS in myocardium and the expression of eNOS mRNA were significantly decreased in H2S donor group (P<0.01), while the myocardial function significantly increased (P<0.05).	Hydrogen Sulfide	115-118	nitric oxide synthase 3	Homo sapiens	73-77
21106532-1	2011	Laminar shear stress (LSS) is known to increase endothelial nitric oxide (NO) production, which is essential for vascular health, through expression and activation of nitric oxide synthase 3 (NOS3).	Nitric Oxide	60-72	nitric oxide synthase 3	Homo sapiens	192-196
21106532-2	2011	Recent studies demonstrated that LSS also increases the expression of argininosuccinate synthetase 1 (ASS1) that regulates the provision of L-arginine, the substrate of NOS3.	Arginine	140-150	nitric oxide synthase 3	Homo sapiens	169-173
22144986-2	2011	These alterations are seen as abnormal expression and activity of the cationic amino acid transporters and endothelial nitric oxide synthase isoform, that is, the "endothelial L-arginine/nitric oxide signalling pathway."	Arginine	176-186	nitric oxide synthase 3	Homo sapiens	107-140
21156160-4	2011	Inhibition of endothelial nitric oxide synthase (eNOS) with N(omega)-nitro-l-arginine methyl ester increased endothelial permeability, indicating a role constitutive NO generation by eNOS in maintaining the permeability barrier.	NG-Nitroarginine Methyl Ester	60-98	nitric oxide synthase 3	Homo sapiens	14-47
21156160-4	2011	Inhibition of endothelial nitric oxide synthase (eNOS) with N(omega)-nitro-l-arginine methyl ester increased endothelial permeability, indicating a role constitutive NO generation by eNOS in maintaining the permeability barrier.	NG-Nitroarginine Methyl Ester	60-98	nitric oxide synthase 3	Homo sapiens	49-53
21156160-8	2011	These results show that endothelial permeability barrier function depends on constitutive generation of NO and that ascorbate-dependent tightening of this barrier involves maintaining NO through the eNOS/guanylate cyclase pathway.	Ascorbic Acid	116-125	nitric oxide synthase 3	Homo sapiens	199-203
21253017-6	2011	We document that apoEdp inhibits vascular endothelial growth factor-induced Flk-1 activation as well as downstream signaling pathways that involve c-Src, Akt, eNOS, FAK, and ERK1/2.	apoedp	17-23	nitric oxide synthase 3	Homo sapiens	159-163
21750782-3	2011	Nitric oxide generated by endothelial nitric oxide synthase (eNOS; EC 1.14.13.39) is an important vasorelaxant.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	26-59
21750782-3	2011	Nitric oxide generated by endothelial nitric oxide synthase (eNOS; EC 1.14.13.39) is an important vasorelaxant.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	61-65
21750782-8	2011	OxLDL, LDL and glucose decreased the eNOS protein level by 74  %, 37  % and 29  %, respectively.	Glucose	15-22	nitric oxide synthase 3	Homo sapiens	37-41
21291370-1	2011	Nitric oxide (NO) is a diatomic free radical produced from L-arginine by constitutive and inducible nitric oxide synthase (cNOS and iNOS) in numerous mammalian cells and tissues.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	123-127
21291370-1	2011	Nitric oxide (NO) is a diatomic free radical produced from L-arginine by constitutive and inducible nitric oxide synthase (cNOS and iNOS) in numerous mammalian cells and tissues.	Arginine	59-69	nitric oxide synthase 3	Homo sapiens	123-127
21196271-2	2011	Generated from L-arginine by the action of endothelial (or type 3) nitric oxide synthase (NOS3), NO regulates vascular tone in humans and causes endothelium-dependent vasodilation.	Arginine	15-25	nitric oxide synthase 3	Homo sapiens	90-94
21644402-1	2011	UNLABELLED: Asymmetric dimethylarginine (ADMA) is an endogenous competitive inhibitor of the endothelial nitric oxide synthase (eNOs).	dimethylarginine	23-39	nitric oxide synthase 3	Homo sapiens	93-126
21644402-1	2011	UNLABELLED: Asymmetric dimethylarginine (ADMA) is an endogenous competitive inhibitor of the endothelial nitric oxide synthase (eNOs).	N,N-dimethylarginine	41-45	nitric oxide synthase 3	Homo sapiens	93-126
20801605-1	2011	OBJECTIVE: Studies have indicated that ginsenoside Rb1 and ghrelin could both prevent homocysteine (Hcy)-induced endothelial dysfunction through the endothelial nitric oxide synthase (eNOS)/nitric oxide (NO) mechanism.	Ghrelin	59-66	nitric oxide synthase 3	Homo sapiens	149-182
21899406-0	2011	Determination of the effects of eNOS gene polymorphisms (T-786C and Glu298Asp) on nitric oxide levels in a methylmercury-exposed population.	Nitric Oxide	82-94	nitric oxide synthase 3	Homo sapiens	32-36
21899406-2	2011	Endothelial NO synthase (eNOS) gene polymorphisms and environmental factors, such as mercury (Hg) exposure, may influence NO levels and increase the risk of cardiovascular damage.	Mercury	85-92	nitric oxide synthase 3	Homo sapiens	25-29
21899406-3	2011	The aim of this study was to determine the role of the T-786C and Glu298Asp polymorphisms of the eNOS gene on nitrite concentrations following Hg exposure in humans.	Nitrites	110-117	nitric oxide synthase 3	Homo sapiens	97-101
20801605-16	2011	The addition of Rb1 to Hcy also greatly reversed Hcy-induced downregulation of ghrelin and eNOS expression.	Homocysteine	23-26	nitric oxide synthase 3	Homo sapiens	91-95
20801605-1	2011	OBJECTIVE: Studies have indicated that ginsenoside Rb1 and ghrelin could both prevent homocysteine (Hcy)-induced endothelial dysfunction through the endothelial nitric oxide synthase (eNOS)/nitric oxide (NO) mechanism.	Ghrelin	59-66	nitric oxide synthase 3	Homo sapiens	184-188
20801605-1	2011	OBJECTIVE: Studies have indicated that ginsenoside Rb1 and ghrelin could both prevent homocysteine (Hcy)-induced endothelial dysfunction through the endothelial nitric oxide synthase (eNOS)/nitric oxide (NO) mechanism.	Homocysteine	86-98	nitric oxide synthase 3	Homo sapiens	149-182
20801605-1	2011	OBJECTIVE: Studies have indicated that ginsenoside Rb1 and ghrelin could both prevent homocysteine (Hcy)-induced endothelial dysfunction through the endothelial nitric oxide synthase (eNOS)/nitric oxide (NO) mechanism.	Homocysteine	100-103	nitric oxide synthase 3	Homo sapiens	149-182
19819117-6	2011	In non-diabetic patients the eNOS 4a allele significantly modulated platelet aggregability in response to arachidonic acid (AA), but not to collagen and adenosine diphosphate (ADP) stimulus, after Bonferroni correction for multiple testing.	Arachidonic Acid	106-122	nitric oxide synthase 3	Homo sapiens	29-33
20978715-0	2011	Effects of Aggrenox and aspirin on plasma endothelial nitric oxide synthase and oxidised low-density lipoproteins in patients after ischaemic stroke.	Aspirin, Dipyridamole Drug Combination	11-19	nitric oxide synthase 3	Homo sapiens	42-75
22216344-3	2011	RESULTS: Endothelial nitric oxide synthase (eNOS) was chronically inhibited either by N(G)-Nitro-L-arginine methyl ester (L-NAME) treatment or its expression was down-regulated by RNA interference.	NG-Nitroarginine Methyl Ester	86-120	nitric oxide synthase 3	Homo sapiens	9-42
22216344-3	2011	RESULTS: Endothelial nitric oxide synthase (eNOS) was chronically inhibited either by N(G)-Nitro-L-arginine methyl ester (L-NAME) treatment or its expression was down-regulated by RNA interference.	NG-Nitroarginine Methyl Ester	122-128	nitric oxide synthase 3	Homo sapiens	9-42
20978715-3	2011	We defined the time course and magnitude of changes of plasma eNOS and oxLDL after Aggrenox or aspirin in post-stroke patients.	Aspirin, Dipyridamole Drug Combination	83-91	nitric oxide synthase 3	Homo sapiens	62-66
20978715-3	2011	We defined the time course and magnitude of changes of plasma eNOS and oxLDL after Aggrenox or aspirin in post-stroke patients.	Aspirin	95-102	nitric oxide synthase 3	Homo sapiens	62-66
20978715-5	2011	Both Aggrenox and aspirin similarly increased plasma eNOS activity.	Aspirin, Dipyridamole Drug Combination	5-13	nitric oxide synthase 3	Homo sapiens	53-57
20978715-5	2011	Both Aggrenox and aspirin similarly increased plasma eNOS activity.	Aspirin	18-25	nitric oxide synthase 3	Homo sapiens	53-57
20978715-7	2011	In the small randomised study, both aspirin and Aggrenox produced fast and sustained recovery of plasma eNOS levels, while only therapy with Aggrenox was associated with oxLDL inhibition late in the trial.	Aspirin	36-43	nitric oxide synthase 3	Homo sapiens	104-108
20978715-7	2011	In the small randomised study, both aspirin and Aggrenox produced fast and sustained recovery of plasma eNOS levels, while only therapy with Aggrenox was associated with oxLDL inhibition late in the trial.	Aspirin, Dipyridamole Drug Combination	48-56	nitric oxide synthase 3	Homo sapiens	104-108
21078410-5	2011	Furthermore, scopoletin was shown to block VEGF-induced autophosphorylation of VEGFR2 but not VEGFR1, and down-regulate the following activation of ERK1/2, p38 MAPK and endothelial nitric oxide synthase (eNOS) as well as the production of nitric oxide (NO) in HUVECs.	Scopoletin	13-23	nitric oxide synthase 3	Homo sapiens	169-202
21147698-9	2010	The reduced affinity of eNOS to the cofactor BH4 may lead to insufficient NO, but increased superoxide production in preeclamptic placentas.	sapropterin	45-48	nitric oxide synthase 3	Homo sapiens	24-28
21147698-9	2010	The reduced affinity of eNOS to the cofactor BH4 may lead to insufficient NO, but increased superoxide production in preeclamptic placentas.	Superoxides	92-102	nitric oxide synthase 3	Homo sapiens	24-28
20883689-6	2010	17beta-Estradiol markedly increased cyclic AMP and cyclic GMP levels, nitric oxide (NO) release, vasodilator-stimulated phosphoprotein (VASP) phosphorylation, and endothelial nitric oxide synthase (eNOS) expression.	Estradiol	0-16	nitric oxide synthase 3	Homo sapiens	163-196
21179168-1	2010	Endothelial nitric oxide synthase (eNOS) is critical in the regulation of vascular function, and can generate both nitric oxide (NO) and superoxide (O(2)( -)), which are key mediators of cellular signalling.	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	35-39
21179168-1	2010	Endothelial nitric oxide synthase (eNOS) is critical in the regulation of vascular function, and can generate both nitric oxide (NO) and superoxide (O(2)( -)), which are key mediators of cellular signalling.	Superoxides	137-147	nitric oxide synthase 3	Homo sapiens	0-33
21179168-1	2010	Endothelial nitric oxide synthase (eNOS) is critical in the regulation of vascular function, and can generate both nitric oxide (NO) and superoxide (O(2)( -)), which are key mediators of cellular signalling.	Superoxides	137-147	nitric oxide synthase 3	Homo sapiens	35-39
21179168-1	2010	Endothelial nitric oxide synthase (eNOS) is critical in the regulation of vascular function, and can generate both nitric oxide (NO) and superoxide (O(2)( -)), which are key mediators of cellular signalling.	o(2)	149-153	nitric oxide synthase 3	Homo sapiens	0-33
21179168-1	2010	Endothelial nitric oxide synthase (eNOS) is critical in the regulation of vascular function, and can generate both nitric oxide (NO) and superoxide (O(2)( -)), which are key mediators of cellular signalling.	o(2)	149-153	nitric oxide synthase 3	Homo sapiens	35-39
21179168-2	2010	In the presence of Ca(2+)/calmodulin, eNOS produces NO, endothelial-derived relaxing factor, from l-arginine (l-Arg) by means of electron transfer from NADPH through a flavin containing reductase domain to oxygen bound at the haem of an oxygenase domain, which also contains binding sites for tetrahydrobiopterin (BH(4)) and l-Arg.	Arginine	98-108	nitric oxide synthase 3	Homo sapiens	38-42
21179168-2	2010	In the presence of Ca(2+)/calmodulin, eNOS produces NO, endothelial-derived relaxing factor, from l-arginine (l-Arg) by means of electron transfer from NADPH through a flavin containing reductase domain to oxygen bound at the haem of an oxygenase domain, which also contains binding sites for tetrahydrobiopterin (BH(4)) and l-Arg.	Arginine	110-115	nitric oxide synthase 3	Homo sapiens	38-42
21179168-2	2010	In the presence of Ca(2+)/calmodulin, eNOS produces NO, endothelial-derived relaxing factor, from l-arginine (l-Arg) by means of electron transfer from NADPH through a flavin containing reductase domain to oxygen bound at the haem of an oxygenase domain, which also contains binding sites for tetrahydrobiopterin (BH(4)) and l-Arg.	NADP	152-157	nitric oxide synthase 3	Homo sapiens	38-42
21179168-2	2010	In the presence of Ca(2+)/calmodulin, eNOS produces NO, endothelial-derived relaxing factor, from l-arginine (l-Arg) by means of electron transfer from NADPH through a flavin containing reductase domain to oxygen bound at the haem of an oxygenase domain, which also contains binding sites for tetrahydrobiopterin (BH(4)) and l-Arg.	Oxygen	206-212	nitric oxide synthase 3	Homo sapiens	38-42
21179168-2	2010	In the presence of Ca(2+)/calmodulin, eNOS produces NO, endothelial-derived relaxing factor, from l-arginine (l-Arg) by means of electron transfer from NADPH through a flavin containing reductase domain to oxygen bound at the haem of an oxygenase domain, which also contains binding sites for tetrahydrobiopterin (BH(4)) and l-Arg.	sapropterin	293-312	nitric oxide synthase 3	Homo sapiens	38-42
21179168-2	2010	In the presence of Ca(2+)/calmodulin, eNOS produces NO, endothelial-derived relaxing factor, from l-arginine (l-Arg) by means of electron transfer from NADPH through a flavin containing reductase domain to oxygen bound at the haem of an oxygenase domain, which also contains binding sites for tetrahydrobiopterin (BH(4)) and l-Arg.	Arginine	325-330	nitric oxide synthase 3	Homo sapiens	38-42
21179168-8	2010	Cysteine residues are critical for the maintenance of eNOS function; we therefore speculated that oxidative stress could alter eNOS activity through S-glutathionylation.	Cysteine	0-8	nitric oxide synthase 3	Homo sapiens	54-58
21179168-8	2010	Cysteine residues are critical for the maintenance of eNOS function; we therefore speculated that oxidative stress could alter eNOS activity through S-glutathionylation.	Cysteine	0-8	nitric oxide synthase 3	Homo sapiens	127-131
21179168-9	2010	Here we show that S-glutathionylation of eNOS reversibly decreases NOS activity with an increase in O(2)( -) generation primarily from the reductase, in which two highly conserved cysteine residues are identified as sites of S-glutathionylation and found to be critical for redox-regulation of eNOS function.	o(2)	100-104	nitric oxide synthase 3	Homo sapiens	41-45
21179168-9	2010	Here we show that S-glutathionylation of eNOS reversibly decreases NOS activity with an increase in O(2)( -) generation primarily from the reductase, in which two highly conserved cysteine residues are identified as sites of S-glutathionylation and found to be critical for redox-regulation of eNOS function.	o(2)	100-104	nitric oxide synthase 3	Homo sapiens	294-298
21179168-9	2010	Here we show that S-glutathionylation of eNOS reversibly decreases NOS activity with an increase in O(2)( -) generation primarily from the reductase, in which two highly conserved cysteine residues are identified as sites of S-glutathionylation and found to be critical for redox-regulation of eNOS function.	Cysteine	180-188	nitric oxide synthase 3	Homo sapiens	41-45
21179168-9	2010	Here we show that S-glutathionylation of eNOS reversibly decreases NOS activity with an increase in O(2)( -) generation primarily from the reductase, in which two highly conserved cysteine residues are identified as sites of S-glutathionylation and found to be critical for redox-regulation of eNOS function.	Cysteine	180-188	nitric oxide synthase 3	Homo sapiens	294-298
21179168-11	2010	In hypertensive vessels, eNOS S-glutathionylation is increased with impaired endothelium-dependent vasodilation that is restored by thiol-specific reducing agents, which reverse this S-glutathionylation.	Sulfhydryl Compounds	132-137	nitric oxide synthase 3	Homo sapiens	25-29
20713168-1	2010	Beyond its vasodilator role, vascular nitric oxide (NO), which is synthesized by endothelial NO synthase (eNOS) via its activation, has been shown to play a number of other beneficial roles in the vascular system; it inhibits proliferation of vascular smooth muscle cells, prevents platelet aggregation, and regulates endothelial apoptosis.	Nitric Oxide	38-50	nitric oxide synthase 3	Homo sapiens	106-110
21127294-5	2010	Inhibition of endothelial nitric oxide synthase (eNOS) with the specific NOS inhibitor L-NAME (N(G)-nitro-l-arginine methyl ester) led to increased APP and BACE1 (beta-site APP-cleaving enzyme1) protein levels, as well as increased secretion of the amyloidogenic peptide amyloid beta (Abeta) (control 10.93 +- 0.70 pg/mL; L-NAME 168.21 +- 27.38 pg/mL; P<0.001).	NG-Nitroarginine Methyl Ester	87-93	nitric oxide synthase 3	Homo sapiens	49-53
21127294-5	2010	Inhibition of endothelial nitric oxide synthase (eNOS) with the specific NOS inhibitor L-NAME (N(G)-nitro-l-arginine methyl ester) led to increased APP and BACE1 (beta-site APP-cleaving enzyme1) protein levels, as well as increased secretion of the amyloidogenic peptide amyloid beta (Abeta) (control 10.93 +- 0.70 pg/mL; L-NAME 168.21 +- 27.38 pg/mL; P<0.001).	NG-Nitroarginine Methyl Ester	95-129	nitric oxide synthase 3	Homo sapiens	49-53
21127294-5	2010	Inhibition of endothelial nitric oxide synthase (eNOS) with the specific NOS inhibitor L-NAME (N(G)-nitro-l-arginine methyl ester) led to increased APP and BACE1 (beta-site APP-cleaving enzyme1) protein levels, as well as increased secretion of the amyloidogenic peptide amyloid beta (Abeta) (control 10.93 +- 0.70 pg/mL; L-NAME 168.21 +- 27.38 pg/mL; P<0.001).	NG-Nitroarginine Methyl Ester	322-328	nitric oxide synthase 3	Homo sapiens	49-53
20858749-4	2010	When tetrahydrobiopterin levels are inadequate, eNOS is no longer coupled to l-arginine oxidation, which results in reactive oxygen species rather than nitric oxide production, thereby inducing vascular endothelial dysfunction.	sapropterin	5-24	nitric oxide synthase 3	Homo sapiens	48-52
20858749-4	2010	When tetrahydrobiopterin levels are inadequate, eNOS is no longer coupled to l-arginine oxidation, which results in reactive oxygen species rather than nitric oxide production, thereby inducing vascular endothelial dysfunction.	Reactive Oxygen Species	116-139	nitric oxide synthase 3	Homo sapiens	48-52
20858749-4	2010	When tetrahydrobiopterin levels are inadequate, eNOS is no longer coupled to l-arginine oxidation, which results in reactive oxygen species rather than nitric oxide production, thereby inducing vascular endothelial dysfunction.	Nitric Oxide	152-164	nitric oxide synthase 3	Homo sapiens	48-52
20926919-0	2010	Genistein activates endothelial nitric oxide synthase in broiler pulmonary arterial endothelial cells by an Akt-dependent mechanism.	Genistein	0-9	nitric oxide synthase 3	Homo sapiens	20-53
21152397-3	2010	METHODOLOGY/PRINCIPAL FINDINGS: We used HPLC and mass spectrometry to identify a primary nitroaromatic glutathione metabolite of PABA/NO and used fluorescent assays to characterize drug effects on calcium and NO homeostasis, relating these to endothelial nitric oxide synthase (eNOS) activity.	Glutathione	103-114	nitric oxide synthase 3	Homo sapiens	243-276
21152397-3	2010	METHODOLOGY/PRINCIPAL FINDINGS: We used HPLC and mass spectrometry to identify a primary nitroaromatic glutathione metabolite of PABA/NO and used fluorescent assays to characterize drug effects on calcium and NO homeostasis, relating these to endothelial nitric oxide synthase (eNOS) activity.	4-Aminobenzoic Acid	129-133	nitric oxide synthase 3	Homo sapiens	243-276
21270942-6	2010	In addition to increased AGE production, there is also evidence of multiple pathways elevating ROS generation in DM, including; enhanced glucose auto-oxidation, increased mitochondrial superoxide production, protein kinase C-dependent activation of NADPH oxidase, uncoupled endothelial nitric oxide synthase (eNOS) activity, increased substrate flux through the polyol pathway and stimulation of eicosanoid metabolism.	Reactive Oxygen Species	95-98	nitric oxide synthase 3	Homo sapiens	274-307
21114867-0	2010	Genetic polymorphisms in the endothelial nitric oxide synthase gene correlate with overall survival in advanced non-small-cell lung cancer patients treated with platinum-based doublet chemotherapy.	Platinum	161-169	nitric oxide synthase 3	Homo sapiens	29-62
21270942-6	2010	In addition to increased AGE production, there is also evidence of multiple pathways elevating ROS generation in DM, including; enhanced glucose auto-oxidation, increased mitochondrial superoxide production, protein kinase C-dependent activation of NADPH oxidase, uncoupled endothelial nitric oxide synthase (eNOS) activity, increased substrate flux through the polyol pathway and stimulation of eicosanoid metabolism.	Reactive Oxygen Species	95-98	nitric oxide synthase 3	Homo sapiens	309-313
21114867-2	2010	Endothelial NO, synthesized from L-arginine by endothelial NO synthase (eNOS), inhibits apoptosis and promotes angiogenesis, tumor cell proliferation and metastasis.	Arginine	33-43	nitric oxide synthase 3	Homo sapiens	72-76
20614130-3	2010	The purpose of this study was to investigate the effect of AEX on the relationship among blood pressure, eNOS gene polymorphism and oxidative stress in pre-hypertensive older people.	N-butyl-9H-beta-carbolin-3-amine	59-62	nitric oxide synthase 3	Homo sapiens	105-109
21076717-1	2010	INTRODUCTION: Continuous treatment with nitroglycerin (GTN) causes tolerance and endothelial dysfunction, both of which may involve endothelial nitric oxide synthase (eNOS) dysfunction.	Nitroglycerin	40-53	nitric oxide synthase 3	Homo sapiens	132-165
21076717-1	2010	INTRODUCTION: Continuous treatment with nitroglycerin (GTN) causes tolerance and endothelial dysfunction, both of which may involve endothelial nitric oxide synthase (eNOS) dysfunction.	Nitroglycerin	55-58	nitric oxide synthase 3	Homo sapiens	132-165
20614130-13	2010	These results suggest the AEX can modulate the NOx concentration, eNOS activity and the relationship among eNOS gene polymorphism, oxidative stress and blood pressure especially in C (T-786C) and T (G-894T) allele carriers.	N-butyl-9H-beta-carbolin-3-amine	26-29	nitric oxide synthase 3	Homo sapiens	66-70
20614130-13	2010	These results suggest the AEX can modulate the NOx concentration, eNOS activity and the relationship among eNOS gene polymorphism, oxidative stress and blood pressure especially in C (T-786C) and T (G-894T) allele carriers.	N-butyl-9H-beta-carbolin-3-amine	26-29	nitric oxide synthase 3	Homo sapiens	107-111
21073768-2	2010	In this study, we examined the potential association of endothelial nitric oxide synthase (eNOS) G894T polymorphism with NAION.	naion	121-126	nitric oxide synthase 3	Homo sapiens	56-89
20691200-0	2010	Ellagic acid protects endothelial cells from oxidized low-density lipoprotein-induced apoptosis by modulating the PI3K/Akt/eNOS pathway.	Ellagic Acid	0-12	nitric oxide synthase 3	Homo sapiens	123-127
20691200-3	2010	Previous studies have shown that the phosphatidylinositol 3-kinase/Akt/endothelial nitric oxide synthase/nitric oxide (PI3K/Akt/eNOS/NO) pathway is involved in oxLDL-induced endothelial apoptosis.	Nitric Oxide	83-95	nitric oxide synthase 3	Homo sapiens	128-132
20691200-8	2010	In addition, the anti-apoptotic effect of ellagic acid was partially inhibited by a PI3K inhibitor (wortmannin) and a specific eNOS inhibitor (cavtratin) but not by an ERK inhibitor (PD98059).	Ellagic Acid	42-54	nitric oxide synthase 3	Homo sapiens	127-131
20691200-9	2010	In exploring the underlying mechanisms of ellagic acid action, we found that oxLDL decreased Akt and eNOS phosphorylation, which in turn activated NF-kappaB and downstream pro-apoptotic signaling events including calcium accumulation, destabilization of mitochondrial permeability, and disruption of the balance between pro- and anti-apoptotic Bcl-2 proteins.	Ellagic Acid	42-54	nitric oxide synthase 3	Homo sapiens	101-105
20691200-11	2010	The inhibition of oxLDL-induced endothelial apoptosis by ellagic acid is due at least in part to its anti-oxidant activity and its ability to modulate the PI3K/Akt/eNOS signaling pathway.	Ellagic Acid	57-69	nitric oxide synthase 3	Homo sapiens	164-168
20693398-5	2010	Despite reduced Hsp90-eNOS interactions, dilation to ACh was enhanced in geldanamycin-treated PRAs from hypoxic, but not normoxic, piglets.	geldanamycin	73-85	nitric oxide synthase 3	Homo sapiens	22-26
20693398-2	2010	We tested the hypotheses that 1) the interaction between Hsp90 and its known client protein, endothelial nitric oxide synthase (eNOS), is impaired in pulmonary resistance arteries (PRAs) from piglets with pulmonary hypertension caused by exposure to 3 or 10 days of hypoxia and 2) Hsp90 interacts with the prostanoid pathway proteins prostacyclin synthase (PGIS) and/or thromboxane synthase (TXAS).	Prostaglandins	306-316	nitric oxide synthase 3	Homo sapiens	93-126
20705923-0	2010	Histone deacetylase 3 antagonizes aspirin-stimulated endothelial nitric oxide production by reversing aspirin-induced lysine acetylation of endothelial nitric oxide synthase.	Aspirin	34-41	nitric oxide synthase 3	Homo sapiens	140-173
20693398-2	2010	We tested the hypotheses that 1) the interaction between Hsp90 and its known client protein, endothelial nitric oxide synthase (eNOS), is impaired in pulmonary resistance arteries (PRAs) from piglets with pulmonary hypertension caused by exposure to 3 or 10 days of hypoxia and 2) Hsp90 interacts with the prostanoid pathway proteins prostacyclin synthase (PGIS) and/or thromboxane synthase (TXAS).	Prostaglandins	306-316	nitric oxide synthase 3	Homo sapiens	128-132
20705923-0	2010	Histone deacetylase 3 antagonizes aspirin-stimulated endothelial nitric oxide production by reversing aspirin-induced lysine acetylation of endothelial nitric oxide synthase.	Nitric Oxide	65-77	nitric oxide synthase 3	Homo sapiens	140-173
20705923-0	2010	Histone deacetylase 3 antagonizes aspirin-stimulated endothelial nitric oxide production by reversing aspirin-induced lysine acetylation of endothelial nitric oxide synthase.	Aspirin	102-109	nitric oxide synthase 3	Homo sapiens	140-173
20705923-0	2010	Histone deacetylase 3 antagonizes aspirin-stimulated endothelial nitric oxide production by reversing aspirin-induced lysine acetylation of endothelial nitric oxide synthase.	Lysine	118-124	nitric oxide synthase 3	Homo sapiens	140-173
20705923-5	2010	OBJECTIVE: To determine the role of lysine acetylation of endothelial nitric oxide synthase (eNOS) in the regulation of endothelial NO production by low-dose aspirin and to examine whether the lysine deacetylase histone deacetylase (HDAC)3 antagonizes the effect of low-dose aspirin on endothelial NO production by reversing acetylation of functionally critical eNOS lysine residues.	Lysine	36-42	nitric oxide synthase 3	Homo sapiens	58-91
20705923-5	2010	OBJECTIVE: To determine the role of lysine acetylation of endothelial nitric oxide synthase (eNOS) in the regulation of endothelial NO production by low-dose aspirin and to examine whether the lysine deacetylase histone deacetylase (HDAC)3 antagonizes the effect of low-dose aspirin on endothelial NO production by reversing acetylation of functionally critical eNOS lysine residues.	Lysine	36-42	nitric oxide synthase 3	Homo sapiens	93-97
20705923-6	2010	METHODS AND RESULTS: Low concentrations of aspirin induce lysine acetylation of eNOS, stimulating eNOS enzymatic activity and endothelial NO production in a cyclooxygenase-1-independent fashion.	Aspirin	43-50	nitric oxide synthase 3	Homo sapiens	80-84
20705923-6	2010	METHODS AND RESULTS: Low concentrations of aspirin induce lysine acetylation of eNOS, stimulating eNOS enzymatic activity and endothelial NO production in a cyclooxygenase-1-independent fashion.	Aspirin	43-50	nitric oxide synthase 3	Homo sapiens	98-102
20705923-6	2010	METHODS AND RESULTS: Low concentrations of aspirin induce lysine acetylation of eNOS, stimulating eNOS enzymatic activity and endothelial NO production in a cyclooxygenase-1-independent fashion.	Lysine	58-64	nitric oxide synthase 3	Homo sapiens	80-84
20705923-7	2010	Low-dose aspirin in vivo also increases bioavailable vascular NO in an eNOS-dependent and cyclooxygenase-1-independent manner.	Aspirin	9-16	nitric oxide synthase 3	Homo sapiens	71-75
20705923-8	2010	Low-dose aspirin promotes the binding of eNOS to calmodulin.	Aspirin	9-16	nitric oxide synthase 3	Homo sapiens	41-45
20705923-10	2010	HDAC3 inhibits aspirin-stimulated (1) lysine acetylation of eNOS, (2) eNOS enzymatic activity, (3) eNOS-derived NO, and (4) binding of eNOS to calmodulin.	Aspirin	15-22	nitric oxide synthase 3	Homo sapiens	60-64
20705923-10	2010	HDAC3 inhibits aspirin-stimulated (1) lysine acetylation of eNOS, (2) eNOS enzymatic activity, (3) eNOS-derived NO, and (4) binding of eNOS to calmodulin.	Aspirin	15-22	nitric oxide synthase 3	Homo sapiens	70-74
20705923-10	2010	HDAC3 inhibits aspirin-stimulated (1) lysine acetylation of eNOS, (2) eNOS enzymatic activity, (3) eNOS-derived NO, and (4) binding of eNOS to calmodulin.	Aspirin	15-22	nitric oxide synthase 3	Homo sapiens	70-74
20705923-10	2010	HDAC3 inhibits aspirin-stimulated (1) lysine acetylation of eNOS, (2) eNOS enzymatic activity, (3) eNOS-derived NO, and (4) binding of eNOS to calmodulin.	Aspirin	15-22	nitric oxide synthase 3	Homo sapiens	70-74
20705923-10	2010	HDAC3 inhibits aspirin-stimulated (1) lysine acetylation of eNOS, (2) eNOS enzymatic activity, (3) eNOS-derived NO, and (4) binding of eNOS to calmodulin.	Lysine	38-44	nitric oxide synthase 3	Homo sapiens	60-64
20513234-0	2010	Grape seed extract enhances eNOS expression and NO production through regulating calcium-mediated AKT phosphorylation in H2O2-treated endothelium.	Calcium	81-88	nitric oxide synthase 3	Homo sapiens	28-32
20705923-11	2010	Conversely, downregulation of HDAC3 promotes lysine acetylation of eNOS and endothelial NO generation.	Lysine	45-51	nitric oxide synthase 3	Homo sapiens	67-71
20513234-0	2010	Grape seed extract enhances eNOS expression and NO production through regulating calcium-mediated AKT phosphorylation in H2O2-treated endothelium.	Hydrogen Peroxide	121-125	nitric oxide synthase 3	Homo sapiens	28-32
20705923-12	2010	CONCLUSIONS: Lysine acetylation of eNOS is a posttranslational protein modification supporting low-dose aspirin-induced vasoprotection.	Lysine	13-19	nitric oxide synthase 3	Homo sapiens	35-39
20513234-3	2010	GSE enhanced eNOS expression and NO release in H2O2-treated cells in a dose-dependent manner.	Hydrogen Peroxide	47-51	nitric oxide synthase 3	Homo sapiens	13-17
20705923-12	2010	CONCLUSIONS: Lysine acetylation of eNOS is a posttranslational protein modification supporting low-dose aspirin-induced vasoprotection.	Aspirin	104-111	nitric oxide synthase 3	Homo sapiens	35-39
20705923-13	2010	HDAC3, by deacetylating aspirin-acetylated eNOS, antagonizes aspirin-stimulated endothelial production of NO.	Aspirin	24-31	nitric oxide synthase 3	Homo sapiens	43-47
20705923-13	2010	HDAC3, by deacetylating aspirin-acetylated eNOS, antagonizes aspirin-stimulated endothelial production of NO.	Aspirin	61-68	nitric oxide synthase 3	Homo sapiens	43-47
20593161-5	2010	Endothelial nitric oxide synthase (eNOS) activation was assessed by evaluating the phosphorylation status of the enzyme and evaluating eNOS activity by citrulline synthesis.	Citrulline	152-162	nitric oxide synthase 3	Homo sapiens	0-33
19908164-1	2010	Endothelial nitric oxide synthase (eNOS) and nitric oxide (NO) may play an important role in attenuating cardiac remodeling and apoptosis after myocardial infarction.	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	35-39
19908164-9	2010	All the protective effects of eNOS were blocked by N(omega)-nitro-L-arginine methyl ester (L-NAME) administration, indicating a NO-mediated event.	NG-Nitroarginine Methyl Ester	51-89	nitric oxide synthase 3	Homo sapiens	30-34
19908164-9	2010	All the protective effects of eNOS were blocked by N(omega)-nitro-L-arginine methyl ester (L-NAME) administration, indicating a NO-mediated event.	NG-Nitroarginine Methyl Ester	91-97	nitric oxide synthase 3	Homo sapiens	30-34
20809399-10	2010	Inhibition of eNOS (by N (omega)-nitro-L: -arginine methyl ester) blocks the NO release, but does not affect the aldosterone-induced changes in K. Application of an eNOS-independent NO donor (NONOate/AM) raises intracellular NO concentration, but, again, does not affect K. Data analysis indicates that a decrease of K by about 10% is sufficient to induce a significant increase of eNOS activity.	NG-Nitroarginine Methyl Ester	23-64	nitric oxide synthase 3	Homo sapiens	14-18
20809399-10	2010	Inhibition of eNOS (by N (omega)-nitro-L: -arginine methyl ester) blocks the NO release, but does not affect the aldosterone-induced changes in K. Application of an eNOS-independent NO donor (NONOate/AM) raises intracellular NO concentration, but, again, does not affect K. Data analysis indicates that a decrease of K by about 10% is sufficient to induce a significant increase of eNOS activity.	pelargonic acid	192-199	nitric oxide synthase 3	Homo sapiens	14-18
20809399-10	2010	Inhibition of eNOS (by N (omega)-nitro-L: -arginine methyl ester) blocks the NO release, but does not affect the aldosterone-induced changes in K. Application of an eNOS-independent NO donor (NONOate/AM) raises intracellular NO concentration, but, again, does not affect K. Data analysis indicates that a decrease of K by about 10% is sufficient to induce a significant increase of eNOS activity.	pelargonic acid	192-199	nitric oxide synthase 3	Homo sapiens	165-169
20809399-10	2010	Inhibition of eNOS (by N (omega)-nitro-L: -arginine methyl ester) blocks the NO release, but does not affect the aldosterone-induced changes in K. Application of an eNOS-independent NO donor (NONOate/AM) raises intracellular NO concentration, but, again, does not affect K. Data analysis indicates that a decrease of K by about 10% is sufficient to induce a significant increase of eNOS activity.	pelargonic acid	192-199	nitric oxide synthase 3	Homo sapiens	165-169
20854685-1	2010	BACKGROUND: Nitric oxide (NO), produced by endothelial nitric oxide synthase (eNOS), plays a key role in the regulation of vascular tone.	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	43-76
20854685-1	2010	BACKGROUND: Nitric oxide (NO), produced by endothelial nitric oxide synthase (eNOS), plays a key role in the regulation of vascular tone.	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	78-82
20540939-0	2010	Impaired calcium influx despite hyper-reactivity in contralateral carotid following balloon injury: eNOS involvement.	Calcium	9-16	nitric oxide synthase 3	Homo sapiens	100-104
20478661-3	2010	Endothelial nitric oxide synthase (eNOS) is a nitric oxide enzyme with a key role in pathologic and physiologic angiogenesis and vasculogenesis.	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	35-39
20540939-10	2010	Results obtained with L-NNA, 1400W, 7-NI, OxyHb, ODQ or Tiron showed that this response was mediated by products from endothelial NOS (eNOS) different from NO and without soluble guanylate cyclase activation, but it involved superoxide anions.	Nitroarginine	22-27	nitric oxide synthase 3	Homo sapiens	118-133
20540939-10	2010	Results obtained with L-NNA, 1400W, 7-NI, OxyHb, ODQ or Tiron showed that this response was mediated by products from endothelial NOS (eNOS) different from NO and without soluble guanylate cyclase activation, but it involved superoxide anions.	Nitroarginine	22-27	nitric oxide synthase 3	Homo sapiens	135-139
20540939-10	2010	Results obtained with L-NNA, 1400W, 7-NI, OxyHb, ODQ or Tiron showed that this response was mediated by products from endothelial NOS (eNOS) different from NO and without soluble guanylate cyclase activation, but it involved superoxide anions.	N-((3-(aminomethyl)phenyl)methyl)ethanimidamide	29-34	nitric oxide synthase 3	Homo sapiens	118-133
20540939-10	2010	Results obtained with L-NNA, 1400W, 7-NI, OxyHb, ODQ or Tiron showed that this response was mediated by products from endothelial NOS (eNOS) different from NO and without soluble guanylate cyclase activation, but it involved superoxide anions.	7-nitroindazole	36-40	nitric oxide synthase 3	Homo sapiens	118-133
20540939-10	2010	Results obtained with L-NNA, 1400W, 7-NI, OxyHb, ODQ or Tiron showed that this response was mediated by products from endothelial NOS (eNOS) different from NO and without soluble guanylate cyclase activation, but it involved superoxide anions.	7-nitroindazole	36-40	nitric oxide synthase 3	Homo sapiens	135-139
20540939-10	2010	Results obtained with L-NNA, 1400W, 7-NI, OxyHb, ODQ or Tiron showed that this response was mediated by products from endothelial NOS (eNOS) different from NO and without soluble guanylate cyclase activation, but it involved superoxide anions.	1H-(1,2,3)oxadiazolo(4,4-a)quinoxalin-1-one	49-52	nitric oxide synthase 3	Homo sapiens	118-133
20540939-10	2010	Results obtained with L-NNA, 1400W, 7-NI, OxyHb, ODQ or Tiron showed that this response was mediated by products from endothelial NOS (eNOS) different from NO and without soluble guanylate cyclase activation, but it involved superoxide anions.	1H-(1,2,3)oxadiazolo(4,4-a)quinoxalin-1-one	49-52	nitric oxide synthase 3	Homo sapiens	135-139
20540939-10	2010	Results obtained with L-NNA, 1400W, 7-NI, OxyHb, ODQ or Tiron showed that this response was mediated by products from endothelial NOS (eNOS) different from NO and without soluble guanylate cyclase activation, but it involved superoxide anions.	1,2-Dihydroxybenzene-3,5-Disulfonic Acid Disodium Salt	56-61	nitric oxide synthase 3	Homo sapiens	118-133
20540939-10	2010	Results obtained with L-NNA, 1400W, 7-NI, OxyHb, ODQ or Tiron showed that this response was mediated by products from endothelial NOS (eNOS) different from NO and without soluble guanylate cyclase activation, but it involved superoxide anions.	1,2-Dihydroxybenzene-3,5-Disulfonic Acid Disodium Salt	56-61	nitric oxide synthase 3	Homo sapiens	135-139
20540939-10	2010	Results obtained with L-NNA, 1400W, 7-NI, OxyHb, ODQ or Tiron showed that this response was mediated by products from endothelial NOS (eNOS) different from NO and without soluble guanylate cyclase activation, but it involved superoxide anions.	Superoxides	225-242	nitric oxide synthase 3	Homo sapiens	118-133
20540939-10	2010	Results obtained with L-NNA, 1400W, 7-NI, OxyHb, ODQ or Tiron showed that this response was mediated by products from endothelial NOS (eNOS) different from NO and without soluble guanylate cyclase activation, but it involved superoxide anions.	Superoxides	225-242	nitric oxide synthase 3	Homo sapiens	135-139
20540939-12	2010	Data suggest that balloon catheter injury promoted eNOS uncoupling in contralateral carotids, which generates superoxide rather than NO, and reduces phenylephrine-induced extracellular calcium mobilization, despite the hyper-reactivity to phenylephrine in contralateral carotids.	Superoxides	110-120	nitric oxide synthase 3	Homo sapiens	51-55
20467051-9	2010	Our findings suggest that the T allele encoding for aspartic acid of the eNOS (Glu298Asp) gene may contribute to poor sperm motility.	Aspartic Acid	52-65	nitric oxide synthase 3	Homo sapiens	73-77
20363286-2	2010	Endothelium regulates these cellular processes by activating endothelial nitric oxide synthase (eNOS) responsible for nitric oxide (NO) production.	Nitric Oxide	73-85	nitric oxide synthase 3	Homo sapiens	96-100
20363286-5	2010	The phosphorylation state of specific serine, threonine and tyrosine residues of the enzyme plays a pivotal role in regulation of eNOS activity.	Serine	38-44	nitric oxide synthase 3	Homo sapiens	130-134
20363286-5	2010	The phosphorylation state of specific serine, threonine and tyrosine residues of the enzyme plays a pivotal role in regulation of eNOS activity.	Threonine	46-55	nitric oxide synthase 3	Homo sapiens	130-134
20363286-5	2010	The phosphorylation state of specific serine, threonine and tyrosine residues of the enzyme plays a pivotal role in regulation of eNOS activity.	Tyrosine	60-68	nitric oxide synthase 3	Homo sapiens	130-134
20565248-8	2010	The distribution of eNOS gene polymorphism genotype frequencies showed a significant difference observed between diabetic patients and healthy controls [CC+CT vs. TT p = 0.05, OR = 1.5 95%CI(0.9-2.5)].	cc+ct	153-158	nitric oxide synthase 3	Homo sapiens	20-24
20211863-8	2010	Ectopic expression of PMCA in endothelial cells resulted in an increase in phosphorylation of the residue Thr-495 of endogenous eNOS.	Threonine	106-109	nitric oxide synthase 3	Homo sapiens	128-132
20409549-0	2010	NOS3 gene polymorphisms are associated with risk markers of cardiovascular disease, and interact with omega-3 polyunsaturated fatty acids.	omega-3 polyunsaturated fatty acids	102-137	nitric oxide synthase 3	Homo sapiens	0-4
20409549-2	2010	Genotype at key genes such as nitric oxide synthase (NOS3) may determine responsiveness to fatty acids.	Fatty Acids	91-102	nitric oxide synthase 3	Homo sapiens	53-57
20409549-7	2010	A significant gene-nutrient interaction was observed between the NOS3 rs1799983 SNP and plasma n-3 PUFA status on plasma triacylglycerol (TAG) concentrations.	Triglycerides	121-136	nitric oxide synthase 3	Homo sapiens	65-69
20489655-5	2010	The experimental results showed that the cytotoxic effects of Ang II on human umbilical vein endothelial cells were significantly ameliorated by atorvastatin pretreatment (LDH tests, MTT assay, and propdium iodide (PI)/Annexin V-stating analysis), and atorvastatin treatment simultaneously enhanced expression of endothelial nitric oxide synthase and yielded of nitric oxide (NO) and cyclic guanosine monophosphate, but both effects were attenuated by the B2Rs antagonist HOE-140.	Atorvastatin	145-157	nitric oxide synthase 3	Homo sapiens	313-346
20547753-1	2010	In damaged or proliferating endothelium, production of nitric oxide (NO) from endothelial nitric oxide synthase (eNOS) is associated with elevated levels of reactive oxygen species (ROS), which are necessary for endothelial migration.	Nitric Oxide	55-67	nitric oxide synthase 3	Homo sapiens	78-111
20547753-1	2010	In damaged or proliferating endothelium, production of nitric oxide (NO) from endothelial nitric oxide synthase (eNOS) is associated with elevated levels of reactive oxygen species (ROS), which are necessary for endothelial migration.	Reactive Oxygen Species	157-180	nitric oxide synthase 3	Homo sapiens	78-111
20547753-1	2010	In damaged or proliferating endothelium, production of nitric oxide (NO) from endothelial nitric oxide synthase (eNOS) is associated with elevated levels of reactive oxygen species (ROS), which are necessary for endothelial migration.	Reactive Oxygen Species	182-185	nitric oxide synthase 3	Homo sapiens	78-111
20546771-0	2010	Ginsenoside Rg3 increases nitric oxide production via increases in phosphorylation and expression of endothelial nitric oxide synthase: essential roles of estrogen receptor-dependent PI3-kinase and AMP-activated protein kinase.	Ginsenosides	0-11	nitric oxide synthase 3	Homo sapiens	101-134
20610538-0	2010	Caveolin 1 is required for the activation of endothelial nitric oxide synthase in response to 17beta-estradiol.	Estradiol	94-110	nitric oxide synthase 3	Homo sapiens	45-78
20472037-6	2010	The eNOS gene polymorphism was determined by polymerase chain reaction-polyacrylamide gel electrophoresis.	polyacrylamide	71-85	nitric oxide synthase 3	Homo sapiens	4-8
20660237-2	2010	Nitric oxide is associated with tumors and has been studied indirectly by nitrotyrosine analysis and with use of the enzymes nitric oxide synthase (NOS)1, NOS2, and NOS3.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	165-169
20435848-8	2010	Three antioxidants, seleno-L-methionine, ginsenoside Rb1, and MnTBAP (superoxide dismutase mimetic), effectively blocked resistin-induced eNOS downregulation.	Selenomethionine	20-39	nitric oxide synthase 3	Homo sapiens	138-142
20462865-3	2010	However, it is not entirely clear why activation of eNOS by certain vasodilatory agents, like acetylcholine, does not affect microvascular permeability, whereas activation of eNOS by other inflammatory agents that increase permeability, like platelet-activating factor, does not cause vasodilation.	Acetylcholine	94-107	nitric oxide synthase 3	Homo sapiens	52-56
20562903-6	2010	RESULTS: Treatment of HUVEC with H(2)O(2) 100 micromol/L for 30 min inhibited the mRNA and protein expression of endothelial nitric oxide synthase (eNOS).	Hydrogen Peroxide	33-41	nitric oxide synthase 3	Homo sapiens	113-146
20562903-6	2010	RESULTS: Treatment of HUVEC with H(2)O(2) 100 micromol/L for 30 min inhibited the mRNA and protein expression of endothelial nitric oxide synthase (eNOS).	Hydrogen Peroxide	33-41	nitric oxide synthase 3	Homo sapiens	148-152
20562903-9	2010	The combination significantly lowered the intracellular ROS level (P&lt;0.05), which was correlated with the increase in eNOS and NO, but there was no visible change in intracellular calcium (P&gt;0.05).	Reactive Oxygen Species	56-59	nitric oxide synthase 3	Homo sapiens	121-125
20562903-10	2010	Compared with individual drug treatment, Akt phosphorylation and the ratio of p-eNOS/eNOS were up-regulated in the combination group, and this effect was inhibited by the phosphatidylinositol 3-kinase (PI3K) inhibitors wortmannin and LY294002.	Wortmannin	219-229	nitric oxide synthase 3	Homo sapiens	80-84
20562903-10	2010	Compared with individual drug treatment, Akt phosphorylation and the ratio of p-eNOS/eNOS were up-regulated in the combination group, and this effect was inhibited by the phosphatidylinositol 3-kinase (PI3K) inhibitors wortmannin and LY294002.	Wortmannin	219-229	nitric oxide synthase 3	Homo sapiens	85-89
20562903-10	2010	Compared with individual drug treatment, Akt phosphorylation and the ratio of p-eNOS/eNOS were up-regulated in the combination group, and this effect was inhibited by the phosphatidylinositol 3-kinase (PI3K) inhibitors wortmannin and LY294002.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	234-242	nitric oxide synthase 3	Homo sapiens	80-84
20562903-10	2010	Compared with individual drug treatment, Akt phosphorylation and the ratio of p-eNOS/eNOS were up-regulated in the combination group, and this effect was inhibited by the phosphatidylinositol 3-kinase (PI3K) inhibitors wortmannin and LY294002.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	234-242	nitric oxide synthase 3	Homo sapiens	85-89
20435848-9	2010	Meanwhile, resistin activated the mitogen-activated protein kinases p38 and c-Jun NH(2)-terminal kinase (JNK), and the specific p38 inhibitor SB-239063 effectively blocked resistin-induced ROS production and eNOS downregulation.	SB 239063	142-151	nitric oxide synthase 3	Homo sapiens	208-212
20435848-11	2010	Thus resistin directly induces eNOS downregulation through overproduction of ROS and activation of p38 and JNK in HCAECs.	Reactive Oxygen Species	77-80	nitric oxide synthase 3	Homo sapiens	31-35
20463056-6	2010	VEGF-induced cell migration requires endogenous nitric oxide (NO) as: 1) VEGF-stimulated phosphorylation of endothelial NO synthase (eNOS) via activation of Akt, JNK1/2, and Src; 2) a NO donor diethylenetriamine-NO-stimulated cell migration; and 3) NO synthase inhibition blocked VEGF-induced cell migration.	Nitric Oxide	48-60	nitric oxide synthase 3	Homo sapiens	133-137
20463056-6	2010	VEGF-induced cell migration requires endogenous nitric oxide (NO) as: 1) VEGF-stimulated phosphorylation of endothelial NO synthase (eNOS) via activation of Akt, JNK1/2, and Src; 2) a NO donor diethylenetriamine-NO-stimulated cell migration; and 3) NO synthase inhibition blocked VEGF-induced cell migration.	diethylenetriamine	193-211	nitric oxide synthase 3	Homo sapiens	133-137
20112298-1	2010	Nitric oxide (NO) produced by the endothelial nitric oxide synthase (eNOS) is an important signaling molecule in the cardiovascular system.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	34-67
20406854-4	2010	LB42708 inhibited VEGF-induced Ras activation and subsequently suppressed angiogenesis in vitro and in vivo by blocking the mitogen-activated protein kinase kinase/extracellular signal-regulated kinase/p38 mitogen-activated protein kinase (MAPK) and phosphatidylinositol 3-kinase (PI3K)/Akt/endothelial nitric-oxide synthase pathways in endothelial cells without altering FAK/Src activation.	LB42708	0-7	nitric oxide synthase 3	Homo sapiens	291-324
20440695-0	2010	The red wine extract-induced activation of endothelial nitric oxide synthase is mediated by a great variety of polyphenolic compounds.	red wine	4-12	nitric oxide synthase 3	Homo sapiens	43-76
20440695-0	2010	The red wine extract-induced activation of endothelial nitric oxide synthase is mediated by a great variety of polyphenolic compounds.	polyphenolic compounds	111-133	nitric oxide synthase 3	Homo sapiens	43-76
20457799-0	2010	Effects of eNOS polymorphisms on nitric oxide formation in healthy pregnancy and in pre-eclampsia.	Nitric Oxide	33-45	nitric oxide synthase 3	Homo sapiens	11-15
20461063-9	2010	Thus, SERCA2a gene transfer increases eNOS expression and activity by modulating calcium homeostasis to improve CF.	Calcium	81-88	nitric oxide synthase 3	Homo sapiens	38-42
20112298-1	2010	Nitric oxide (NO) produced by the endothelial nitric oxide synthase (eNOS) is an important signaling molecule in the cardiovascular system.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	69-73
20112298-3	2010	We aimed to examine whether the model Maillard reaction product 3-hydroxy-2-methyl-1-propyl-4(1H)-pyridone (HMPP), formed from maltol or starch and propylamine, affects the eNOS system.	3-hydroxy-2-methyl-1-propyl-4(1h)-pyridone	64-106	nitric oxide synthase 3	Homo sapiens	173-177
20112298-3	2010	We aimed to examine whether the model Maillard reaction product 3-hydroxy-2-methyl-1-propyl-4(1H)-pyridone (HMPP), formed from maltol or starch and propylamine, affects the eNOS system.	hmpp	108-112	nitric oxide synthase 3	Homo sapiens	173-177
20112298-3	2010	We aimed to examine whether the model Maillard reaction product 3-hydroxy-2-methyl-1-propyl-4(1H)-pyridone (HMPP), formed from maltol or starch and propylamine, affects the eNOS system.	maltol	127-133	nitric oxide synthase 3	Homo sapiens	173-177
20112298-3	2010	We aimed to examine whether the model Maillard reaction product 3-hydroxy-2-methyl-1-propyl-4(1H)-pyridone (HMPP), formed from maltol or starch and propylamine, affects the eNOS system.	Propylamines	148-159	nitric oxide synthase 3	Homo sapiens	173-177
20112298-4	2010	Incubation of EA.hy926 endothelial cells with 30-300 microM HMPP for 18 h enhanced endothelial NO release measured with the fluorescent probe diaminofluorescein-2 and eNOS activity determined by the [14C]L-arginine-[14C]L-citrulline conversion assay.	hmpp	60-64	nitric oxide synthase 3	Homo sapiens	167-171
20112298-7	2010	HMPP inhibited eNOS activity within the first 2-4 h, whereas it potently increased eNOS activity after 12-24 h. Levels of eNOS phosphorylation, expression of heat-shock protein 90, caveolin-1 and various antioxidant enzymes were not affected.	hmpp	0-4	nitric oxide synthase 3	Homo sapiens	15-19
20112298-7	2010	HMPP inhibited eNOS activity within the first 2-4 h, whereas it potently increased eNOS activity after 12-24 h. Levels of eNOS phosphorylation, expression of heat-shock protein 90, caveolin-1 and various antioxidant enzymes were not affected.	hmpp	0-4	nitric oxide synthase 3	Homo sapiens	83-87
20112298-7	2010	HMPP inhibited eNOS activity within the first 2-4 h, whereas it potently increased eNOS activity after 12-24 h. Levels of eNOS phosphorylation, expression of heat-shock protein 90, caveolin-1 and various antioxidant enzymes were not affected.	hmpp	0-4	nitric oxide synthase 3	Homo sapiens	83-87
20309548-2	2010	We examined the hypothesis that AVE3085, a novel compound that enhances eNOS transcription, may protect coronary endothelium against hypoxia-reoxygenation (H-R) injury during cardioplegic arrest and the possible mechanism by which this occurs.	2,2-difluorobenzo(1,3)dioxole-5-carboxylic acid indan-2-ylamide	32-39	nitric oxide synthase 3	Homo sapiens	72-76
20309548-8	2010	eNOS and p-eNOS(Ser1177) expressions in coronary endothelial cells were significantly increased by the addition of AVE3085 in ST solution during hypoxia (p &lt; 0.05).	2,2-difluorobenzo(1,3)dioxole-5-carboxylic acid indan-2-ylamide	115-122	nitric oxide synthase 3	Homo sapiens	0-4
20309548-8	2010	eNOS and p-eNOS(Ser1177) expressions in coronary endothelial cells were significantly increased by the addition of AVE3085 in ST solution during hypoxia (p &lt; 0.05).	2,2-difluorobenzo(1,3)dioxole-5-carboxylic acid indan-2-ylamide	115-122	nitric oxide synthase 3	Homo sapiens	11-15
20309548-9	2010	Protection of endothelium-dependent relaxation from H-R by AVE3085 (70.3 +/- 7.2% vs. 90.5 +/- 2.4%, p &lt; 0.05) also reached a level similar to that by L-arginine (69.9 +/- 9.0% vs. 94.7 +/- 3.9%, p &lt; 0.05) at 4 degrees C. CONCLUSIONS: We have demonstrated a new mechanism to protect coronary endothelium from H-R injury by using eNOS enhancers.	2,2-difluorobenzo(1,3)dioxole-5-carboxylic acid indan-2-ylamide	59-66	nitric oxide synthase 3	Homo sapiens	335-339
20371606-6	2010	Trans-activation of wild-type NOS3 promoter by FGF2 was significantly inhibited when either the AP-1 or the cAMP-response element (CRE)-like sequence (TGCGTCA, -752 to -758) was mutated and was completely blocked when both were mutated.	Cyclic AMP	108-112	nitric oxide synthase 3	Homo sapiens	30-34
23961079-1	2010	Endothelium-derived nitric oxide (NO) is synthesized from l-arginine by endothelial nitric oxide synthase (eNOS) encoded by the NOS3 gene on chromosome7.	Nitric Oxide	20-32	nitric oxide synthase 3	Homo sapiens	72-105
23961079-1	2010	Endothelium-derived nitric oxide (NO) is synthesized from l-arginine by endothelial nitric oxide synthase (eNOS) encoded by the NOS3 gene on chromosome7.	Nitric Oxide	20-32	nitric oxide synthase 3	Homo sapiens	107-111
23961079-1	2010	Endothelium-derived nitric oxide (NO) is synthesized from l-arginine by endothelial nitric oxide synthase (eNOS) encoded by the NOS3 gene on chromosome7.	Nitric Oxide	20-32	nitric oxide synthase 3	Homo sapiens	128-132
23961079-1	2010	Endothelium-derived nitric oxide (NO) is synthesized from l-arginine by endothelial nitric oxide synthase (eNOS) encoded by the NOS3 gene on chromosome7.	Arginine	58-68	nitric oxide synthase 3	Homo sapiens	72-105
23961079-1	2010	Endothelium-derived nitric oxide (NO) is synthesized from l-arginine by endothelial nitric oxide synthase (eNOS) encoded by the NOS3 gene on chromosome7.	Arginine	58-68	nitric oxide synthase 3	Homo sapiens	107-111
23961079-1	2010	Endothelium-derived nitric oxide (NO) is synthesized from l-arginine by endothelial nitric oxide synthase (eNOS) encoded by the NOS3 gene on chromosome7.	Arginine	58-68	nitric oxide synthase 3	Homo sapiens	128-132
20230881-0	2010	Molecular mechanism of endothelial nitric-oxide synthase activation by Platycodon grandiflorum root-derived saponins.	Saponins	108-116	nitric oxide synthase 3	Homo sapiens	23-56
20525309-10	2010	Simvastatin markedly increased NO release, vasodilator-stimulated phosphoprotein (VASP) phosphorylation, and endothelial nitric oxide synthase (eNOS) expression.	Simvastatin	0-11	nitric oxide synthase 3	Homo sapiens	109-142
20230881-1	2010	Nitric oxide (NO) produced by endothelial nitric-oxide synthase (eNOS) has antithrombotic and antiatherosclerotic properties in the vasculature.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	30-63
20404222-0	2010	(-)-epicatechin activation of endothelial cell endothelial nitric oxide synthase, nitric oxide, and related signaling pathways.	Catechin	0-15	nitric oxide synthase 3	Homo sapiens	47-80
20416296-1	2010	Icariin, a flavonoid isolated from Epimedii herba, stimulated phosphorylation of endothelial nitric oxide synthase (eNOS) at Ser1177, Akt (Ser473) and ERK1/2 (Thr202/Tyr204).	icariin	0-7	nitric oxide synthase 3	Homo sapiens	81-114
20300066-9	2010	At the polymorphism T-786C in the endothelial nitric oxide (NO) synthase (eNOS) gene, the subjects with TT genotype had lower BRS than subjects carrying either the TC or the CC genotype.	Nitric Oxide	46-58	nitric oxide synthase 3	Homo sapiens	74-78
20392826-8	2010	In particular, endothelium-dependent vasodilatation by estradiol-induced activation of endothelial nitric oxide synthase has proven to be an uniquely informative model to study sex steroid signaling via classical sex steroid receptors localized to the cell membrane.	Estradiol	55-64	nitric oxide synthase 3	Homo sapiens	87-120
20392826-8	2010	In particular, endothelium-dependent vasodilatation by estradiol-induced activation of endothelial nitric oxide synthase has proven to be an uniquely informative model to study sex steroid signaling via classical sex steroid receptors localized to the cell membrane.	Steroids	181-188	nitric oxide synthase 3	Homo sapiens	87-120
20404222-1	2010	Recent reports indicate that (-)-epicatechin can exert cardioprotective actions, which may involve endothelial nitric oxide synthase (eNOS)-mediated nitric oxide production in endothelial cells.	Catechin	29-44	nitric oxide synthase 3	Homo sapiens	99-132
21234858-8	2010	Western blotting studies revealed that AGEs decreased NOS-3 phosphorylation on serine-1177, increased NOS-3 O-glycosylation, and decreased serine phosphorylation of protein kinase Akt; all of these changes were abrogated by pyridoxine.	Pyridoxine	224-234	nitric oxide synthase 3	Homo sapiens	54-59
21234858-5	2010	Serine-1177-specific phosphorylation of NOS type 3 (NOS-3) and phosphorylation of protein kinase Akt were determined in platelets by Western blotting.	Serine	0-6	nitric oxide synthase 3	Homo sapiens	40-50
21234858-5	2010	Serine-1177-specific phosphorylation of NOS type 3 (NOS-3) and phosphorylation of protein kinase Akt were determined in platelets by Western blotting.	Serine	0-6	nitric oxide synthase 3	Homo sapiens	52-57
21234858-10	2010	We conclude that pyridoxine is effective in ameliorating the dysfunction of platelet NO signaling in response to AGEs, through improving PI3K activity, and hence downstream Akt phosphorylation and in turn serine-1177 phosphorylation of NOS-3.	Pyridoxine	17-27	nitric oxide synthase 3	Homo sapiens	236-241
21234858-8	2010	Western blotting studies revealed that AGEs decreased NOS-3 phosphorylation on serine-1177, increased NOS-3 O-glycosylation, and decreased serine phosphorylation of protein kinase Akt; all of these changes were abrogated by pyridoxine.	Serine	79-85	nitric oxide synthase 3	Homo sapiens	54-59
20144727-0	2010	Activation of endothelial nitric oxide synthase by the pro-apoptotic drug embelin: Striking discrepancy between nitric oxide-mediated cyclic GMP accumulation and L-citrulline formation.	Citrulline	162-174	nitric oxide synthase 3	Homo sapiens	14-47
20598027-0	2010	Glu298Asp polymorphism of the endothelial nitric oxide synthase gene and plasma concentrations of asymmetric dimethylarginine in Turkish pre-eclamptic women without fetal growth retardation.	dimethylarginine	109-125	nitric oxide synthase 3	Homo sapiens	30-63
20144727-5	2010	The apparent discrepancy between NO/cGMP and l-citrulline formation in embelin-treated cells was not due to enhanced metabolism and/or efflux of l-citrulline, increased NO bioavailability, inhibition of cGMP hydrolysis, sensitization of soluble guanylate cyclase (sGC) to NO, or enhanced formation of a sGC/eNOS complex.	embelin	71-78	nitric oxide synthase 3	Homo sapiens	307-311
20188080-4	2010	In previous investigations, we have conclusively established calreticulin transacetylase catalyzed activation of endothelial nitric oxide synthase (eNOS) by polyphenolic acetates.	polyphenolic acetates	157-178	nitric oxide synthase 3	Homo sapiens	113-146
20299462-4	2010	We hypothesized that Ang II stimulates TAL NO production via AT(2)-mediated Akt1 activation, which phosphorylates NOS3 at serine 1177.	Serine	122-128	nitric oxide synthase 3	Homo sapiens	114-118
20299462-15	2010	Ang II increased phospho-NOS3 at serine 1177 by 130% (p &lt; 0.01) and 150% after 5 and 10 min (p &lt; 0.02).	Serine	33-39	nitric oxide synthase 3	Homo sapiens	25-29
20299462-18	2010	We concluded that Ang II enhances TAL NO production via activation of AT(2) and Akt1-dependent phosphorylation of NOS3 at serines 1177 and 633.	Serine	122-129	nitric oxide synthase 3	Homo sapiens	114-118
20114041-1	2010	BACKGROUND: Endothelium derived nitric oxide is formed from l-arginine by endothelial nitric oxide synthase encoded by the nitric oxide synthase 3 (NOS3) gene.	Nitric Oxide	32-44	nitric oxide synthase 3	Homo sapiens	123-146
20210789-2	2010	This key signalling molecule is synthesised by a family of nitric oxide synthases (NOS), and the endothelial isoform (eNOS) is the most important for nitric oxide formation in the cardiovascular system.	Nitric Oxide	59-71	nitric oxide synthase 3	Homo sapiens	118-122
20114041-1	2010	BACKGROUND: Endothelium derived nitric oxide is formed from l-arginine by endothelial nitric oxide synthase encoded by the nitric oxide synthase 3 (NOS3) gene.	Nitric Oxide	32-44	nitric oxide synthase 3	Homo sapiens	148-152
20114041-1	2010	BACKGROUND: Endothelium derived nitric oxide is formed from l-arginine by endothelial nitric oxide synthase encoded by the nitric oxide synthase 3 (NOS3) gene.	Arginine	60-70	nitric oxide synthase 3	Homo sapiens	123-146
20114041-1	2010	BACKGROUND: Endothelium derived nitric oxide is formed from l-arginine by endothelial nitric oxide synthase encoded by the nitric oxide synthase 3 (NOS3) gene.	Arginine	60-70	nitric oxide synthase 3	Homo sapiens	148-152
20114041-2	2010	Nitric oxide possesses a variety of protective effects on endothelial cells and therefore NOS3 is a logical candidate gene to be investigated for the susceptibility of deep vein thrombosis (DVT).	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	90-94
20348139-0	2010	Translocation of protein kinase C isoforms is involved in propofol-induced endothelial nitric oxide synthase activation.	Propofol	58-66	nitric oxide synthase 3	Homo sapiens	75-108
20021702-4	2010	Resveratrol and quercetin (0.1-1 microm) increased eNOS and VEGF mRNA expression particularly in the absence of H2O2 (50 microm) and decreased H2O2-induced ET-1 mRNA expression (P &lt; 0.001 for polyphenol x H2O2 interactions).	Resveratrol	0-11	nitric oxide synthase 3	Homo sapiens	51-55
20021702-4	2010	Resveratrol and quercetin (0.1-1 microm) increased eNOS and VEGF mRNA expression particularly in the absence of H2O2 (50 microm) and decreased H2O2-induced ET-1 mRNA expression (P &lt; 0.001 for polyphenol x H2O2 interactions).	Quercetin	16-25	nitric oxide synthase 3	Homo sapiens	51-55
20021702-6	2010	Of the nine other polyphenols tested, only epigallocatechin gallate had similar effects on both the eNOS and ET-1 mRNA expression, but to a lesser extent than resveratrol at an equimolar concentration (0.1 microm).	epigallocatechin gallate	43-67	nitric oxide synthase 3	Homo sapiens	100-104
20186148-1	2010	We investigated the variations in genes encoding endothelial nitric oxide synthase (NOS3), angiotensin-converting enzyme (ACE) and angiotensinogen (AGT) in hypertensive disorders of pregnancy and the relationship between the polymorphisms and circulating nitric oxide (NO) and ACE levels in pregnant north Indian women.	Nitric Oxide	61-73	nitric oxide synthase 3	Homo sapiens	84-88
20372828-9	2010	These results indicate that eNOS polymorphisms and haplotypes serve as risk factors for SBI, and three different polymorphic loci in the eNOS gene play interactively, thereby leading to synergistic effects for the generation of SBI.	sorbinil	88-91	nitric oxide synthase 3	Homo sapiens	28-32
20375905-1	2010	OBJECTIVE: We hypothesized a possible mechanism for atherosclerosis in which interleukin-6 (IL-6) might affect the endothelial nitric oxide synthase (eNOS)-caveolin-1 interaction and result in decreased nitric oxide bioavailability in the setting of low-grade inflammation.	Nitric Oxide	127-139	nitric oxide synthase 3	Homo sapiens	150-154
20375905-7	2010	IL-6 treatment was found to stabilize caveolin-1 protein and its half-life was estimated to prolong from 7.5 h to longer than 12 h. Furthermore, treatment with PD98059 and short interference RNA of extracellular signal-regulated kinase gene reversed the effects of IL-6 on eNOS and caveolin-1.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	160-167	nitric oxide synthase 3	Homo sapiens	273-277
20213497-5	2010	Mechanisms involved include binding to repressor response elements on the eNOS gene, competing for co-regulators common to hormones with positive genomic actions, regulating eNOS co-factors, decreasing substrate for eNOS, and increasing production of oxygen-derived free radicals.	Oxygen	251-257	nitric oxide synthase 3	Homo sapiens	74-78
20213743-0	2010	CDK5 phosphorylates eNOS at Ser-113 and regulates NO production.	Serine	28-31	nitric oxide synthase 3	Homo sapiens	20-24
20213743-2	2010	Through protein nitration by peroxynitrite, eNOS is believed to be responsible for the major abnormalities in several important neurodegenerative diseases including Alzheimer"s (AD) and Parkinson"s diseases (PD).	Peroxynitrous Acid	29-42	nitric oxide synthase 3	Homo sapiens	44-48
20213743-7	2010	Most interestingly, the nitrite production was significantly reduced in eNOS and Cdk5/p35 co-transfected SH-SY5Y cells when compared with co-transfection of Cdk5/p35 and S113A.	Nitrites	24-31	nitric oxide synthase 3	Homo sapiens	72-76
20213743-8	2010	Together, our data suggest that Cdk5 can phosphorylate eNOS at the Ser-113 site and down-regulate eNOS-derived NO levels.	Serine	67-70	nitric oxide synthase 3	Homo sapiens	55-59
19913857-4	2010	Plasma homocysteine levels were enhanced 2-fold in the subjects with the MTHFR 677T/T compared with the others (P = .0001) and also enhanced in the subjects with the endothelial nitric oxide synthase -786C allele (P = .031).	Homocysteine	7-19	nitric oxide synthase 3	Homo sapiens	166-199
20213497-5	2010	Mechanisms involved include binding to repressor response elements on the eNOS gene, competing for co-regulators common to hormones with positive genomic actions, regulating eNOS co-factors, decreasing substrate for eNOS, and increasing production of oxygen-derived free radicals.	Free Radicals	266-279	nitric oxide synthase 3	Homo sapiens	74-78
20184376-0	2010	Peroxynitrite induces destruction of the tetrahydrobiopterin and heme in endothelial nitric oxide synthase: transition from reversible to irreversible enzyme inhibition.	Peroxynitrous Acid	0-13	nitric oxide synthase 3	Homo sapiens	73-106
20448437-8	2010	In contrast, endothelial nitric oxide synthase (eNOS) was expressed in both types of EPCs, and both cell types could produce nitric oxide (NO), as judged by measuring the total amounts of nitrites and nitrates in culture media.	Nitrites	188-196	nitric oxide synthase 3	Homo sapiens	13-46
20448437-8	2010	In contrast, endothelial nitric oxide synthase (eNOS) was expressed in both types of EPCs, and both cell types could produce nitric oxide (NO), as judged by measuring the total amounts of nitrites and nitrates in culture media.	Nitrates	201-209	nitric oxide synthase 3	Homo sapiens	13-46
20184376-0	2010	Peroxynitrite induces destruction of the tetrahydrobiopterin and heme in endothelial nitric oxide synthase: transition from reversible to irreversible enzyme inhibition.	sapropterin	41-60	nitric oxide synthase 3	Homo sapiens	73-106
20184376-0	2010	Peroxynitrite induces destruction of the tetrahydrobiopterin and heme in endothelial nitric oxide synthase: transition from reversible to irreversible enzyme inhibition.	Heme	65-69	nitric oxide synthase 3	Homo sapiens	73-106
20083095-1	2010	BACKGROUND: The polymorphism Glu298Asp of endothelial nitric oxide (eNOS) gene has been associated with hypertension and coronary artery disease in several populations worldwide, but results are still controversial.	Nitric Oxide	54-66	nitric oxide synthase 3	Homo sapiens	68-72
20305680-7	2010	In addition, PGE(1) significantly increased NO content, eNOS protein, and mRNA expression.	Prostaglandins E	13-16	nitric oxide synthase 3	Homo sapiens	56-60
20960276-9	2010	Resveratrol also counteracted other pro-atherosclerotic effects of high glucose, including the up-regulating roles of high glucose on the expression of endothelin-1 mRNA and E-selectin mRNA, and the down-regulating roles of high glucose on the expression of eNOS mRNA and the basal NO secretion without the stimulating of insulin.	Resveratrol	0-11	nitric oxide synthase 3	Homo sapiens	258-262
20093623-9	2010	Incubation with nitric oxide donor sodium nitroprusside significantly ameliorated the inhibition of tumor necrosis factor-alpha on EPC proliferation, but incubation with endothelial nitric oxide synthase inhibitor l-NAME and PI3K inhibitor markedly attenuated the effect of RW on EPC proliferation.	NG-Nitroarginine Methyl Ester	214-220	nitric oxide synthase 3	Homo sapiens	170-203
20382774-8	2010	In this respect, ADMA could serve as a re-coupling agent overcoming endothelial nitric oxide synthase (eNOS) uncoupling in patients with diabetes.	N,N-dimethylarginine	17-21	nitric oxide synthase 3	Homo sapiens	68-101
20367485-1	2010	Endothelial nitric oxide synthase (eNOS) is a vascular enzyme that produces nitric oxide, a transient signaling molecule that by vasodilatation regulates blood flow and pressure.	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	35-39
20367485-6	2010	Taken together, our data suggest that this variant in NOS3, which has been previously associated with higher levels of nitric oxide, contributes to both acclimatization and adaptation to altitude.	Nitric Oxide	119-131	nitric oxide synthase 3	Homo sapiens	54-58
20375793-3	2010	METHODS: The expression of endothelial nitric oxide synthase was tested in formalin-fixed, paraffin-embedded tissues from specimens including 8 first trimester placentas, 3 partial hydatidiform moles, 20 complete hydatidiform moles, 2 invasive moles, and 5 choriocarcinomas.	Formaldehyde	75-83	nitric oxide synthase 3	Homo sapiens	27-60
20375793-3	2010	METHODS: The expression of endothelial nitric oxide synthase was tested in formalin-fixed, paraffin-embedded tissues from specimens including 8 first trimester placentas, 3 partial hydatidiform moles, 20 complete hydatidiform moles, 2 invasive moles, and 5 choriocarcinomas.	Paraffin	91-99	nitric oxide synthase 3	Homo sapiens	27-60
19913548-1	2010	The balance between endothelial nitric oxide synthase (eNOS)-derived nitric oxide (NO) and reactive oxygen species (ROS) production determines endothelial-mediated vascular homeostasis.	Nitric Oxide	32-44	nitric oxide synthase 3	Homo sapiens	55-59
20354497-1	2010	AIM: The endothelial nitric oxide (eNOS) gene T-786C polymorphism may influence as a genetic risk factor cardiovascular diseases and shows association with cardiovascular mortality.	Nitric Oxide	21-33	nitric oxide synthase 3	Homo sapiens	35-39
19913548-5	2010	We demonstrate here that serum deprivation of CVEC increased eNOS-mediated ROS levels, activated caspase-3, reduced Akt phosphorylation and cell number.	Reactive Oxygen Species	75-78	nitric oxide synthase 3	Homo sapiens	61-65
19913548-6	2010	Treatment with either the deltaPKC inhibitor, deltaV1-1, or the varepsilonPKC activator, psivarepsilonRACK, inhibited these effects, restoring cell survival through inhibition of eNOS activity.	psivarepsilonrack	89-106	nitric oxide synthase 3	Homo sapiens	179-183
19913548-9	2010	Together our data demonstrate that (1) in endothelial dysfunction, ROS and reactive nitrogen species (RNS) formation result from uncontrolled eNOS activity mediated by activation of deltaPKC or inhibition of varepsilonPKC; (2) inhibition of deltaPKC or activation of varepsilonPKC corrects the perturbed phosphorylation state of eNOS, thus increasing cell survival.	Reactive Oxygen Species	67-70	nitric oxide synthase 3	Homo sapiens	142-146
19913548-9	2010	Together our data demonstrate that (1) in endothelial dysfunction, ROS and reactive nitrogen species (RNS) formation result from uncontrolled eNOS activity mediated by activation of deltaPKC or inhibition of varepsilonPKC; (2) inhibition of deltaPKC or activation of varepsilonPKC corrects the perturbed phosphorylation state of eNOS, thus increasing cell survival.	Reactive Oxygen Species	67-70	nitric oxide synthase 3	Homo sapiens	329-333
19913548-9	2010	Together our data demonstrate that (1) in endothelial dysfunction, ROS and reactive nitrogen species (RNS) formation result from uncontrolled eNOS activity mediated by activation of deltaPKC or inhibition of varepsilonPKC; (2) inhibition of deltaPKC or activation of varepsilonPKC corrects the perturbed phosphorylation state of eNOS, thus increasing cell survival.	Reactive Nitrogen Species	75-100	nitric oxide synthase 3	Homo sapiens	142-146
19913548-9	2010	Together our data demonstrate that (1) in endothelial dysfunction, ROS and reactive nitrogen species (RNS) formation result from uncontrolled eNOS activity mediated by activation of deltaPKC or inhibition of varepsilonPKC; (2) inhibition of deltaPKC or activation of varepsilonPKC corrects the perturbed phosphorylation state of eNOS, thus increasing cell survival.	Reactive Nitrogen Species	102-105	nitric oxide synthase 3	Homo sapiens	142-146
19913548-9	2010	Together our data demonstrate that (1) in endothelial dysfunction, ROS and reactive nitrogen species (RNS) formation result from uncontrolled eNOS activity mediated by activation of deltaPKC or inhibition of varepsilonPKC; (2) inhibition of deltaPKC or activation of varepsilonPKC corrects the perturbed phosphorylation state of eNOS, thus increasing cell survival.	Reactive Nitrogen Species	102-105	nitric oxide synthase 3	Homo sapiens	329-333
20185342-1	2010	OBJECTIVE: We hypothesized that, similar to idiopathic hip osteonecrosis, the T-786C mutation of the endothelial nitric oxide synthase (eNOS) gene affecting nitric oxide (NO) production was associated with neuralgia-inducing cavitational osteonecrosis of the jaws (NICO).	Nitric Oxide	113-125	nitric oxide synthase 3	Homo sapiens	136-140
19952778-1	2010	BACKGROUND: Considering that the role of nitric oxide as a vasodilator is increased after an acute bout of exercise and that the 894G&gt;T polymorphism of the endothelial nitric oxide synthase seems to reduce the nitric oxide release in response to shear stress, the present study investigated the 894G&gt;T polymorphism in relation to vascular reactivity following maximal dynamic exercise.	Nitric Oxide	41-53	nitric oxide synthase 3	Homo sapiens	159-192
20185342-7	2010	CONCLUSIONS: The eNOS T-786C polymorphism affecting NO production is associated with NICO, may contribute to the pathogenesis of NICO, and may open therapeutic medical approaches to treatment of NICO through provision of L-arginine, the amino-acid precursor of NO.	Arginine	221-231	nitric oxide synthase 3	Homo sapiens	17-21
20044991-9	2010	These data revealed an estrogen receptor alpha-dependent modulation of Ca(2+) homeostasis accompanying the enhancement of endothelial nitric oxide synthase expression in 17 beta-estradiol-treated human endothelial cells.	Estradiol	173-187	nitric oxide synthase 3	Homo sapiens	122-155
20387553-3	2010	We have also demonstrated that endothelial nitric oxide synthase (eNOS) is a major source of EDHF/H2(0)2, where Cu, Zn-SOD is involved.	edhf	93-97	nitric oxide synthase 3	Homo sapiens	31-64
20387553-3	2010	We have also demonstrated that endothelial nitric oxide synthase (eNOS) is a major source of EDHF/H2(0)2, where Cu, Zn-SOD is involved.	Hydrogen	98-100	nitric oxide synthase 3	Homo sapiens	31-64
20448349-5	2010	The expression of PI3K, PKB, and eNOS in the intermittent high glucose group was significantly lower than that in the constant high glucose group (P&lt;0.05).	Glucose	63-70	nitric oxide synthase 3	Homo sapiens	33-37
20448349-5	2010	The expression of PI3K, PKB, and eNOS in the intermittent high glucose group was significantly lower than that in the constant high glucose group (P&lt;0.05).	Glucose	132-139	nitric oxide synthase 3	Homo sapiens	33-37
20448349-6	2010	CONCLUSION: Intermittent high glucose could be more deleterious to endothelial cells than constant high glucose, and may lead to decrease synthesis of NO by inhibiting PI3K/PKB/eNOS pathway activation.	Glucose	30-37	nitric oxide synthase 3	Homo sapiens	177-181
20044991-3	2010	Hence, we investigated the effect of chronic 17 beta-estradiol treatment on the intracellular Ca(2+) concentration and endothelial nitric oxide synthase protein expression in the human endothelial cell line, EA.hy926, using spectrofluorometry and Western blot, respectively.	Estradiol	45-62	nitric oxide synthase 3	Homo sapiens	119-152
20044991-6	2010	In addition, 17 beta-estradiol-treated cells expressed higher levels of endothelial nitric oxide synthase protein in comparison to vehicle-treated cells.	Estradiol	16-30	nitric oxide synthase 3	Homo sapiens	72-105
20044991-7	2010	The chronic effect of 17 beta-estradiol on Ca(2+) homeostasis and endothelial nitric oxide synthase expression was attenuated with the nonselective estrogen receptor inhibitor, ICI 182,780 (10muM, 7alpha, 17beta-[9-[(4,4,5,5,5-Pentafluoropentyl)sulfinyl]nonyl] estra-1,3,5(10)-triene-3,17-diol).	Estradiol	22-39	nitric oxide synthase 3	Homo sapiens	66-99
20044991-7	2010	The chronic effect of 17 beta-estradiol on Ca(2+) homeostasis and endothelial nitric oxide synthase expression was attenuated with the nonselective estrogen receptor inhibitor, ICI 182,780 (10muM, 7alpha, 17beta-[9-[(4,4,5,5,5-Pentafluoropentyl)sulfinyl]nonyl] estra-1,3,5(10)-triene-3,17-diol).	ici	177-180	nitric oxide synthase 3	Homo sapiens	66-99
20044991-7	2010	The chronic effect of 17 beta-estradiol on Ca(2+) homeostasis and endothelial nitric oxide synthase expression was attenuated with the nonselective estrogen receptor inhibitor, ICI 182,780 (10muM, 7alpha, 17beta-[9-[(4,4,5,5,5-Pentafluoropentyl)sulfinyl]nonyl] estra-1,3,5(10)-triene-3,17-diol).	7alpha, 17beta-[9-[(4,4,5,5,5-pentafluoropentyl)sulfinyl]nonyl] estra-1,3,5(10)-triene-3,17-diol	197-293	nitric oxide synthase 3	Homo sapiens	66-99
20149802-9	2010	The higher [TPEN] also induced cNOS uncoupling.	N,N,N',N'-tetrakis(2-pyridylmethyl)ethylenediamine	12-16	nitric oxide synthase 3	Homo sapiens	31-35
20149802-6	2010	The UVB-induced intracellular Zn(2+) elevation was dependent on the increase of constitutive nitric oxide synthase (cNOS) activity and production of superoxide.	Zinc	30-36	nitric oxide synthase 3	Homo sapiens	116-120
20149802-12	2010	SIGNIFICANCE: Our findings not only advance our understanding of the correlations between cNOS activation and Zn elevation, but also elucidated the role of cNOS in regulation of oxidative stress and apoptosis upon UVB-irradiation.	Zinc	110-112	nitric oxide synthase 3	Homo sapiens	90-94
20149802-12	2010	SIGNIFICANCE: Our findings not only advance our understanding of the correlations between cNOS activation and Zn elevation, but also elucidated the role of cNOS in regulation of oxidative stress and apoptosis upon UVB-irradiation.	Zinc	110-112	nitric oxide synthase 3	Homo sapiens	156-160
20093168-4	2010	We recently reported that nitric oxide (NO) synthesized by endothelial NO synthase (eNOS) slows down functional recovery and axon regeneration after XIIth nerve crushing.	Nitric Oxide	26-38	nitric oxide synthase 3	Homo sapiens	84-88
20042732-0	2010	Shear stress-induced ATP-mediated endothelial constitutive nitric oxide synthase expression in human lymphatic endothelial cells.	Adenosine Triphosphate	21-24	nitric oxide synthase 3	Homo sapiens	34-80
20042732-4	2010	Exogenous ATP ranging in concentration from 10(-9) to 10(-6) M produced a significant increase in ecNOS immunohistochemical expression in a dose-dependent manner.	Adenosine Triphosphate	10-13	nitric oxide synthase 3	Homo sapiens	98-103
20042732-5	2010	The increase in ecNOS expression mediated by 10(-6)M ATP was significantly reduced by 10(-5) M suramin.	Adenosine Triphosphate	53-56	nitric oxide synthase 3	Homo sapiens	16-21
20042732-5	2010	The increase in ecNOS expression mediated by 10(-6)M ATP was significantly reduced by 10(-5) M suramin.	Suramin	95-102	nitric oxide synthase 3	Homo sapiens	16-21
20393589-12	2010	Overproduction of ROS resulting from mitochondrial dysfunction or NOX activation is associated with uncoupling of endothelial nitric oxide synthase, which leads to reduced production of nitric oxide and endothelial-dependent vasodilation.	Reactive Oxygen Species	18-21	nitric oxide synthase 3	Homo sapiens	114-147
20042732-6	2010	Suramin (10(-5) M) caused a significant reduction in the shear stress-mediated increases in ecNOS immunohistochemical staining and mRNA expression.	Suramin	0-7	nitric oxide synthase 3	Homo sapiens	92-97
20042732-7	2010	The shear stress-mediated increases in ecNOS expression were significantly reduced by 3 mM tetraethylammonium, 10(-4) M apamin, 10(-9) M iberiotoxin, 10(-5) M 2-aminoethoxydephenyl borate, or 10(-5)M xestospongin C, but not 10(-5) M glybenclamide or 10(-5) M nifedipine.	Tetraethylammonium	91-109	nitric oxide synthase 3	Homo sapiens	39-44
19687739-0	2010	Propofol induces endothelial nitric oxide synthase phosphorylation and activation in human umbilical vein endothelial cells by inhibiting protein kinase C delta expression.	Propofol	0-8	nitric oxide synthase 3	Homo sapiens	17-50
20042732-7	2010	The shear stress-mediated increases in ecNOS expression were significantly reduced by 3 mM tetraethylammonium, 10(-4) M apamin, 10(-9) M iberiotoxin, 10(-5) M 2-aminoethoxydephenyl borate, or 10(-5)M xestospongin C, but not 10(-5) M glybenclamide or 10(-5) M nifedipine.	iberiotoxin	137-148	nitric oxide synthase 3	Homo sapiens	39-44
20042732-7	2010	The shear stress-mediated increases in ecNOS expression were significantly reduced by 3 mM tetraethylammonium, 10(-4) M apamin, 10(-9) M iberiotoxin, 10(-5) M 2-aminoethoxydephenyl borate, or 10(-5)M xestospongin C, but not 10(-5) M glybenclamide or 10(-5) M nifedipine.	2-aminoethoxydephenyl borate	159-187	nitric oxide synthase 3	Homo sapiens	39-44
20042732-7	2010	The shear stress-mediated increases in ecNOS expression were significantly reduced by 3 mM tetraethylammonium, 10(-4) M apamin, 10(-9) M iberiotoxin, 10(-5) M 2-aminoethoxydephenyl borate, or 10(-5)M xestospongin C, but not 10(-5) M glybenclamide or 10(-5) M nifedipine.	xestospongin C	200-214	nitric oxide synthase 3	Homo sapiens	39-44
20042732-7	2010	The shear stress-mediated increases in ecNOS expression were significantly reduced by 3 mM tetraethylammonium, 10(-4) M apamin, 10(-9) M iberiotoxin, 10(-5) M 2-aminoethoxydephenyl borate, or 10(-5)M xestospongin C, but not 10(-5) M glybenclamide or 10(-5) M nifedipine.	Glyburide	233-246	nitric oxide synthase 3	Homo sapiens	39-44
20042732-7	2010	The shear stress-mediated increases in ecNOS expression were significantly reduced by 3 mM tetraethylammonium, 10(-4) M apamin, 10(-9) M iberiotoxin, 10(-5) M 2-aminoethoxydephenyl borate, or 10(-5)M xestospongin C, but not 10(-5) M glybenclamide or 10(-5) M nifedipine.	Nifedipine	259-269	nitric oxide synthase 3	Homo sapiens	39-44
20042732-8	2010	The shear stress-mediated increases in ecNOS expression were significantly potentiated by pinacidil or NS1619 in a dose-dependent manner.	Pinacidil	90-99	nitric oxide synthase 3	Homo sapiens	39-44
20042732-8	2010	The shear stress-mediated increases in ecNOS expression were significantly potentiated by pinacidil or NS1619 in a dose-dependent manner.	NS 1619	103-109	nitric oxide synthase 3	Homo sapiens	39-44
20042732-10	2010	These findings suggest that shear stress produces a significant release of ATP from LEC, which activates the purinergic P2X/2Y receptor, thereby facilitating ecNOS mRNA and protein expression through inositol 1,4,5-trisphosphate-mediated release of intracellular Ca(2+) ions and the activation of Ca(2+)-activated K(+) channels in LEC.	Adenosine Triphosphate	75-78	nitric oxide synthase 3	Homo sapiens	158-163
20042732-10	2010	These findings suggest that shear stress produces a significant release of ATP from LEC, which activates the purinergic P2X/2Y receptor, thereby facilitating ecNOS mRNA and protein expression through inositol 1,4,5-trisphosphate-mediated release of intracellular Ca(2+) ions and the activation of Ca(2+)-activated K(+) channels in LEC.	5-trisphosphate	213-228	nitric oxide synthase 3	Homo sapiens	158-163
20406610-1	2010	OBJECTIVES: An impaired availability of nitric oxide (NO), related to polymorphisms in endothelial nitric oxide synthase (eNOS) gene, may influence the microvasculature in systemic Sclerosis (SSc).	Nitric Oxide	40-52	nitric oxide synthase 3	Homo sapiens	87-120
20406610-1	2010	OBJECTIVES: An impaired availability of nitric oxide (NO), related to polymorphisms in endothelial nitric oxide synthase (eNOS) gene, may influence the microvasculature in systemic Sclerosis (SSc).	Nitric Oxide	40-52	nitric oxide synthase 3	Homo sapiens	122-126
20184449-0	2010	Mass spectroscopy and molecular modeling predict endothelial nitric oxide synthase dimer collapse by hydrogen peroxide through zinc tetrathiolate metal-binding site disruption.	Hydrogen Peroxide	101-118	nitric oxide synthase 3	Homo sapiens	49-82
20184449-0	2010	Mass spectroscopy and molecular modeling predict endothelial nitric oxide synthase dimer collapse by hydrogen peroxide through zinc tetrathiolate metal-binding site disruption.	zinc tetrathiolate	127-145	nitric oxide synthase 3	Homo sapiens	49-82
20184449-0	2010	Mass spectroscopy and molecular modeling predict endothelial nitric oxide synthase dimer collapse by hydrogen peroxide through zinc tetrathiolate metal-binding site disruption.	Metals	146-151	nitric oxide synthase 3	Homo sapiens	49-82
20184449-1	2010	Endothelial nitric oxide synthase (eNOS) is inhibited by hydrogen peroxide (H(2)O(2)), but the mechanism has not been determined.	Hydrogen Peroxide	57-74	nitric oxide synthase 3	Homo sapiens	0-33
20184449-1	2010	Endothelial nitric oxide synthase (eNOS) is inhibited by hydrogen peroxide (H(2)O(2)), but the mechanism has not been determined.	Hydrogen Peroxide	57-74	nitric oxide synthase 3	Homo sapiens	35-39
20184449-2	2010	Thus, the purpose of this study was to delineate the mechanism by which H(2)O(2) inhibits eNOS activity.	Hydrogen Peroxide	72-80	nitric oxide synthase 3	Homo sapiens	90-94
20506636-0	2010	[Protein kinase C activation is required for free fatty acid-induced impairment of endothelial nitric oxide synthase].	Fatty Acids, Nonesterified	45-60	nitric oxide synthase 3	Homo sapiens	83-116
19968769-2	2010	The gene encoding endothelial nitric oxide synthase (eNOS) is an interesting candidate gene for understanding the physiopathology of ED, as it is involved in the catalytic production of nitric oxide (NO), the neurotransmitter that plays a critical role in penile tumescence and erection.	Nitric Oxide	30-42	nitric oxide synthase 3	Homo sapiens	53-57
20506636-1	2010	OBJECTIVE: To observe whether the impairment of endothelial nitric oxide synthase (eNOS) activity by elevated level of free fatty acid (FFA) is associated with activation of protein kinase C (PKC).	Fatty Acids, Nonesterified	119-134	nitric oxide synthase 3	Homo sapiens	48-81
20102704-4	2010	However, the role of SIRT1 in regulation of eNOS by CS and oxidants are not known.	Cesium	52-54	nitric oxide synthase 3	Homo sapiens	44-48
20560249-1	2010	Genetic polymorphisms in the gene that codes for endothelial nitric oxide synthase (eNOS) have been associated with less nitric oxide availability and with various cardiovascular diseases in humans.	Nitric Oxide	61-73	nitric oxide synthase 3	Homo sapiens	84-88
20102704-5	2010	We hypothesized that CS-mediated oxidative stress downregulates SIRT1 leading to acetylation of eNOS which results in reduced nitric oxide (NO)-mediated signaling and endothelial dysfunction.	Cesium	21-23	nitric oxide synthase 3	Homo sapiens	96-100
20102704-5	2010	We hypothesized that CS-mediated oxidative stress downregulates SIRT1 leading to acetylation of eNOS which results in reduced nitric oxide (NO)-mediated signaling and endothelial dysfunction.	Nitric Oxide	126-138	nitric oxide synthase 3	Homo sapiens	96-100
20102704-7	2010	Pre-treatment of endothelial cells with resveratrol significantly attenuated the CSE- and oxidant-mediated SIRT1 levels and eNOS acetylation.	Resveratrol	40-51	nitric oxide synthase 3	Homo sapiens	124-128
20102704-8	2010	These findings suggest that CS- and oxidant-mediated reduction of SIRT1 is associated with acetylation of eNOS which have implications in endothelial dysfunction.	Cesium	28-30	nitric oxide synthase 3	Homo sapiens	106-110
20117080-0	2010	The EGCg-induced redox-sensitive activation of endothelial nitric oxide synthase and relaxation are critically dependent on hydroxyl moieties.	epigallocatechin gallate	4-8	nitric oxide synthase 3	Homo sapiens	47-80
20117080-0	2010	The EGCg-induced redox-sensitive activation of endothelial nitric oxide synthase and relaxation are critically dependent on hydroxyl moieties.	Hydroxyl Radical	124-132	nitric oxide synthase 3	Homo sapiens	47-80
19946124-7	2010	Site-directed mutagenesis of the actin-binding domain of eNOS replacing leucine and tryptophan with alanine yielded an eNOS mutant that exhibited reduced eNOS-beta-actin association, decreased NO production, and increased superoxide formation in COS-7 cells.	Alanine	100-107	nitric oxide synthase 3	Homo sapiens	119-123
19946124-0	2010	Beta-actin association with endothelial nitric-oxide synthase modulates nitric oxide and superoxide generation from the enzyme.	Nitric Oxide	72-84	nitric oxide synthase 3	Homo sapiens	28-61
19946124-7	2010	Site-directed mutagenesis of the actin-binding domain of eNOS replacing leucine and tryptophan with alanine yielded an eNOS mutant that exhibited reduced eNOS-beta-actin association, decreased NO production, and increased superoxide formation in COS-7 cells.	Alanine	100-107	nitric oxide synthase 3	Homo sapiens	119-123
19946124-0	2010	Beta-actin association with endothelial nitric-oxide synthase modulates nitric oxide and superoxide generation from the enzyme.	Superoxides	89-99	nitric oxide synthase 3	Homo sapiens	28-61
19946124-7	2010	Site-directed mutagenesis of the actin-binding domain of eNOS replacing leucine and tryptophan with alanine yielded an eNOS mutant that exhibited reduced eNOS-beta-actin association, decreased NO production, and increased superoxide formation in COS-7 cells.	Superoxides	222-232	nitric oxide synthase 3	Homo sapiens	57-61
19946124-2	2010	We have previously reported that beta-actin is associated with eNOS oxygenase domain and that association of eNOS with beta-actin increases eNOS activity and nitric oxide (NO) production.	Nitric Oxide	158-170	nitric oxide synthase 3	Homo sapiens	109-113
19946124-7	2010	Site-directed mutagenesis of the actin-binding domain of eNOS replacing leucine and tryptophan with alanine yielded an eNOS mutant that exhibited reduced eNOS-beta-actin association, decreased NO production, and increased superoxide formation in COS-7 cells.	Superoxides	222-232	nitric oxide synthase 3	Homo sapiens	119-123
19946124-2	2010	We have previously reported that beta-actin is associated with eNOS oxygenase domain and that association of eNOS with beta-actin increases eNOS activity and nitric oxide (NO) production.	Nitric Oxide	158-170	nitric oxide synthase 3	Homo sapiens	109-113
19946124-4	2010	A synthetic actin-binding sequence (ABS) peptide 326 with amino acid sequence corresponding to residues 326-333 of human eNOS, one of the putative ABSs, specifically bound to beta-actin and prevented eNOS association with beta-actin in vitro.	Peptides	41-48	nitric oxide synthase 3	Homo sapiens	121-125
19946124-7	2010	Site-directed mutagenesis of the actin-binding domain of eNOS replacing leucine and tryptophan with alanine yielded an eNOS mutant that exhibited reduced eNOS-beta-actin association, decreased NO production, and increased superoxide formation in COS-7 cells.	Superoxides	222-232	nitric oxide synthase 3	Homo sapiens	119-123
19946124-4	2010	A synthetic actin-binding sequence (ABS) peptide 326 with amino acid sequence corresponding to residues 326-333 of human eNOS, one of the putative ABSs, specifically bound to beta-actin and prevented eNOS association with beta-actin in vitro.	Peptides	41-48	nitric oxide synthase 3	Homo sapiens	200-204
19946124-7	2010	Site-directed mutagenesis of the actin-binding domain of eNOS replacing leucine and tryptophan with alanine yielded an eNOS mutant that exhibited reduced eNOS-beta-actin association, decreased NO production, and increased superoxide formation in COS-7 cells.	carbonyl sulfide	246-249	nitric oxide synthase 3	Homo sapiens	57-61
19946124-7	2010	Site-directed mutagenesis of the actin-binding domain of eNOS replacing leucine and tryptophan with alanine yielded an eNOS mutant that exhibited reduced eNOS-beta-actin association, decreased NO production, and increased superoxide formation in COS-7 cells.	Leucine	72-79	nitric oxide synthase 3	Homo sapiens	57-61
19946124-7	2010	Site-directed mutagenesis of the actin-binding domain of eNOS replacing leucine and tryptophan with alanine yielded an eNOS mutant that exhibited reduced eNOS-beta-actin association, decreased NO production, and increased superoxide formation in COS-7 cells.	Leucine	72-79	nitric oxide synthase 3	Homo sapiens	119-123
19946124-7	2010	Site-directed mutagenesis of the actin-binding domain of eNOS replacing leucine and tryptophan with alanine yielded an eNOS mutant that exhibited reduced eNOS-beta-actin association, decreased NO production, and increased superoxide formation in COS-7 cells.	carbonyl sulfide	246-249	nitric oxide synthase 3	Homo sapiens	119-123
19946124-7	2010	Site-directed mutagenesis of the actin-binding domain of eNOS replacing leucine and tryptophan with alanine yielded an eNOS mutant that exhibited reduced eNOS-beta-actin association, decreased NO production, and increased superoxide formation in COS-7 cells.	Leucine	72-79	nitric oxide synthase 3	Homo sapiens	119-123
19946124-7	2010	Site-directed mutagenesis of the actin-binding domain of eNOS replacing leucine and tryptophan with alanine yielded an eNOS mutant that exhibited reduced eNOS-beta-actin association, decreased NO production, and increased superoxide formation in COS-7 cells.	Tryptophan	84-94	nitric oxide synthase 3	Homo sapiens	57-61
19946124-7	2010	Site-directed mutagenesis of the actin-binding domain of eNOS replacing leucine and tryptophan with alanine yielded an eNOS mutant that exhibited reduced eNOS-beta-actin association, decreased NO production, and increased superoxide formation in COS-7 cells.	Tryptophan	84-94	nitric oxide synthase 3	Homo sapiens	119-123
19946124-7	2010	Site-directed mutagenesis of the actin-binding domain of eNOS replacing leucine and tryptophan with alanine yielded an eNOS mutant that exhibited reduced eNOS-beta-actin association, decreased NO production, and increased superoxide formation in COS-7 cells.	Tryptophan	84-94	nitric oxide synthase 3	Homo sapiens	119-123
19946124-7	2010	Site-directed mutagenesis of the actin-binding domain of eNOS replacing leucine and tryptophan with alanine yielded an eNOS mutant that exhibited reduced eNOS-beta-actin association, decreased NO production, and increased superoxide formation in COS-7 cells.	Alanine	100-107	nitric oxide synthase 3	Homo sapiens	57-61
19946124-7	2010	Site-directed mutagenesis of the actin-binding domain of eNOS replacing leucine and tryptophan with alanine yielded an eNOS mutant that exhibited reduced eNOS-beta-actin association, decreased NO production, and increased superoxide formation in COS-7 cells.	carbonyl sulfide	246-249	nitric oxide synthase 3	Homo sapiens	119-123
19946124-8	2010	Disruption of eNOS-beta-actin interaction in endothelial cells using ABS peptide 326 resulted in decreased NO production, increased superoxide formation, and decreased endothelial monolayer wound repair, which was prevented by PEG-SOD and NO donor NOC-18.	Superoxides	132-142	nitric oxide synthase 3	Homo sapiens	14-18
19946124-9	2010	Taken together, this novel finding indicates that beta-actin binding to eNOS through residues 326-333 in the eNOS protein results in shifting the enzymatic activity from superoxide formation toward NO production.	Superoxides	170-180	nitric oxide synthase 3	Homo sapiens	72-76
19946124-9	2010	Taken together, this novel finding indicates that beta-actin binding to eNOS through residues 326-333 in the eNOS protein results in shifting the enzymatic activity from superoxide formation toward NO production.	Superoxides	170-180	nitric oxide synthase 3	Homo sapiens	109-113
19946124-10	2010	Modulation of NO and superoxide formation from eNOS by beta-actin plays an important role in endothelial function.	Superoxides	21-31	nitric oxide synthase 3	Homo sapiens	47-51
19878672-0	2010	Effect of apocynin on NADPH oxidase-mediated oxidative stress-LOX-1-eNOS pathway in human endothelial cells exposed to high glucose.	acetovanillone	10-18	nitric oxide synthase 3	Homo sapiens	68-72
20036714-2	2010	Preliminary in vitro studies have shown that the selective serotonin reuptake inhibitor (SSRI) antidepressant paroxetine inhibits constitutive nitric oxide synthase (cNOS) activity in animals and humans and that another SSRI such as fluoxetine reduced NO release in the media of synovial cells.	Paroxetine	110-120	nitric oxide synthase 3	Homo sapiens	166-170
20036714-2	2010	Preliminary in vitro studies have shown that the selective serotonin reuptake inhibitor (SSRI) antidepressant paroxetine inhibits constitutive nitric oxide synthase (cNOS) activity in animals and humans and that another SSRI such as fluoxetine reduced NO release in the media of synovial cells.	Fluoxetine	233-243	nitric oxide synthase 3	Homo sapiens	166-170
19878672-9	2010	Furthermore, high glucose attenuated eNOS protein and total nitrite levels.	Glucose	18-25	nitric oxide synthase 3	Homo sapiens	37-41
19878672-11	2010	Collectively, our study demonstrates that high glucose-induced oxidative stress via NADPH oxidase activation and this contributed to LOX-1 upregulation and eNOS downregulation in human endothelial cells.	Glucose	47-54	nitric oxide synthase 3	Homo sapiens	156-160
19931521-1	2010	BACKGROUND: Nitric oxide (NO) from the endothelium, produced by oxidation of l-arginine to l-citruline for the action at the endothelial nitric oxide synthase (eNOS) is considered an important atheroprotective factor.	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	125-158
19931521-1	2010	BACKGROUND: Nitric oxide (NO) from the endothelium, produced by oxidation of l-arginine to l-citruline for the action at the endothelial nitric oxide synthase (eNOS) is considered an important atheroprotective factor.	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	160-164
19931521-1	2010	BACKGROUND: Nitric oxide (NO) from the endothelium, produced by oxidation of l-arginine to l-citruline for the action at the endothelial nitric oxide synthase (eNOS) is considered an important atheroprotective factor.	Arginine	77-87	nitric oxide synthase 3	Homo sapiens	125-158
19931521-1	2010	BACKGROUND: Nitric oxide (NO) from the endothelium, produced by oxidation of l-arginine to l-citruline for the action at the endothelial nitric oxide synthase (eNOS) is considered an important atheroprotective factor.	Arginine	77-87	nitric oxide synthase 3	Homo sapiens	160-164
19931521-1	2010	BACKGROUND: Nitric oxide (NO) from the endothelium, produced by oxidation of l-arginine to l-citruline for the action at the endothelial nitric oxide synthase (eNOS) is considered an important atheroprotective factor.	DL-Citrulline	91-102	nitric oxide synthase 3	Homo sapiens	125-158
19931521-1	2010	BACKGROUND: Nitric oxide (NO) from the endothelium, produced by oxidation of l-arginine to l-citruline for the action at the endothelial nitric oxide synthase (eNOS) is considered an important atheroprotective factor.	DL-Citrulline	91-102	nitric oxide synthase 3	Homo sapiens	160-164
19960019-8	2010	We found a significant relationship between NOS3 Glu298Asp and triglycerides in African Americans.	Triglycerides	63-76	nitric oxide synthase 3	Homo sapiens	44-48
19960019-10	2010	We recommend further exploration of the relationship between NOS3 Glu298Asp and triglycerides in African Americans.	Triglycerides	80-93	nitric oxide synthase 3	Homo sapiens	61-65
19906781-9	2010	In human umbilical vein endothelial cells, L-165041 and GW0742 increased nitric oxide (NO) production and Akt and endothelial NOS (eNOS) phosphorylation, which were sensitive to PI3K inhibition and PPAR-beta blockade.	4-(3-(2-propyl-3-hydroxy-4-acetyl)phenoxy)propyloxyphenoxy acetic acid	43-51	nitric oxide synthase 3	Homo sapiens	114-129
19906781-9	2010	In human umbilical vein endothelial cells, L-165041 and GW0742 increased nitric oxide (NO) production and Akt and endothelial NOS (eNOS) phosphorylation, which were sensitive to PI3K inhibition and PPAR-beta blockade.	GW0742	56-62	nitric oxide synthase 3	Homo sapiens	114-129
19837105-3	2010	The study evaluated the involvement of Ca2+ on the regulation of NO synthase (NOS)-3 expression during N-acetylcysteine (NAC) cytoprotection against GCDCA-induced cell death in hepatocytes.	Acetylcysteine	103-119	nitric oxide synthase 3	Homo sapiens	65-84
19925457-0	2010	Insulin-stimulated phosphorylation of endothelial nitric oxide synthase at serine-615 contributes to nitric oxide synthesis.	Serine	75-81	nitric oxide synthase 3	Homo sapiens	38-71
19837105-10	2010	The stimulation of Ca2+ entrance by A23187 reduced cell death and enhanced NOS-3 expression in GCDCA-treated HepG2 cells.	Calcimycin	36-42	nitric oxide synthase 3	Homo sapiens	75-80
19837105-3	2010	The study evaluated the involvement of Ca2+ on the regulation of NO synthase (NOS)-3 expression during N-acetylcysteine (NAC) cytoprotection against GCDCA-induced cell death in hepatocytes.	Acetylcysteine	121-124	nitric oxide synthase 3	Homo sapiens	65-84
19837105-11	2010	The cytoprotective properties of NAC were related to the recovery of intracellular Ca2+ concentration, NOS-3 expression and NO production induced by GCDCA-treated HepG2 cells.	Acetylcysteine	33-36	nitric oxide synthase 3	Homo sapiens	103-108
19837105-7	2010	GCDCA reduced intracellular Ca2+ concentration and NOS-3 expression, and enhanced cell death in HepG2.	Glycochenodeoxycholic Acid	0-5	nitric oxide synthase 3	Homo sapiens	51-56
19837105-12	2010	The increase of NO production by Ca2+-dependent NOS-3 expression during NAC administration reduces cell death in GCDCA-treated hepatocytes.	Acetylcysteine	72-75	nitric oxide synthase 3	Homo sapiens	48-53
21188246-2	2010	Tetrahydrobiopterin (BH(4)) is an essential cofactor of endothelial NO synthase (eNOS) to produce NO, whereas dihydrobiopterin (BH(2)) can shift the eNOS product profile from NO to superoxide, which is further converted to hydrogen peroxide (H(2)O(2)) and cause I/R injury.	sapropterin	0-19	nitric oxide synthase 3	Homo sapiens	81-85
19880524-2	2010	Here we present evidence that hypoxia causes a rapid decrease in the transcription of the eNOS/NOS3 gene, accompanied by decreased acetylation and lysine 4 (histone H3) methylation of eNOS proximal promoter histones.	Lysine	147-153	nitric oxide synthase 3	Homo sapiens	90-94
19880524-2	2010	Here we present evidence that hypoxia causes a rapid decrease in the transcription of the eNOS/NOS3 gene, accompanied by decreased acetylation and lysine 4 (histone H3) methylation of eNOS proximal promoter histones.	Lysine	147-153	nitric oxide synthase 3	Homo sapiens	95-99
19880524-2	2010	Here we present evidence that hypoxia causes a rapid decrease in the transcription of the eNOS/NOS3 gene, accompanied by decreased acetylation and lysine 4 (histone H3) methylation of eNOS proximal promoter histones.	Lysine	147-153	nitric oxide synthase 3	Homo sapiens	184-188
21188246-2	2010	Tetrahydrobiopterin (BH(4)) is an essential cofactor of endothelial NO synthase (eNOS) to produce NO, whereas dihydrobiopterin (BH(2)) can shift the eNOS product profile from NO to superoxide, which is further converted to hydrogen peroxide (H(2)O(2)) and cause I/R injury.	sapropterin	0-19	nitric oxide synthase 3	Homo sapiens	149-153
21188246-2	2010	Tetrahydrobiopterin (BH(4)) is an essential cofactor of endothelial NO synthase (eNOS) to produce NO, whereas dihydrobiopterin (BH(2)) can shift the eNOS product profile from NO to superoxide, which is further converted to hydrogen peroxide (H(2)O(2)) and cause I/R injury.	7,8-dihydrobiopterin	110-126	nitric oxide synthase 3	Homo sapiens	149-153
21188246-2	2010	Tetrahydrobiopterin (BH(4)) is an essential cofactor of endothelial NO synthase (eNOS) to produce NO, whereas dihydrobiopterin (BH(2)) can shift the eNOS product profile from NO to superoxide, which is further converted to hydrogen peroxide (H(2)O(2)) and cause I/R injury.	bh(2)	128-133	nitric oxide synthase 3	Homo sapiens	149-153
20503475-1	2010	The purported effects of "circulation-improving" herbs used in traditional Chinese medicine (TCM) show striking similarities with the vascular actions of nitric oxide (NO) produced by the endothelial NO synthase (eNOS).	Nitric Oxide	154-166	nitric oxide synthase 3	Homo sapiens	213-217
21188246-2	2010	Tetrahydrobiopterin (BH(4)) is an essential cofactor of endothelial NO synthase (eNOS) to produce NO, whereas dihydrobiopterin (BH(2)) can shift the eNOS product profile from NO to superoxide, which is further converted to hydrogen peroxide (H(2)O(2)) and cause I/R injury.	Superoxides	181-191	nitric oxide synthase 3	Homo sapiens	81-85
21188246-2	2010	Tetrahydrobiopterin (BH(4)) is an essential cofactor of endothelial NO synthase (eNOS) to produce NO, whereas dihydrobiopterin (BH(2)) can shift the eNOS product profile from NO to superoxide, which is further converted to hydrogen peroxide (H(2)O(2)) and cause I/R injury.	Hydrogen Peroxide	223-240	nitric oxide synthase 3	Homo sapiens	81-85
20503475-5	2010	We have previously shown that ursolic acid (a constituent of Salviae miltiorrhizae radix), betulinic acid (a compound present in Zizyphi spinosae semen), luteolin and cynaroside (ingredients of artichoke, Cynara scolymus L.) are capable of enhancing eNOS gene expression.	luteolin-7-glucoside	167-177	nitric oxide synthase 3	Homo sapiens	250-254
21188246-2	2010	Tetrahydrobiopterin (BH(4)) is an essential cofactor of endothelial NO synthase (eNOS) to produce NO, whereas dihydrobiopterin (BH(2)) can shift the eNOS product profile from NO to superoxide, which is further converted to hydrogen peroxide (H(2)O(2)) and cause I/R injury.	Water	242-247	nitric oxide synthase 3	Homo sapiens	81-85
21188246-6	2010	In conclusion, these results suggest that promoting eNOS coupling to produce NO and decrease H(2)O(2) may be a key mechanism to restore postreperfused organ function during early reperfusion.	Water	93-98	nitric oxide synthase 3	Homo sapiens	52-56
19855060-1	2010	Nitric oxide (NO), synthesized by endothelial nitric oxide synthase (eNOS), exerts control over vascular function via two distinct mechanisms, the activation of soluble guanylate cyclase (sGC)/cGMP-dependent signaling or through S-nitrosylation of proteins with reactive thiols (S-nitrosylation).	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	34-67
19855060-1	2010	Nitric oxide (NO), synthesized by endothelial nitric oxide synthase (eNOS), exerts control over vascular function via two distinct mechanisms, the activation of soluble guanylate cyclase (sGC)/cGMP-dependent signaling or through S-nitrosylation of proteins with reactive thiols (S-nitrosylation).	Cyclic GMP	193-197	nitric oxide synthase 3	Homo sapiens	34-67
19855060-1	2010	Nitric oxide (NO), synthesized by endothelial nitric oxide synthase (eNOS), exerts control over vascular function via two distinct mechanisms, the activation of soluble guanylate cyclase (sGC)/cGMP-dependent signaling or through S-nitrosylation of proteins with reactive thiols (S-nitrosylation).	Sulfhydryl Compounds	271-277	nitric oxide synthase 3	Homo sapiens	34-67
19741206-2	2010	Uterine artery endothelial cells from nonpregnant (NP-UAECs) or pregnant (P-UAECs) ewes maintained in culture still show a pregnancy-enhanced difference in ATP-stimulated endothelial NO synthase (eNOS; official symbol NOS3) activation, even though NOS3 protein, purinergic receptors, and associated cell signaling proteins are expressed at equal levels.	Adenosine Triphosphate	156-159	nitric oxide synthase 3	Homo sapiens	218-222
20103956-1	2010	BACKGROUND AND OBJECTIVES: Endo-derived nitric oxide (NO) is synthesized from L-arginine by endothelial nitric oxide synthase (NOS3).	Nitric Oxide	40-52	nitric oxide synthase 3	Homo sapiens	92-125
20103956-1	2010	BACKGROUND AND OBJECTIVES: Endo-derived nitric oxide (NO) is synthesized from L-arginine by endothelial nitric oxide synthase (NOS3).	Nitric Oxide	40-52	nitric oxide synthase 3	Homo sapiens	127-131
20103956-1	2010	BACKGROUND AND OBJECTIVES: Endo-derived nitric oxide (NO) is synthesized from L-arginine by endothelial nitric oxide synthase (NOS3).	Arginine	78-88	nitric oxide synthase 3	Homo sapiens	92-125
20103956-1	2010	BACKGROUND AND OBJECTIVES: Endo-derived nitric oxide (NO) is synthesized from L-arginine by endothelial nitric oxide synthase (NOS3).	Arginine	78-88	nitric oxide synthase 3	Homo sapiens	127-131
19741206-2	2010	Uterine artery endothelial cells from nonpregnant (NP-UAECs) or pregnant (P-UAECs) ewes maintained in culture still show a pregnancy-enhanced difference in ATP-stimulated endothelial NO synthase (eNOS; official symbol NOS3) activation, even though NOS3 protein, purinergic receptors, and associated cell signaling proteins are expressed at equal levels.	Adenosine Triphosphate	156-159	nitric oxide synthase 3	Homo sapiens	248-252
19741206-7	2010	The relationship between Ca(2+) bursts and NOS3 activation is further established by the finding that (43,37)GAP27 inhibits ATP-stimulated NOS3 activation but has no effect on cell mitogenesis.	Adenosine Triphosphate	124-127	nitric oxide synthase 3	Homo sapiens	43-47
19741206-7	2010	The relationship between Ca(2+) bursts and NOS3 activation is further established by the finding that (43,37)GAP27 inhibits ATP-stimulated NOS3 activation but has no effect on cell mitogenesis.	Adenosine Triphosphate	124-127	nitric oxide synthase 3	Homo sapiens	139-143
20110684-6	2010	LPC concentration- and time-dependently decreased eNOS levels, but this effect was blocked by antioxidants and SOD and potentiated by the SOD1 inhibitor, ammonium tetrathiomolybdate.	tetrathiomolybdate	154-181	nitric oxide synthase 3	Homo sapiens	50-54
19917268-4	2010	The MEK inhibitor PD98059 and the PI3K inhibitor Wortmannin specifically inhibited sesamin-induced activation of the ERK and Akt/eNOS pathways.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	18-25	nitric oxide synthase 3	Homo sapiens	129-133
19917268-4	2010	The MEK inhibitor PD98059 and the PI3K inhibitor Wortmannin specifically inhibited sesamin-induced activation of the ERK and Akt/eNOS pathways.	Wortmannin	49-59	nitric oxide synthase 3	Homo sapiens	129-133
19917268-4	2010	The MEK inhibitor PD98059 and the PI3K inhibitor Wortmannin specifically inhibited sesamin-induced activation of the ERK and Akt/eNOS pathways.	sesamin	83-90	nitric oxide synthase 3	Homo sapiens	129-133
19917268-9	2010	These results suggest that sesamin stimulates angiogenesis in vitro and in vivo through the activation of MEK/ERK-, PI3K/Akt/eNOS-, p125(FAK)-, and p38 MAPK-dependent pathways, without increasing vascular inflammation, and may be used for treating ischemic diseases and tissue regeneration.	sesamin	27-34	nitric oxide synthase 3	Homo sapiens	125-129
20460711-0	2010	Vinegar intake enhances flow-mediated vasodilatation via upregulation of endothelial nitric oxide synthase activity.	Acetic Acid	0-7	nitric oxide synthase 3	Homo sapiens	73-106
20460711-1	2010	This study examined the effect of acetate on endothelial nitric oxide synthase (eNOS) in human umbilical vein endothelial cells (HUVECs) by immunoblotting assay and the ability of acetic acid to upregulate flow-mediated vasodilatation in humans.	Acetates	34-41	nitric oxide synthase 3	Homo sapiens	45-78
20110684-1	2010	We examined the mechanism through which lysophosphatidylcholine (LPC) induces endothelial nitric oxide (eNOS) downregulation.	Lysophosphatidylcholines	40-63	nitric oxide synthase 3	Homo sapiens	104-108
20110684-1	2010	We examined the mechanism through which lysophosphatidylcholine (LPC) induces endothelial nitric oxide (eNOS) downregulation.	Lysophosphatidylcholines	65-68	nitric oxide synthase 3	Homo sapiens	104-108
20110684-1	2010	We examined the mechanism through which lysophosphatidylcholine (LPC) induces endothelial nitric oxide (eNOS) downregulation.	Nitric Oxide	90-102	nitric oxide synthase 3	Homo sapiens	104-108
20110684-6	2010	LPC concentration- and time-dependently decreased eNOS levels, but this effect was blocked by antioxidants and SOD and potentiated by the SOD1 inhibitor, ammonium tetrathiomolybdate.	Lysophosphatidylcholines	0-3	nitric oxide synthase 3	Homo sapiens	50-54
20675897-1	2010	Previous reports have demonstrated that red blood cells (RBC) have an active nitric oxide (NO) synthesizing mechanism which has properties similar to endothelial nitric oxide synthase (eNOS).	Nitric Oxide	77-89	nitric oxide synthase 3	Homo sapiens	150-183
21063103-0	2010	Opposite effect of Hsp90alpha and Hsp90beta on eNOS ability to produce nitric oxide or superoxide anion in human embryonic kidney cells.	Nitric Oxide	71-83	nitric oxide synthase 3	Homo sapiens	47-51
21063103-0	2010	Opposite effect of Hsp90alpha and Hsp90beta on eNOS ability to produce nitric oxide or superoxide anion in human embryonic kidney cells.	Superoxides	87-103	nitric oxide synthase 3	Homo sapiens	47-51
21063103-8	2010	The Hsp90alpha over-expression induced a significant increase in NO(2)/NO(3) levels, an effect that was associated with increased phosphorylation of eNOS Ser 1177 and Akt/PKB Ser473, as well as with a greater Hsp90alpha dimerization.	Serine	154-157	nitric oxide synthase 3	Homo sapiens	149-153
19022425-9	2010	Cigarette smoking and nicotine stimulated the expression of endothelial NO synthase (eNOS) and inducible NO synthase (iNOS) whereas benzo[a]pyrene (BP) only stimulated the expression of eNOS in HES cells.	Nicotine	22-30	nitric oxide synthase 3	Homo sapiens	60-83
19022425-9	2010	Cigarette smoking and nicotine stimulated the expression of endothelial NO synthase (eNOS) and inducible NO synthase (iNOS) whereas benzo[a]pyrene (BP) only stimulated the expression of eNOS in HES cells.	Nicotine	22-30	nitric oxide synthase 3	Homo sapiens	186-190
19022425-9	2010	Cigarette smoking and nicotine stimulated the expression of endothelial NO synthase (eNOS) and inducible NO synthase (iNOS) whereas benzo[a]pyrene (BP) only stimulated the expression of eNOS in HES cells.	Nicotine	22-30	nitric oxide synthase 3	Homo sapiens	85-89
19022425-9	2010	Cigarette smoking and nicotine stimulated the expression of endothelial NO synthase (eNOS) and inducible NO synthase (iNOS) whereas benzo[a]pyrene (BP) only stimulated the expression of eNOS in HES cells.	Benzo(a)pyrene	132-146	nitric oxide synthase 3	Homo sapiens	186-190
19876820-1	2010	Hemodynamic shear stress is the most powerful physiological regulator of endothelial Nitric Oxide Synthase (eNOS), leading to rapid rises in nitric oxide (NO).	Nitric Oxide	141-153	nitric oxide synthase 3	Homo sapiens	73-106
19022425-9	2010	Cigarette smoking and nicotine stimulated the expression of endothelial NO synthase (eNOS) and inducible NO synthase (iNOS) whereas benzo[a]pyrene (BP) only stimulated the expression of eNOS in HES cells.	Benzo(a)pyrene	148-150	nitric oxide synthase 3	Homo sapiens	186-190
19022425-11	2010	The effect of CS on eNOS/iNOS expression in HES cells was blocked by ascorbic acid but not by glutathione.	Cesium	14-16	nitric oxide synthase 3	Homo sapiens	20-24
19022425-11	2010	The effect of CS on eNOS/iNOS expression in HES cells was blocked by ascorbic acid but not by glutathione.	Helium	44-47	nitric oxide synthase 3	Homo sapiens	20-24
19022425-11	2010	The effect of CS on eNOS/iNOS expression in HES cells was blocked by ascorbic acid but not by glutathione.	Ascorbic Acid	69-82	nitric oxide synthase 3	Homo sapiens	20-24
19876820-1	2010	Hemodynamic shear stress is the most powerful physiological regulator of endothelial Nitric Oxide Synthase (eNOS), leading to rapid rises in nitric oxide (NO).	Nitric Oxide	141-153	nitric oxide synthase 3	Homo sapiens	108-112
19907345-1	2010	Nitric oxide is a key mediator of endothelial function and is synthesized by endothelial nitric oxide synthase (eNOS).	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	77-110
19907424-0	2010	Increased cyclic guanosine monophosphate production and endothelial nitric oxide synthase level in mononuclear cells from sildenafil citrate-treated patients with erectile dysfunction.	Sildenafil Citrate	122-140	nitric oxide synthase 3	Homo sapiens	56-89
19907424-6	2010	In the mononuclear cells, the protein level of endothelial NO synthase (eNOS) was higher after sildenafil citrate treatment.	Sildenafil Citrate	95-113	nitric oxide synthase 3	Homo sapiens	47-70
19907424-6	2010	In the mononuclear cells, the protein level of endothelial NO synthase (eNOS) was higher after sildenafil citrate treatment.	Sildenafil Citrate	95-113	nitric oxide synthase 3	Homo sapiens	72-76
19907424-10	2010	In conclusion, in mononuclear cells from patients with ED sildenafil citrate administration increased the level of eNOS protein and increased cGMP production in response to NO.	Sildenafil Citrate	58-76	nitric oxide synthase 3	Homo sapiens	115-119
20308789-6	2010	Addition of high concentration Abeta{1-42} (200, 2000 ng/mL) to the CAC culture reduced CAC counts and endothelial nitric oxide synthase/Akt phosphorylation and induced apoptosis.	UNII-042A8N37WH	31-36	nitric oxide synthase 3	Homo sapiens	103-136
19907345-1	2010	Nitric oxide is a key mediator of endothelial function and is synthesized by endothelial nitric oxide synthase (eNOS).	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	112-116
20459417-10	2010	In addition Glu allele of the polymorphic locus Glu298Asp of eNOS gene in the homozygous state was associated with the severity and unfavorable development of CHF.	Glutamic Acid	12-15	nitric oxide synthase 3	Homo sapiens	61-65
20459417-11	2010	The endothelial-dependent dysfunction was more severe in homozygotes of Glu allele of the polymorphic locus Glu298Asp of eNOS gene than in carrier of allele 298Asp.	Glutamic Acid	72-75	nitric oxide synthase 3	Homo sapiens	121-125
20632820-1	2010	AIMS: Recent study indicates that the binding of caveolin-1 (CAV1), the essential constituent of caveolae, to endothelial nitric oxide synthase (eNOS) prevents nitric oxide (NO) production in cirrhotic human liver.	Nitric Oxide	122-134	nitric oxide synthase 3	Homo sapiens	145-149
20043715-1	2010	OBJECT: Studies have shown decreased levels of nitric oxide (NO), the product of endothelial NO synthase (eNOS) gene activity, in infants with respiratory conditions and intraventricular hemorrhage (IVH).	Nitric Oxide	47-59	nitric oxide synthase 3	Homo sapiens	81-104
20043715-1	2010	OBJECT: Studies have shown decreased levels of nitric oxide (NO), the product of endothelial NO synthase (eNOS) gene activity, in infants with respiratory conditions and intraventricular hemorrhage (IVH).	Nitric Oxide	47-59	nitric oxide synthase 3	Homo sapiens	106-110
20360620-3	2010	Incubation of HUVECs with fluvastatin, lovastatin or cerivastatin for 24 h caused an approximately 3-fold upregulation of eNOS expression that was associated with increased eNOS activity and accumulation of cGMP.	Fluvastatin	26-37	nitric oxide synthase 3	Homo sapiens	122-126
20360620-3	2010	Incubation of HUVECs with fluvastatin, lovastatin or cerivastatin for 24 h caused an approximately 3-fold upregulation of eNOS expression that was associated with increased eNOS activity and accumulation of cGMP.	Fluvastatin	26-37	nitric oxide synthase 3	Homo sapiens	173-177
20360620-3	2010	Incubation of HUVECs with fluvastatin, lovastatin or cerivastatin for 24 h caused an approximately 3-fold upregulation of eNOS expression that was associated with increased eNOS activity and accumulation of cGMP.	Lovastatin	39-49	nitric oxide synthase 3	Homo sapiens	122-126
20360620-3	2010	Incubation of HUVECs with fluvastatin, lovastatin or cerivastatin for 24 h caused an approximately 3-fold upregulation of eNOS expression that was associated with increased eNOS activity and accumulation of cGMP.	Lovastatin	39-49	nitric oxide synthase 3	Homo sapiens	173-177
20360620-3	2010	Incubation of HUVECs with fluvastatin, lovastatin or cerivastatin for 24 h caused an approximately 3-fold upregulation of eNOS expression that was associated with increased eNOS activity and accumulation of cGMP.	cerivastatin	53-65	nitric oxide synthase 3	Homo sapiens	122-126
20360620-3	2010	Incubation of HUVECs with fluvastatin, lovastatin or cerivastatin for 24 h caused an approximately 3-fold upregulation of eNOS expression that was associated with increased eNOS activity and accumulation of cGMP.	cerivastatin	53-65	nitric oxide synthase 3	Homo sapiens	173-177
20360620-3	2010	Incubation of HUVECs with fluvastatin, lovastatin or cerivastatin for 24 h caused an approximately 3-fold upregulation of eNOS expression that was associated with increased eNOS activity and accumulation of cGMP.	Cyclic GMP	207-211	nitric oxide synthase 3	Homo sapiens	122-126
19917066-0	2009	Rosiglitazone via upregulation of Akt/eNOS pathways attenuates dysfunction of endothelial progenitor cells, induced by advanced glycation end products.	Rosiglitazone	0-13	nitric oxide synthase 3	Homo sapiens	38-42
19632222-0	2009	Basal endothelial nitric oxide synthase (eNOS) phosphorylation on Ser(1177) occurs in a stable microtubule- and tubulin acetylation-dependent manner.	Serine	66-69	nitric oxide synthase 3	Homo sapiens	6-39
20020783-5	2009	GCDCA reduced the intracellular Ca(2+) concentration and NOS-3 expression and enhanced cell death in HepG2.	Glycochenodeoxycholic Acid	0-5	nitric oxide synthase 3	Homo sapiens	57-62
20020783-7	2009	The reduction of Ca(2+) entry by EGTA, but not its release from intracellular stores by BAPTA-AM, reduced the expression of NOS-3 and enhanced cell death in control and GCDCA-treated cells.	Egtazic Acid	33-37	nitric oxide synthase 3	Homo sapiens	124-129
20020783-8	2009	Mito Q prevented the reduction of intracellular Ca(2+) concentration, NOS-3 expression, NO production, and cell death in GCDCA-treated HepG2 cells.	mito q	0-6	nitric oxide synthase 3	Homo sapiens	70-75
20020783-9	2009	The conclusion is that the recovery of Ca(2+)-dependent NOS-3 expression by Mito Q may be considered an additional cytoprotective property of an antioxidant.	mito q	76-82	nitric oxide synthase 3	Homo sapiens	56-61
19917066-6	2009	KEY RESULTS: Number, proliferation/migration capacities, eNOS and Akt phosphorylation as well as NO synthesized by EPCs were increased by rosiglitazone and reduced by AGEs.	Rosiglitazone	138-151	nitric oxide synthase 3	Homo sapiens	57-61
19917066-10	2009	CONCLUSIONS AND IMPLICATIONS: The PPARgamma agonist rosiglitazone increased EPC function and attenuated EPC dysfunction induced by AGEs via upregulating the Akt-eNOS signal pathways of EPCs.	Rosiglitazone	52-65	nitric oxide synthase 3	Homo sapiens	161-165
19838132-2	2009	Increasing evidence suggests a dysfunctional platelet nitric oxide synthase type 3 (NOS3) pathway in essential hypertension, whereas for endothelial-derived nitric oxide the picture is more complicated, with many studies suggesting an impairment of endothelial nitric oxide generation, whilst others have suggested that the endothelial nitric oxide pathway is preserved.	Nitric Oxide	54-66	nitric oxide synthase 3	Homo sapiens	84-88
19797052-7	2009	We hypothesize that under redox stress, when the availability of tetrahydrobiopterin, a pivotal stoichiometric cofactor for eNOS, is limited, activation of Nrf2 leads (a) to transient reduction of eNOS protein levels and (b) to an antioxidant defense in human umbilical vein endothelial cells.	sapropterin	65-84	nitric oxide synthase 3	Homo sapiens	124-128
19330466-4	2009	We have identified polymorphisms in the NOS 3 gene and one of these polymorphisms, Glu(298--&gt;)Asp, was found to be a major risk factor for carotid artery disease and myocardial infarction.	Glutamic Acid	83-86	nitric oxide synthase 3	Homo sapiens	40-45
19330466-4	2009	We have identified polymorphisms in the NOS 3 gene and one of these polymorphisms, Glu(298--&gt;)Asp, was found to be a major risk factor for carotid artery disease and myocardial infarction.	Aspartic Acid	97-100	nitric oxide synthase 3	Homo sapiens	40-45
19891529-1	2009	Nitric Oxide (NO) plays a relevant role in regulating platelet recruitment and eNOS is the major isoform known to be expressed in platelets.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	79-83
20005399-4	2009	A reduction in basal nitric oxide (NO) release as a result of genetic variation in endothelial NO synthase (eNOS) function may predispose to hypertension, thrombosis, vasospasm, and atherosclerosis, all contributing to the development of CAN.	Nitric Oxide	21-33	nitric oxide synthase 3	Homo sapiens	108-112
19797052-7	2009	We hypothesize that under redox stress, when the availability of tetrahydrobiopterin, a pivotal stoichiometric cofactor for eNOS, is limited, activation of Nrf2 leads (a) to transient reduction of eNOS protein levels and (b) to an antioxidant defense in human umbilical vein endothelial cells.	sapropterin	65-84	nitric oxide synthase 3	Homo sapiens	197-201
19479297-7	2009	Functional studies revealed that in the presence of defined growth conditions, compared to the untransfected and GFP-transfected cells, eNOS-EPCs from patients with CAD have a significant increase in [3H] thymidine-labeled DNA (P &lt; 0.01), migration (14.6 +/- 1.8 and 16.5 +/- 1.9 vs. 23.5 +/- 3.4 cells/field, P &lt; 0.01), ability to differentiate into endothelial-like spindle-shaped cells (46 +/- 4.5 and 56.5 +/- 2.1 vs. 93.2 +/- 6.6 cells/field, P &lt; 0.001) and also incorporation into tube-like structures on the matrigel (GFP-EPCs: 21.25 +/- 2.9 vs. GFP-eNOS-EPCs: 34.5 +/- 5.5 cells/field, P &lt; 0.05).	Tritium	201-203	nitric oxide synthase 3	Homo sapiens	136-140
19479297-7	2009	Functional studies revealed that in the presence of defined growth conditions, compared to the untransfected and GFP-transfected cells, eNOS-EPCs from patients with CAD have a significant increase in [3H] thymidine-labeled DNA (P &lt; 0.01), migration (14.6 +/- 1.8 and 16.5 +/- 1.9 vs. 23.5 +/- 3.4 cells/field, P &lt; 0.01), ability to differentiate into endothelial-like spindle-shaped cells (46 +/- 4.5 and 56.5 +/- 2.1 vs. 93.2 +/- 6.6 cells/field, P &lt; 0.001) and also incorporation into tube-like structures on the matrigel (GFP-EPCs: 21.25 +/- 2.9 vs. GFP-eNOS-EPCs: 34.5 +/- 5.5 cells/field, P &lt; 0.05).	Thymidine	205-214	nitric oxide synthase 3	Homo sapiens	136-140
19468830-0	2009	The 27-bp repeat polymorphism in intron 4 (27 bp-VNTR) of endothelial nitric oxide synthase (eNOS) gene is associated with albumin to creatinine ratio in Mexican Americans.	Creatinine	134-144	nitric oxide synthase 3	Homo sapiens	58-91
19881294-5	2009	However, resveratrol markedly suppressed VEGF-induced eNOS phosphorylation.	Resveratrol	9-20	nitric oxide synthase 3	Homo sapiens	54-58
19409716-1	2009	Reduced folates have been shown to reconstitute the proper activity of "uncoupled" endothelial nitric oxide synthase in inflamed endothlelium.	Folic Acid	8-15	nitric oxide synthase 3	Homo sapiens	83-116
19468830-0	2009	The 27-bp repeat polymorphism in intron 4 (27 bp-VNTR) of endothelial nitric oxide synthase (eNOS) gene is associated with albumin to creatinine ratio in Mexican Americans.	Creatinine	134-144	nitric oxide synthase 3	Homo sapiens	93-97
19468830-1	2009	The T-786C, Glu298Asp, and 27 bp variable number of tandem repeats (27 bp-VNTR-a/b) polymorphsims of the endothelial nitric oxide synthase (eNOS) gene are thought to alter nitric oxide production and contribute to the development of vascular and renal disease risk.	Nitric Oxide	117-129	nitric oxide synthase 3	Homo sapiens	140-144
19666465-0	2009	Critical role for tetrahydrobiopterin recycling by dihydrofolate reductase in regulation of endothelial nitric-oxide synthase coupling: relative importance of the de novo biopterin synthesis versus salvage pathways.	sapropterin	18-37	nitric oxide synthase 3	Homo sapiens	92-125
19682597-6	2009	Treatment with the nitric oxide donor, propylamine propylamine NONOate (PAPA-NO; 1 microM for 1 h) increased Akt and GSK-3beta phosphorylation, and induced NFATc1 nuclear translocation in WT and eNOS(-/-) myotubes, and eliminated differences from WT in the NOS knockout cultures.	Nitric Oxide	19-31	nitric oxide synthase 3	Homo sapiens	195-199
19682597-6	2009	Treatment with the nitric oxide donor, propylamine propylamine NONOate (PAPA-NO; 1 microM for 1 h) increased Akt and GSK-3beta phosphorylation, and induced NFATc1 nuclear translocation in WT and eNOS(-/-) myotubes, and eliminated differences from WT in the NOS knockout cultures.	propylamine propylamine nonoate	39-70	nitric oxide synthase 3	Homo sapiens	195-199
19682597-6	2009	Treatment with the nitric oxide donor, propylamine propylamine NONOate (PAPA-NO; 1 microM for 1 h) increased Akt and GSK-3beta phosphorylation, and induced NFATc1 nuclear translocation in WT and eNOS(-/-) myotubes, and eliminated differences from WT in the NOS knockout cultures.	PAPA-NO	72-79	nitric oxide synthase 3	Homo sapiens	195-199
20447567-3	2009	The conventional notion that endothelial NO synthase (eNOS)-derived NO is largely responsible for both effects has been challenged by first-in-human studies with a selective inhibitor of neuronal NOS (nNOS), S-methyl-l-thiocitrulline (SMTC).	S-methylthiocitrulline	208-233	nitric oxide synthase 3	Homo sapiens	54-58
20447567-3	2009	The conventional notion that endothelial NO synthase (eNOS)-derived NO is largely responsible for both effects has been challenged by first-in-human studies with a selective inhibitor of neuronal NOS (nNOS), S-methyl-l-thiocitrulline (SMTC).	S-methylthiocitrulline	235-239	nitric oxide synthase 3	Homo sapiens	54-58
19666465-0	2009	Critical role for tetrahydrobiopterin recycling by dihydrofolate reductase in regulation of endothelial nitric-oxide synthase coupling: relative importance of the de novo biopterin synthesis versus salvage pathways.	Biopterin	28-37	nitric oxide synthase 3	Homo sapiens	92-125
19666465-1	2009	Tetrahyrobiopterin (BH4) is a required cofactor for the synthesis of nitric oxide by endothelial nitric-oxide synthase (eNOS), and BH4 bioavailability within the endothelium is a critical factor in regulating the balance between NO and superoxide production by eNOS (eNOS coupling).	tetrahyrobiopterin	0-18	nitric oxide synthase 3	Homo sapiens	85-118
19666465-1	2009	Tetrahyrobiopterin (BH4) is a required cofactor for the synthesis of nitric oxide by endothelial nitric-oxide synthase (eNOS), and BH4 bioavailability within the endothelium is a critical factor in regulating the balance between NO and superoxide production by eNOS (eNOS coupling).	sapropterin	20-23	nitric oxide synthase 3	Homo sapiens	85-118
19666465-1	2009	Tetrahyrobiopterin (BH4) is a required cofactor for the synthesis of nitric oxide by endothelial nitric-oxide synthase (eNOS), and BH4 bioavailability within the endothelium is a critical factor in regulating the balance between NO and superoxide production by eNOS (eNOS coupling).	Nitric Oxide	69-81	nitric oxide synthase 3	Homo sapiens	85-118
19531501-2	2009	The genotypes of eNOS gene (NOS3) may be responsible for variation in its enzymatic activity as well as plasma concentration of nitric oxide.	Nitric Oxide	128-140	nitric oxide synthase 3	Homo sapiens	17-21
19505886-2	2009	INTRODUCTION: Nitric oxide (NO) produced by endothelial nitric oxide synthase (eNOS) is a potent vasodilator.	Nitric Oxide	14-26	nitric oxide synthase 3	Homo sapiens	44-77
19505886-2	2009	INTRODUCTION: Nitric oxide (NO) produced by endothelial nitric oxide synthase (eNOS) is a potent vasodilator.	Nitric Oxide	14-26	nitric oxide synthase 3	Homo sapiens	79-83
19775216-3	2009	Nitric oxide is a potent vasomodulator, and variants in the gene that encodes endothelial nitric oxide synthase (NOS3) have been shown to affect blood pressure.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	78-111
19775216-3	2009	Nitric oxide is a potent vasomodulator, and variants in the gene that encodes endothelial nitric oxide synthase (NOS3) have been shown to affect blood pressure.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	113-117
19526276-2	2009	NO is synthesized through the conversion of L-arginine to L-citrulline by the enzyme NO synthase (NOS), which is found in three isoforms classified as neuronal (nNOS), inducible (iNOS), and endothelial (eNOS).	Arginine	44-54	nitric oxide synthase 3	Homo sapiens	203-207
19531501-2	2009	The genotypes of eNOS gene (NOS3) may be responsible for variation in its enzymatic activity as well as plasma concentration of nitric oxide.	Nitric Oxide	128-140	nitric oxide synthase 3	Homo sapiens	28-32
19531501-9	2009	CONCLUSION: These findings suggest that the T allele, encoding aspartic acid, of the Glu298Asp polymorphism of the NOS3 may be associated with advanced stage endometriosis in the Korean population.	Aspartic Acid	63-76	nitric oxide synthase 3	Homo sapiens	115-119
19551451-6	2009	ACh exhibited significant inhibitory effects towards NO, endothelial nitric oxide synthase (eNOS), and IL-1beta secretion especially by tumor cells derived form Duke"s C stage of colon carcinoma.	Acetylcholine	0-3	nitric oxide synthase 3	Homo sapiens	57-90
19730129-2	2009	It is synthesized by endothelium from arginine with the catalytic help of endothelial NO synthase (eNOS).	Arginine	38-46	nitric oxide synthase 3	Homo sapiens	99-103
19526276-2	2009	NO is synthesized through the conversion of L-arginine to L-citrulline by the enzyme NO synthase (NOS), which is found in three isoforms classified as neuronal (nNOS), inducible (iNOS), and endothelial (eNOS).	Citrulline	58-70	nitric oxide synthase 3	Homo sapiens	203-207
19717511-4	2009	CPB1 tyrosine nitration and loss of activity by the concerted action of NOS-3 and XO were also confirmed in vitro using both the NO donor 3-morpholinosydnonimine and peroxynitrite.	linsidomine	138-161	nitric oxide synthase 3	Homo sapiens	72-77
19549586-3	2009	This includes estrogen-stimulated, rapid activation of endothelial nitric oxide synthase (eNOS), resulting in elaboration of the athero-protective, angiogenesis-promoting product nitric oxide (NO).	Nitric Oxide	67-79	nitric oxide synthase 3	Homo sapiens	90-94
19717511-4	2009	CPB1 tyrosine nitration and loss of activity by the concerted action of NOS-3 and XO were also confirmed in vitro using both the NO donor 3-morpholinosydnonimine and peroxynitrite.	Peroxynitrous Acid	166-179	nitric oxide synthase 3	Homo sapiens	72-77
19690675-5	2009	Unlike iNOS, eNOS and nNOS isoforms are controlled by calmodulin (CaM) binding through facilitating catalytically significant IET processes.	1-(4-CYANO-PHENYL)-3-[2-(2,6-DICHLORO-PHENYL)-1-IMINO-ETHYL]-THIOUREA	126-129	nitric oxide synthase 3	Homo sapiens	13-17
19577623-0	2009	Gomisin A induces Ca2+-dependent activation of eNOS in human coronary artery endothelial cells.	schizandrol B	0-9	nitric oxide synthase 3	Homo sapiens	47-51
19722703-8	2009	Concentration-dependent correlations between enhanced NO level and endothelial nitric oxide synthase (eNOS) expression were demonstrated for the three polyphenols tested (resveratrol, ECg, and EGCg).	Polyphenols	151-162	nitric oxide synthase 3	Homo sapiens	67-100
19722703-8	2009	Concentration-dependent correlations between enhanced NO level and endothelial nitric oxide synthase (eNOS) expression were demonstrated for the three polyphenols tested (resveratrol, ECg, and EGCg).	Resveratrol	171-182	nitric oxide synthase 3	Homo sapiens	67-100
19722703-8	2009	Concentration-dependent correlations between enhanced NO level and endothelial nitric oxide synthase (eNOS) expression were demonstrated for the three polyphenols tested (resveratrol, ECg, and EGCg).	epicatechin gallate	184-187	nitric oxide synthase 3	Homo sapiens	67-100
19722703-8	2009	Concentration-dependent correlations between enhanced NO level and endothelial nitric oxide synthase (eNOS) expression were demonstrated for the three polyphenols tested (resveratrol, ECg, and EGCg).	epigallocatechin gallate	193-197	nitric oxide synthase 3	Homo sapiens	67-100
19577623-5	2009	Both GA-induced NO production and eNOS activation were attenuated by pretreatment of the cells with EGTA, an extracellular Ca(2+) chelator, and BAPTA-AM, an intracellular Ca(2+) chelator, but not by LY 294002, a PI3-kinase/Akt inhibitor, suggesting involvement of Ca(2+).	Egtazic Acid	100-104	nitric oxide synthase 3	Homo sapiens	34-38
19577623-5	2009	Both GA-induced NO production and eNOS activation were attenuated by pretreatment of the cells with EGTA, an extracellular Ca(2+) chelator, and BAPTA-AM, an intracellular Ca(2+) chelator, but not by LY 294002, a PI3-kinase/Akt inhibitor, suggesting involvement of Ca(2+).	1,2-bis(2-aminophenoxy)ethane N,N,N',N'-tetraacetic acid acetoxymethyl ester	144-152	nitric oxide synthase 3	Homo sapiens	34-38
19577623-5	2009	Both GA-induced NO production and eNOS activation were attenuated by pretreatment of the cells with EGTA, an extracellular Ca(2+) chelator, and BAPTA-AM, an intracellular Ca(2+) chelator, but not by LY 294002, a PI3-kinase/Akt inhibitor, suggesting involvement of Ca(2+).	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	199-208	nitric oxide synthase 3	Homo sapiens	34-38
19577623-7	2009	CONCLUSION: Taken together, our results suggest that GA induces Ca(2+)-dependent activation and translocation of eNOS in HCAEC, events linked to NO production and thereby endothelial-dependent vasorelaxation.	schizandrol B	53-55	nitric oxide synthase 3	Homo sapiens	113-117
19617312-2	2009	NO is produced by endothelial NO synthase (eNOS) in the pulmonary vascular endothelium using l-arginine as a substrate and producing l-citrulline as a byproduct.	Arginine	93-103	nitric oxide synthase 3	Homo sapiens	43-47
19617312-2	2009	NO is produced by endothelial NO synthase (eNOS) in the pulmonary vascular endothelium using l-arginine as a substrate and producing l-citrulline as a byproduct.	Citrulline	133-145	nitric oxide synthase 3	Homo sapiens	43-47
19617312-3	2009	l-Citrulline is metabolized to l-arginine by two enzymes that are colocated with eNOS in pulmonary vascular endothelial cells.	Citrulline	0-12	nitric oxide synthase 3	Homo sapiens	81-85
19617312-3	2009	l-Citrulline is metabolized to l-arginine by two enzymes that are colocated with eNOS in pulmonary vascular endothelial cells.	Arginine	31-41	nitric oxide synthase 3	Homo sapiens	81-85
19268941-2	2009	We have previously shown that CRP decreases endothelial nitric oxide synthase (eNOS) activity in endothelial cells and inhibits endothelium-dependent nitric oxide (NO)-mediated vasodilation in vitro.	Nitric Oxide	56-68	nitric oxide synthase 3	Homo sapiens	79-83
19809994-1	2009	BACKGROUND: Asymmetric dimethylarginine (ADMA)is an endogenous amino acid similar to l-arginine and able to inhibit the enzyme endothelial nitric oxide synthase (eNOS).	dimethylarginine	23-39	nitric oxide synthase 3	Homo sapiens	127-160
19809994-1	2009	BACKGROUND: Asymmetric dimethylarginine (ADMA)is an endogenous amino acid similar to l-arginine and able to inhibit the enzyme endothelial nitric oxide synthase (eNOS).	N,N-dimethylarginine	41-45	nitric oxide synthase 3	Homo sapiens	127-160
19809994-1	2009	BACKGROUND: Asymmetric dimethylarginine (ADMA)is an endogenous amino acid similar to l-arginine and able to inhibit the enzyme endothelial nitric oxide synthase (eNOS).	Arginine	85-95	nitric oxide synthase 3	Homo sapiens	127-160
19481100-2	2009	Endothelial nitric oxide synthase (eNOS) mediates nitric oxide (NO) production; polymorphism of the eNOS gene may affect response to the PORH process.	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	35-39
19481100-2	2009	Endothelial nitric oxide synthase (eNOS) mediates nitric oxide (NO) production; polymorphism of the eNOS gene may affect response to the PORH process.	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	100-104
19525401-6	2009	Expression of eNOS was significantly greater in the LTH group compared with control.	L-threonic acid	52-55	nitric oxide synthase 3	Homo sapiens	14-18
19525401-8	2009	We conclude that LTH enhances eNOS expression in the inner adrenal cortex which may play a role in regulation of cortisol biosynthesis in the LTH fetus.	Hydrocortisone	113-121	nitric oxide synthase 3	Homo sapiens	30-34
19644064-1	2009	BACKGROUND AND PURPOSE: Asymmetrical dimethylarginine (ADMA), an inhibitor of endothelial nitric oxide synthase, is a marker of endothelial dysfunction.	dimethylarginine	37-53	nitric oxide synthase 3	Homo sapiens	78-111
19644064-1	2009	BACKGROUND AND PURPOSE: Asymmetrical dimethylarginine (ADMA), an inhibitor of endothelial nitric oxide synthase, is a marker of endothelial dysfunction.	N,N-dimethylarginine	55-59	nitric oxide synthase 3	Homo sapiens	78-111
19767824-0	2009	Cadmium attenuates bradykinin-driven nitric oxide production by interplaying with the localization pattern of endothelial nitric oxide synthase.	Cadmium	0-7	nitric oxide synthase 3	Homo sapiens	110-143
18830972-8	2009	We confirmed that reduction of Nitrate levels in Jurkat cells was due to down-regulation of inducible nitric oxide synthase (iNOS), not endothelial nitric oxide synthase (eNOS).	Nitrates	31-38	nitric oxide synthase 3	Homo sapiens	136-169
19603529-2	2009	Investigators have identified associations of genetic polymorphisms in nitric oxide synthase genes (NOS1 and NOS3) with FeNO levels; however, none have explored whether these polymorphisms modify the relationship of environmental exposures with FeNO.	flubendiamide	120-124	nitric oxide synthase 3	Homo sapiens	109-113
19603529-8	2009	In contrast, there was an interaction of the NOS3 polymorphism and airborne nicotine concentration with FeNO levels (P = 0.01).	Nicotine	76-84	nitric oxide synthase 3	Homo sapiens	45-49
19603529-8	2009	In contrast, there was an interaction of the NOS3 polymorphism and airborne nicotine concentration with FeNO levels (P = 0.01).	flubendiamide	104-108	nitric oxide synthase 3	Homo sapiens	45-49
19419976-3	2009	Variation in the endothelial nitric oxide (NO) synthase (eNOS) gene has been implicated in CV and outcome after SAH.	Nitric Oxide	29-41	nitric oxide synthase 3	Homo sapiens	57-61
19767878-0	2009	Rosiglitazone inhibits high glucose-induced apoptosis in human umbilical vein endothelial cells through the PI3K/Akt/eNOS pathway.	Rosiglitazone	0-13	nitric oxide synthase 3	Homo sapiens	117-121
19767878-0	2009	Rosiglitazone inhibits high glucose-induced apoptosis in human umbilical vein endothelial cells through the PI3K/Akt/eNOS pathway.	Glucose	28-35	nitric oxide synthase 3	Homo sapiens	117-121
19767878-1	2009	Previous studies have shown that the phosphatidylinositol 3-kinase / Akt / endothelial nitric oxide synthase / NO (PI3K/Akt/eNOS/NO) pathway is involved in high glucose-induced endothelial cell apoptosis and rosiglitazone has a protective effect on endothelium.	Glucose	161-168	nitric oxide synthase 3	Homo sapiens	75-108
19767878-1	2009	Previous studies have shown that the phosphatidylinositol 3-kinase / Akt / endothelial nitric oxide synthase / NO (PI3K/Akt/eNOS/NO) pathway is involved in high glucose-induced endothelial cell apoptosis and rosiglitazone has a protective effect on endothelium.	Glucose	161-168	nitric oxide synthase 3	Homo sapiens	124-128
19767878-1	2009	Previous studies have shown that the phosphatidylinositol 3-kinase / Akt / endothelial nitric oxide synthase / NO (PI3K/Akt/eNOS/NO) pathway is involved in high glucose-induced endothelial cell apoptosis and rosiglitazone has a protective effect on endothelium.	Rosiglitazone	208-221	nitric oxide synthase 3	Homo sapiens	75-108
19767878-1	2009	Previous studies have shown that the phosphatidylinositol 3-kinase / Akt / endothelial nitric oxide synthase / NO (PI3K/Akt/eNOS/NO) pathway is involved in high glucose-induced endothelial cell apoptosis and rosiglitazone has a protective effect on endothelium.	Rosiglitazone	208-221	nitric oxide synthase 3	Homo sapiens	124-128
19767878-4	2009	High glucose treatment also decreased Akt and eNOS phosphorylation levels with subsequent NO production.	Glucose	5-12	nitric oxide synthase 3	Homo sapiens	46-50
19767878-8	2009	These findings suggest that rosiglitazone inhibits high glucose-induced apoptosis in HUVECs through the PI3K/Akt/eNOS pathway.	Rosiglitazone	28-41	nitric oxide synthase 3	Homo sapiens	113-117
19767878-8	2009	These findings suggest that rosiglitazone inhibits high glucose-induced apoptosis in HUVECs through the PI3K/Akt/eNOS pathway.	Glucose	56-63	nitric oxide synthase 3	Homo sapiens	113-117
19373110-9	2009	With regard to the Glu298Asp polymorphism in NOS3, the odds ratio for the presence of hypertension in individuals having the Glu/Glu genotype of NOS3 when compared with those having the other genotypes (Asp/Asp and Asp/Glu) was 2.79.	Glutamic Acid	19-22	nitric oxide synthase 3	Homo sapiens	45-49
19373110-9	2009	With regard to the Glu298Asp polymorphism in NOS3, the odds ratio for the presence of hypertension in individuals having the Glu/Glu genotype of NOS3 when compared with those having the other genotypes (Asp/Asp and Asp/Glu) was 2.79.	Glutamic Acid	19-22	nitric oxide synthase 3	Homo sapiens	145-149
19373110-9	2009	With regard to the Glu298Asp polymorphism in NOS3, the odds ratio for the presence of hypertension in individuals having the Glu/Glu genotype of NOS3 when compared with those having the other genotypes (Asp/Asp and Asp/Glu) was 2.79.	Glutamic Acid	125-128	nitric oxide synthase 3	Homo sapiens	45-49
19373110-9	2009	With regard to the Glu298Asp polymorphism in NOS3, the odds ratio for the presence of hypertension in individuals having the Glu/Glu genotype of NOS3 when compared with those having the other genotypes (Asp/Asp and Asp/Glu) was 2.79.	Glutamic Acid	125-128	nitric oxide synthase 3	Homo sapiens	145-149
19373110-9	2009	With regard to the Glu298Asp polymorphism in NOS3, the odds ratio for the presence of hypertension in individuals having the Glu/Glu genotype of NOS3 when compared with those having the other genotypes (Asp/Asp and Asp/Glu) was 2.79.	Aspartic Acid	25-28	nitric oxide synthase 3	Homo sapiens	45-49
19373110-9	2009	With regard to the Glu298Asp polymorphism in NOS3, the odds ratio for the presence of hypertension in individuals having the Glu/Glu genotype of NOS3 when compared with those having the other genotypes (Asp/Asp and Asp/Glu) was 2.79.	Aspartic Acid	25-28	nitric oxide synthase 3	Homo sapiens	145-149
19373110-9	2009	With regard to the Glu298Asp polymorphism in NOS3, the odds ratio for the presence of hypertension in individuals having the Glu/Glu genotype of NOS3 when compared with those having the other genotypes (Asp/Asp and Asp/Glu) was 2.79.	Glutamic Acid	125-128	nitric oxide synthase 3	Homo sapiens	45-49
19373110-9	2009	With regard to the Glu298Asp polymorphism in NOS3, the odds ratio for the presence of hypertension in individuals having the Glu/Glu genotype of NOS3 when compared with those having the other genotypes (Asp/Asp and Asp/Glu) was 2.79.	Glutamic Acid	125-128	nitric oxide synthase 3	Homo sapiens	145-149
19373110-10	2009	Interestingly, the odds ratio was 7.64 for individuals having a combination of the Gly/Gly genotype of ADRB2 and Glu/Glu genotype of NOS3 when compared with those having a combination of Arg/Arg and Arg/Gly genotypes of ADRB2 and Asp/Asp and Asp/Glu genotypes of NOS3.	Glycine	83-86	nitric oxide synthase 3	Homo sapiens	263-267
19373110-10	2009	Interestingly, the odds ratio was 7.64 for individuals having a combination of the Gly/Gly genotype of ADRB2 and Glu/Glu genotype of NOS3 when compared with those having a combination of Arg/Arg and Arg/Gly genotypes of ADRB2 and Asp/Asp and Asp/Glu genotypes of NOS3.	Glutamic Acid	113-116	nitric oxide synthase 3	Homo sapiens	133-137
19520256-5	2009	RESULTS: Treatment with paclitaxel, sirolimus, and everolimus significantly caused a senescent phenotype and PAI-1 up-regulation, associated with a decrease in endothelial nitric oxide synthase (eNOS) and Sirt1 expression.	Paclitaxel	24-34	nitric oxide synthase 3	Homo sapiens	160-193
19520256-5	2009	RESULTS: Treatment with paclitaxel, sirolimus, and everolimus significantly caused a senescent phenotype and PAI-1 up-regulation, associated with a decrease in endothelial nitric oxide synthase (eNOS) and Sirt1 expression.	Sirolimus	36-45	nitric oxide synthase 3	Homo sapiens	160-193
19520256-5	2009	RESULTS: Treatment with paclitaxel, sirolimus, and everolimus significantly caused a senescent phenotype and PAI-1 up-regulation, associated with a decrease in endothelial nitric oxide synthase (eNOS) and Sirt1 expression.	Everolimus	51-61	nitric oxide synthase 3	Homo sapiens	160-193
19307231-0	2009	Valsartan regulates the interaction of angiotensin II type 1 receptor and endothelial nitric oxide synthase via Src/PI3K/Akt signalling.	Valsartan	0-9	nitric oxide synthase 3	Homo sapiens	74-107
19385062-9	2009	Small interfering RNA-mediated knockdown of Epac1 suppressed forskolin-induced angiogenesis and phosphorylation of ERK, Akt, and eNOS, but not CREB phosphorylation and VEGF expression.	Colforsin	61-70	nitric oxide synthase 3	Homo sapiens	129-133
19385062-10	2009	These results suggest that forskolin stimulates angiogenesis through coordinated cross-talk between two distinct pathways, PKA-dependent VEGF expression and Epac-dependent ERKactivation and PI3K/Akt/eNOS/NO signaling.	Colforsin	27-36	nitric oxide synthase 3	Homo sapiens	199-203
19486510-1	2009	BACKGROUND: Asymmetric dimethylarginine (ADMA) is a competitive inhibitor of endothelial nitric oxide synthase (eNOS) that is associated with endothelial dysfunction, and is a risk marker for cardiovascular disease, a significant problem in Type 1 diabetes.	dimethylarginine	23-39	nitric oxide synthase 3	Homo sapiens	77-110
19486510-1	2009	BACKGROUND: Asymmetric dimethylarginine (ADMA) is a competitive inhibitor of endothelial nitric oxide synthase (eNOS) that is associated with endothelial dysfunction, and is a risk marker for cardiovascular disease, a significant problem in Type 1 diabetes.	N,N-dimethylarginine	41-45	nitric oxide synthase 3	Homo sapiens	77-110
19513607-3	2009	In the present study, we investigated if simvastatin increases eNOS activity through its phosphorylation in 293 cells (293-eNOS) with stable expression of eNOS.	Simvastatin	41-52	nitric oxide synthase 3	Homo sapiens	123-127
19513607-3	2009	In the present study, we investigated if simvastatin increases eNOS activity through its phosphorylation in 293 cells (293-eNOS) with stable expression of eNOS.	Simvastatin	41-52	nitric oxide synthase 3	Homo sapiens	123-127
19513607-4	2009	The results showed that incubation of 293-eNOS cells with simvastatin (10 microm/L) for 2 h significantly increased in the activity of eNOS as shown by the conversion of L-arginine to L-citrulline (2889.70+/-201.51 versus 5630.18+/-218.75 pmol/min .	Simvastatin	58-69	nitric oxide synthase 3	Homo sapiens	42-46
19513607-4	2009	The results showed that incubation of 293-eNOS cells with simvastatin (10 microm/L) for 2 h significantly increased in the activity of eNOS as shown by the conversion of L-arginine to L-citrulline (2889.70+/-201.51 versus 5630.18+/-218.75 pmol/min .	Simvastatin	58-69	nitric oxide synthase 3	Homo sapiens	135-139
19513607-4	2009	The results showed that incubation of 293-eNOS cells with simvastatin (10 microm/L) for 2 h significantly increased in the activity of eNOS as shown by the conversion of L-arginine to L-citrulline (2889.70+/-201.51 versus 5630.18+/-218.75 pmol/min .	Arginine	170-180	nitric oxide synthase 3	Homo sapiens	42-46
19513607-4	2009	The results showed that incubation of 293-eNOS cells with simvastatin (10 microm/L) for 2 h significantly increased in the activity of eNOS as shown by the conversion of L-arginine to L-citrulline (2889.70+/-201.51 versus 5630.18+/-218.75 pmol/min .	Arginine	170-180	nitric oxide synthase 3	Homo sapiens	135-139
19513607-4	2009	The results showed that incubation of 293-eNOS cells with simvastatin (10 microm/L) for 2 h significantly increased in the activity of eNOS as shown by the conversion of L-arginine to L-citrulline (2889.70+/-201.51 versus 5630.18+/-218.75 pmol/min .	Citrulline	184-196	nitric oxide synthase 3	Homo sapiens	135-139
19513607-6	2009	Western blotting revealed that simvastatin increased phosphorylation of eNOS at 1177 (ser) and also 495 (thr) but did not affect the overall expression of eNOS or inducible NOS.	Simvastatin	31-42	nitric oxide synthase 3	Homo sapiens	72-76
19513607-6	2009	Western blotting revealed that simvastatin increased phosphorylation of eNOS at 1177 (ser) and also 495 (thr) but did not affect the overall expression of eNOS or inducible NOS.	Serine	86-89	nitric oxide synthase 3	Homo sapiens	72-76
19513607-8	2009	These results suggest that simvastatin could stimulate the activity of eNOS via its phosphorylation by Akt and AMPK, which provides a new mechanism, other than lipid-lowering effect, for the cardiovascular protection of statins.	Simvastatin	27-38	nitric oxide synthase 3	Homo sapiens	71-75
19433760-1	2009	BACKGROUND: Nitric oxide (NO)-mediated local regulation of vascular tone is considered to involve endothelial NO synthase (eNOS).	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	123-127
19433760-2	2009	However, we recently reported that human forearm basal microvascular tone in vivo is tonically regulated by neuronal NO synthase (nNOS), in contrast to an acetylcholine-stimulated reduction in tone, which is eNOS dependent.	Acetylcholine	155-168	nitric oxide synthase 3	Homo sapiens	208-212
19286667-0	2009	Tetrahydrobiopterin recycling, a key determinant of endothelial nitric-oxide synthase-dependent signaling pathways in cultured vascular endothelial cells.	sapropterin	0-19	nitric oxide synthase 3	Homo sapiens	52-85
19488614-2	2009	The nitric oxide produced by the endothelium under the action of endothelial nitric oxide synthase has important antiatherogenic functions.	Nitric Oxide	4-16	nitric oxide synthase 3	Homo sapiens	65-98
18710710-7	2009	RESULT(S): Progesterone induced a concentration- and time-dependent stimulation of endothelial NOS (eNOS), inducible NOS (iNOS), and peNOS protein in HES cells.	Progesterone	11-23	nitric oxide synthase 3	Homo sapiens	83-98
19393035-7	2009	We then examined the activity of Ca2+-dependent enzymes that are known to generate RONS and found that ammonia significantly increased the activities of NADPH oxidase (NOX), constitutive nitric oxide synthase (cNOS), and phospholipase A2 (PLA2) and such increases in activity were significantly diminished by BAPTA.	Ammonia	103-110	nitric oxide synthase 3	Homo sapiens	210-214
19393035-8	2009	Pre-treatment of cultures with 7-nitroindazole, apocyanin, and quinacrine, respective inhibitors of cNOS, NOX, and PLA2, all significantly diminished RONS production.	7-nitroindazole	31-46	nitric oxide synthase 3	Homo sapiens	100-104
19393035-8	2009	Pre-treatment of cultures with 7-nitroindazole, apocyanin, and quinacrine, respective inhibitors of cNOS, NOX, and PLA2, all significantly diminished RONS production.	apocyanin	48-57	nitric oxide synthase 3	Homo sapiens	100-104
19393035-8	2009	Pre-treatment of cultures with 7-nitroindazole, apocyanin, and quinacrine, respective inhibitors of cNOS, NOX, and PLA2, all significantly diminished RONS production.	Quinacrine	63-73	nitric oxide synthase 3	Homo sapiens	100-104
19393035-9	2009	Additionally, treatment of cultures with BAPTA or with inhibitors of cNOS, NOX, and PLA2 reduced ammonia-induced astrocyte swelling.	Ammonia	97-104	nitric oxide synthase 3	Homo sapiens	69-73
19764340-0	2009	Alteration of nitric oxide gas on gene expression of endothelin-1 and endothelial nitric oxide synthase by a time- and dose-dependent manner in human endothelial cells.	Nitric Oxide	14-26	nitric oxide synthase 3	Homo sapiens	70-103
19104789-0	2009	eNOS T-786C polymorphism affects atorvastatin-induced changes in erythrocyte membrane fluidity.	Atorvastatin	33-45	nitric oxide synthase 3	Homo sapiens	0-4
19104789-1	2009	PURPOSE: Statins have pleiotropic effects, including endothelial nitric oxide synthase (eNOS) upregulation and increased nitric oxide formation, which can be modulated by a genetic polymorphism in the promoter region of the eNOS gene (T-786C).	Nitric Oxide	65-77	nitric oxide synthase 3	Homo sapiens	88-92
19104789-1	2009	PURPOSE: Statins have pleiotropic effects, including endothelial nitric oxide synthase (eNOS) upregulation and increased nitric oxide formation, which can be modulated by a genetic polymorphism in the promoter region of the eNOS gene (T-786C).	Nitric Oxide	65-77	nitric oxide synthase 3	Homo sapiens	224-228
19115208-1	2009	Endothelial-derived nitric oxide, which is produced by endothelial nitric oxide synthase (eNOS), may play an important role in colorectal carcinogenesis.	Nitric Oxide	20-32	nitric oxide synthase 3	Homo sapiens	55-88
19115208-1	2009	Endothelial-derived nitric oxide, which is produced by endothelial nitric oxide synthase (eNOS), may play an important role in colorectal carcinogenesis.	Nitric Oxide	20-32	nitric oxide synthase 3	Homo sapiens	90-94
19429543-5	2009	The induced eNOS and p-Akt expression was inhibited by LY294002, indicating that the effect of nanocomposites could be attributed to the PI3K pathway.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	55-63	nitric oxide synthase 3	Homo sapiens	12-16
19136580-10	2009	ACh failed to stimulate Hsp90-eNOS binding in 2-day-old but induced a significant increase in Hsp90-eNOS coimmunoprecipitation in PRA from the older age groups, which was blocked by Hsp90 antagonism.	Acetylcholine	0-3	nitric oxide synthase 3	Homo sapiens	100-104
19036824-11	2009	Inhibition of protein phosphatase 1 (PP1) by calyculin A, tautomycetin, or siRNA against PP1 reversed NF-induced eNOS-Thr495 dephosphorylation.	tautomycetin	58-70	nitric oxide synthase 3	Homo sapiens	113-117
19331593-1	2009	Asymmetric dimethylarginine (ADMA), an endogenous methylated form of the amino acid L-arginine, inhibits the activity of the enzyme endothelial nitric oxide synthase, with consequent reduced synthesis of nitric oxide.	dimethylarginine	11-27	nitric oxide synthase 3	Homo sapiens	132-165
19331593-1	2009	Asymmetric dimethylarginine (ADMA), an endogenous methylated form of the amino acid L-arginine, inhibits the activity of the enzyme endothelial nitric oxide synthase, with consequent reduced synthesis of nitric oxide.	N,N-dimethylarginine	29-33	nitric oxide synthase 3	Homo sapiens	132-165
19331593-1	2009	Asymmetric dimethylarginine (ADMA), an endogenous methylated form of the amino acid L-arginine, inhibits the activity of the enzyme endothelial nitric oxide synthase, with consequent reduced synthesis of nitric oxide.	amino acid l-arginine	73-94	nitric oxide synthase 3	Homo sapiens	132-165
20108211-13	2009	In conclusion, pyridoxine is effective in elevating platelet NO biosynthesis, through improving PI3K activity and hence downstream Akt phosphorylation, and in turn serine-1177 phosphorylation of NOS-3.	Pyridoxine	15-25	nitric oxide synthase 3	Homo sapiens	195-200
20108211-13	2009	In conclusion, pyridoxine is effective in elevating platelet NO biosynthesis, through improving PI3K activity and hence downstream Akt phosphorylation, and in turn serine-1177 phosphorylation of NOS-3.	Serine	164-170	nitric oxide synthase 3	Homo sapiens	195-200
18974424-18	2009	These findings suggest the following: 1) elements responsible for PAL include endothelial nitric oxide synthase, soluble guanylate cyclase, and type II protein kinase G; 2) the resting state of the nitric oxide/cGMP/protein kinase G pathway is a determinant of acrosomal status; 3) PPCM and nitric oxide donors induce acrosomal loss via nitric oxide, but through independent pathways; and 4) covalent attachment of a nitric oxide donor to PPCM provides synergistic efficacy as a stimulus of acrosomal loss.	Nitric Oxide	198-210	nitric oxide synthase 3	Homo sapiens	78-111
19188511-1	2009	BACKGROUND: Decreased endothelial nitric oxide (NO) synthase (eNOS) activity and NO production are critical contributors to the endothelial dysfunction and vascular complications observed in many diseases, including diabetes mellitus.	nitric	34-40	nitric oxide synthase 3	Homo sapiens	62-66
19188511-3	2009	METHODS AND RESULTS: To elucidate the signaling pathway(s) leading to nucleotide-mediated eNOS phosphorylation at Ser-1177, human umbilical vein endothelial cells were treated with several nucleotides, including ATP, UTP, and ADP, in the presence or absence of selective inhibitors.	Serine	114-117	nitric oxide synthase 3	Homo sapiens	90-94
19188511-4	2009	These experiments identified P2Y1, P2Y2, and possibly P2Y4 as the purinergic receptors involved in eNOS phosphorylation and demonstrated that this process was adenosine independent.	Adenosine	159-168	nitric oxide synthase 3	Homo sapiens	99-103
19188511-5	2009	Nucleotide-induced eNOS phosphorylation and activity were inhibited by BAPTA-AM (an intracellular free calcium chelator), rottlerin (a protein kinase Cdelta inhibitor), and protein kinase Cdelta siRNA.	1,2-bis(2-aminophenoxy)ethane N,N,N',N'-tetraacetic acid acetoxymethyl ester	71-79	nitric oxide synthase 3	Homo sapiens	19-23
19188511-5	2009	Nucleotide-induced eNOS phosphorylation and activity were inhibited by BAPTA-AM (an intracellular free calcium chelator), rottlerin (a protein kinase Cdelta inhibitor), and protein kinase Cdelta siRNA.	Calcium	103-110	nitric oxide synthase 3	Homo sapiens	19-23
19188511-5	2009	Nucleotide-induced eNOS phosphorylation and activity were inhibited by BAPTA-AM (an intracellular free calcium chelator), rottlerin (a protein kinase Cdelta inhibitor), and protein kinase Cdelta siRNA.	rottlerin	122-131	nitric oxide synthase 3	Homo sapiens	19-23
19036874-9	2009	CNP-induced hyperpolarization was mimicked by the PKG agonist, 8-bromo-cGMP, and attenuated by both the endothelial nitric oxide synthase (eNOS) inhibitor, N(omega)-nitro-l-arginine methyl ester (l-NAME), and the soluble guanylyl cyclase (sGC) inhibitor, 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one.	nitro-l-arginine methyl ester	165-194	nitric oxide synthase 3	Homo sapiens	139-143
19036874-9	2009	CNP-induced hyperpolarization was mimicked by the PKG agonist, 8-bromo-cGMP, and attenuated by both the endothelial nitric oxide synthase (eNOS) inhibitor, N(omega)-nitro-l-arginine methyl ester (l-NAME), and the soluble guanylyl cyclase (sGC) inhibitor, 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one.	NG-Nitroarginine Methyl Ester	196-202	nitric oxide synthase 3	Homo sapiens	139-143
19036874-9	2009	CNP-induced hyperpolarization was mimicked by the PKG agonist, 8-bromo-cGMP, and attenuated by both the endothelial nitric oxide synthase (eNOS) inhibitor, N(omega)-nitro-l-arginine methyl ester (l-NAME), and the soluble guanylyl cyclase (sGC) inhibitor, 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one.	1H-(1,2,4)oxadiazolo(4,3-a)quinoxalin-1-one	255-298	nitric oxide synthase 3	Homo sapiens	139-143
18564176-0	2009	Glimepiride upregulates eNOS activity and inhibits cytokine-induced NF-kappaB activation through a phosphoinoside 3-kinase-Akt-dependent pathway.	glimepiride	0-11	nitric oxide synthase 3	Homo sapiens	24-28
18564176-5	2009	A significant increase in endothelial NO synthase (eNOS) activity, measured in terms of citrulline production, was observed with glimepiride treatment.	Citrulline	88-98	nitric oxide synthase 3	Homo sapiens	51-55
18564176-5	2009	A significant increase in endothelial NO synthase (eNOS) activity, measured in terms of citrulline production, was observed with glimepiride treatment.	glimepiride	129-140	nitric oxide synthase 3	Homo sapiens	51-55
18564176-6	2009	Akt phosphorylation followed by phosphorylation of eNOS (Ser1177) was observed with glimepiride treatment in HUVEC.	glimepiride	84-95	nitric oxide synthase 3	Homo sapiens	51-55
19008412-7	2009	The results of this study cumulatively indicate that gene therapy with human eNOS decreased fructose-induced hypertension and insulin resistance in rats and suggest potential signaling pathways that mediate these effects.	Fructose	92-100	nitric oxide synthase 3	Homo sapiens	77-81
18221806-0	2009	Short-term withdrawal of simvastatin induces endothelial dysfunction in patients with coronary artery disease: a dose-response effect dependent on endothelial nitric oxide synthase.	Simvastatin	25-36	nitric oxide synthase 3	Homo sapiens	147-180
19011239-6	2009	Doxycycline abolished GTPCH mRNA expression and GTPCH protein, leading to markedly diminished total biopterin levels and a decreased ratio of BH4 to oxidized biopterins in cells expressing eNOS.	Doxycycline	0-11	nitric oxide synthase 3	Homo sapiens	189-193
19011239-6	2009	Doxycycline abolished GTPCH mRNA expression and GTPCH protein, leading to markedly diminished total biopterin levels and a decreased ratio of BH4 to oxidized biopterins in cells expressing eNOS.	sapropterin	142-145	nitric oxide synthase 3	Homo sapiens	189-193
19011239-6	2009	Doxycycline abolished GTPCH mRNA expression and GTPCH protein, leading to markedly diminished total biopterin levels and a decreased ratio of BH4 to oxidized biopterins in cells expressing eNOS.	Biopterin	158-168	nitric oxide synthase 3	Homo sapiens	189-193
19011239-7	2009	Intracellular BH4 deficiency induced superoxide generation from eNOS, as assessed by N-nitro-L-arginine methyl ester inhibitable 2-hydroxyethidium generation, and attenuated NO production.	sapropterin	14-17	nitric oxide synthase 3	Homo sapiens	64-68
19011239-7	2009	Intracellular BH4 deficiency induced superoxide generation from eNOS, as assessed by N-nitro-L-arginine methyl ester inhibitable 2-hydroxyethidium generation, and attenuated NO production.	Superoxides	37-47	nitric oxide synthase 3	Homo sapiens	64-68
19011239-7	2009	Intracellular BH4 deficiency induced superoxide generation from eNOS, as assessed by N-nitro-L-arginine methyl ester inhibitable 2-hydroxyethidium generation, and attenuated NO production.	n-nitro-l-arginine methyl ester	85-116	nitric oxide synthase 3	Homo sapiens	64-68
19011239-7	2009	Intracellular BH4 deficiency induced superoxide generation from eNOS, as assessed by N-nitro-L-arginine methyl ester inhibitable 2-hydroxyethidium generation, and attenuated NO production.	2-hydroxyethidium	129-146	nitric oxide synthase 3	Homo sapiens	64-68
19011239-8	2009	Quantitative analysis of cellular BH4 versus superoxide production between GCH/eNOS-LOW and GCH/eNOS-HIGH cells revealed a striking linear relationship between eNOS protein and cellular BH4 stoichiometry, with eNOS uncoupling at eNOS:BH4 molar ratio &gt;1.	sapropterin	34-37	nitric oxide synthase 3	Homo sapiens	79-83
19011239-8	2009	Quantitative analysis of cellular BH4 versus superoxide production between GCH/eNOS-LOW and GCH/eNOS-HIGH cells revealed a striking linear relationship between eNOS protein and cellular BH4 stoichiometry, with eNOS uncoupling at eNOS:BH4 molar ratio &gt;1.	sapropterin	186-189	nitric oxide synthase 3	Homo sapiens	96-100
19011239-8	2009	Quantitative analysis of cellular BH4 versus superoxide production between GCH/eNOS-LOW and GCH/eNOS-HIGH cells revealed a striking linear relationship between eNOS protein and cellular BH4 stoichiometry, with eNOS uncoupling at eNOS:BH4 molar ratio &gt;1.	sapropterin	186-189	nitric oxide synthase 3	Homo sapiens	96-100
19011239-8	2009	Quantitative analysis of cellular BH4 versus superoxide production between GCH/eNOS-LOW and GCH/eNOS-HIGH cells revealed a striking linear relationship between eNOS protein and cellular BH4 stoichiometry, with eNOS uncoupling at eNOS:BH4 molar ratio &gt;1.	sapropterin	186-189	nitric oxide synthase 3	Homo sapiens	96-100
19011239-8	2009	Quantitative analysis of cellular BH4 versus superoxide production between GCH/eNOS-LOW and GCH/eNOS-HIGH cells revealed a striking linear relationship between eNOS protein and cellular BH4 stoichiometry, with eNOS uncoupling at eNOS:BH4 molar ratio &gt;1.	sapropterin	186-189	nitric oxide synthase 3	Homo sapiens	96-100
19011239-8	2009	Quantitative analysis of cellular BH4 versus superoxide production between GCH/eNOS-LOW and GCH/eNOS-HIGH cells revealed a striking linear relationship between eNOS protein and cellular BH4 stoichiometry, with eNOS uncoupling at eNOS:BH4 molar ratio &gt;1.	sapropterin	186-189	nitric oxide synthase 3	Homo sapiens	96-100
19011239-8	2009	Quantitative analysis of cellular BH4 versus superoxide production between GCH/eNOS-LOW and GCH/eNOS-HIGH cells revealed a striking linear relationship between eNOS protein and cellular BH4 stoichiometry, with eNOS uncoupling at eNOS:BH4 molar ratio &gt;1.	sapropterin	186-189	nitric oxide synthase 3	Homo sapiens	96-100
19011239-8	2009	Quantitative analysis of cellular BH4 versus superoxide production between GCH/eNOS-LOW and GCH/eNOS-HIGH cells revealed a striking linear relationship between eNOS protein and cellular BH4 stoichiometry, with eNOS uncoupling at eNOS:BH4 molar ratio &gt;1.	sapropterin	186-189	nitric oxide synthase 3	Homo sapiens	96-100
19011239-8	2009	Quantitative analysis of cellular BH4 versus superoxide production between GCH/eNOS-LOW and GCH/eNOS-HIGH cells revealed a striking linear relationship between eNOS protein and cellular BH4 stoichiometry, with eNOS uncoupling at eNOS:BH4 molar ratio &gt;1.	sapropterin	186-189	nitric oxide synthase 3	Homo sapiens	96-100
19011239-9	2009	Furthermore, increasing the intracellular BH2 concentration in the presence of a constant eNOS:BH4 ratio was sufficient to induce eNOS-dependent superoxide production.	bh2	42-45	nitric oxide synthase 3	Homo sapiens	90-94
19011239-9	2009	Furthermore, increasing the intracellular BH2 concentration in the presence of a constant eNOS:BH4 ratio was sufficient to induce eNOS-dependent superoxide production.	bh2	42-45	nitric oxide synthase 3	Homo sapiens	130-134
19011239-9	2009	Furthermore, increasing the intracellular BH2 concentration in the presence of a constant eNOS:BH4 ratio was sufficient to induce eNOS-dependent superoxide production.	sapropterin	95-98	nitric oxide synthase 3	Homo sapiens	130-134
19011239-9	2009	Furthermore, increasing the intracellular BH2 concentration in the presence of a constant eNOS:BH4 ratio was sufficient to induce eNOS-dependent superoxide production.	Superoxides	145-155	nitric oxide synthase 3	Homo sapiens	90-94
19011239-9	2009	Furthermore, increasing the intracellular BH2 concentration in the presence of a constant eNOS:BH4 ratio was sufficient to induce eNOS-dependent superoxide production.	Superoxides	145-155	nitric oxide synthase 3	Homo sapiens	130-134
19011239-10	2009	This specific, reductionist approach in a cell-based system reveals that eNOS:BH4 reaction stoichiometry together with the intracellular BH4:BH2 ratio, rather than absolute concentrations of BH4, are the key determinants of eNOS uncoupling, even in the absence of exogenous oxidative stress.	sapropterin	78-81	nitric oxide synthase 3	Homo sapiens	73-77
19011239-10	2009	This specific, reductionist approach in a cell-based system reveals that eNOS:BH4 reaction stoichiometry together with the intracellular BH4:BH2 ratio, rather than absolute concentrations of BH4, are the key determinants of eNOS uncoupling, even in the absence of exogenous oxidative stress.	sapropterin	78-81	nitric oxide synthase 3	Homo sapiens	224-228
19803415-1	2009	Asymmetric dimethylarginine (ADMA), an endogenous methylated form of the amino acid L-arginine, inhibits the activity of the enzyme endothelial nitric oxide synthase (eNOS), with consequent reduced synthesis of nitric oxide (NO).	dimethylarginine	11-27	nitric oxide synthase 3	Homo sapiens	132-165
19803415-1	2009	Asymmetric dimethylarginine (ADMA), an endogenous methylated form of the amino acid L-arginine, inhibits the activity of the enzyme endothelial nitric oxide synthase (eNOS), with consequent reduced synthesis of nitric oxide (NO).	N,N-dimethylarginine	29-33	nitric oxide synthase 3	Homo sapiens	132-165
19803415-1	2009	Asymmetric dimethylarginine (ADMA), an endogenous methylated form of the amino acid L-arginine, inhibits the activity of the enzyme endothelial nitric oxide synthase (eNOS), with consequent reduced synthesis of nitric oxide (NO).	amino acid l-arginine	73-94	nitric oxide synthase 3	Homo sapiens	132-165
18945937-9	2009	Blocking of IKKbeta expression by IKK inhibitor II (15 microM wedelolactone) or small interferring RNA (siRNA) improved Hsp-90-eNOS interaction and NO production under conditions of HG.	wedelolactone	62-75	nitric oxide synthase 3	Homo sapiens	127-131
19104173-8	2009	On the contrary, nitric oxide production, endothelial nitric oxide synthase activity, and protein kinase B phosphorylation were enhanced by propofol treatment.	Propofol	140-148	nitric oxide synthase 3	Homo sapiens	42-75
18838165-6	2009	The high percentage of viable cells on the biomaterial and the preservation of endothelial nitric oxide synthase (eNOS) expression, eNOS activity and mitochondrial membrane potential (Deltapsi(m)), demonstrate the good biocompatibility of hydroxyapatite-betaTCP/agarose disks and its potential utility for bone substitution and repair.	Durapatite	239-253	nitric oxide synthase 3	Homo sapiens	79-112
18716005-4	2009	Deletion analysis of the eNOS promoter indicated that the segment within -119 bp upstream from the transcription start site was significantly involved in the effect of cortisol.	Hydrocortisone	168-176	nitric oxide synthase 3	Homo sapiens	25-29
18716005-8	2009	The suppression of 11 beta-HSD1 abolished the inhibition of eNOS expression by cortisol.	Hydrocortisone	79-87	nitric oxide synthase 3	Homo sapiens	60-64
19275271-10	2009	One year of treatment with perindopril upregulated eNOS protein expression and activity (19% and 27% vs placebo; p &lt; 0.05).	Perindopril	27-38	nitric oxide synthase 3	Homo sapiens	51-55
19273095-5	2009	Key to this dysfunction are changes in the following: nitric oxide signaling secondary to changes in eNOS and iNOS expression and activity, cyclooxygenase function with increases in pro-inflammatory COX-2 activity, alterations in Protein Kinase C and Mitogen Activated Protein Kinase signaling, and an increase in Vascular Endothelial Growth Factor expression increasing vascular permeability and dilatation.	Nitric Oxide	54-66	nitric oxide synthase 3	Homo sapiens	101-105
19246848-2	2009	We investigated whether telmisartan improves vascular endothelial function in patients with essential hypertension with the production of endothelial nitric oxide synthase (eNOS) through PPAR-gamma.Telmisartan was administered to 15 patients with essential hypertension.	Telmisartan	24-35	nitric oxide synthase 3	Homo sapiens	138-171
19246848-2	2009	We investigated whether telmisartan improves vascular endothelial function in patients with essential hypertension with the production of endothelial nitric oxide synthase (eNOS) through PPAR-gamma.Telmisartan was administered to 15 patients with essential hypertension.	Telmisartan	198-209	nitric oxide synthase 3	Homo sapiens	138-171
19229826-0	2009	Effect of glucose degradation products, glucose-containing dialysate and icodextrin on AQP1 and eNOS expression in cultured endothelial cells.	Glucose	40-47	nitric oxide synthase 3	Homo sapiens	96-100
19229826-0	2009	Effect of glucose degradation products, glucose-containing dialysate and icodextrin on AQP1 and eNOS expression in cultured endothelial cells.	Icodextrin	73-83	nitric oxide synthase 3	Homo sapiens	96-100
19229826-3	2009	We aimed at examining the effect of peritoneal dialysis solutions (PDSs) and glucose degradation products (GDPs) on the expression of AQP1 and eNOS in cultured endothelial cells.	Glucose	77-84	nitric oxide synthase 3	Homo sapiens	143-147
19229826-3	2009	We aimed at examining the effect of peritoneal dialysis solutions (PDSs) and glucose degradation products (GDPs) on the expression of AQP1 and eNOS in cultured endothelial cells.	gdps	107-111	nitric oxide synthase 3	Homo sapiens	143-147
19229826-6	2009	RESULTS: Fur and MGly at concentrations reported in traditional PDSs (Fur 0.8 microM; MGly 35 microM) significantly up-regulated eNOS mRNA and tended to down-regulate AQP1 mRNA in cultured endothelial cells.	Furaldehyde	9-12	nitric oxide synthase 3	Homo sapiens	129-133
19229826-6	2009	RESULTS: Fur and MGly at concentrations reported in traditional PDSs (Fur 0.8 microM; MGly 35 microM) significantly up-regulated eNOS mRNA and tended to down-regulate AQP1 mRNA in cultured endothelial cells.	Pyruvaldehyde	17-21	nitric oxide synthase 3	Homo sapiens	129-133
19229826-6	2009	RESULTS: Fur and MGly at concentrations reported in traditional PDSs (Fur 0.8 microM; MGly 35 microM) significantly up-regulated eNOS mRNA and tended to down-regulate AQP1 mRNA in cultured endothelial cells.	Furaldehyde	70-73	nitric oxide synthase 3	Homo sapiens	129-133
19229826-6	2009	RESULTS: Fur and MGly at concentrations reported in traditional PDSs (Fur 0.8 microM; MGly 35 microM) significantly up-regulated eNOS mRNA and tended to down-regulate AQP1 mRNA in cultured endothelial cells.	Pyruvaldehyde	86-90	nitric oxide synthase 3	Homo sapiens	129-133
19229826-7	2009	Glucose-based PDS as well as icodextrin PDS significantly up-regulated basal AQP1 and eNOS mRNA.	Glucose	0-7	nitric oxide synthase 3	Homo sapiens	86-90
19229826-7	2009	Glucose-based PDS as well as icodextrin PDS significantly up-regulated basal AQP1 and eNOS mRNA.	Icodextrin	29-39	nitric oxide synthase 3	Homo sapiens	86-90
19155632-0	2009	eNOS activation induced by a polyphenol-rich grape skin extract in porcine coronary arteries.	Polyphenols	29-39	nitric oxide synthase 3	Homo sapiens	0-4
19155632-5	2009	RESULTS: GSE-induced endothelium-dependent relaxations were abolished by N(G)-nitro-L-arginine (an eNOS inhibitor) and ODQ (a soluble guanylyl cyclase inhibitor), and they were reduced by MnTMPyP, polyethyleneglycol catalase, PP2 (an inhibitor of Src kinase) and wortmannin (an inhibitor of phosphoinositide 3-kinase).	Nitroarginine	73-94	nitric oxide synthase 3	Homo sapiens	99-103
19155632-7	2009	It also caused phosphorylation of Akt and eNOS, which were prevented by MnTMPyP, polyethyleneglycol catalase, PP2, wortmannin and LY294002.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	130-138	nitric oxide synthase 3	Homo sapiens	42-46
19155632-10	2009	This effect involves the intracellular formation of ROS in endothelial cells leading to the Src kinase/phosphoinositide 3-kinase/Akt-dependent phosphorylation of eNOS.	Reactive Oxygen Species	52-55	nitric oxide synthase 3	Homo sapiens	162-166
18957297-1	2008	AIMS: Low concentrations of nitric oxide (NO) produced by constitutive NO synthase (cNOS) in pancreatic beta-cells have been suggested to be a physiological regulator of insulin secretion.	Nitric Oxide	28-40	nitric oxide synthase 3	Homo sapiens	84-88
18931031-3	2008	Akt and its downstream target nitric oxide (NO) synthase (NOS)3 can protect barrier integrity during ROS stress, but little work has studied these oxidant stress responses in human cardiac microvascular endothelial cells (HCMVEC).	Nitric Oxide	30-42	nitric oxide synthase 3	Homo sapiens	58-63
18931031-3	2008	Akt and its downstream target nitric oxide (NO) synthase (NOS)3 can protect barrier integrity during ROS stress, but little work has studied these oxidant stress responses in human cardiac microvascular endothelial cells (HCMVEC).	Reactive Oxygen Species	101-104	nitric oxide synthase 3	Homo sapiens	58-63
18931031-4	2008	We, therefore, studied how ROS affects barrier function and NO generation via Akt and its downstream target NOS3 in HCMVEC.	Reactive Oxygen Species	27-30	nitric oxide synthase 3	Homo sapiens	108-112
18931031-6	2008	H2O2 also induced NO generation that was associated with NOS3 Ser-1177 site phosphorylation and Thr-495 dephosphorylation, with Ser-1177 effects attenuated by LY-294002 and an Akt inhibitor, Akt/PKB signaling inhibitor-2 (API-2).	Hydrogen Peroxide	0-4	nitric oxide synthase 3	Homo sapiens	57-61
18931031-6	2008	H2O2 also induced NO generation that was associated with NOS3 Ser-1177 site phosphorylation and Thr-495 dephosphorylation, with Ser-1177 effects attenuated by LY-294002 and an Akt inhibitor, Akt/PKB signaling inhibitor-2 (API-2).	Serine	62-65	nitric oxide synthase 3	Homo sapiens	57-61
18678642-3	2008	We also analysed the expression of NO synthase 3 (NOS3) in patients with CAF.	cafestol palmitate	73-76	nitric oxide synthase 3	Homo sapiens	35-48
18678642-3	2008	We also analysed the expression of NO synthase 3 (NOS3) in patients with CAF.	cafestol palmitate	73-76	nitric oxide synthase 3	Homo sapiens	50-54
18682551-0	2008	Effects of dietary decosahexaenoic acid (DHA) on eNOS in human coronary artery endothelial cells.	decosahexaenoic acid	19-39	nitric oxide synthase 3	Homo sapiens	49-53
18682551-0	2008	Effects of dietary decosahexaenoic acid (DHA) on eNOS in human coronary artery endothelial cells.	Dihydroalprenolol	41-44	nitric oxide synthase 3	Homo sapiens	49-53
18682551-3	2008	This study determined if DHA enhances expression and activity of eNOS in cultured human coronary artery endothelial cells (HCAEC).	Dihydroalprenolol	25-28	nitric oxide synthase 3	Homo sapiens	65-69
18682551-5	2008	A trend for increased expression of endothelial nitric oxide synthase (eNOS) and phospho-eNOS was observed with 5 and 50 nM DHA.	Dihydroalprenolol	124-127	nitric oxide synthase 3	Homo sapiens	36-69
18682551-5	2008	A trend for increased expression of endothelial nitric oxide synthase (eNOS) and phospho-eNOS was observed with 5 and 50 nM DHA.	Dihydroalprenolol	124-127	nitric oxide synthase 3	Homo sapiens	71-75
18682551-5	2008	A trend for increased expression of endothelial nitric oxide synthase (eNOS) and phospho-eNOS was observed with 5 and 50 nM DHA.	Dihydroalprenolol	124-127	nitric oxide synthase 3	Homo sapiens	89-93
18682551-6	2008	DHA also enhanced expression of 2 proteins instrumental in activation of eNOS: phospho-Akt (5 and 50 nM) and HSP90 (50 nM and 1 microM).	Dihydroalprenolol	0-3	nitric oxide synthase 3	Homo sapiens	73-77
18682551-8	2008	Findings suggest that DHA enhances eNOS and Akt activity, augments HSP90 expression, and increases NO bioavailability in response to Akt kinase activation.	Dihydroalprenolol	22-25	nitric oxide synthase 3	Homo sapiens	35-39
18941922-4	2008	Endothelium-derived nitric oxide (eNO), produced by eNO synthase (eNOS), is a key regulator of vessel wall function and cardiovascular homeostasis.	Nitric Oxide	20-32	nitric oxide synthase 3	Homo sapiens	66-70
18804337-1	2008	OBJECTIVES: To investigate the association of two common genetic polymorphisms of the gene encoding for endothelial nitric oxide synthase (Nos3), the enzyme catalyzing the production of nitric oxide (NO), with occurrence of the polycystic ovary syndrome (PCOS).	Nitric Oxide	116-128	nitric oxide synthase 3	Homo sapiens	139-143
18789310-0	2008	Icariin stimulates angiogenesis by activating the MEK/ERK- and PI3K/Akt/eNOS-dependent signal pathways in human endothelial cells.	icariin	0-7	nitric oxide synthase 3	Homo sapiens	72-76
18789310-3	2008	Icariin activated the angiogenic signal modulators, ERK, phosphatidylinositol 3-kinase (PI3K), Akt, and endothelial nitric oxide synthase (eNOS), and increased NO production, without affecting VEGF expression, indicating that icariin may directly stimulate angiogenesis.	icariin	0-7	nitric oxide synthase 3	Homo sapiens	104-137
18789310-3	2008	Icariin activated the angiogenic signal modulators, ERK, phosphatidylinositol 3-kinase (PI3K), Akt, and endothelial nitric oxide synthase (eNOS), and increased NO production, without affecting VEGF expression, indicating that icariin may directly stimulate angiogenesis.	icariin	0-7	nitric oxide synthase 3	Homo sapiens	139-143
18719233-3	2008	The activation/upregulation of arginase appears to be an important contributor to age-related endothelial dysfunction by a mechanism that involves substrate (L-arginine) limitation for NO synthase (NOS) 3 and therefore NO synthesis.	Arginine	158-168	nitric oxide synthase 3	Homo sapiens	185-204
18682401-0	2008	Functional role of HSP90 complexes with endothelial nitric-oxide synthase (eNOS) and calpain on nitric oxide generation in endothelial cells.	Nitric Oxide	96-108	nitric oxide synthase 3	Homo sapiens	40-73
18682401-0	2008	Functional role of HSP90 complexes with endothelial nitric-oxide synthase (eNOS) and calpain on nitric oxide generation in endothelial cells.	Nitric Oxide	96-108	nitric oxide synthase 3	Homo sapiens	75-79
18682401-4	2008	Furthermore, in the presence of the HSP90 inhibitor geldanamycin, a significant decrease in NO production and an extensive degradation of eNOS protein occurs, indicating that dissociation from membranes and association with the chaperone is correlated to the protection of the synthase.	geldanamycin	52-64	nitric oxide synthase 3	Homo sapiens	138-142
18818408-6	2008	Thus, XOR and eNOS are ideally situated on the membranes of RBCs and blood vessels to generate intravascular vasodilator NO from nitrite during ischemic episodes.	Nitrites	129-136	nitric oxide synthase 3	Homo sapiens	14-18
18693249-3	2008	Exposure of human umbilical vein endothelial cells (HUVECs) to NO donors caused an increase in phosphorylation of both Thr-172 of AMPK and Ser-1177 of endothelial nitric oxide synthase, a downstream enzyme of AMPK.	Serine	139-142	nitric oxide synthase 3	Homo sapiens	151-184
18687367-0	2008	Mechanism of thrombin mediated eNOS phosphorylation in endothelial cells is dependent on ATP levels after stimulation.	Adenosine Triphosphate	89-92	nitric oxide synthase 3	Homo sapiens	31-35
18687367-4	2008	In culture medium 1640 the level of intracellular ATP was unchanged after thrombin stimulation and the CaMKK inhibitor STO-609 totally inhibited phosphorylation of AMPK and acetyl coenzyme A carboxylase (ACC) but not eNOS.	STO 609	119-126	nitric oxide synthase 3	Homo sapiens	217-221
18687367-7	2008	Thus, conditions subjecting endothelial cells to a fall in ATP after thrombin stimulation facilitate activation of pathways partly dependent on AMPK causing downstream phosphorylation of eNOS.	Adenosine Triphosphate	59-62	nitric oxide synthase 3	Homo sapiens	187-191
18713021-1	2008	Nitric oxide (NO) is synthesized by endothelial nitric oxide synthase (eNOS) and plays an important role in vascular homeostasis and cardiovascular diseases.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	36-69
18713021-1	2008	Nitric oxide (NO) is synthesized by endothelial nitric oxide synthase (eNOS) and plays an important role in vascular homeostasis and cardiovascular diseases.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	71-75
18841076-5	2008	Cytoprotective rLE substantially reduced high glucose-induced expression of endothelial nitric oxide synthase (eNOS), and hence attenuated the formation of peroxynitrite radicals derived from NO.	Glucose	46-53	nitric oxide synthase 3	Homo sapiens	76-109
18435486-0	2008	Tannin 1-alpha-O-galloylpunicalagin induces the calcium-dependent activation of endothelial nitric-oxide synthase via the phosphatidylinositol 3-kinase/Akt pathway in endothelial cells.	tannin 1-alpha-O-galloylpunicalagin	0-35	nitric oxide synthase 3	Homo sapiens	80-113
18435486-0	2008	Tannin 1-alpha-O-galloylpunicalagin induces the calcium-dependent activation of endothelial nitric-oxide synthase via the phosphatidylinositol 3-kinase/Akt pathway in endothelial cells.	Calcium	48-55	nitric oxide synthase 3	Homo sapiens	80-113
18435486-2	2008	In our present study, we investigated the effects of 1-alpha-O-galloylpunicalagin upon endothelial nitric oxide synthase (eNOS) activity in endothelial cells (ECs).	1-alpha-o-galloylpunicalagin	53-81	nitric oxide synthase 3	Homo sapiens	87-120
18435486-2	2008	In our present study, we investigated the effects of 1-alpha-O-galloylpunicalagin upon endothelial nitric oxide synthase (eNOS) activity in endothelial cells (ECs).	1-alpha-o-galloylpunicalagin	53-81	nitric oxide synthase 3	Homo sapiens	122-126
18435486-6	2008	The Ca(2+) ionophore A23187 stimulated eNOS phosphorylation and augmented NO production.	Calcimycin	21-27	nitric oxide synthase 3	Homo sapiens	39-43
18435486-7	2008	Pretreatment with Ca(2+) chelators inhibited 1-alpha-O-galloylpunicalagin-induced eNOS phosphorylation and NO production.	1-alpha-o-galloylpunicalagin	45-73	nitric oxide synthase 3	Homo sapiens	82-86
18435486-8	2008	Treatment with 1-alpha-O-galloylpunicalagin did not alter the eNOS protein levels but, unlike punicalagin, induced a sustained activation of eNOS Ser(1179) phosphorylation.	1-alpha-o-galloylpunicalagin	15-43	nitric oxide synthase 3	Homo sapiens	141-145
18435486-8	2008	Treatment with 1-alpha-O-galloylpunicalagin did not alter the eNOS protein levels but, unlike punicalagin, induced a sustained activation of eNOS Ser(1179) phosphorylation.	punicalagin	32-43	nitric oxide synthase 3	Homo sapiens	141-145
18435486-8	2008	Treatment with 1-alpha-O-galloylpunicalagin did not alter the eNOS protein levels but, unlike punicalagin, induced a sustained activation of eNOS Ser(1179) phosphorylation.	Serine	146-149	nitric oxide synthase 3	Homo sapiens	141-145
18435486-12	2008	Our present results thus indicate that the 1-alpha-O-galloylpunicalagin-induced calcium-dependent activation of eNOS is primarily mediated via a phosphatidylinositol 3-kinase/Akt-dependent increase in eNOS activity, and occurs independently of the eNOS protein content.	1-alpha-o-galloylpunicalagin	43-71	nitric oxide synthase 3	Homo sapiens	112-116
18435486-12	2008	Our present results thus indicate that the 1-alpha-O-galloylpunicalagin-induced calcium-dependent activation of eNOS is primarily mediated via a phosphatidylinositol 3-kinase/Akt-dependent increase in eNOS activity, and occurs independently of the eNOS protein content.	1-alpha-o-galloylpunicalagin	43-71	nitric oxide synthase 3	Homo sapiens	201-205
18435486-12	2008	Our present results thus indicate that the 1-alpha-O-galloylpunicalagin-induced calcium-dependent activation of eNOS is primarily mediated via a phosphatidylinositol 3-kinase/Akt-dependent increase in eNOS activity, and occurs independently of the eNOS protein content.	1-alpha-o-galloylpunicalagin	43-71	nitric oxide synthase 3	Homo sapiens	201-205
18435486-12	2008	Our present results thus indicate that the 1-alpha-O-galloylpunicalagin-induced calcium-dependent activation of eNOS is primarily mediated via a phosphatidylinositol 3-kinase/Akt-dependent increase in eNOS activity, and occurs independently of the eNOS protein content.	Calcium	80-87	nitric oxide synthase 3	Homo sapiens	112-116
18435486-12	2008	Our present results thus indicate that the 1-alpha-O-galloylpunicalagin-induced calcium-dependent activation of eNOS is primarily mediated via a phosphatidylinositol 3-kinase/Akt-dependent increase in eNOS activity, and occurs independently of the eNOS protein content.	Calcium	80-87	nitric oxide synthase 3	Homo sapiens	201-205
18435486-12	2008	Our present results thus indicate that the 1-alpha-O-galloylpunicalagin-induced calcium-dependent activation of eNOS is primarily mediated via a phosphatidylinositol 3-kinase/Akt-dependent increase in eNOS activity, and occurs independently of the eNOS protein content.	Calcium	80-87	nitric oxide synthase 3	Homo sapiens	201-205
18663495-1	2008	Nitric oxide synthase (NOS) genes (NOS1, NOS2A, and NOS3) may create excess nitric oxide that contributes to neurodegeneration in Parkinson"s disease (PD).	Nitric Oxide	76-88	nitric oxide synthase 3	Homo sapiens	52-56
18325557-4	2008	This includes estrogen-stimulated rapid activation of endothelial nitric oxide synthase (eNOS), resulting in the elaboration of the athero-protective, angiogenesis-promoting product nitric oxide (NO).	Nitric Oxide	66-78	nitric oxide synthase 3	Homo sapiens	89-93
18692595-1	2008	Nitric oxide (NO) is a gaseous lipophilic free radical generated by three distinct isoforms of nitric oxide synthases (NOS), type 1 or neuronal (nNOS), type 2 or inducible (iNOS) and type 3 or endothelial NOS (eNOS).	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	193-208
18617528-0	2008	Bidirectional actions of hydrogen peroxide on endothelial nitric-oxide synthase phosphorylation and function: co-commitment and interplay of Akt and AMPK.	Hydrogen Peroxide	25-42	nitric oxide synthase 3	Homo sapiens	46-79
18617528-2	2008	Reactive oxygen species such as H(2)O(2) was reported to activate Akt, leading to increased eNOS Ser(1179) phosphorylation and activity.	Reactive Oxygen Species	0-23	nitric oxide synthase 3	Homo sapiens	92-96
18617528-2	2008	Reactive oxygen species such as H(2)O(2) was reported to activate Akt, leading to increased eNOS Ser(1179) phosphorylation and activity.	Hydrogen Peroxide	32-40	nitric oxide synthase 3	Homo sapiens	92-96
18617528-2	2008	Reactive oxygen species such as H(2)O(2) was reported to activate Akt, leading to increased eNOS Ser(1179) phosphorylation and activity.	Serine	97-100	nitric oxide synthase 3	Homo sapiens	92-96
18617528-3	2008	But reactive oxygen species are also known to attenuate eNOS function in cardiovascular diseases.	Reactive Oxygen Species	4-27	nitric oxide synthase 3	Homo sapiens	56-60
18617528-4	2008	Prior studies showing H(2)O(2)-stimulated eNOS phosphorylation were performed on serum-starved cells, and only the short term effect of H(2)O(2) was examined.	Hydrogen Peroxide	22-30	nitric oxide synthase 3	Homo sapiens	42-46
18617528-5	2008	Here we found that the effects of H(2)O(2) on eNOS Ser(1179) phosphorylation and function were bidirectional.	Hydrogen Peroxide	34-42	nitric oxide synthase 3	Homo sapiens	46-50
18617528-5	2008	Here we found that the effects of H(2)O(2) on eNOS Ser(1179) phosphorylation and function were bidirectional.	Serine	51-54	nitric oxide synthase 3	Homo sapiens	46-50
18617528-6	2008	With endothelial cells cultured with serum, H(2)O(2) initially raised eNOS Ser(1179) phosphorylation and activity.	Hydrogen Peroxide	44-52	nitric oxide synthase 3	Homo sapiens	70-74
18617528-6	2008	With endothelial cells cultured with serum, H(2)O(2) initially raised eNOS Ser(1179) phosphorylation and activity.	Serine	75-78	nitric oxide synthase 3	Homo sapiens	70-74
18617528-7	2008	However, after the peak increase at 30 min, eNOS Ser(1179) phosphorylation dramatically declined.	Serine	49-52	nitric oxide synthase 3	Homo sapiens	44-48
18617528-8	2008	Parallel to the alterations of eNOS Ser(1179) phosphorylation, Akt was transiently activated by H(2)O(2) and subsequently became dormant.	Serine	36-39	nitric oxide synthase 3	Homo sapiens	31-35
18617528-8	2008	Parallel to the alterations of eNOS Ser(1179) phosphorylation, Akt was transiently activated by H(2)O(2) and subsequently became dormant.	Hydrogen Peroxide	96-104	nitric oxide synthase 3	Homo sapiens	31-35
18556569-1	2008	OBJECTIVE: Increased formation of reactive oxygen species (ROS) has been identified as a causative factor in endothelial dysfunction by reducing NO bioavailability and uncoupling endothelial nitric oxide synthase (eNOS).	Reactive Oxygen Species	34-57	nitric oxide synthase 3	Homo sapiens	179-212
18556569-1	2008	OBJECTIVE: Increased formation of reactive oxygen species (ROS) has been identified as a causative factor in endothelial dysfunction by reducing NO bioavailability and uncoupling endothelial nitric oxide synthase (eNOS).	Reactive Oxygen Species	59-62	nitric oxide synthase 3	Homo sapiens	179-212
18556572-6	2008	Cilostazol increased phosphorylation of Akt at Ser(473) and of endothelial nitric oxide synthase (eNOS) at Ser(1177), with a dose-dependent increase in Sirt1 expression.	Cilostazol	0-10	nitric oxide synthase 3	Homo sapiens	63-96
18556572-6	2008	Cilostazol increased phosphorylation of Akt at Ser(473) and of endothelial nitric oxide synthase (eNOS) at Ser(1177), with a dose-dependent increase in Sirt1 expression.	Serine	107-110	nitric oxide synthase 3	Homo sapiens	63-96
18716157-7	2008	Resveratrol in vitro enhanced significantly the production of NO by stimulated platelets, the activity of platelet NO synthase (NOS), phosphorylation of protein kinase B, an activator of the endothelial NOS (eNOS), and phosphorylation of vasodilator-activated protein (VASP), an expression of the biologic activity of NO in platelets.	Resveratrol	0-11	nitric oxide synthase 3	Homo sapiens	191-206
18556800-1	2008	Previously, we have reported that endothelial nitric oxide synthase (eNOS) promoter activity is decreased in pulmonary arterial endothelial cells (PAECs) in response to hydrogen peroxide (H(2)O(2)).	Hydrogen Peroxide	169-186	nitric oxide synthase 3	Homo sapiens	34-67
18556800-1	2008	Previously, we have reported that endothelial nitric oxide synthase (eNOS) promoter activity is decreased in pulmonary arterial endothelial cells (PAECs) in response to hydrogen peroxide (H(2)O(2)).	Hydrogen Peroxide	169-186	nitric oxide synthase 3	Homo sapiens	69-73
18516617-4	2008	Combined endothelial nitric oxide synthase (eNOS) and cyclooxygenase (COX) inhibition was achieved by an intradermal injection (10 microl) of the eNOS inhibitor, L(omega)-monomethyl L-arginine (L-NMMA, 10 mM) and the COX inhibitor, diclofenac (10 mM); saline was injected as a control.	l(omega)-monomethyl l-arginine	162-192	nitric oxide synthase 3	Homo sapiens	9-42
18516617-4	2008	Combined endothelial nitric oxide synthase (eNOS) and cyclooxygenase (COX) inhibition was achieved by an intradermal injection (10 microl) of the eNOS inhibitor, L(omega)-monomethyl L-arginine (L-NMMA, 10 mM) and the COX inhibitor, diclofenac (10 mM); saline was injected as a control.	omega-N-Methylarginine	194-200	nitric oxide synthase 3	Homo sapiens	9-42
18516617-4	2008	Combined endothelial nitric oxide synthase (eNOS) and cyclooxygenase (COX) inhibition was achieved by an intradermal injection (10 microl) of the eNOS inhibitor, L(omega)-monomethyl L-arginine (L-NMMA, 10 mM) and the COX inhibitor, diclofenac (10 mM); saline was injected as a control.	Diclofenac	232-242	nitric oxide synthase 3	Homo sapiens	9-42
18516617-4	2008	Combined endothelial nitric oxide synthase (eNOS) and cyclooxygenase (COX) inhibition was achieved by an intradermal injection (10 microl) of the eNOS inhibitor, L(omega)-monomethyl L-arginine (L-NMMA, 10 mM) and the COX inhibitor, diclofenac (10 mM); saline was injected as a control.	Sodium Chloride	252-258	nitric oxide synthase 3	Homo sapiens	9-42
18622262-2	2008	To analyze the functional significance of the G894T polymorphism of NOS3, the gene encoding endothelial nitric oxide synthase (NOS), we assessed basal nitric oxide activity and the amount of oxidative stress in the renal circulation of patients with type 2 diabetes.	Nitric Oxide	104-116	nitric oxide synthase 3	Homo sapiens	68-72
18550157-1	2008	OBJECTIVE: To assess whether the Glu298Asp polymorphism of the endothelial nitric oxide synthase (eNOS) gene possibly mediates the relation of blood pressure and serum cholesterol.	Cholesterol	168-179	nitric oxide synthase 3	Homo sapiens	63-96
18550157-1	2008	OBJECTIVE: To assess whether the Glu298Asp polymorphism of the endothelial nitric oxide synthase (eNOS) gene possibly mediates the relation of blood pressure and serum cholesterol.	Cholesterol	168-179	nitric oxide synthase 3	Homo sapiens	98-102
18550157-4	2008	After adjustment for age, sex, BMI, and lifestyle (drinking, smoking, exercise and stress), the odds ratio (OR) of hypertension associated with high (&gt; or = 220 mg/dl or under treatment) total cholesterol was 2.08 (95% Confidence Interval (CI) 1.02-4.24) among carriers of the eNOS 298Asp allele versus 1.18 (95% CI 0.89-1.55, p for interaction=0.50) among non-carriers.	Cholesterol	196-207	nitric oxide synthase 3	Homo sapiens	280-284
18578689-1	2008	BACKGROUND: Nitric oxide (NO) - a major signalling molecule of the vascular system - is constitutively produced in endothelial cells (EC) by the endothelial NO synthase (eNOS).	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	170-174
18578689-4	2008	RESULTS: Short-term (20-30 min) detNO treatment of EC increases the Ser(1177) phosphorylation of the constitutively expressed endothelial NOS and the production of endogenous NO generated by eNOS from [(3)H]arginine.	detno	32-37	nitric oxide synthase 3	Homo sapiens	191-195
18578689-5	2008	The phosphorylation of eNOS is Akt-dependent and completely reverted by the phosphatidylinositol-3 kinase (PI-3K) inhibitor LY294002.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	124-132	nitric oxide synthase 3	Homo sapiens	23-27
18422522-4	2008	The TNF-alpha-dependent eNOS activation occurred through generation, by sphingosine-kinase-1, of sphingosine-1-phosphate, stimulation of its membrane receptors and activation of Akt, as determined using small interference RNA and dominant negative constructs specific for the enzymes and receptors.	sphingosine 1-phosphate	97-120	nitric oxide synthase 3	Homo sapiens	24-28
18422522-5	2008	eNOS activation by TNF-alpha conferred cytoprotection from excitotoxicity and neurotoxic cues such as reactive oxygen species, endoplasmic reticulum stress, DNA damage, and mutated alsin itself.	oxygen species	111-125	nitric oxide synthase 3	Homo sapiens	0-4
19140434-1	2008	Nitric oxide (NO) is synthesized from 1-arginine by endothelial nitric oxide synthase (eNOS).	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	52-85
19140434-1	2008	Nitric oxide (NO) is synthesized from 1-arginine by endothelial nitric oxide synthase (eNOS).	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	87-91
19140434-1	2008	Nitric oxide (NO) is synthesized from 1-arginine by endothelial nitric oxide synthase (eNOS).	1-arginine	38-48	nitric oxide synthase 3	Homo sapiens	52-85
19140434-1	2008	Nitric oxide (NO) is synthesized from 1-arginine by endothelial nitric oxide synthase (eNOS).	1-arginine	38-48	nitric oxide synthase 3	Homo sapiens	87-91
17588688-1	2008	BACKGROUND: L-arginine, the substrate for endothelial nitric oxide synthase, is essential for normal endothelial function.	Arginine	12-22	nitric oxide synthase 3	Homo sapiens	42-75
18001743-1	2008	OBJECTIVE: We examined the endothelial nitric oxide (eNOS) gene Glu298Asp polymorphism to assess its possible association with the extent of coronary collaterals.	Nitric Oxide	39-51	nitric oxide synthase 3	Homo sapiens	53-57
18064606-1	2008	High D-glucose reduces human equilibrative nucleoside transporter 1 (hENT1)-mediated adenosine uptake involving endothelial nitric oxide synthase (eNOS), mitogen-activated protein (MAP) kinase kinases 1 and 2/MAP kinases p42/44 (MEK/ERKs), and protein kinase C (PKC) activation in human umbilical vein endothelium (HUVEC).	Glucose	5-14	nitric oxide synthase 3	Homo sapiens	112-145
18064606-1	2008	High D-glucose reduces human equilibrative nucleoside transporter 1 (hENT1)-mediated adenosine uptake involving endothelial nitric oxide synthase (eNOS), mitogen-activated protein (MAP) kinase kinases 1 and 2/MAP kinases p42/44 (MEK/ERKs), and protein kinase C (PKC) activation in human umbilical vein endothelium (HUVEC).	Adenosine	85-94	nitric oxide synthase 3	Homo sapiens	112-145
18331440-1	2008	AIM: Nitric oxide (NO), produced by the polymorphic endothelial nitric oxide synthase (NOS3), plays an important role in endothelial function.	Nitric Oxide	5-17	nitric oxide synthase 3	Homo sapiens	52-85
18331440-1	2008	AIM: Nitric oxide (NO), produced by the polymorphic endothelial nitric oxide synthase (NOS3), plays an important role in endothelial function.	Nitric Oxide	5-17	nitric oxide synthase 3	Homo sapiens	87-91
18375203-1	2008	Vascular endothelial nitric oxide (NO) production via the citrulline-NO cycle not only involves the regulation of endothelial nitric oxide synthase (eNOS), but also regulation of caveolar-localized endothelial argininosuccinate synthase (AS), which catalyzes the rate-limiting step of the cycle.	Nitric Oxide	21-33	nitric oxide synthase 3	Homo sapiens	114-147
18375203-1	2008	Vascular endothelial nitric oxide (NO) production via the citrulline-NO cycle not only involves the regulation of endothelial nitric oxide synthase (eNOS), but also regulation of caveolar-localized endothelial argininosuccinate synthase (AS), which catalyzes the rate-limiting step of the cycle.	Citrulline	58-68	nitric oxide synthase 3	Homo sapiens	114-147
21478289-1	2011	Endothelial nitric oxide synthase (eNOS) catalyses the production of nitric oxide, which has been shown to participate in the pathogenesis of systemic lupus erythematosus (SLE).	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	35-39
19779107-6	2009	RESULTS: Elevated expression of ecNOS was found to be coupled with significantly lower SOD activity and glutathione level, and increased lipid peroxidation in IUGR neonates.	Glutathione	104-115	nitric oxide synthase 3	Homo sapiens	32-37
19721393-0	2009	Ceramide mediates inhibition of the AKT/eNOS signaling pathway by palmitate in human vascular endothelial cells.	Ceramides	0-8	nitric oxide synthase 3	Homo sapiens	40-44
19721393-7	2009	Preventing de novo ceramide synthesis abolished the antagonistic effect of palmitate toward the Akt/ eNOS pathway.	Ceramides	19-27	nitric oxide synthase 3	Homo sapiens	101-105
19721393-7	2009	Preventing de novo ceramide synthesis abolished the antagonistic effect of palmitate toward the Akt/ eNOS pathway.	Palmitates	75-84	nitric oxide synthase 3	Homo sapiens	101-105
19721393-9	2009	CONCLUSIONS: Taken together, we have demonstrated that palmitic acid induces accumulation of ceramide, which appears to mediate palmitic acid"s inhibitory effects on the Akt/eNOS pathway, leading to a significant decrease in NO generation.	Palmitic Acid	55-68	nitric oxide synthase 3	Homo sapiens	174-178
19721393-9	2009	CONCLUSIONS: Taken together, we have demonstrated that palmitic acid induces accumulation of ceramide, which appears to mediate palmitic acid"s inhibitory effects on the Akt/eNOS pathway, leading to a significant decrease in NO generation.	Ceramides	93-101	nitric oxide synthase 3	Homo sapiens	174-178
19721393-9	2009	CONCLUSIONS: Taken together, we have demonstrated that palmitic acid induces accumulation of ceramide, which appears to mediate palmitic acid"s inhibitory effects on the Akt/eNOS pathway, leading to a significant decrease in NO generation.	Palmitic Acid	128-141	nitric oxide synthase 3	Homo sapiens	174-178
19721393-10	2009	Therefore, ceramide is a necessary and sufficient intermediate mediating the inhibition of the AKT/eNOS signaling pathway by palmitate in endothelial cells.	Ceramides	11-19	nitric oxide synthase 3	Homo sapiens	99-103
19721393-10	2009	Therefore, ceramide is a necessary and sufficient intermediate mediating the inhibition of the AKT/eNOS signaling pathway by palmitate in endothelial cells.	Palmitates	125-134	nitric oxide synthase 3	Homo sapiens	99-103
19671875-8	2009	When NOS3 genotypes were combined, women with genotypes encoding for lower nitric oxide who received chemotherapy had a &gt;2-fold increase in hazard of progression (hazard ratio, 2.32; 95% confidence interval, 1.26-4.25), whereas there was reduced risk for those who did not receive adjuvant therapy (hazard ratio, 0.42; 95% confidence interval, 0.19-0.95).	Nitric Oxide	75-87	nitric oxide synthase 3	Homo sapiens	5-9
19583242-2	2009	In this study, we note the functional platform of caveolae with dual functions, internalization of external substances and cell signalings leading to nitric oxide release, and hypothesize that the switching of enzyme activity of endothelial nitric oxide synthase can be achieved by targeting caveolae with nanoparticles.	Nitric Oxide	150-162	nitric oxide synthase 3	Homo sapiens	229-262
19447893-3	2009	The pteridine cofactor tetrahydrobiopterin (BH(4)) is a critical determinant of endothelial NOS (eNOS) activity and coupling, and GTP cyclohydrolase I (GCH1) is the rate-limiting enzyme in its generation.	Pteridines	4-13	nitric oxide synthase 3	Homo sapiens	80-95
19447893-3	2009	The pteridine cofactor tetrahydrobiopterin (BH(4)) is a critical determinant of endothelial NOS (eNOS) activity and coupling, and GTP cyclohydrolase I (GCH1) is the rate-limiting enzyme in its generation.	sapropterin	23-42	nitric oxide synthase 3	Homo sapiens	80-95
19727605-3	2009	Thus, the conversion of nitrite into NO during cellular stress may be an evolutionarily conserved and redundant means for NO generation at a time when endothelial nitric oxide synthase is non-functional.	Nitrites	24-31	nitric oxide synthase 3	Homo sapiens	151-184
19650200-9	2009	The plasma testosterone and osteocalcin concentrations in the subjects of eNOS G894T G/T genotype were evidently higher than those in the subjects of other genotypes (P&lt;0.05); the plasma estradiol concentration in the subjects of eNOS 27 bp-VNTR a/a genotype was obviously higher than that in the subjects of b/b genotype (P&lt;0.01).	Testosterone	11-23	nitric oxide synthase 3	Homo sapiens	74-78
19650200-16	2009	CONCLUSION: eNOS G894T G/T genotype influenced the plasma testosterone and osteocalcin concentrations, and T/T genotype influenced BMD.	Testosterone	58-70	nitric oxide synthase 3	Homo sapiens	12-16
19650200-17	2009	eNOS 27 bp-VNTR a/a genotype increased plasma estradiol concentration to have a protective effect on osteoporosis.	Estradiol	46-55	nitric oxide synthase 3	Homo sapiens	0-4
19395011-4	2009	Presence of endothelial nitric oxide-generating enzyme NO synthase (NOS3) was also investigated, as it is known that the vasodilator NOS3 might be involved in the development of uterine edema.	Nitric Oxide	24-36	nitric oxide synthase 3	Homo sapiens	68-72
19502286-4	2009	Statins appear to have actions on vascular nitric oxide through the balance of inducible and endothelial nitric oxide synthase.	Nitric Oxide	43-55	nitric oxide synthase 3	Homo sapiens	93-126
19377066-2	2009	The aim of the present study was to determine the mechanism by which aspirin acutely increases the activity of NO synthase type 3 (NOS-3), the predominant NOS isoform expressed by platelets, and specifically whether this occurs through an increase in its acetylation.	Aspirin	69-76	nitric oxide synthase 3	Homo sapiens	111-136
19377066-5	2009	Following immunoprecipitation of NOS-3 from platelet lysates, its activity was determined from l-[(3)H]arginine to l-[(3)H]citrulline conversion, and its serine phosphorylation quantified by western blotting.	l-[(3)h]arginine	95-111	nitric oxide synthase 3	Homo sapiens	33-38
19377066-5	2009	Following immunoprecipitation of NOS-3 from platelet lysates, its activity was determined from l-[(3)H]arginine to l-[(3)H]citrulline conversion, and its serine phosphorylation quantified by western blotting.	l-[(3)h]citrulline	115-133	nitric oxide synthase 3	Homo sapiens	33-38
19377066-5	2009	Following immunoprecipitation of NOS-3 from platelet lysates, its activity was determined from l-[(3)H]arginine to l-[(3)H]citrulline conversion, and its serine phosphorylation quantified by western blotting.	Serine	154-160	nitric oxide synthase 3	Homo sapiens	33-38
19377066-6	2009	Acetylation of NOS-3 in platelets was assessed by the incorporation of radioactivity into the immunoprecipitated enzyme from [acetyl-(14)C]aspirin.	acetyl-(14)c]aspirin	126-146	nitric oxide synthase 3	Homo sapiens	15-20
19377066-8	2009	At all concentrations tested, aspirin increased the activity of NOS-3 from platelets.	Aspirin	30-37	nitric oxide synthase 3	Homo sapiens	64-69
19377066-10	2009	Serine phosphorylation of NOS-3 in platelets was decreased, and this was especially marked for serine-1177 phosphorylation, whereas acetylation of NOS-3 was increased, by aspirin incubation.	Serine	0-6	nitric oxide synthase 3	Homo sapiens	26-31
19377066-10	2009	Serine phosphorylation of NOS-3 in platelets was decreased, and this was especially marked for serine-1177 phosphorylation, whereas acetylation of NOS-3 was increased, by aspirin incubation.	Serine	95-101	nitric oxide synthase 3	Homo sapiens	26-31
19377066-10	2009	Serine phosphorylation of NOS-3 in platelets was decreased, and this was especially marked for serine-1177 phosphorylation, whereas acetylation of NOS-3 was increased, by aspirin incubation.	Aspirin	171-178	nitric oxide synthase 3	Homo sapiens	26-31
19377066-10	2009	Serine phosphorylation of NOS-3 in platelets was decreased, and this was especially marked for serine-1177 phosphorylation, whereas acetylation of NOS-3 was increased, by aspirin incubation.	Aspirin	171-178	nitric oxide synthase 3	Homo sapiens	147-152
19377066-11	2009	HeLa cells transfected with NOS-3 exhibited an increase in NO biosynthesis following aspirin exposure, and this was associated with acetylation of the enzyme on both serine-765 and serine-771.	Aspirin	85-92	nitric oxide synthase 3	Homo sapiens	28-33
19377066-11	2009	HeLa cells transfected with NOS-3 exhibited an increase in NO biosynthesis following aspirin exposure, and this was associated with acetylation of the enzyme on both serine-765 and serine-771.	Serine	166-172	nitric oxide synthase 3	Homo sapiens	28-33
19377066-11	2009	HeLa cells transfected with NOS-3 exhibited an increase in NO biosynthesis following aspirin exposure, and this was associated with acetylation of the enzyme on both serine-765 and serine-771.	Serine	181-187	nitric oxide synthase 3	Homo sapiens	28-33
19377066-12	2009	CONCLUSION: Aspirin acetylates NOS-3 acutely in platelets, and this causes an increase in its activity as well as a decrease in its phosphorylation.	Aspirin	12-19	nitric oxide synthase 3	Homo sapiens	31-36
19377066-13	2009	It is also possible that aspirin indirectly affects NOS-3 activity by acetylating other substrates within the platelet, but this remains to be determined.	Aspirin	25-32	nitric oxide synthase 3	Homo sapiens	52-57
19435422-1	2009	Interethnic disparities in the distribution of endothelial nitric oxide synthase (eNOS) polymorphisms may affect nitric oxide (NO)-mediated effects of and responses to drugs.	Nitric Oxide	59-71	nitric oxide synthase 3	Homo sapiens	82-86
19401197-10	2009	The EMPs in vitro led to diminished eNOS protein expression in HUVECs and this EMP-mediated detrimental effect was markedly inhibited by berberine.	Berberine	137-146	nitric oxide synthase 3	Homo sapiens	36-40
19501907-7	2009	IUGR cells in normoxia or hypoxia, and normal cells in hypoxia exhibited reduced l-arginine transport, hCAT-1 expression, NO synthesis and eNOS phosphorylation at Serine(1177), effects reversed by calphostin C (PKC inhibitor) and S-nitroso-N-acetyl-l,d-penicillamine (SNAP, NO donor).	Serine	163-169	nitric oxide synthase 3	Homo sapiens	139-143
19501907-11	2009	Thus, IUGR- and hypoxia-reduced l-arginine transport could result from increased PKCalpha, but reduced eNOS activity leading to a lower hCAT-1 expression in HUVEC.	Arginine	32-42	nitric oxide synthase 3	Homo sapiens	103-107
19351806-9	2009	Visfatin increased total Akt and Ser(473)-phospho-Akt expression with concomitant rises in eNOS phosphorylation at Ser(1177); these effects were blocked by LY-2940002.	Serine	115-118	nitric oxide synthase 3	Homo sapiens	91-95
19351806-9	2009	Visfatin increased total Akt and Ser(473)-phospho-Akt expression with concomitant rises in eNOS phosphorylation at Ser(1177); these effects were blocked by LY-2940002.	Lysine	156-158	nitric oxide synthase 3	Homo sapiens	91-95
19385062-0	2009	Forskolin increases angiogenesis through the coordinated cross-talk of  PKA-dependent VEGF expression and Epac-mediated PI3K/Akt/eNOS signaling.	Colforsin	0-9	nitric oxide synthase 3	Homo sapiens	129-133
19385062-3	2009	Forskolin stimulated angiogenesis of human endothelial cells and in vivo neovascularization, which was accompanied by phosphorylation of CREB, ERK, Akt, and endothelial nitric oxide synthase (eNOS) as well as NO production and VEGF expression.	Colforsin	0-9	nitric oxide synthase 3	Homo sapiens	157-190
19385062-3	2009	Forskolin stimulated angiogenesis of human endothelial cells and in vivo neovascularization, which was accompanied by phosphorylation of CREB, ERK, Akt, and endothelial nitric oxide synthase (eNOS) as well as NO production and VEGF expression.	Colforsin	0-9	nitric oxide synthase 3	Homo sapiens	192-196
19385062-5	2009	The forskolin-induced Akt/eNOS/NO pathway was completely inhibited by the phosphatidylinositol 3-kinase (PI3K) inhibitor LY294002, but not significantly suppressed by PKI.	Colforsin	4-13	nitric oxide synthase 3	Homo sapiens	26-30
19385062-5	2009	The forskolin-induced Akt/eNOS/NO pathway was completely inhibited by the phosphatidylinositol 3-kinase (PI3K) inhibitor LY294002, but not significantly suppressed by PKI.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	121-129	nitric oxide synthase 3	Homo sapiens	26-30
19385062-7	2009	The exchange protein directly activated by cAMP (Epac) activator, 8CPT-2Me-cAMP, promoted the Akt/eNOS/NO pathway and ERK phosphorylation,but did not induce CREB phosphorylation and VEGF expression.	Cyclic AMP	43-47	nitric oxide synthase 3	Homo sapiens	98-102
19385062-7	2009	The exchange protein directly activated by cAMP (Epac) activator, 8CPT-2Me-cAMP, promoted the Akt/eNOS/NO pathway and ERK phosphorylation,but did not induce CREB phosphorylation and VEGF expression.	8cpt-2me	66-74	nitric oxide synthase 3	Homo sapiens	98-102
19385062-7	2009	The exchange protein directly activated by cAMP (Epac) activator, 8CPT-2Me-cAMP, promoted the Akt/eNOS/NO pathway and ERK phosphorylation,but did not induce CREB phosphorylation and VEGF expression.	Cyclic AMP	75-79	nitric oxide synthase 3	Homo sapiens	98-102
19111531-1	2009	OBJECTIVES: Nitric oxide (NO) produced by endothelial nitric oxide synthase (eNOS) mediates endothelium-dependent vasodilatation and antithrombotic action.	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	42-75
19111531-1	2009	OBJECTIVES: Nitric oxide (NO) produced by endothelial nitric oxide synthase (eNOS) mediates endothelium-dependent vasodilatation and antithrombotic action.	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	77-81
19490210-2	2009	Endothelium-derived NO is formed from L-arginine by endothelial NO synthase (eNOS), and earlier studies have provided evidence for altered NO metabolism and impaired endothelial function in diabetes, probably due to polymorphisms in eNOS gene.	Arginine	38-48	nitric oxide synthase 3	Homo sapiens	77-81
19490210-2	2009	Endothelium-derived NO is formed from L-arginine by endothelial NO synthase (eNOS), and earlier studies have provided evidence for altered NO metabolism and impaired endothelial function in diabetes, probably due to polymorphisms in eNOS gene.	Arginine	38-48	nitric oxide synthase 3	Homo sapiens	233-237
18624763-0	2009	Lysophosphatidylcholine up-regulates human endothelial nitric oxide synthase gene transactivity by c-Jun N-terminal kinase signalling pathway.	Lysophosphatidylcholines	0-23	nitric oxide synthase 3	Homo sapiens	43-76
18624763-4	2009	In this study, eNOS gene transactivity in human umbilical vein endothelial cells was up-regulated by stimulation of lysophosphatidylcholine (LPC).	Lysophosphatidylcholines	116-139	nitric oxide synthase 3	Homo sapiens	15-19
18624763-4	2009	In this study, eNOS gene transactivity in human umbilical vein endothelial cells was up-regulated by stimulation of lysophosphatidylcholine (LPC).	Lysophosphatidylcholines	141-144	nitric oxide synthase 3	Homo sapiens	15-19
19513607-0	2009	Simvastatin increases the activity of endothelial nitric oxide synthase via enhancing phosphorylation.	Simvastatin	0-11	nitric oxide synthase 3	Homo sapiens	38-71
19513607-3	2009	In the present study, we investigated if simvastatin increases eNOS activity through its phosphorylation in 293 cells (293-eNOS) with stable expression of eNOS.	Simvastatin	41-52	nitric oxide synthase 3	Homo sapiens	63-67
19320461-2	2009	Central to endothelial dysfunction is a decrease in the bioavailability of nitric oxide (NO) synthesized by endothelial NO synthase (NOS-3).	Nitric Oxide	75-87	nitric oxide synthase 3	Homo sapiens	133-138
19398669-8	2009	Both MTHFR genotype and vascular 5-MTHF were associated with vascular nitric oxide bioavailability and superoxide generated by uncoupled endothelial nitric oxide synthase.	5-methyltetrahydrofolate	33-39	nitric oxide synthase 3	Homo sapiens	137-170
19398669-8	2009	Both MTHFR genotype and vascular 5-MTHF were associated with vascular nitric oxide bioavailability and superoxide generated by uncoupled endothelial nitric oxide synthase.	Superoxides	103-113	nitric oxide synthase 3	Homo sapiens	137-170
19398669-11	2009	Vascular 5-MTHF, rather than plasma or vascular homocysteine, is a key regulator of endothelial nitric oxide synthase coupling and nitric oxide bioavailability in human vessels, suggesting that plasma homocysteine is an indirect marker of 5-MTHF rather than a primary regulator of endothelial function.	5-methyltetrahydrofolate	9-15	nitric oxide synthase 3	Homo sapiens	84-117
18849028-1	2009	Diminished levels of L-arginine and endothelial nitric oxide synthase (eNOS) uncoupling through deficiency of tetrahydrobiopterin (BH(4)) may contribute to endothelial dysfunction.	sapropterin	110-129	nitric oxide synthase 3	Homo sapiens	36-69
19297385-0	2009	Association of plasma asymmetrical dimethylarginine (ADMA) with elevated vascular superoxide production and endothelial nitric oxide synthase uncoupling: implications for endothelial function in human atherosclerosis.	dimethylarginine	35-51	nitric oxide synthase 3	Homo sapiens	108-141
19297385-0	2009	Association of plasma asymmetrical dimethylarginine (ADMA) with elevated vascular superoxide production and endothelial nitric oxide synthase uncoupling: implications for endothelial function in human atherosclerosis.	N,N-dimethylarginine	53-57	nitric oxide synthase 3	Homo sapiens	108-141
19297385-1	2009	BACKGROUND: Asymmetrical dimethylarginine (ADMA), an endogenous inhibitor of endothelial nitric oxide synthase (eNOS), is considered to be a risk factor for atherosclerosis.	dimethylarginine	25-41	nitric oxide synthase 3	Homo sapiens	77-110
19297385-1	2009	BACKGROUND: Asymmetrical dimethylarginine (ADMA), an endogenous inhibitor of endothelial nitric oxide synthase (eNOS), is considered to be a risk factor for atherosclerosis.	N,N-dimethylarginine	43-47	nitric oxide synthase 3	Homo sapiens	77-110
19210708-9	2009	BCN induced massive penile hypoxia, decreased muscle/fiber ratio, nNOS, eNOS, PDE5 expression, increased sensitivity to the nitric oxide donor, sodium nitroprusside (SNP), and reduced the relaxant response to acetylcholine (Ach), as well as unresponsiveness to acute Tad dosing.	bcn	0-3	nitric oxide synthase 3	Homo sapiens	72-76
19332631-3	2009	Endothelial dysfunction can be assessed by quantifying plasma asymmetric dimethylarginine (ADMA), an endogenous inhibitor of endothelial nitric oxide synthase.	dimethylarginine	73-89	nitric oxide synthase 3	Homo sapiens	125-158
19332631-3	2009	Endothelial dysfunction can be assessed by quantifying plasma asymmetric dimethylarginine (ADMA), an endogenous inhibitor of endothelial nitric oxide synthase.	N,N-dimethylarginine	91-95	nitric oxide synthase 3	Homo sapiens	125-158
19473288-8	2009	The frequency of the eNOS gene intron 4 genotype was found as bb: 55 (67.1%), ab: 26 (31.7%), and aa: 1 (1.2%) in the controls and bb: 43 (67.2%), ab: 19 (29.7%), and aa: 2 (3.1%) in the patient group.	boeravinone B	62-64	nitric oxide synthase 3	Homo sapiens	21-25
19342481-5	2009	We also observed that anchoring caveolar eNOS to the plasma membrane uncouples eNOS phosphorylation at Ser-1177 from NO production.	Serine	103-106	nitric oxide synthase 3	Homo sapiens	41-45
19342481-5	2009	We also observed that anchoring caveolar eNOS to the plasma membrane uncouples eNOS phosphorylation at Ser-1177 from NO production.	Serine	103-106	nitric oxide synthase 3	Homo sapiens	79-83
19342481-7	2009	PAF induced Ser-1177-eNOS phosphorylation in ECV-CD8eNOSGFP and CVEC transfected with dyn2K44A, but it dephosphorylated eNOS at Ser-1177 in CVEC transfected with cav1Y14F.	Platelet Activating Factor	0-3	nitric oxide synthase 3	Homo sapiens	21-25
19342481-7	2009	PAF induced Ser-1177-eNOS phosphorylation in ECV-CD8eNOSGFP and CVEC transfected with dyn2K44A, but it dephosphorylated eNOS at Ser-1177 in CVEC transfected with cav1Y14F.	Platelet Activating Factor	0-3	nitric oxide synthase 3	Homo sapiens	52-56
19342481-7	2009	PAF induced Ser-1177-eNOS phosphorylation in ECV-CD8eNOSGFP and CVEC transfected with dyn2K44A, but it dephosphorylated eNOS at Ser-1177 in CVEC transfected with cav1Y14F.	Serine	12-15	nitric oxide synthase 3	Homo sapiens	21-25
19342481-7	2009	PAF induced Ser-1177-eNOS phosphorylation in ECV-CD8eNOSGFP and CVEC transfected with dyn2K44A, but it dephosphorylated eNOS at Ser-1177 in CVEC transfected with cav1Y14F.	Serine	12-15	nitric oxide synthase 3	Homo sapiens	52-56
19096000-5	2009	Medroxyprogesterone acetate (MPA), progesterone, levonorgestrel, and nomegestrol acetate prevented the 17beta-estradiol (17beta-E)-induced expression of eNOS mRNA and protein.	Medroxyprogesterone Acetate	0-27	nitric oxide synthase 3	Homo sapiens	153-157
19096000-5	2009	Medroxyprogesterone acetate (MPA), progesterone, levonorgestrel, and nomegestrol acetate prevented the 17beta-estradiol (17beta-E)-induced expression of eNOS mRNA and protein.	Medroxyprogesterone Acetate	29-32	nitric oxide synthase 3	Homo sapiens	153-157
19096000-5	2009	Medroxyprogesterone acetate (MPA), progesterone, levonorgestrel, and nomegestrol acetate prevented the 17beta-estradiol (17beta-E)-induced expression of eNOS mRNA and protein.	Progesterone	7-19	nitric oxide synthase 3	Homo sapiens	153-157
19096000-5	2009	Medroxyprogesterone acetate (MPA), progesterone, levonorgestrel, and nomegestrol acetate prevented the 17beta-estradiol (17beta-E)-induced expression of eNOS mRNA and protein.	Levonorgestrel	49-63	nitric oxide synthase 3	Homo sapiens	153-157
19096000-5	2009	Medroxyprogesterone acetate (MPA), progesterone, levonorgestrel, and nomegestrol acetate prevented the 17beta-estradiol (17beta-E)-induced expression of eNOS mRNA and protein.	nomegestrol acetate	69-88	nitric oxide synthase 3	Homo sapiens	153-157
19096000-5	2009	Medroxyprogesterone acetate (MPA), progesterone, levonorgestrel, and nomegestrol acetate prevented the 17beta-estradiol (17beta-E)-induced expression of eNOS mRNA and protein.	Estradiol	103-119	nitric oxide synthase 3	Homo sapiens	153-157
19096000-9	2009	CONCLUSIONS: Certain progestins, including MPA, attenuate the 17beta-E-induced NO-mediated inhibition of platelet aggregation by endothelial cells through preventing both eNOS and GTPCH I expression most likely via activation of glucocorticoid receptors.	Estradiol	62-70	nitric oxide synthase 3	Homo sapiens	171-175
19176602-1	2009	AIMS: The requirement of endothelial NO synthase (NOS3) calcium to produce NO is well described, although the effect of NO on intracellular calcium levels [Ca(2+)](i) is still confusing.	Calcium	56-63	nitric oxide synthase 3	Homo sapiens	50-54
19176602-4	2009	Activity of NOS3 was characterized by conversion of arginine to citrulline, BH(4) intracellular availability, cGMP, and superoxide anion production.	Arginine	52-60	nitric oxide synthase 3	Homo sapiens	12-16
19176602-4	2009	Activity of NOS3 was characterized by conversion of arginine to citrulline, BH(4) intracellular availability, cGMP, and superoxide anion production.	Citrulline	64-74	nitric oxide synthase 3	Homo sapiens	12-16
19176602-4	2009	Activity of NOS3 was characterized by conversion of arginine to citrulline, BH(4) intracellular availability, cGMP, and superoxide anion production.	Cyclic GMP	110-114	nitric oxide synthase 3	Homo sapiens	12-16
19176602-4	2009	Activity of NOS3 was characterized by conversion of arginine to citrulline, BH(4) intracellular availability, cGMP, and superoxide anion production.	Superoxides	120-136	nitric oxide synthase 3	Homo sapiens	12-16
19176602-7	2009	In aged cells with an uncoupled NOS3 as shown by the reduced BH(4) level, the increase in superoxide anion and the lower production of cGMP and the decrease in NO bioavailability were linearly correlated with the increase in basal [Ca(2+)](i).	Superoxides	90-106	nitric oxide synthase 3	Homo sapiens	32-36
19176602-7	2009	In aged cells with an uncoupled NOS3 as shown by the reduced BH(4) level, the increase in superoxide anion and the lower production of cGMP and the decrease in NO bioavailability were linearly correlated with the increase in basal [Ca(2+)](i).	Cyclic GMP	135-139	nitric oxide synthase 3	Homo sapiens	32-36
19165164-7	2009	However, the expression levels of two transcripts involved in vasodilation (natriuretic peptide receptor A/guanylate cyclase A (NPRA) and endothelial nitric oxide synthase (eNOS)) were positively associated with postprandial ATBF (r = 0.53 and r = 0.55, P &lt; 0.01, respectively).	atbf	225-229	nitric oxide synthase 3	Homo sapiens	138-171
19203270-2	2009	Six compounds were found to be selective for iNOS over endothelial nitric oxide synthase (eNOS), and among them, the most active and selective compound was the N-benzylacetamidine 2.	n-benzylacetamidine	160-179	nitric oxide synthase 3	Homo sapiens	55-88
19118090-9	2009	Finally, we found that mutating the STAT3 binding site sequence within the eNOS promoter increased promoter activity in response to shear and that this was no longer inhibited by bryostatin.	Bryostatins	179-189	nitric oxide synthase 3	Homo sapiens	75-79
19218343-5	2009	Five HAART drugs (ritonavir, indinavir, lamivudine, abacavir, and AZT) significantly decreased endothelial nitric oxide synthase (eNOS) expression and increased superoxide anion levels in both vessels and HPAECs.	Ritonavir	18-27	nitric oxide synthase 3	Homo sapiens	95-128
19218343-5	2009	Five HAART drugs (ritonavir, indinavir, lamivudine, abacavir, and AZT) significantly decreased endothelial nitric oxide synthase (eNOS) expression and increased superoxide anion levels in both vessels and HPAECs.	Ritonavir	18-27	nitric oxide synthase 3	Homo sapiens	130-134
19218343-5	2009	Five HAART drugs (ritonavir, indinavir, lamivudine, abacavir, and AZT) significantly decreased endothelial nitric oxide synthase (eNOS) expression and increased superoxide anion levels in both vessels and HPAECs.	Indinavir	29-38	nitric oxide synthase 3	Homo sapiens	95-128
19218343-5	2009	Five HAART drugs (ritonavir, indinavir, lamivudine, abacavir, and AZT) significantly decreased endothelial nitric oxide synthase (eNOS) expression and increased superoxide anion levels in both vessels and HPAECs.	Indinavir	29-38	nitric oxide synthase 3	Homo sapiens	130-134
19218343-5	2009	Five HAART drugs (ritonavir, indinavir, lamivudine, abacavir, and AZT) significantly decreased endothelial nitric oxide synthase (eNOS) expression and increased superoxide anion levels in both vessels and HPAECs.	Lamivudine	40-50	nitric oxide synthase 3	Homo sapiens	95-128
19218343-5	2009	Five HAART drugs (ritonavir, indinavir, lamivudine, abacavir, and AZT) significantly decreased endothelial nitric oxide synthase (eNOS) expression and increased superoxide anion levels in both vessels and HPAECs.	Lamivudine	40-50	nitric oxide synthase 3	Homo sapiens	130-134
19218343-5	2009	Five HAART drugs (ritonavir, indinavir, lamivudine, abacavir, and AZT) significantly decreased endothelial nitric oxide synthase (eNOS) expression and increased superoxide anion levels in both vessels and HPAECs.	abacavir	52-60	nitric oxide synthase 3	Homo sapiens	95-128
19218343-5	2009	Five HAART drugs (ritonavir, indinavir, lamivudine, abacavir, and AZT) significantly decreased endothelial nitric oxide synthase (eNOS) expression and increased superoxide anion levels in both vessels and HPAECs.	abacavir	52-60	nitric oxide synthase 3	Homo sapiens	130-134
19218343-5	2009	Five HAART drugs (ritonavir, indinavir, lamivudine, abacavir, and AZT) significantly decreased endothelial nitric oxide synthase (eNOS) expression and increased superoxide anion levels in both vessels and HPAECs.	Zidovudine	66-69	nitric oxide synthase 3	Homo sapiens	95-128
19218343-5	2009	Five HAART drugs (ritonavir, indinavir, lamivudine, abacavir, and AZT) significantly decreased endothelial nitric oxide synthase (eNOS) expression and increased superoxide anion levels in both vessels and HPAECs.	Zidovudine	66-69	nitric oxide synthase 3	Homo sapiens	130-134
19218343-7	2009	Additionally, the antioxidants ginsenoside Rb1 and ginkgolide A effectively reversed HAART drug-induced vasomotor dysfunction and eNOS down-regulation.	ginkgolide A	51-63	nitric oxide synthase 3	Homo sapiens	130-134
19218343-8	2009	Inhibition of ERK1/2 also partially blocked ritonavir- and AZT-induced down-regulation of eNOS and vasomotor dysfunction.	Ritonavir	44-53	nitric oxide synthase 3	Homo sapiens	90-94
19218343-8	2009	Inhibition of ERK1/2 also partially blocked ritonavir- and AZT-induced down-regulation of eNOS and vasomotor dysfunction.	Zidovudine	59-62	nitric oxide synthase 3	Homo sapiens	90-94
19153832-0	2009	N-acetyl cysteine enhances imatinib-induced apoptosis of Bcr-Abl+ cells by endothelial nitric oxide synthase-mediated production of nitric oxide.	Acetylcysteine	0-17	nitric oxide synthase 3	Homo sapiens	75-108
19153832-0	2009	N-acetyl cysteine enhances imatinib-induced apoptosis of Bcr-Abl+ cells by endothelial nitric oxide synthase-mediated production of nitric oxide.	Imatinib Mesylate	27-35	nitric oxide synthase 3	Homo sapiens	75-108
19153832-9	2009	Co-treatment with NAC leads to enhanced production of nitric oxide (NO) by endothelial nitric oxide synthase (eNOS).	Acetylcysteine	18-21	nitric oxide synthase 3	Homo sapiens	75-108
19153832-9	2009	Co-treatment with NAC leads to enhanced production of nitric oxide (NO) by endothelial nitric oxide synthase (eNOS).	Nitric Oxide	54-66	nitric oxide synthase 3	Homo sapiens	75-108
19153832-12	2009	CONCLUSION: NAC enhances imatinib-induced apoptosis of Bcr-Abl(+) cells by endothelial nitric oxide synthase-mediated production of nitric oxide.	Acetylcysteine	12-15	nitric oxide synthase 3	Homo sapiens	75-108
19153832-12	2009	CONCLUSION: NAC enhances imatinib-induced apoptosis of Bcr-Abl(+) cells by endothelial nitric oxide synthase-mediated production of nitric oxide.	Imatinib Mesylate	25-33	nitric oxide synthase 3	Homo sapiens	75-108
19036824-0	2009	Norfuraneol dephosphorylates eNOS at threonine 495 and enhances eNOS activity in human endothelial cells.	4-hydroxy-5-methyl-3(2H)-furanone	0-11	nitric oxide synthase 3	Homo sapiens	29-33
19036824-0	2009	Norfuraneol dephosphorylates eNOS at threonine 495 and enhances eNOS activity in human endothelial cells.	4-hydroxy-5-methyl-3(2H)-furanone	0-11	nitric oxide synthase 3	Homo sapiens	64-68
19036824-0	2009	Norfuraneol dephosphorylates eNOS at threonine 495 and enhances eNOS activity in human endothelial cells.	Threonine	37-46	nitric oxide synthase 3	Homo sapiens	29-33
19105596-0	2009	Hydrogen peroxide decreases endothelial nitric oxide synthase promoter activity through the inhibition of Sp1 activity.	Hydrogen Peroxide	0-17	nitric oxide synthase 3	Homo sapiens	28-61
19105596-1	2009	We have previously shown that endothelial nitric oxide synthase (eNOS) promoter activity is decreased in endothelial cells in response to the addition of hydrogen peroxide (H(2)O(2)), and this involves, at least in part, the inhibition of AP-1 activity.	Hydrogen Peroxide	154-171	nitric oxide synthase 3	Homo sapiens	30-63
19105596-1	2009	We have previously shown that endothelial nitric oxide synthase (eNOS) promoter activity is decreased in endothelial cells in response to the addition of hydrogen peroxide (H(2)O(2)), and this involves, at least in part, the inhibition of AP-1 activity.	Hydrogen Peroxide	154-171	nitric oxide synthase 3	Homo sapiens	65-69
19105596-3	2009	Our initial experiments indicated that although H(2)O(2) treatment increased eNOS mRNA levels in ovine pulmonary arterial endothelial cells (OPAECs), there was a significant decrease in the promoter activity of an eNOS promoter construct containing 840 bp of upstream sequence.	Hydrogen Peroxide	48-56	nitric oxide synthase 3	Homo sapiens	77-81
20108211-8	2009	Serine-1177-specific phosphorylation of NO synthase type 3 (NOS-3) and phosphorylation of protein kinase Akt were determined in platelets by Western blotting.	Serine	0-6	nitric oxide synthase 3	Homo sapiens	40-65
20108211-11	2009	It also increased NOS-3 phosphorylation on serine-1177, and increased Akt serine phosphorylation.	Serine	43-49	nitric oxide synthase 3	Homo sapiens	18-23
18974424-18	2009	These findings suggest the following: 1) elements responsible for PAL include endothelial nitric oxide synthase, soluble guanylate cyclase, and type II protein kinase G; 2) the resting state of the nitric oxide/cGMP/protein kinase G pathway is a determinant of acrosomal status; 3) PPCM and nitric oxide donors induce acrosomal loss via nitric oxide, but through independent pathways; and 4) covalent attachment of a nitric oxide donor to PPCM provides synergistic efficacy as a stimulus of acrosomal loss.	Nitric Oxide	198-210	nitric oxide synthase 3	Homo sapiens	78-111
18974424-18	2009	These findings suggest the following: 1) elements responsible for PAL include endothelial nitric oxide synthase, soluble guanylate cyclase, and type II protein kinase G; 2) the resting state of the nitric oxide/cGMP/protein kinase G pathway is a determinant of acrosomal status; 3) PPCM and nitric oxide donors induce acrosomal loss via nitric oxide, but through independent pathways; and 4) covalent attachment of a nitric oxide donor to PPCM provides synergistic efficacy as a stimulus of acrosomal loss.	Nitric Oxide	198-210	nitric oxide synthase 3	Homo sapiens	78-111
19247195-5	2009	Functional analysis showed that thymosin beta4-induced EPC migration was blocked by phosphatidylinositol 3-kinase inhibitors (LY294002 or wortmannin) or eNOS inhibitor (Nomega-nitro-L-arginine methyl ester) but was not significantly attenuated by mitogen-activated protein kinase (MAPK)/ERK inhibitor (PD98059).	NG-Nitroarginine Methyl Ester	169-205	nitric oxide synthase 3	Homo sapiens	153-157
19176751-0	2009	Salt inactivates endothelial nitric oxide synthase in endothelial cells.	Salts	0-4	nitric oxide synthase 3	Homo sapiens	17-50
19176751-2	2009	In this study, we used 3 independent assays to determine whether such a small increase in sodium concentrations per se alters endothelial nitric oxide synthase (eNOS) function and contributes to hypertension.	Sodium	90-96	nitric oxide synthase 3	Homo sapiens	126-159
19176751-2	2009	In this study, we used 3 independent assays to determine whether such a small increase in sodium concentrations per se alters endothelial nitric oxide synthase (eNOS) function and contributes to hypertension.	Sodium	90-96	nitric oxide synthase 3	Homo sapiens	161-165
19176751-6	2009	Using Chinese hamster ovary cells stably expressing eNOS, we confirmed the inhibitory effects of salt on eNOS activity.	Salts	97-101	nitric oxide synthase 3	Homo sapiens	52-56
19176751-6	2009	Using Chinese hamster ovary cells stably expressing eNOS, we confirmed the inhibitory effects of salt on eNOS activity.	Salts	97-101	nitric oxide synthase 3	Homo sapiens	105-109
19176751-10	2009	In conclusion, our findings demonstrated that eNOS is sensitive to changes in salt concentration.	Salts	78-82	nitric oxide synthase 3	Homo sapiens	46-50
19176751-11	2009	A 5-mmol/L rise in salt concentration, within the range observed in essential hypertension patients or in individuals with high salt intake, could significantly suppress eNOS activity.	Salts	19-23	nitric oxide synthase 3	Homo sapiens	170-174
19176751-11	2009	A 5-mmol/L rise in salt concentration, within the range observed in essential hypertension patients or in individuals with high salt intake, could significantly suppress eNOS activity.	Salts	128-132	nitric oxide synthase 3	Homo sapiens	170-174
19052844-1	2009	Nitric oxide (NO) produced by the action of endothelial nitric oxide synthase (eNOS) plays an important role in the regulation of vascular tone, cell survival, and angiogenesis.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	44-77
19537035-10	2009	In the AD group, the platelet-derived nitric oxide level was positively correlated with the activity level of eNOS (r = 0.326, P < 0.05).	Nitric Oxide	38-50	nitric oxide synthase 3	Homo sapiens	110-114
19011239-0	2009	Quantitative regulation of intracellular endothelial nitric-oxide synthase (eNOS) coupling by both tetrahydrobiopterin-eNOS stoichiometry and biopterin redox status: insights from cells with tet-regulated GTP cyclohydrolase I expression.	sapropterin	99-118	nitric oxide synthase 3	Homo sapiens	41-74
19011239-0	2009	Quantitative regulation of intracellular endothelial nitric-oxide synthase (eNOS) coupling by both tetrahydrobiopterin-eNOS stoichiometry and biopterin redox status: insights from cells with tet-regulated GTP cyclohydrolase I expression.	sapropterin	99-118	nitric oxide synthase 3	Homo sapiens	76-80
19011239-0	2009	Quantitative regulation of intracellular endothelial nitric-oxide synthase (eNOS) coupling by both tetrahydrobiopterin-eNOS stoichiometry and biopterin redox status: insights from cells with tet-regulated GTP cyclohydrolase I expression.	Biopterin	109-118	nitric oxide synthase 3	Homo sapiens	41-74
19011239-0	2009	Quantitative regulation of intracellular endothelial nitric-oxide synthase (eNOS) coupling by both tetrahydrobiopterin-eNOS stoichiometry and biopterin redox status: insights from cells with tet-regulated GTP cyclohydrolase I expression.	Biopterin	109-118	nitric oxide synthase 3	Homo sapiens	76-80
19011239-0	2009	Quantitative regulation of intracellular endothelial nitric-oxide synthase (eNOS) coupling by both tetrahydrobiopterin-eNOS stoichiometry and biopterin redox status: insights from cells with tet-regulated GTP cyclohydrolase I expression.	tetramethylenedisulfotetramine	99-102	nitric oxide synthase 3	Homo sapiens	41-74
19011239-0	2009	Quantitative regulation of intracellular endothelial nitric-oxide synthase (eNOS) coupling by both tetrahydrobiopterin-eNOS stoichiometry and biopterin redox status: insights from cells with tet-regulated GTP cyclohydrolase I expression.	tetramethylenedisulfotetramine	99-102	nitric oxide synthase 3	Homo sapiens	76-80
19011239-1	2009	Tetrahydrobiopterin (BH4) is a critical determinant of endothelial nitric-oxide synthase (eNOS) activity.	sapropterin	0-19	nitric oxide synthase 3	Homo sapiens	55-88
19011239-1	2009	Tetrahydrobiopterin (BH4) is a critical determinant of endothelial nitric-oxide synthase (eNOS) activity.	sapropterin	0-19	nitric oxide synthase 3	Homo sapiens	90-94
19011239-1	2009	Tetrahydrobiopterin (BH4) is a critical determinant of endothelial nitric-oxide synthase (eNOS) activity.	sapropterin	21-24	nitric oxide synthase 3	Homo sapiens	55-88
19011239-1	2009	Tetrahydrobiopterin (BH4) is a critical determinant of endothelial nitric-oxide synthase (eNOS) activity.	sapropterin	21-24	nitric oxide synthase 3	Homo sapiens	90-94
19011239-2	2009	In the absence of BH4, eNOS becomes "uncoupled" and generates superoxide rather than NO.	sapropterin	18-21	nitric oxide synthase 3	Homo sapiens	23-27
19011239-2	2009	In the absence of BH4, eNOS becomes "uncoupled" and generates superoxide rather than NO.	Superoxides	62-72	nitric oxide synthase 3	Homo sapiens	23-27
19038867-7	2009	AKT, AMP-dependent kinase (AMPK), and endothelial nitric oxide synthase (eNOS)(s1179) phosphorylations in VEGF-stimulated endothelial cells were markedly enhanced, which were however significantly attenuated by either ALLN, Calpeptin, or ezrin small interfering RNA, as well as by Wortmannin or compound C (respectively for phosphatidylinositol 3-kinase [PI3K] or AMPK).	Wortmannin	281-291	nitric oxide synthase 3	Homo sapiens	73-77
19227443-3	2009	Effects of additional O2*- production from dysfunctional endothelial nitric oxide synthase (eNOS) were also simulated.	o2*	22-25	nitric oxide synthase 3	Homo sapiens	57-90
19546528-7	2009	The simultaneous presence of the DD and GG variants of the ACE and eNOS genes was related to an unfavorable outcome as compared with other combinations [hazard ratio ranging from 4.7 (95% CI 1.52-14.33) to 8.4 (95% CI 2.45-29.10)] after controlling for proteinuria, mean arterial pressure and baseline histological lesions.	Fumigant 93	33-35	nitric oxide synthase 3	Homo sapiens	67-71
18162361-3	2009	Rosuvastatin rapidly phosphorylated Akt and endothelial nitric oxide synthase (eNOS) in human endothelial cells.	Rosuvastatin Calcium	0-12	nitric oxide synthase 3	Homo sapiens	44-77
19407362-5	2009	We examined the impact of the -949 A/G, the -716 C/T and the Glu298Asp polymorphisms in the NOS3 gene on the risk of clinical restenosis in a previously described subpopulation of the GENDER-study, a multicenter prospective study design that enrolled consecutive patients after successful PCI.	Tetrahydrocortisone	12-15	nitric oxide synthase 3	Homo sapiens	92-96
19287060-4	2009	The objective of the present study was to determine the presence of genotype frequencies of Glu298--&gt;Asp (G894T) single nucleotide polymorphism in the eNOS gene among south Indian male Tamil speaking population.	Aspartic Acid	104-107	nitric oxide synthase 3	Homo sapiens	154-158
19287060-5	2009	METHODS: Polymerase chain reaction and restriction fragmant analysis was done to detect the presence of Glu298--&gt;Asp (G894T) variant of the eNOS gene in 105 healthy male volunteers.	Aspartic Acid	116-119	nitric oxide synthase 3	Homo sapiens	143-147
20445800-5	2009	As hypothesized, patients carrying low ROS producing eNOS Glu298Asp asparagine allele showed an increased hazard of death compared to homozygous carriers of the glutamine allele (hazard ratio (HR): 2.10, 95% confidence interval (CI): 1.01-4.38).	Reactive Oxygen Species	39-42	nitric oxide synthase 3	Homo sapiens	53-57
20445800-5	2009	As hypothesized, patients carrying low ROS producing eNOS Glu298Asp asparagine allele showed an increased hazard of death compared to homozygous carriers of the glutamine allele (hazard ratio (HR): 2.10, 95% confidence interval (CI): 1.01-4.38).	Asparagine	68-78	nitric oxide synthase 3	Homo sapiens	53-57
19028051-12	2009	Homocysteine significantly reduced eNOS expression, whereas ghrelin cotreatment effectively restored eNOS expression to the control levels.	Homocysteine	0-12	nitric oxide synthase 3	Homo sapiens	35-39
19028051-12	2009	Homocysteine significantly reduced eNOS expression, whereas ghrelin cotreatment effectively restored eNOS expression to the control levels.	Ghrelin	60-67	nitric oxide synthase 3	Homo sapiens	101-105
19028051-14	2009	Ghrelin also effectively blocked the Hcy-induced decrease of eNOS protein levels in HCAECs in a concentration-dependent manner.	Ghrelin	0-7	nitric oxide synthase 3	Homo sapiens	61-65
19028051-14	2009	Ghrelin also effectively blocked the Hcy-induced decrease of eNOS protein levels in HCAECs in a concentration-dependent manner.	Homocysteine	37-40	nitric oxide synthase 3	Homo sapiens	61-65
19028051-16	2009	CONCLUSION: Ghrelin has a protective effect in the porcine coronary artery by blocking Hcy-induced endothelial dysfunction, improving eNOS expression, and reducing oxidative stress.	Ghrelin	12-19	nitric oxide synthase 3	Homo sapiens	134-138
19028051-17	2009	Ghrelin also shows a protective effect on HCACEs from the Hcy-induced decrease in eNOS protein levels.	Ghrelin	0-7	nitric oxide synthase 3	Homo sapiens	82-86
19028051-17	2009	Ghrelin also shows a protective effect on HCACEs from the Hcy-induced decrease in eNOS protein levels.	hcaces	42-48	nitric oxide synthase 3	Homo sapiens	82-86
19028051-17	2009	Ghrelin also shows a protective effect on HCACEs from the Hcy-induced decrease in eNOS protein levels.	Homocysteine	58-61	nitric oxide synthase 3	Homo sapiens	82-86
19155632-7	2009	It also caused phosphorylation of Akt and eNOS, which were prevented by MnTMPyP, polyethyleneglycol catalase, PP2, wortmannin and LY294002.	Wortmannin	115-125	nitric oxide synthase 3	Homo sapiens	42-46
19468800-0	2009	Therapeutic approach against intimal hyperplasia of vein grafts through endothelial nitric oxide synthase/nitric oxide (eNOS/NO) and the Rho/Rho-kinase pathway.	Nitric Oxide	84-96	nitric oxide synthase 3	Homo sapiens	120-124
19468800-2	2009	Endothelial nitric oxide synthase (eNOS) is an enzyme that synthesizes nitric oxide (NO).	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	35-39
18790993-10	2008	Thus therapies designed to decrease oxidative stress and restore eNOS coupling, such as rhSOD, may prove useful in the treatment of PPHN in newborn infants.	pphn	132-136	nitric oxide synthase 3	Homo sapiens	65-69
18925469-3	2008	Nitric oxide (NO) derived from endothelial nitric oxide synthase (eNOS) is an important regulator of angiogenesis.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	31-64
18925469-3	2008	Nitric oxide (NO) derived from endothelial nitric oxide synthase (eNOS) is an important regulator of angiogenesis.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	66-70
18925469-10	2008	NG-nitro-L-arginine-methyl-ester (L-NAME) and L-N5-(1-lminoethyl)ornithine,dihydochloride (L-NIO) (specific inhibitors of eNOS) also abolished HB-EGF-induced HUVEC migration and angiogenesis.	NG-Nitroarginine Methyl Ester	0-32	nitric oxide synthase 3	Homo sapiens	122-126
18925469-10	2008	NG-nitro-L-arginine-methyl-ester (L-NAME) and L-N5-(1-lminoethyl)ornithine,dihydochloride (L-NIO) (specific inhibitors of eNOS) also abolished HB-EGF-induced HUVEC migration and angiogenesis.	l-n5-(1-lminoethyl)ornithine	46-74	nitric oxide synthase 3	Homo sapiens	122-126
18941922-4	2008	Endothelium-derived nitric oxide (eNO), produced by eNO synthase (eNOS), is a key regulator of vessel wall function and cardiovascular homeostasis.	Nitric Oxide	20-32	nitric oxide synthase 3	Homo sapiens	52-64
18926858-0	2008	Autoinhibition of endothelial nitric oxide synthase (eNOS) in gut smooth muscle by nitric oxide.	Nitric Oxide	30-42	nitric oxide synthase 3	Homo sapiens	53-57
18926858-1	2008	Nitric oxide in the gut is produced by nNOS in enteric neurons and by eNOS in smooth muscle cells.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	70-74
18926858-3	2008	In the present study, we examined the effect of nitric oxide on VIP-induced eNOS activation in smooth muscle cells isolated from human intestine and rabbit stomach.	Nitric Oxide	48-60	nitric oxide synthase 3	Homo sapiens	76-80
18926858-10	2008	The results suggest that NO produced in smooth muscle cells as a result of the activation of eNOS by VIP exerts an autoinhibitory restraint on eNOS thereby regulating the balance of the VIP/cAMP/PKA and NO/cGMP/PKG pathways that regulate the relaxation of gut smooth muscle.	Cyclic GMP	206-210	nitric oxide synthase 3	Homo sapiens	93-97
18926858-10	2008	The results suggest that NO produced in smooth muscle cells as a result of the activation of eNOS by VIP exerts an autoinhibitory restraint on eNOS thereby regulating the balance of the VIP/cAMP/PKA and NO/cGMP/PKG pathways that regulate the relaxation of gut smooth muscle.	Cyclic GMP	206-210	nitric oxide synthase 3	Homo sapiens	143-147
18789310-5	2008	The PI3K inhibitor Wortmannin suppressed icariin-mediated angiogenesis and Akt and eNOS activation without affecting ERK phosphorylation.	Wortmannin	19-29	nitric oxide synthase 3	Homo sapiens	83-87
18789310-7	2008	These results suggest that icariin stimulated angiogenesis by activating the MEK/ERK- and PI3K/Akt/eNOS-dependent signal pathways and may be a useful drug for angiogenic therapy.	icariin	27-34	nitric oxide synthase 3	Homo sapiens	99-103
18718910-2	2008	We previously reported that DHEA has opposing actions in endothelial cells to stimulate phosphatidylinositol (PI) 3-kinase/Akt/endothelial nitric-oxide synthase leading to increased production of nitric oxide while simultaneously stimulating MAPK-dependent secretion of the vasoconstrictor ET-1.	Dehydroepiandrosterone	28-32	nitric oxide synthase 3	Homo sapiens	127-160
18718910-2	2008	We previously reported that DHEA has opposing actions in endothelial cells to stimulate phosphatidylinositol (PI) 3-kinase/Akt/endothelial nitric-oxide synthase leading to increased production of nitric oxide while simultaneously stimulating MAPK-dependent secretion of the vasoconstrictor ET-1.	Phosphatidylinositols	88-108	nitric oxide synthase 3	Homo sapiens	127-160
18658029-7	2008	Antioxidant seleno-l-methionine; chemical inhibitors of p38, ERK1/2, and mitochondrial complex II; as well as dominant negative mutant forms of IkappaBalpha and NOX4 effectively blocked sCD40L-induced eNOS down-regulation in HCAECs.	Selenomethionine	12-31	nitric oxide synthase 3	Homo sapiens	201-205
18622039-0	2008	Phosphorylation of endothelial nitric-oxide synthase regulates superoxide generation from the enzyme.	Superoxides	63-73	nitric oxide synthase 3	Homo sapiens	19-52
18786089-7	2008	When blood vessel and cultured endothelial cells from hypertensive animals are treated with nebivolol, there is a decrease in superoxide production and an increase in the expression and activity of endothelial NOS (eNOS).	Nebivolol	92-101	nitric oxide synthase 3	Homo sapiens	198-213
18667411-8	2008	Endothelial nitric-oxide synthase Ser-1177 did not change over the time period evaluated with breast or leiomyoma tissue.	Serine	34-37	nitric oxide synthase 3	Homo sapiens	0-33
18242654-4	2008	Disrupting the endothelium as well as blockade of endothelial NO synthase (eNOS) augmented aldosterone-induced vasoconstriction in this study.	Aldosterone	91-102	nitric oxide synthase 3	Homo sapiens	50-73
18242654-4	2008	Disrupting the endothelium as well as blockade of endothelial NO synthase (eNOS) augmented aldosterone-induced vasoconstriction in this study.	Aldosterone	91-102	nitric oxide synthase 3	Homo sapiens	75-79
18242654-9	2008	Co-infusion of the eNOS inhibitor N(G)-monomethyl-L-arginine (L-NMMA) changed the effect of aldosterone on renal hemodynamics.	omega-N-Methylarginine	34-60	nitric oxide synthase 3	Homo sapiens	19-23
18242654-9	2008	Co-infusion of the eNOS inhibitor N(G)-monomethyl-L-arginine (L-NMMA) changed the effect of aldosterone on renal hemodynamics.	omega-N-Methylarginine	62-68	nitric oxide synthase 3	Homo sapiens	19-23
18242654-9	2008	Co-infusion of the eNOS inhibitor N(G)-monomethyl-L-arginine (L-NMMA) changed the effect of aldosterone on renal hemodynamics.	Aldosterone	92-103	nitric oxide synthase 3	Homo sapiens	19-23
18617528-10	2008	Blocking Akt activation abolished the initial rise of eNOS Ser(1179) phosphorylation after H(2)O(2) treatment.	Serine	59-62	nitric oxide synthase 3	Homo sapiens	54-58
18617528-11	2008	In long term H(2)O(2)-treated cells where Akt was deactivated, significant amounts of Ser(1179)-phosphorylated eNOS remained.	Hydrogen Peroxide	13-21	nitric oxide synthase 3	Homo sapiens	111-115
18617528-11	2008	In long term H(2)O(2)-treated cells where Akt was deactivated, significant amounts of Ser(1179)-phosphorylated eNOS remained.	Serine	86-89	nitric oxide synthase 3	Homo sapiens	111-115
18617528-12	2008	AMPK inhibition eradicated the remaining eNOS Ser(1179) phosphorylation.	Serine	46-49	nitric oxide synthase 3	Homo sapiens	41-45
18617528-13	2008	Taken together, these studies revealed that Akt and AMPK orchestrated a bidirectional action on eNOS Ser(1179) phosphorylation in H(2)O(2)-treated cells.	Serine	101-104	nitric oxide synthase 3	Homo sapiens	96-100
18617528-13	2008	Taken together, these studies revealed that Akt and AMPK orchestrated a bidirectional action on eNOS Ser(1179) phosphorylation in H(2)O(2)-treated cells.	Hydrogen Peroxide	130-138	nitric oxide synthase 3	Homo sapiens	96-100
18617528-14	2008	Long term H(2)O(2) exposure decreased eNOS Ser(1179) phosphorylation, and this might account for the loss of eNOS function in cardiovascular diseases where chronic oxidative injury occurs.	Serine	43-46	nitric oxide synthase 3	Homo sapiens	38-42
18716321-0	2008	Targeted increases in endothelial cell superoxide anion production stimulate eNOS-dependent nitric oxide production, not uncoupled eNOS activity.	Superoxides	39-55	nitric oxide synthase 3	Homo sapiens	77-81
18716321-0	2008	Targeted increases in endothelial cell superoxide anion production stimulate eNOS-dependent nitric oxide production, not uncoupled eNOS activity.	Nitric Oxide	92-104	nitric oxide synthase 3	Homo sapiens	77-81
18792879-1	2008	Asymmetric dimethylarginine (ADMA) and NG-monomethyl- L-arginine ( L-NMMA) are important endogenous endothelial nitric oxide synthase (eNOS) inhibitors.	dimethylarginine	11-27	nitric oxide synthase 3	Homo sapiens	100-133
18792879-1	2008	Asymmetric dimethylarginine (ADMA) and NG-monomethyl- L-arginine ( L-NMMA) are important endogenous endothelial nitric oxide synthase (eNOS) inhibitors.	N,N-dimethylarginine	29-33	nitric oxide synthase 3	Homo sapiens	100-133
18792879-1	2008	Asymmetric dimethylarginine (ADMA) and NG-monomethyl- L-arginine ( L-NMMA) are important endogenous endothelial nitric oxide synthase (eNOS) inhibitors.	omega-N-Methylarginine	39-64	nitric oxide synthase 3	Homo sapiens	100-133
18792879-1	2008	Asymmetric dimethylarginine (ADMA) and NG-monomethyl- L-arginine ( L-NMMA) are important endogenous endothelial nitric oxide synthase (eNOS) inhibitors.	omega-N-Methylarginine	67-73	nitric oxide synthase 3	Homo sapiens	100-133
18413207-1	2008	BACKGROUND: Nitric oxide (NO) produced by endothelial NO synthase (eNOS) mediates a wide range of processes, and abnormal NO production mediated diabetes complications, including diabetic nephropathy (DN).	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	67-71
18695006-2	2008	We have previously demonstrated in animals and humans that endothelium-derived hydrogen peroxide (H(2)O(2)) is an EDHF that is produced in part by endothelial NO synthase (eNOS).	Hydrogen Peroxide	79-96	nitric oxide synthase 3	Homo sapiens	172-176
18695006-2	2008	We have previously demonstrated in animals and humans that endothelium-derived hydrogen peroxide (H(2)O(2)) is an EDHF that is produced in part by endothelial NO synthase (eNOS).	h(2)	98-102	nitric oxide synthase 3	Homo sapiens	172-176
18695006-2	2008	We have previously demonstrated in animals and humans that endothelium-derived hydrogen peroxide (H(2)O(2)) is an EDHF that is produced in part by endothelial NO synthase (eNOS).	edhf	114-118	nitric oxide synthase 3	Homo sapiens	172-176
18556800-0	2008	Hydrogen peroxide decreases endothelial nitric oxide synthase promoter activity through the inhibition of AP-1 activity.	Hydrogen Peroxide	0-17	nitric oxide synthase 3	Homo sapiens	28-61
18537053-4	2008	Vasoreactivity induced by L-arginine, which is the substrate for endothelial nitric oxide synthase, is a parameter of endothelial function and has been shown to be altered in patients with cerebrovascular disease.	Arginine	26-36	nitric oxide synthase 3	Homo sapiens	65-98
19124426-4	2008	Nitric oxide (NO), which is synthesized from L-arginine in endothelial cells by the endothelial nitric oxide synthase (eNOS), provides a tonic dilator tone and regulates the adhesion of white blood cells and platelet aggregation.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	84-117
19124426-4	2008	Nitric oxide (NO), which is synthesized from L-arginine in endothelial cells by the endothelial nitric oxide synthase (eNOS), provides a tonic dilator tone and regulates the adhesion of white blood cells and platelet aggregation.	Arginine	45-55	nitric oxide synthase 3	Homo sapiens	84-117
18641128-2	2008	We recently reported that endothelial nitric oxide synthase (eNOS)-derived NO regulates T cell receptor (TCR)-dependent ERK activation by a cGMP-independent mechanism.	Cyclic GMP	140-144	nitric oxide synthase 3	Homo sapiens	26-59
18641128-2	2008	We recently reported that endothelial nitric oxide synthase (eNOS)-derived NO regulates T cell receptor (TCR)-dependent ERK activation by a cGMP-independent mechanism.	Cyclic GMP	140-144	nitric oxide synthase 3	Homo sapiens	61-65
18641128-7	2008	We further show that activation of N-Ras involves eNOS-dependent S-nitrosylation on Cys(118), suggesting that upon TCR engagement, eNOS-derived NO directly activates N-Ras on the Golgi.	Cysteine	84-87	nitric oxide synthase 3	Homo sapiens	50-54
18641128-7	2008	We further show that activation of N-Ras involves eNOS-dependent S-nitrosylation on Cys(118), suggesting that upon TCR engagement, eNOS-derived NO directly activates N-Ras on the Golgi.	Cysteine	84-87	nitric oxide synthase 3	Homo sapiens	131-135
18645335-5	2008	A decline in nitric oxide bioavailability may be caused by decreased expression of the endothelial nitric oxide synthase, a reduction of substrate or cofactors for this enzyme, alterations of cellular signaling, enzyme inhibition by asymmetric dimethyl arginine, and, finally, accelerated nitric oxide degradation by reactive oxygen species.	Nitric Oxide	13-25	nitric oxide synthase 3	Homo sapiens	87-120
18551021-9	2008	In human umbilical endothelial cells, candesartan increased the eNOS protein level AT2-R dependently, inhibited the expression of nicotinamide adenine dinucleotide phosphate oxidase subunits and angiotensin II-induced intracellular reactive oxygen species and nitric oxide, and promoted the extracellular release of nitric oxide, suggesting that it augmented the bioavailability of nitric oxide.	candesartan	38-49	nitric oxide synthase 3	Homo sapiens	64-68
18401556-11	2008	These results suggest that the eNOS gene locus is associated with diabetic nephropathy and the functional polymorphisms (-786T &gt; C &amp; 894G &gt; T) might lead to a decreased expression of eNOS gene.	Adenosine Monophosphate	135-138	nitric oxide synthase 3	Homo sapiens	31-35
18401556-11	2008	These results suggest that the eNOS gene locus is associated with diabetic nephropathy and the functional polymorphisms (-786T &gt; C &amp; 894G &gt; T) might lead to a decreased expression of eNOS gene.	Adenosine Monophosphate	135-138	nitric oxide synthase 3	Homo sapiens	193-197
18483407-2	2008	We found that fluid shear stress induces the association of eNOS with the proline-rich tyrosine kinase 2 (PYK2) in endothelial cells and that the eNOS immunoprecipitated from eNOS- and PYK2-overexpressing HEK293 cells was tyrosine-phosphorylated on Tyr657.	Tyrosine	87-95	nitric oxide synthase 3	Homo sapiens	60-64
18397880-6	2008	The increase in eNOS mRNA caused by shear was completely blocked by pharmacological inhibition of p300/HAT activity with curcumin or by p300 small interfering RNA.	Curcumin	121-129	nitric oxide synthase 3	Homo sapiens	16-20
18385287-5	2008	Furthermore, we found that this endothelial NOS (eNOS) uncoupling increased 3-nitrotyrosine levels preferentially in the mitochondria of PAEC due to a redistribution of eNOS from the plasma membrane to the mitochondria.	3-nitrotyrosine	76-91	nitric oxide synthase 3	Homo sapiens	32-47
18385287-5	2008	Furthermore, we found that this endothelial NOS (eNOS) uncoupling increased 3-nitrotyrosine levels preferentially in the mitochondria of PAEC due to a redistribution of eNOS from the plasma membrane to the mitochondria.	3-nitrotyrosine	76-91	nitric oxide synthase 3	Homo sapiens	49-53
18385287-5	2008	Furthermore, we found that this endothelial NOS (eNOS) uncoupling increased 3-nitrotyrosine levels preferentially in the mitochondria of PAEC due to a redistribution of eNOS from the plasma membrane to the mitochondria.	3-nitrotyrosine	76-91	nitric oxide synthase 3	Homo sapiens	169-173
18385287-7	2008	Finally, we found that the decrease in ATP resulted in a reduction in the chaperone activity of HSP90 resulting in a decrease in its interaction with eNOS.	Adenosine Triphosphate	39-42	nitric oxide synthase 3	Homo sapiens	150-154
18385287-8	2008	In conclusion increased levels of ADMA causes mitochondrial dysfunction and a loss of heat shock protein-90 chaperone activity secondary to an uncoupling of eNOS.	N,N-dimethylarginine	34-38	nitric oxide synthase 3	Homo sapiens	157-161
18396156-1	2008	BACKGROUND: Nitric oxide (NO) synthesized by endothelial nitric oxide synthase (eNOS) plays a key role in vascular regulation and atherosclerosis, therefore, eNOS may be a candidate gene for ischemic stroke (IS).	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	45-78
18396156-1	2008	BACKGROUND: Nitric oxide (NO) synthesized by endothelial nitric oxide synthase (eNOS) plays a key role in vascular regulation and atherosclerosis, therefore, eNOS may be a candidate gene for ischemic stroke (IS).	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	80-84
18396156-1	2008	BACKGROUND: Nitric oxide (NO) synthesized by endothelial nitric oxide synthase (eNOS) plays a key role in vascular regulation and atherosclerosis, therefore, eNOS may be a candidate gene for ischemic stroke (IS).	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	158-162
18622047-4	2008	The loss in countering capacity of leptin on the ethanol-induced cytotoxicity was attained with cyclooxygenase inhibitor, indomethacin and nitric oxide synthase (cNOS) inhibitor, L-NAME, as well as PP2, an inhibitor of Src kinase.	Ethanol	49-56	nitric oxide synthase 3	Homo sapiens	162-166
18622047-7	2008	Moreover, the stimulatory effect of leptin on the mucosal cells cNOS activity was inhibited not only by PP2, but also by Akt inhibitor, SH-5.	SH-5	136-140	nitric oxide synthase 3	Homo sapiens	64-68
18510731-1	2008	BACKGROUND: Nitric oxide (NO) synthesized by endothelial nitric oxide synthase (eNOS) plays an important role in regulation of endothelial function and in the control of blood pressure.	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	45-78
18510731-1	2008	BACKGROUND: Nitric oxide (NO) synthesized by endothelial nitric oxide synthase (eNOS) plays an important role in regulation of endothelial function and in the control of blood pressure.	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	80-84
18390539-0	2008	Biogenesis of short intronic repeat 27-nucleotide small RNA from endothelial nitric-oxide synthase gene.	27-nucleotide	36-49	nitric oxide synthase 3	Homo sapiens	65-98
18390539-2	2008	Previously, we reported that the 27-nucleotide (nt) repeat polymorphism in eNOS intron 4, a source of 27-nt small RNA, which inhibits eNOS expression, were associated with cardiovascular risk and expression of the eNOS gene.	27-nucleotide	33-46	nitric oxide synthase 3	Homo sapiens	75-79
18390539-2	2008	Previously, we reported that the 27-nucleotide (nt) repeat polymorphism in eNOS intron 4, a source of 27-nt small RNA, which inhibits eNOS expression, were associated with cardiovascular risk and expression of the eNOS gene.	27-nucleotide	33-46	nitric oxide synthase 3	Homo sapiens	134-138
18390539-2	2008	Previously, we reported that the 27-nucleotide (nt) repeat polymorphism in eNOS intron 4, a source of 27-nt small RNA, which inhibits eNOS expression, were associated with cardiovascular risk and expression of the eNOS gene.	27-nucleotide	33-46	nitric oxide synthase 3	Homo sapiens	134-138
18326799-6	2008	Compared with normal cells in unmodified plasma, perfusion with suspensions of poloxamer-coated RBC in normal plasma resulted in decreased levels of NO metabolites and serine 1177 phosphorylation of endothelial nitric oxide synthase (eNOS).	Serine	168-174	nitric oxide synthase 3	Homo sapiens	199-232
18375715-1	2008	Folic acid (FA) is a member of the B-vitamin family with cardiovascular roles in homocysteine regulation and endothelial nitric oxide synthase (eNOS) activity.	Folic Acid	0-10	nitric oxide synthase 3	Homo sapiens	109-142
18403947-1	2008	BACKGROUND: Helicobacter pylori (H. pylori) infection induces nitric acid (NO) overproduction through inducible NO synthase (NOS) expression, subsequent DNA damage and enhanced antiapoptosis signal transduction sequence in the human gastric mucosa, whereas its possible effect on endothelial nitric oxide synthase (eNOS) expression has not as yet been investigated.	Nitric Acid	62-73	nitric oxide synthase 3	Homo sapiens	280-313
18403947-1	2008	BACKGROUND: Helicobacter pylori (H. pylori) infection induces nitric acid (NO) overproduction through inducible NO synthase (NOS) expression, subsequent DNA damage and enhanced antiapoptosis signal transduction sequence in the human gastric mucosa, whereas its possible effect on endothelial nitric oxide synthase (eNOS) expression has not as yet been investigated.	Nitric Acid	62-73	nitric oxide synthase 3	Homo sapiens	315-319
18387520-7	2008	While overnight incubation of HCMC with IgE significantly increased the expression of NOS2 and NOS3, only NOS2 expression was up-regulated after overnight incubation with a mixture of TNF-alpha, IFN-gamma and IL-1beta.	hcmc	30-34	nitric oxide synthase 3	Homo sapiens	95-99
19240311-0	2008	Lack of association between Glu(298) asp polymorphism of endothelial nitric oxide synthase (eNOS) gene and coronary artery disease in Tamilian population.	Glutamic Acid	28-31	nitric oxide synthase 3	Homo sapiens	57-90
19240311-0	2008	Lack of association between Glu(298) asp polymorphism of endothelial nitric oxide synthase (eNOS) gene and coronary artery disease in Tamilian population.	Glutamic Acid	28-31	nitric oxide synthase 3	Homo sapiens	92-96
19240311-0	2008	Lack of association between Glu(298) asp polymorphism of endothelial nitric oxide synthase (eNOS) gene and coronary artery disease in Tamilian population.	Aspartic Acid	37-40	nitric oxide synthase 3	Homo sapiens	57-90
19240311-0	2008	Lack of association between Glu(298) asp polymorphism of endothelial nitric oxide synthase (eNOS) gene and coronary artery disease in Tamilian population.	Aspartic Acid	37-40	nitric oxide synthase 3	Homo sapiens	92-96
18252813-6	2008	Enhanced transcription of eNOS by AVE9488 in primary human umbilical vein endothelial cells was associated with increased levels of eNOS mRNA and protein expression, as well as increased bradykinin-stimulated NO production.	4-fluoro-N-indan-2-yl-benzamide	34-41	nitric oxide synthase 3	Homo sapiens	26-30
18252813-6	2008	Enhanced transcription of eNOS by AVE9488 in primary human umbilical vein endothelial cells was associated with increased levels of eNOS mRNA and protein expression, as well as increased bradykinin-stimulated NO production.	4-fluoro-N-indan-2-yl-benzamide	34-41	nitric oxide synthase 3	Homo sapiens	132-136
18468205-0	2008	Lack of evidence for contribution of intron4a/b polymorphism of endothelial nitric oxide synthase (NOS3) gene to plasma nitric oxide levels.	Nitric Oxide	76-88	nitric oxide synthase 3	Homo sapiens	99-103
18504217-0	2008	[Effect of propofol on the transcription activity of endothelial nitric oxide synthase gene promoter in human umbilic vein endothelial cells induced by lipopolysaccharide].	Propofol	11-19	nitric oxide synthase 3	Homo sapiens	53-86
18504217-1	2008	OBJECTIVE: To observe the effect of propofol on the transcription activity of endothelial nitric oxide synthase (heNOS) gene promoter in human umbilic vein endothelial cells (HUVECs) induced by lipopolysaccharide (LPS).	Propofol	36-44	nitric oxide synthase 3	Homo sapiens	78-111
18468205-1	2008	OBJECTIVE: Nitric oxide (NO) is synthesized from L-arginine by endothelium nitric oxide synthase (NOS3).	Nitric Oxide	11-23	nitric oxide synthase 3	Homo sapiens	98-102
18468205-1	2008	OBJECTIVE: Nitric oxide (NO) is synthesized from L-arginine by endothelium nitric oxide synthase (NOS3).	Arginine	49-59	nitric oxide synthase 3	Homo sapiens	98-102
18414637-8	2008	Increased endothelial nitric oxide synthase (eNOS) activity was observed for roxarsone but not for As(III)-induced angiogenesis.	Roxarsone	77-86	nitric oxide synthase 3	Homo sapiens	10-43
18079107-0	2008	Rapamycin modulates the eNOS vs. shear stress relationship.	Sirolimus	0-9	nitric oxide synthase 3	Homo sapiens	24-28
18079107-2	2008	We evaluated in this study whether rapamycin affects endothelial nitric oxide synthase (eNOS) responsiveness to shear stress under normo- and hypercholesteraemic conditions to explain these findings.	Sirolimus	35-44	nitric oxide synthase 3	Homo sapiens	53-86
18079107-2	2008	We evaluated in this study whether rapamycin affects endothelial nitric oxide synthase (eNOS) responsiveness to shear stress under normo- and hypercholesteraemic conditions to explain these findings.	Sirolimus	35-44	nitric oxide synthase 3	Homo sapiens	88-92
18079107-8	2008	In control carotid arteries, eNOS expression increased by 1.8 +/- 0.3-fold in response to rapamycin.	Sirolimus	90-99	nitric oxide synthase 3	Homo sapiens	29-33
17973941-1	2008	OBJECTIVE: The possible association between the endothelial nitric oxide (eNOS) gene T-786C (promoter region), 27-bp repeat 4b/4a (intron 4), and Glu298Asp (exon 7) polymorphisms with diabetic retinopathy (DR) was investigated.	Nitric Oxide	60-72	nitric oxide synthase 3	Homo sapiens	74-78
18414637-8	2008	Increased endothelial nitric oxide synthase (eNOS) activity was observed for roxarsone but not for As(III)-induced angiogenesis.	Roxarsone	77-86	nitric oxide synthase 3	Homo sapiens	45-49
18340408-4	2008	The loss in countering capacity of leptin on the ethanol-induced cytotoxicity was attained with cyclooxygenase inhibitor, indomethacin and nitric oxide synthase (cNOS) inhibitor, L-NAME, as well as PP2, an inhibitor of Src kinase.	Ethanol	49-56	nitric oxide synthase 3	Homo sapiens	162-166
18340408-7	2008	Further, leptin suppression of ethanol cytotoxicity was reflected in the increased Akt and cNOS phosphorylation that was sensitive to PP2.	Ethanol	31-38	nitric oxide synthase 3	Homo sapiens	91-95
18340408-8	2008	Moreover, the stimulatory effect of leptin on the acinar cell cNOS activity was inhibited not only by PP2, but also by Akt inhibitor, SH-5, while wortmannin had no effect.	SH-5	134-138	nitric oxide synthase 3	Homo sapiens	62-66
18242595-0	2008	Geldanamycin enhances hepatocyte growth factor stimulation of eNOS phosphorylation in endothelial cells.	geldanamycin	0-12	nitric oxide synthase 3	Homo sapiens	62-66
18242595-1	2008	Previously, we demonstrated that hepatocyte growth factor (HGF) potently stimulates endothelial nitric oxide synthase (eNOS) activity and nitric oxide (NO) production through a calcium- and Akt-mediated phosphorylation at Ser-1179 (Ser-1177 human) in bovine aortic endothelial cells.	Nitric Oxide	96-108	nitric oxide synthase 3	Homo sapiens	119-123
18242595-4	2008	Treatment of endothelial cells with geldanamycin, a commonly used HSP90 inhibitor, augmented HGF-stimulated eNOS phosphorylation at Ser-1179, while it did not alter eNOS phosphorylation at Thr-497.	geldanamycin	36-48	nitric oxide synthase 3	Homo sapiens	108-112
18242595-4	2008	Treatment of endothelial cells with geldanamycin, a commonly used HSP90 inhibitor, augmented HGF-stimulated eNOS phosphorylation at Ser-1179, while it did not alter eNOS phosphorylation at Thr-497.	Serine	132-135	nitric oxide synthase 3	Homo sapiens	108-112
18242595-1	2008	Previously, we demonstrated that hepatocyte growth factor (HGF) potently stimulates endothelial nitric oxide synthase (eNOS) activity and nitric oxide (NO) production through a calcium- and Akt-mediated phosphorylation at Ser-1179 (Ser-1177 human) in bovine aortic endothelial cells.	Calcium	177-184	nitric oxide synthase 3	Homo sapiens	84-117
18242595-9	2008	These results suggest that geldanamycin, but neither 17-AAG nor radicicol, may enhance HGF-mediated eNOS Ser-1179 phosphorylation by some as yet unknown mechanisms independently of HSP90 inhibition.	geldanamycin	27-39	nitric oxide synthase 3	Homo sapiens	100-104
18242595-1	2008	Previously, we demonstrated that hepatocyte growth factor (HGF) potently stimulates endothelial nitric oxide synthase (eNOS) activity and nitric oxide (NO) production through a calcium- and Akt-mediated phosphorylation at Ser-1179 (Ser-1177 human) in bovine aortic endothelial cells.	Calcium	177-184	nitric oxide synthase 3	Homo sapiens	119-123
18242595-9	2008	These results suggest that geldanamycin, but neither 17-AAG nor radicicol, may enhance HGF-mediated eNOS Ser-1179 phosphorylation by some as yet unknown mechanisms independently of HSP90 inhibition.	Serine	105-108	nitric oxide synthase 3	Homo sapiens	100-104
18242595-1	2008	Previously, we demonstrated that hepatocyte growth factor (HGF) potently stimulates endothelial nitric oxide synthase (eNOS) activity and nitric oxide (NO) production through a calcium- and Akt-mediated phosphorylation at Ser-1179 (Ser-1177 human) in bovine aortic endothelial cells.	Serine	222-225	nitric oxide synthase 3	Homo sapiens	84-117
18160488-2	2008	Our purpose was to evaluate the effects of spatial colocalization of endothelial nitric oxide synthase (eNOS) and capacitative calcium entry (CCE) channels in caveolae on eNOS activation in response to ATP.	Adenosine Triphosphate	202-205	nitric oxide synthase 3	Homo sapiens	69-102
18339887-7	2008	Antiangiogenic effect of silibinin was coupled with a strong decrease in inducible nitric oxide synthase (NOS) and NOS3, cyclooxygenase-1 (COX-1) and COX-2, and hypoxia-inducing factor-1 alpha (HIF-1 alpha) and vascular endothelial growth factor (VEGF).	Silybin	25-34	nitric oxide synthase 3	Homo sapiens	115-119
18246059-1	2008	BACKGROUND: The endothelial nitric-oxide synthase (NOS3) gene encodes the enzyme (eNOS) that synthesizes the molecule nitric oxide, which facilitates endothelium-dependent vasodilation in response to physical activity.	Nitric Oxide	118-130	nitric oxide synthase 3	Homo sapiens	16-49
18246059-1	2008	BACKGROUND: The endothelial nitric-oxide synthase (NOS3) gene encodes the enzyme (eNOS) that synthesizes the molecule nitric oxide, which facilitates endothelium-dependent vasodilation in response to physical activity.	Nitric Oxide	118-130	nitric oxide synthase 3	Homo sapiens	51-55
18409050-5	2008	High glucose attenuated activation of Akt and endothelial nitric oxide synthase (eNOS).	Glucose	5-12	nitric oxide synthase 3	Homo sapiens	46-79
18409050-5	2008	High glucose attenuated activation of Akt and endothelial nitric oxide synthase (eNOS).	Glucose	5-12	nitric oxide synthase 3	Homo sapiens	81-85
18409050-6	2008	Crocetin (0.1 microM, 1.0 microM) prevented high glucose-induced apoptosis, which correlates with the increase of activation of p-Akt, following the up-regulation of eNOS and NO production.	crocetin	0-8	nitric oxide synthase 3	Homo sapiens	166-170
18409050-7	2008	Pretreatment with phosphatidylinositol 3" kinase (Pl3K) inhibitor LY294002 or eNOS inhibitor NG-nitro-arginine methyl ester (LN or L-NAME) inhibited crocetin effect on p-Akt or eNOS, respectively.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	66-74	nitric oxide synthase 3	Homo sapiens	177-181
18409050-7	2008	Pretreatment with phosphatidylinositol 3" kinase (Pl3K) inhibitor LY294002 or eNOS inhibitor NG-nitro-arginine methyl ester (LN or L-NAME) inhibited crocetin effect on p-Akt or eNOS, respectively.	NG-Nitroarginine Methyl Ester	93-123	nitric oxide synthase 3	Homo sapiens	78-82
18409050-7	2008	Pretreatment with phosphatidylinositol 3" kinase (Pl3K) inhibitor LY294002 or eNOS inhibitor NG-nitro-arginine methyl ester (LN or L-NAME) inhibited crocetin effect on p-Akt or eNOS, respectively.	NG-Nitroarginine Methyl Ester	93-123	nitric oxide synthase 3	Homo sapiens	177-181
18409050-7	2008	Pretreatment with phosphatidylinositol 3" kinase (Pl3K) inhibitor LY294002 or eNOS inhibitor NG-nitro-arginine methyl ester (LN or L-NAME) inhibited crocetin effect on p-Akt or eNOS, respectively.	NG-Nitroarginine Methyl Ester	131-137	nitric oxide synthase 3	Homo sapiens	177-181
18409050-8	2008	For the first time, results of our study suggest that crocetin inhibits high glucose-induced apoptosis, at least partly, via Pl3K/Akt/eNOS pathway in HUVECs and crocetin may exert a beneficial effect in preventing diabetes-associated cardiovascular complications.	crocetin	54-62	nitric oxide synthase 3	Homo sapiens	134-138
18409050-8	2008	For the first time, results of our study suggest that crocetin inhibits high glucose-induced apoptosis, at least partly, via Pl3K/Akt/eNOS pathway in HUVECs and crocetin may exert a beneficial effect in preventing diabetes-associated cardiovascular complications.	Glucose	77-84	nitric oxide synthase 3	Homo sapiens	134-138
18409050-8	2008	For the first time, results of our study suggest that crocetin inhibits high glucose-induced apoptosis, at least partly, via Pl3K/Akt/eNOS pathway in HUVECs and crocetin may exert a beneficial effect in preventing diabetes-associated cardiovascular complications.	crocetin	161-169	nitric oxide synthase 3	Homo sapiens	134-138
18551994-8	2008	Analysis of the gene polymorphism revealed that the frequency of the eNOS gene variant containing a 27-bp repeat in intron 4 is similar between control subjects (aa:ab:bb = 0%:21.8%:78.2%), and patients with CVD (aa:ab:bb = 3.3%:21.7%:75.0%).	boeravinone B	168-170	nitric oxide synthase 3	Homo sapiens	69-73
18551994-8	2008	Analysis of the gene polymorphism revealed that the frequency of the eNOS gene variant containing a 27-bp repeat in intron 4 is similar between control subjects (aa:ab:bb = 0%:21.8%:78.2%), and patients with CVD (aa:ab:bb = 3.3%:21.7%:75.0%).	boeravinone B	219-221	nitric oxide synthase 3	Homo sapiens	69-73
18211539-1	2008	PROBLEM: Polymorphisms of the endothelial nitric oxide synthase (eNOS) gene have been associated with reduced vascular NO production or increased level of homocysteine, and evaluated as risk factors for recurrent pregnancy loss (RPL).	Homocysteine	155-167	nitric oxide synthase 3	Homo sapiens	30-63
18211539-1	2008	PROBLEM: Polymorphisms of the endothelial nitric oxide synthase (eNOS) gene have been associated with reduced vascular NO production or increased level of homocysteine, and evaluated as risk factors for recurrent pregnancy loss (RPL).	Homocysteine	155-167	nitric oxide synthase 3	Homo sapiens	65-69
18364740-0	2008	Cadmium reduces nitric oxide production by impairing phosphorylation of endothelial nitric oxide synthase.	Cadmium	0-7	nitric oxide synthase 3	Homo sapiens	72-105
18364740-0	2008	Cadmium reduces nitric oxide production by impairing phosphorylation of endothelial nitric oxide synthase.	Nitric Oxide	16-28	nitric oxide synthase 3	Homo sapiens	72-105
17892503-0	2008	Regulation of endothelial nitric oxide synthase: involvement of protein kinase G 1 beta, serine 116 phosphorylation and lipid structures.	Serine	89-95	nitric oxide synthase 3	Homo sapiens	14-47
17892503-15	2008	Nitric oxide production decreased by approximately 20% with 300 nmol/L and 3 micromol/L 8-Br cGMP (P &lt; 0.05) and increased by 20.8 +/- 3.7% with 3 micromol/L BPC (P &lt; 0.001), indicating that both stimulated and basal PKG activity has inhibitory effects on basal NOS3 function.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	268-272
18398337-10	2008	CYBA C242T and NOS3 G894T polymorphisms had additive effects on vascular superoxide generation (P = 0.026) and xanthine oxidase activity was increased in patients with CAD (P = 0.043).	Superoxides	73-83	nitric oxide synthase 3	Homo sapiens	15-19
18160488-5	2008	To achieve a quantitative understanding of the mechanisms of microdomain calcium signaling and the preferential sensitivity of eNOS to calcium entering the cell through CCE channels, we constructed a mathematical model incorporating the cell morphology and cellular physiological processes.	Calcium	135-142	nitric oxide synthase 3	Homo sapiens	127-131
18160488-2	2008	Our purpose was to evaluate the effects of spatial colocalization of endothelial nitric oxide synthase (eNOS) and capacitative calcium entry (CCE) channels in caveolae on eNOS activation in response to ATP.	Adenosine Triphosphate	202-205	nitric oxide synthase 3	Homo sapiens	104-108
18160488-2	2008	Our purpose was to evaluate the effects of spatial colocalization of endothelial nitric oxide synthase (eNOS) and capacitative calcium entry (CCE) channels in caveolae on eNOS activation in response to ATP.	Adenosine Triphosphate	202-205	nitric oxide synthase 3	Homo sapiens	171-175
18203895-0	2008	Genistein, a soy phytoestrogen, upregulates the expression of human endothelial nitric oxide synthase and lowers blood pressure in spontaneously hypertensive rats.	Genistein	0-9	nitric oxide synthase 3	Homo sapiens	68-101
18203895-6	2008	Genistein, at physiologically achievable concentrations in individuals consuming soy products, enhanced the expression of eNOS and subsequently elevated NO synthesis in both HAEC and HUVEC, with 1-10 micromol/L genistein inducing the maximal effects.	Genistein	0-9	nitric oxide synthase 3	Homo sapiens	122-126
18203895-7	2008	However, the effects of genistein on eNOS and NO were not mediated by activation of estrogen signaling or inhibition of tyrosine kinases, 2 known biological actions of genistein.	Genistein	24-33	nitric oxide synthase 3	Homo sapiens	37-41
18203895-8	2008	Genistein (1-10 micromol/L) increased eNOS gene expression (1.8- to 2.6-fold of control) and significantly increased eNOS promoter activity of the human eNOS gene in HAEC and HUVEC, suggesting that genistein activates eNOS transcription.	Genistein	0-9	nitric oxide synthase 3	Homo sapiens	38-42
18203895-8	2008	Genistein (1-10 micromol/L) increased eNOS gene expression (1.8- to 2.6-fold of control) and significantly increased eNOS promoter activity of the human eNOS gene in HAEC and HUVEC, suggesting that genistein activates eNOS transcription.	Genistein	0-9	nitric oxide synthase 3	Homo sapiens	117-121
18203895-8	2008	Genistein (1-10 micromol/L) increased eNOS gene expression (1.8- to 2.6-fold of control) and significantly increased eNOS promoter activity of the human eNOS gene in HAEC and HUVEC, suggesting that genistein activates eNOS transcription.	Genistein	0-9	nitric oxide synthase 3	Homo sapiens	117-121
18203895-8	2008	Genistein (1-10 micromol/L) increased eNOS gene expression (1.8- to 2.6-fold of control) and significantly increased eNOS promoter activity of the human eNOS gene in HAEC and HUVEC, suggesting that genistein activates eNOS transcription.	Genistein	0-9	nitric oxide synthase 3	Homo sapiens	117-121
17570544-1	2008	Endothelial nitric oxide synthase (eNOS), the main source of endothelium-derived nitric oxide (NO), appears to be a rational therapeutic target in atherosclerosis.	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	35-39
18180853-3	2008	The caveolar coordination of NOS3, more specifically its interaction with caveolin-1 (Cav-1), plays a major role in normal endothelial NOS3 activity and vascular bioavailability of nitric oxide.	Nitric Oxide	181-193	nitric oxide synthase 3	Homo sapiens	29-33
18180853-7	2008	We observed that in the Glu/Asp and Asp/Asp mutant genotypes, the amount of NOS3 associated with Cav-1 was significantly lower.	Glutamic Acid	24-27	nitric oxide synthase 3	Homo sapiens	76-80
18180853-7	2008	We observed that in the Glu/Asp and Asp/Asp mutant genotypes, the amount of NOS3 associated with Cav-1 was significantly lower.	Aspartic Acid	28-31	nitric oxide synthase 3	Homo sapiens	76-80
18382884-4	2008	Superoxide produced by the NADPH oxidase may react with NO released by the endothelial nitric oxide synthase (eNOS) thereby generating peroxynitrite (ONOO-), leading to eNOS uncoupling and therefore eNOS-mediated superoxide production.	Superoxides	0-10	nitric oxide synthase 3	Homo sapiens	75-108
18180853-7	2008	We observed that in the Glu/Asp and Asp/Asp mutant genotypes, the amount of NOS3 associated with Cav-1 was significantly lower.	Aspartic Acid	36-39	nitric oxide synthase 3	Homo sapiens	76-80
18180853-7	2008	We observed that in the Glu/Asp and Asp/Asp mutant genotypes, the amount of NOS3 associated with Cav-1 was significantly lower.	Aspartic Acid	36-39	nitric oxide synthase 3	Homo sapiens	76-80
18456999-1	2008	Nitric oxide (NO), also known as endothelium-derived relaxing factor, is produced by endothelial nitric oxide synthase (eNOS) in the intima and by neuronal nitric oxide synthase (nNOS) in the adventitia of cerebral vessels.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	85-118
18382884-4	2008	Superoxide produced by the NADPH oxidase may react with NO released by the endothelial nitric oxide synthase (eNOS) thereby generating peroxynitrite (ONOO-), leading to eNOS uncoupling and therefore eNOS-mediated superoxide production.	Peroxynitrous Acid	135-148	nitric oxide synthase 3	Homo sapiens	75-108
18382884-4	2008	Superoxide produced by the NADPH oxidase may react with NO released by the endothelial nitric oxide synthase (eNOS) thereby generating peroxynitrite (ONOO-), leading to eNOS uncoupling and therefore eNOS-mediated superoxide production.	oxido nitrite	150-155	nitric oxide synthase 3	Homo sapiens	75-108
18382884-4	2008	Superoxide produced by the NADPH oxidase may react with NO released by the endothelial nitric oxide synthase (eNOS) thereby generating peroxynitrite (ONOO-), leading to eNOS uncoupling and therefore eNOS-mediated superoxide production.	Superoxides	213-223	nitric oxide synthase 3	Homo sapiens	75-108
18343248-0	2008	A case-control study of the association between polymorphisms of the endothelial nitric oxide synthase and glycoprotein IIIa genes and upper gastrointestinal bleeding in users of low-dose aspirin.	Aspirin	188-195	nitric oxide synthase 3	Homo sapiens	69-102
17977947-0	2008	Diabetic HDL-associated myristic acid inhibits acetylcholine-induced nitric oxide generation by preventing the association of endothelial nitric oxide synthase with calmodulin.	Myristic Acid	24-37	nitric oxide synthase 3	Homo sapiens	126-159
17977947-0	2008	Diabetic HDL-associated myristic acid inhibits acetylcholine-induced nitric oxide generation by preventing the association of endothelial nitric oxide synthase with calmodulin.	Acetylcholine	47-60	nitric oxide synthase 3	Homo sapiens	126-159
17977947-0	2008	Diabetic HDL-associated myristic acid inhibits acetylcholine-induced nitric oxide generation by preventing the association of endothelial nitric oxide synthase with calmodulin.	Nitric Oxide	69-81	nitric oxide synthase 3	Homo sapiens	126-159
17980690-3	2008	Endothelial nitric oxide synthase (eNOS or NOS3) is the predominant constitutive isoform of nitric NOS within bone.	nitric	12-18	nitric oxide synthase 3	Homo sapiens	43-47
18006482-5	2008	In macrovascular endothelial cells derived from aortas, CaM Kinase II mediates redox-sensitive upregulation of endothelial nitric oxide synthase (eNOS) gene expression by hydrogen peroxide (H2O2) and oscillatory shear stress, and a rapid activation of eNOS in response to bradykinin.	Hydrogen Peroxide	171-188	nitric oxide synthase 3	Homo sapiens	111-144
18006482-5	2008	In macrovascular endothelial cells derived from aortas, CaM Kinase II mediates redox-sensitive upregulation of endothelial nitric oxide synthase (eNOS) gene expression by hydrogen peroxide (H2O2) and oscillatory shear stress, and a rapid activation of eNOS in response to bradykinin.	Hydrogen Peroxide	171-188	nitric oxide synthase 3	Homo sapiens	146-150
18006482-5	2008	In macrovascular endothelial cells derived from aortas, CaM Kinase II mediates redox-sensitive upregulation of endothelial nitric oxide synthase (eNOS) gene expression by hydrogen peroxide (H2O2) and oscillatory shear stress, and a rapid activation of eNOS in response to bradykinin.	Hydrogen Peroxide	190-194	nitric oxide synthase 3	Homo sapiens	111-144
18006482-5	2008	In macrovascular endothelial cells derived from aortas, CaM Kinase II mediates redox-sensitive upregulation of endothelial nitric oxide synthase (eNOS) gene expression by hydrogen peroxide (H2O2) and oscillatory shear stress, and a rapid activation of eNOS in response to bradykinin.	Hydrogen Peroxide	190-194	nitric oxide synthase 3	Homo sapiens	146-150
18230825-6	2008	The Asp298 allele carriers of the eNOS gene presented significantly higher plasma low density lipoprotein (LDL) cholesterol, LDL particle size, malondialdehyde-modified LDL (MDA-LDL), and fasting insulin levels and lower plasma high density lipoprotein (HDL) cholesterol, apolipoprotein A-I levels, and endothelium-dependent vasodilation when compared with noncarriers.	Cholesterol	112-123	nitric oxide synthase 3	Homo sapiens	34-38
18230825-6	2008	The Asp298 allele carriers of the eNOS gene presented significantly higher plasma low density lipoprotein (LDL) cholesterol, LDL particle size, malondialdehyde-modified LDL (MDA-LDL), and fasting insulin levels and lower plasma high density lipoprotein (HDL) cholesterol, apolipoprotein A-I levels, and endothelium-dependent vasodilation when compared with noncarriers.	Malondialdehyde	144-159	nitric oxide synthase 3	Homo sapiens	34-38
18230825-6	2008	The Asp298 allele carriers of the eNOS gene presented significantly higher plasma low density lipoprotein (LDL) cholesterol, LDL particle size, malondialdehyde-modified LDL (MDA-LDL), and fasting insulin levels and lower plasma high density lipoprotein (HDL) cholesterol, apolipoprotein A-I levels, and endothelium-dependent vasodilation when compared with noncarriers.	Cholesterol	259-270	nitric oxide synthase 3	Homo sapiens	34-38
17906677-6	2008	In addition, Ang II diminished insulin-stimulated phosphorylation of Akt (at Ser(473)) and eNOS (at Ser(1177)) and NO generation, effects which were reversed by ACE2 gene transfer and anti-MIF treatment in endothelial cells.	Serine	100-103	nitric oxide synthase 3	Homo sapiens	91-95
18343248-10	2008	CONCLUSION: In this small, selected population of individuals taking low-dose aspirin for secondary prevention, carriage of the "a" allele of the eNOS gene was associated with a decreased risk for upper GI bleeding.	Aspirin	78-85	nitric oxide synthase 3	Homo sapiens	146-150
19169966-8	2008	The influence of APOE epsilon4 and NOS3 G alleles on the risk of AD was independent of homocysteine, vitamin B12 levels and MTHFR status.	Homocysteine	87-99	nitric oxide synthase 3	Homo sapiens	35-39
17941803-8	2008	All these cysteine residues identified were found to be located on the surface of the protein according to the available X-ray structure of the oxygenase domain of eNOS.	Cysteine	10-18	nitric oxide synthase 3	Homo sapiens	164-168
17941803-9	2008	Among those identified were Cys 93 and 98, the residues involved in the formation of the eNOS dimer through a Zn tetrathiolate cluster.	Cysteine	28-31	nitric oxide synthase 3	Homo sapiens	89-93
17941803-9	2008	Among those identified were Cys 93 and 98, the residues involved in the formation of the eNOS dimer through a Zn tetrathiolate cluster.	zn tetrathiolate	110-126	nitric oxide synthase 3	Homo sapiens	89-93
17941803-14	2008	These cysteines are located in regions of eNOS that have not been implicated in any known biochemical functions and the significance of their S-nitrosylation is not clear from this study.	Cysteine	6-15	nitric oxide synthase 3	Homo sapiens	42-46
17941803-15	2008	Thus, our data indicate that the eNOS protein can be S-nitrosylated at multiple sites other than within the Zn tetrathiolate cluster, suggesting that S-nitrosylation may regulate eNOS function in ways other than simply by inducing dimer collapse.	zn tetrathiolate	108-124	nitric oxide synthase 3	Homo sapiens	33-37
17941803-0	2008	Identification of the cysteine nitrosylation sites in human endothelial nitric oxide synthase.	Cysteine	22-30	nitric oxide synthase 3	Homo sapiens	60-93
17941803-2	2008	In our previous work we have shown that S-nitrosylation is involved in the disruption of the endothelial nitric oxide synthase (eNOS) dimer and that this involves the disruption of the zinc (Zn) tetrathiolate cluster due to the S-nitrosylation of Cysteine 98.	zinc (zn) tetrathiolate	185-208	nitric oxide synthase 3	Homo sapiens	93-126
17941803-2	2008	In our previous work we have shown that S-nitrosylation is involved in the disruption of the endothelial nitric oxide synthase (eNOS) dimer and that this involves the disruption of the zinc (Zn) tetrathiolate cluster due to the S-nitrosylation of Cysteine 98.	zinc (zn) tetrathiolate	185-208	nitric oxide synthase 3	Homo sapiens	128-132
17941803-2	2008	In our previous work we have shown that S-nitrosylation is involved in the disruption of the endothelial nitric oxide synthase (eNOS) dimer and that this involves the disruption of the zinc (Zn) tetrathiolate cluster due to the S-nitrosylation of Cysteine 98.	Cysteine	247-255	nitric oxide synthase 3	Homo sapiens	93-126
17941803-2	2008	In our previous work we have shown that S-nitrosylation is involved in the disruption of the endothelial nitric oxide synthase (eNOS) dimer and that this involves the disruption of the zinc (Zn) tetrathiolate cluster due to the S-nitrosylation of Cysteine 98.	Cysteine	247-255	nitric oxide synthase 3	Homo sapiens	128-132
17941803-3	2008	However, human eNOS contains 28 other cysteine residues whose potential to undergo S-nitrosylation has not been determined.	Cysteine	38-46	nitric oxide synthase 3	Homo sapiens	15-19
17941803-4	2008	Thus, the goal of this study was to identify the cysteine residues within eNOS that are susceptible to S-nitrosylation in vitro.	Cysteine	49-57	nitric oxide synthase 3	Homo sapiens	74-78
17965142-2	2008	In healthy vessels, the endothelium expresses constitutive forms of nitric oxide synthase (NOSIII) and cyclo-oxygenase (COX-1), which produce the vasoactive hormones NO and prostacyclin, respectively.	Epoprostenol	173-185	nitric oxide synthase 3	Homo sapiens	91-97
19169966-8	2008	The influence of APOE epsilon4 and NOS3 G alleles on the risk of AD was independent of homocysteine, vitamin B12 levels and MTHFR status.	Vitamin B 12	101-112	nitric oxide synthase 3	Homo sapiens	35-39
18703855-1	2008	OBJECTIVE: To investigate the effects of the potent immunosuppressive agent cyclosporin A (CsA) on the proliferation of human endothelial progenitor cells (EPCs) and endothelial nitric oxide synthase (eNOS) expression in EPCs.	Cyclosporine	76-89	nitric oxide synthase 3	Homo sapiens	166-199
18703855-6	2008	The effects of CsA on EPC proliferation, apoptosis, and eNOS/NO production were dose dependent in the concentration ranging from 0.1 microg/mL to 10 microg/mL.	Cyclosporine	15-18	nitric oxide synthase 3	Homo sapiens	56-60
18191076-4	2008	Constant high glucose levels increased p47-phox, p67-phox, and p22-phox expression [components of the Nicotinamide adenine dinucleotide phosphate [NAD(P)H] oxidase complex]; endothelial nitric oxide synthase, nitric oxide, and O(2)(-) production; nitrotyrosine, 8-hydroxy-2"-deoxyguanosine, and caspase-3 expression; and reduced Bcl-2 expression.	Glucose	14-21	nitric oxide synthase 3	Homo sapiens	174-207
18703855-7	2008	Treatment with VEGF (50 ng/mL) significantly promoted EPC proliferation and eNOS/NO production, which were completely abrogated by pre-incubation with CsA (10 microg/mL).	Cyclosporine	151-154	nitric oxide synthase 3	Homo sapiens	76-80
18703855-9	2008	CONCLUSION: CsA significantly inhibited proliferation, eNOS mRNA expression and NO production of human EPCs, in a dose-dependent manner.	Cyclosporine	12-15	nitric oxide synthase 3	Homo sapiens	55-59
18209570-9	2008	The cardioprotective effects of pravastatin were closely associated with the downregulation of collagen I, transforming growth factor-beta, matrix metalloproteinases-2 and -3, atrial natriuretic factor, interleukin-6, tumor necrosis factor-alpha, ROCK1 gene expression, and the upregulation of endothelial nitric oxide synthase gene expression.	Pravastatin	32-43	nitric oxide synthase 3	Homo sapiens	294-327
18776599-8	2008	RESULTS: Both single gene and MDR analyses revealed the NOS3 (ENOS) p.Glu298Asp polymorphism as significantly associated with GM-induced vestibular dysfunction (both p &lt;or= 0.03).	Gentamicins	126-128	nitric oxide synthase 3	Homo sapiens	56-60
18776599-9	2008	MDR analysis revealed a three-gene combination, consisting of NOS3 (p.Glu298Asp), GSTZ1 (p.Lys32Glu), and GSTP1 (p.Ile105Val), that provided the highest predictive model for GM-induced vestibular dysfunction (64% accuracy; p=0.009).	Gentamicins	174-176	nitric oxide synthase 3	Homo sapiens	62-66
18064439-6	2008	In blood from healthy donors, propofol increased NO production and cNOS activity.	Propofol	30-38	nitric oxide synthase 3	Homo sapiens	67-71
18064439-7	2008	The concentration of propofol that increased NO production by 50% (EC(50)) was 23.5 microM, and the EC(50) of propofol for cNOS was 18.6 microM.	Propofol	110-118	nitric oxide synthase 3	Homo sapiens	123-127
18040031-1	2007	BACKGROUND: Tetrahydrobiopterin (BH4) is a key regulator of endothelial nitric oxide synthase (eNOS) activity and coupling.	sapropterin	12-31	nitric oxide synthase 3	Homo sapiens	60-93
18220263-8	2008	The induced eNOS expression was inhibited by LY294002, indicating that the effect of laser on EC could be attributed to the up-regulation of eNOS expression through PI3K pathway at the cellular and molecular levels as a result of the He-Ne laser.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	45-53	nitric oxide synthase 3	Homo sapiens	12-16
18220263-8	2008	The induced eNOS expression was inhibited by LY294002, indicating that the effect of laser on EC could be attributed to the up-regulation of eNOS expression through PI3K pathway at the cellular and molecular levels as a result of the He-Ne laser.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	45-53	nitric oxide synthase 3	Homo sapiens	141-145
18421850-10	2008	Results of conditional logistic regression demonstrated that eNOS A-922G genetic polymorphism also had significant effects on ischemic stroke (OR = 2.156, 95% CI 1.081-4.299) after adjusting smoking, alcohol drinking, waist-to-hipratio, body mass index and history of hypertension, et al.	Alcohols	200-207	nitric oxide synthase 3	Homo sapiens	61-65
18077344-6	2007	Importantly, NOS1(-/-) and NOS1/NOS3(-/-) myocytes also exhibited spontaneous calcium waves.	Calcium	78-85	nitric oxide synthase 3	Homo sapiens	32-36
18167189-2	2007	Dimethylarginine dimethylaminohydrolase (DDAH) is the key enzyme for degrading asymmetric dimethylarginine (ADMA), which is an endogenous inhibitor of endothelial nitric oxide (NO) synthase (eNOS).	dimethylarginine	90-106	nitric oxide synthase 3	Homo sapiens	191-195
18167189-2	2007	Dimethylarginine dimethylaminohydrolase (DDAH) is the key enzyme for degrading asymmetric dimethylarginine (ADMA), which is an endogenous inhibitor of endothelial nitric oxide (NO) synthase (eNOS).	N,N-dimethylarginine	108-112	nitric oxide synthase 3	Homo sapiens	191-195
18167189-2	2007	Dimethylarginine dimethylaminohydrolase (DDAH) is the key enzyme for degrading asymmetric dimethylarginine (ADMA), which is an endogenous inhibitor of endothelial nitric oxide (NO) synthase (eNOS).	Nitric Oxide	163-175	nitric oxide synthase 3	Homo sapiens	191-195
18167189-10	2007	The inhibition of DDAH2 activity, the increase of ADMA concentration, the reduction of eNOS activity and the decrease of NO production were all consistently relevant to the alteration of Hcy concentration.	Homocysteine	187-190	nitric oxide synthase 3	Homo sapiens	87-91
18056530-6	2007	The effects of progesterone were mediated by nitric oxide released via nongenomic activation of endothelial nitric oxide synthase; this signal transduction likely takes place in the caveolae because sucrose density gradient fractionation experiments showed colocalization of the progesterone receptor c-Src, phosphoinositide 3-kinase, Akt, and endothelial nitric oxide synthase with KCNQ1, KCNE1, and Ca(V)1.2 in the caveolae fraction.	Nitric Oxide	45-57	nitric oxide synthase 3	Homo sapiens	96-129
18056530-6	2007	The effects of progesterone were mediated by nitric oxide released via nongenomic activation of endothelial nitric oxide synthase; this signal transduction likely takes place in the caveolae because sucrose density gradient fractionation experiments showed colocalization of the progesterone receptor c-Src, phosphoinositide 3-kinase, Akt, and endothelial nitric oxide synthase with KCNQ1, KCNE1, and Ca(V)1.2 in the caveolae fraction.	Nitric Oxide	45-57	nitric oxide synthase 3	Homo sapiens	344-377
17784906-8	2007	Phosphorylation of eNOS was unaltered in normoxia vs. hyperoxia, but phosphorylation of eNOS-Ser(1177) was increased and phosphorylation of eNOS-Thr(495) decreased by U46619.	Serine	93-96	nitric oxide synthase 3	Homo sapiens	88-92
17784906-8	2007	Phosphorylation of eNOS was unaltered in normoxia vs. hyperoxia, but phosphorylation of eNOS-Ser(1177) was increased and phosphorylation of eNOS-Thr(495) decreased by U46619.	Serine	93-96	nitric oxide synthase 3	Homo sapiens	88-92
18040031-1	2007	BACKGROUND: Tetrahydrobiopterin (BH4) is a key regulator of endothelial nitric oxide synthase (eNOS) activity and coupling.	sapropterin	33-36	nitric oxide synthase 3	Homo sapiens	60-93
17933968-0	2007	The role of caveolin-1 in PCB77-induced eNOS phosphorylation in human-derived endothelial cells.	3,4,3',4'-tetrachlorobiphenyl	26-31	nitric oxide synthase 3	Homo sapiens	40-44
17827260-1	2007	Emerging evidence supports the idea that arginase, expressed in the vascular endothelial cells of humans and other species, modulates endothelial nitric oxide (NO) synthase-3 (NOS-3) activity by regulating intracellular L-arginine bioavailability.	Arginine	220-230	nitric oxide synthase 3	Homo sapiens	146-181
17916773-3	2007	METHODS AND RESULTS: Endothelial cells treated with statins had a time- and dose-dependent increase in eNOS transcripts with long poly(A) tails (75 to 160 adenosines).	Poly A	130-137	nitric oxide synthase 3	Homo sapiens	103-107
17916773-3	2007	METHODS AND RESULTS: Endothelial cells treated with statins had a time- and dose-dependent increase in eNOS transcripts with long poly(A) tails (75 to 160 adenosines).	Adenosine	155-165	nitric oxide synthase 3	Homo sapiens	103-107
17916773-6	2007	The effect of statins on eNOS polyadenylation was related to cytoskeleton organization; there was increased eNOS mRNA polyadenylation after Rho inhibition and cytochalasin D treatment.	Cytochalasin D	159-173	nitric oxide synthase 3	Homo sapiens	25-29
17916773-6	2007	The effect of statins on eNOS polyadenylation was related to cytoskeleton organization; there was increased eNOS mRNA polyadenylation after Rho inhibition and cytochalasin D treatment.	Cytochalasin D	159-173	nitric oxide synthase 3	Homo sapiens	108-112
17262178-1	2007	Endothelial nitric oxide synthase (NOS3) produces nitric oxide which is a mediator of cytotoxic effects potentially associated with breast cancer.	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	35-39
17933968-3	2007	PCBs may be proatherogenic by causing dysfunctional eNOS signaling.	Polychlorinated Biphenyls	0-4	nitric oxide synthase 3	Homo sapiens	52-56
17933968-5	2007	Cells derived from an immortalized human vascular endothelial cell line were treated with PCB77 to study nitrotyrosine formation through eNOS signaling.	3-nitrotyrosine	105-118	nitric oxide synthase 3	Homo sapiens	137-141
17933968-8	2007	Cellular exposure to PCB77 increased eNOS phosphorylation and nitric oxide production, as well as peroxynitrite levels.	3,4,3',4'-tetrachlorobiphenyl	21-26	nitric oxide synthase 3	Homo sapiens	37-41
17933968-10	2007	The activation of eNOS by PCB77 treatment was blocked by inhibitors of the Src/PI3K/Akt pathway.	3,4,3',4'-tetrachlorobiphenyl	26-31	nitric oxide synthase 3	Homo sapiens	18-22
17933968-13	2007	These findings suggest that PCB77 induces eNOS phosphorylation in endothelial cells through a Src/PI3K/Akt-dependent mechanism, events regulated by functional caveolin-1.	3,4,3',4'-tetrachlorobiphenyl	28-33	nitric oxide synthase 3	Homo sapiens	42-46
18231735-0	2007	Effect of Troglitazone on expression of adhesion molecules and eNOS in human saphenous vein graft.	Troglitazone	10-22	nitric oxide synthase 3	Homo sapiens	63-67
17869551-1	2007	Nitric oxide (NO) is an important vasorelaxant produced along with L-citrulline from L-arginine in a reaction catalyzed by endothelial nitric oxide synthase (eNOS).	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	123-156
17977009-1	2007	Asymmetric dimethylarginine (ADMA) has been reported to affect the synthesis of nitric oxide (NO) in endothelial cells by inhibiting endothelial NO synthase (eNOS) activity and to cause endothelial dysfunction in humans.	dimethylarginine	11-27	nitric oxide synthase 3	Homo sapiens	158-162
17977009-1	2007	Asymmetric dimethylarginine (ADMA) has been reported to affect the synthesis of nitric oxide (NO) in endothelial cells by inhibiting endothelial NO synthase (eNOS) activity and to cause endothelial dysfunction in humans.	N,N-dimethylarginine	29-33	nitric oxide synthase 3	Homo sapiens	158-162
17977009-1	2007	Asymmetric dimethylarginine (ADMA) has been reported to affect the synthesis of nitric oxide (NO) in endothelial cells by inhibiting endothelial NO synthase (eNOS) activity and to cause endothelial dysfunction in humans.	Nitric Oxide	80-92	nitric oxide synthase 3	Homo sapiens	158-162
17888559-2	2007	Activity of all nNOS, iNOS and eNOS was inhibited by NaHS (IC(50): 0.13-0.21 mM).	sodium bisulfide	53-57	nitric oxide synthase 3	Homo sapiens	31-35
17888559-4	2007	Increasing concentrations of tetrahydrobiopterin (BH(4)) reversed the NaHS inhibition of nNOS and eNOS, but not iNOS.	sapropterin	29-48	nitric oxide synthase 3	Homo sapiens	98-102
17888559-4	2007	Increasing concentrations of tetrahydrobiopterin (BH(4)) reversed the NaHS inhibition of nNOS and eNOS, but not iNOS.	sodium bisulfide	70-74	nitric oxide synthase 3	Homo sapiens	98-102
17974890-2	2007	Nitric oxide production is impaired by the T-786C eNOS single nucleotide polymorphism, with a substitution of the nucleotide thymine by cytosine at a locus 786 base pairs upstream of the eNOS gene.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	50-54
17974890-2	2007	Nitric oxide production is impaired by the T-786C eNOS single nucleotide polymorphism, with a substitution of the nucleotide thymine by cytosine at a locus 786 base pairs upstream of the eNOS gene.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	187-191
17974890-2	2007	Nitric oxide production is impaired by the T-786C eNOS single nucleotide polymorphism, with a substitution of the nucleotide thymine by cytosine at a locus 786 base pairs upstream of the eNOS gene.	Thymine Nucleotides	114-132	nitric oxide synthase 3	Homo sapiens	187-191
17974890-2	2007	Nitric oxide production is impaired by the T-786C eNOS single nucleotide polymorphism, with a substitution of the nucleotide thymine by cytosine at a locus 786 base pairs upstream of the eNOS gene.	Cytosine	136-144	nitric oxide synthase 3	Homo sapiens	50-54
17974890-2	2007	Nitric oxide production is impaired by the T-786C eNOS single nucleotide polymorphism, with a substitution of the nucleotide thymine by cytosine at a locus 786 base pairs upstream of the eNOS gene.	Cytosine	136-144	nitric oxide synthase 3	Homo sapiens	187-191
17974890-10	2007	CONCLUSIONS: The T-786C eNOS polymorphism and resultant reduction of nitric oxide production is associated with, and may contribute to, the pathogenesis of idiopathic osteonecrosis of the femoral head.	Nitric Oxide	69-81	nitric oxide synthase 3	Homo sapiens	24-28
18062898-8	2007	Acute leptin exposure increased eNOS serine 1177 phosphorylation and caused Erk activation.	Serine	37-43	nitric oxide synthase 3	Homo sapiens	32-36
18021704-4	2007	We hereby present evidence that prolonged exposure to CO(2) impairs developmental retinal neovascularisation through a mechanism involving increased endothelial nitric oxide synthase and induction of a nitrative stress; effects of hypercapnia are independent of its hyperaemic effects.	Carbon Dioxide	54-59	nitric oxide synthase 3	Homo sapiens	149-182
18086002-2	2007	It is synthesized from the oxidation of L-arginine by the enzyme, endothelial nitric oxide synthase (eNOS).	Arginine	40-50	nitric oxide synthase 3	Homo sapiens	66-99
18086002-2	2007	It is synthesized from the oxidation of L-arginine by the enzyme, endothelial nitric oxide synthase (eNOS).	Arginine	40-50	nitric oxide synthase 3	Homo sapiens	101-105
18086002-3	2007	The eNOS gene has a number of polymorphic sites, including SNPs, dinucleotide repeats and variable number tandem repeat sequences, and the opportunity exists to investigate polymorphic functional correlates as well as disease-specific associations, especially in cardiovascular disease, including coronary artery disease, and its most severe consequence, myocardial infarction.	Dinucleoside Phosphates	65-77	nitric oxide synthase 3	Homo sapiens	4-8
17916362-6	2007	Sirt1 inhibition by sirtinol or Sirt1 siRNA increased PAI-1 expression and decreased both protein expression and activity of eNOS.	sirtinol	20-28	nitric oxide synthase 3	Homo sapiens	125-129
17916362-9	2007	Conversely, overexpression of Sirt1 prevented hydrogen peroxide-induced SA-beta-gal activity, morphological changes and deranged expression of PAI-1 and eNOS.	Hydrogen Peroxide	46-63	nitric oxide synthase 3	Homo sapiens	153-157
17855507-1	2007	Nitric oxide (NO) release from endothelial cells, via endothelial NO synthase (eNOS) activation, is central to the proangiogenic actions of vascular endothelial growth factor (VEGF).	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	79-83
17869551-1	2007	Nitric oxide (NO) is an important vasorelaxant produced along with L-citrulline from L-arginine in a reaction catalyzed by endothelial nitric oxide synthase (eNOS).	Citrulline	67-79	nitric oxide synthase 3	Homo sapiens	123-156
17869551-1	2007	Nitric oxide (NO) is an important vasorelaxant produced along with L-citrulline from L-arginine in a reaction catalyzed by endothelial nitric oxide synthase (eNOS).	Arginine	85-95	nitric oxide synthase 3	Homo sapiens	123-156
17996131-0	2007	[Association of endothelial nitric oxide synthase gene polymorphism with level of uric acid in serum for acute coronary syndrome].	Uric Acid	82-91	nitric oxide synthase 3	Homo sapiens	16-49
17996131-1	2007	OBJECTIVE: To evaluate the association of elevation in serum uric acid with the development of coronary artery disease, and to determine the relationship between uric acid and Glu(298) Asp polymorphism of the endothelial nitric oxide synthase (eNOS) gene in acute coronary syndrome (ACS) in the Chinese Han Nationality.	Uric Acid	162-171	nitric oxide synthase 3	Homo sapiens	209-242
17996131-5	2007	In comparison with subjects who had Glu(298) allele in the eNOS gene, the risk of ACS was not increased among Asp/Asp carriers (odds ratio 1.34, 95% confidence interval 0.479 to 3.755, P = 0.575).	Glutamic Acid	36-39	nitric oxide synthase 3	Homo sapiens	59-63
17996131-7	2007	CONCLUSION: Glu(298) Asp polymorphism of the eNOS gene appears to have no association with ACS in the Chinese Han Nationality, but a significant association between the eNOS Glu(298) Asp variant and the serum uric acid level is found in patients with ACS.	Uric Acid	209-218	nitric oxide synthase 3	Homo sapiens	45-49
17996131-7	2007	CONCLUSION: Glu(298) Asp polymorphism of the eNOS gene appears to have no association with ACS in the Chinese Han Nationality, but a significant association between the eNOS Glu(298) Asp variant and the serum uric acid level is found in patients with ACS.	Uric Acid	209-218	nitric oxide synthase 3	Homo sapiens	169-173
17898383-0	2007	Propofol reduces apoptosis and up-regulates endothelial nitric oxide synthase protein expression in hydrogen peroxide-stimulated human umbilical vein endothelial cells.	Propofol	0-8	nitric oxide synthase 3	Homo sapiens	44-77
17719164-9	2007	RT-PCR detection showed that NHEK expressed both iNOS and cNOS mRNA by TCE exposure.	Trichloroethylene	71-74	nitric oxide synthase 3	Homo sapiens	58-62
17898383-0	2007	Propofol reduces apoptosis and up-regulates endothelial nitric oxide synthase protein expression in hydrogen peroxide-stimulated human umbilical vein endothelial cells.	Hydrogen Peroxide	100-117	nitric oxide synthase 3	Homo sapiens	44-77
18025053-0	2007	Polychlorinated biphenyls alter the expression of endothelial nitric oxide synthase mRNA in human umbilical vein endothelial cells.	Polychlorinated Biphenyls	0-25	nitric oxide synthase 3	Homo sapiens	50-83
17719164-10	2007	Whereas a concentration- and time-dependent up-regulation of the mRNA expression was observed for iNOS and cNOS following TCE exposure, changes to iNOS were more marked.	Trichloroethylene	122-125	nitric oxide synthase 3	Homo sapiens	107-111
17719164-11	2007	These results suggest that TCE caused increase in NO production, attributed to activation of iNOS as well as cNOS, and expression of iNOS and cNOS mRNA.	Trichloroethylene	27-30	nitric oxide synthase 3	Homo sapiens	109-113
17719164-11	2007	These results suggest that TCE caused increase in NO production, attributed to activation of iNOS as well as cNOS, and expression of iNOS and cNOS mRNA.	Trichloroethylene	27-30	nitric oxide synthase 3	Homo sapiens	142-146
17714081-12	2007	Despite no effect on NOS-3 expression, AGE-albumin decreased and 17beta-oestradiol increased phosphoserine-1177-NOS-3 and 17beta-oestradiol largely prevented the decrease in phosphoserine-1177-NOS-3 induced by AGE-albumin.	Estradiol	65-82	nitric oxide synthase 3	Homo sapiens	112-117
17714081-12	2007	Despite no effect on NOS-3 expression, AGE-albumin decreased and 17beta-oestradiol increased phosphoserine-1177-NOS-3 and 17beta-oestradiol largely prevented the decrease in phosphoserine-1177-NOS-3 induced by AGE-albumin.	Estradiol	65-82	nitric oxide synthase 3	Homo sapiens	112-117
17714081-12	2007	Despite no effect on NOS-3 expression, AGE-albumin decreased and 17beta-oestradiol increased phosphoserine-1177-NOS-3 and 17beta-oestradiol largely prevented the decrease in phosphoserine-1177-NOS-3 induced by AGE-albumin.	Phosphoserine	93-106	nitric oxide synthase 3	Homo sapiens	112-117
17714081-12	2007	Despite no effect on NOS-3 expression, AGE-albumin decreased and 17beta-oestradiol increased phosphoserine-1177-NOS-3 and 17beta-oestradiol largely prevented the decrease in phosphoserine-1177-NOS-3 induced by AGE-albumin.	Phosphoserine	93-106	nitric oxide synthase 3	Homo sapiens	112-117
17714081-12	2007	Despite no effect on NOS-3 expression, AGE-albumin decreased and 17beta-oestradiol increased phosphoserine-1177-NOS-3 and 17beta-oestradiol largely prevented the decrease in phosphoserine-1177-NOS-3 induced by AGE-albumin.	Estradiol	122-139	nitric oxide synthase 3	Homo sapiens	21-26
17714081-13	2007	Alone, AGE-albumin increased O-glycosylation of NOS-3 by N-acetylglucosamine, an effect largely inhibited by 17beta-oestradiol.	Acetylglucosamine	57-76	nitric oxide synthase 3	Homo sapiens	48-53
17714081-13	2007	Alone, AGE-albumin increased O-glycosylation of NOS-3 by N-acetylglucosamine, an effect largely inhibited by 17beta-oestradiol.	Estradiol	109-126	nitric oxide synthase 3	Homo sapiens	48-53
18025053-3	2007	The mRNA levels of eNOS, aryl hydrocarbon receptor (AhR) and cytochrome P450 (CYP) 1A1 in cells treated with 5 microM PCBs for 24 hours were analysed by real-time RT-PCR.	Polychlorinated Biphenyls	118-122	nitric oxide synthase 3	Homo sapiens	19-23
18025053-6	2007	ERs were also suspected of altering eNOS levels because ICI 182780 treatment resulted in a decrease in the eNOS level.	Fulvestrant	56-66	nitric oxide synthase 3	Homo sapiens	36-40
18025053-6	2007	ERs were also suspected of altering eNOS levels because ICI 182780 treatment resulted in a decrease in the eNOS level.	Fulvestrant	56-66	nitric oxide synthase 3	Homo sapiens	107-111
18025053-7	2007	These results suggest that the eNOS mRNA expression increases due to the action of PCBs related to both AhR and ERs in HUVECs, and that maternal PCB exposure could influence fetal circulation.	Polychlorinated Biphenyls	83-87	nitric oxide synthase 3	Homo sapiens	31-35
17698846-4	2007	In the presence of both L-arginine and tetrahydrobiopterin, eNOS is highly coupled (&gt;90%), and the measured stoichiometry of O(2)/NADPH is very close to the theoretical value.	Arginine	24-34	nitric oxide synthase 3	Homo sapiens	60-64
17408626-11	2007	RESULT(S): Ghrelin negatively affected PGs release as well as COX2, ECNOS, and INOS mRNA expressions in HUVEC.	Ghrelin	11-18	nitric oxide synthase 3	Homo sapiens	68-73
17716867-0	2007	Alpha-linolenic acid attenuates high glucose-induced apoptosis in cultured human umbilical vein endothelial cells via PI3K/Akt/eNOS pathway.	alpha-Linolenic Acid	0-20	nitric oxide synthase 3	Homo sapiens	127-131
17716867-0	2007	Alpha-linolenic acid attenuates high glucose-induced apoptosis in cultured human umbilical vein endothelial cells via PI3K/Akt/eNOS pathway.	Glucose	37-44	nitric oxide synthase 3	Homo sapiens	127-131
17716867-6	2007	Furthermore, high glucose reduced phosphorylation of Akt and endothelial nitric oxide synthase (eNOS) with subsequent nitric oxide production, whereas ALA treatment attenuated the reduction caused by high glucose.	Glucose	18-25	nitric oxide synthase 3	Homo sapiens	61-94
17716867-6	2007	Furthermore, high glucose reduced phosphorylation of Akt and endothelial nitric oxide synthase (eNOS) with subsequent nitric oxide production, whereas ALA treatment attenuated the reduction caused by high glucose.	Glucose	18-25	nitric oxide synthase 3	Homo sapiens	96-100
17716867-6	2007	Furthermore, high glucose reduced phosphorylation of Akt and endothelial nitric oxide synthase (eNOS) with subsequent nitric oxide production, whereas ALA treatment attenuated the reduction caused by high glucose.	Nitric Oxide	73-85	nitric oxide synthase 3	Homo sapiens	96-100
17716867-8	2007	CONCLUSION: ALA exerts an antiapoptotic effect by the phosphatidylinositol 3"-kinase/Akt/eNOS pathway in HUVECs exposed to high glucose and thus may represent a candidate therapeutic agent for diabetic cardiovascular complications.	alpha-Linolenic Acid	12-15	nitric oxide synthase 3	Homo sapiens	89-93
17716867-8	2007	CONCLUSION: ALA exerts an antiapoptotic effect by the phosphatidylinositol 3"-kinase/Akt/eNOS pathway in HUVECs exposed to high glucose and thus may represent a candidate therapeutic agent for diabetic cardiovascular complications.	Glucose	128-135	nitric oxide synthase 3	Homo sapiens	89-93
18049306-4	2007	An imbalance between [NO]/[ONOO-] concentrations was used as an indicator of endothelial dysfunction and correlated with endothelial nitric oxide synthase (eNOS) expression.	oxido nitrite	27-32	nitric oxide synthase 3	Homo sapiens	121-154
18049306-4	2007	An imbalance between [NO]/[ONOO-] concentrations was used as an indicator of endothelial dysfunction and correlated with endothelial nitric oxide synthase (eNOS) expression.	oxido nitrite	27-32	nitric oxide synthase 3	Homo sapiens	156-160
18049306-8	2007	Treatment with statins reversed eNOS uncoupling, induced by oxidized-LDL and significantly increased the [NO]/[ONOO-] balance to 1.2 +/- 0.1.	onoo	111-115	nitric oxide synthase 3	Homo sapiens	32-36
17545677-6	2007	The eNOS activity was measured by the conversion of [(14)C]arginine to [(14)C]citrulline.	[(14)c]arginine	52-67	nitric oxide synthase 3	Homo sapiens	4-8
17545677-6	2007	The eNOS activity was measured by the conversion of [(14)C]arginine to [(14)C]citrulline.	[(14)c]citrulline	71-88	nitric oxide synthase 3	Homo sapiens	4-8
17545677-10	2007	The addition of calphostin C (PKC inhibitor) or Rp-cAMP (PKA inhibitor) reduced the eNOS mRNA, protein expression and activity of PTH-stimulated HUVEC.	calphostin C	16-28	nitric oxide synthase 3	Homo sapiens	84-88
17545677-10	2007	The addition of calphostin C (PKC inhibitor) or Rp-cAMP (PKA inhibitor) reduced the eNOS mRNA, protein expression and activity of PTH-stimulated HUVEC.	Cyclic AMP	51-55	nitric oxide synthase 3	Homo sapiens	84-88
17545677-11	2007	The combined treatment of calphostin C and Rp-cAMP abolished the eNOS protein expression and activity.	Cyclic AMP	46-50	nitric oxide synthase 3	Homo sapiens	65-69
17698846-4	2007	In the presence of both L-arginine and tetrahydrobiopterin, eNOS is highly coupled (&gt;90%), and the measured stoichiometry of O(2)/NADPH is very close to the theoretical value.	sapropterin	39-58	nitric oxide synthase 3	Homo sapiens	60-64
17698846-4	2007	In the presence of both L-arginine and tetrahydrobiopterin, eNOS is highly coupled (&gt;90%), and the measured stoichiometry of O(2)/NADPH is very close to the theoretical value.	Oxygen	128-132	nitric oxide synthase 3	Homo sapiens	60-64
17698846-4	2007	In the presence of both L-arginine and tetrahydrobiopterin, eNOS is highly coupled (&gt;90%), and the measured stoichiometry of O(2)/NADPH is very close to the theoretical value.	NADP	133-138	nitric oxide synthase 3	Homo sapiens	60-64
17698846-5	2007	We report for the first time that the presence of L-arginine stimulates oxygen uptake by eNOS.	Arginine	50-60	nitric oxide synthase 3	Homo sapiens	89-93
17698846-5	2007	We report for the first time that the presence of L-arginine stimulates oxygen uptake by eNOS.	Oxygen	72-78	nitric oxide synthase 3	Homo sapiens	89-93
17698846-8	2007	These results reveal different mechanisms for oxygen metabolism for eNOS as opposed to nNOS and, perhaps, partially explain their functional differences.	Oxygen	46-52	nitric oxide synthase 3	Homo sapiens	68-72
17878410-5	2007	Studies examining the interactions between NOS-3, beta-actin, and Hsp90 could potentially lead to the discovery of effective peptides for the treatment of diseases associated with impaired NOS-3 activity and nitric oxide release, such as systemic and pulmonary hypertension, atherosclerosis, and thrombotic diseases.	Nitric Oxide	208-220	nitric oxide synthase 3	Homo sapiens	43-48
18007078-0	2007	[Effect of rosiglitazone on NO and eNOS via PI3K/PKB signal pathways in cultured human umbilical vein endothelial cells].	Rosiglitazone	11-24	nitric oxide synthase 3	Homo sapiens	35-39
18007078-4	2007	RESULTS: Rosiglitazone increased the endothelial NO production in a dose- and time-dependent manner in cultured HUVECs, and also increased the expression of PI3K mRNA and the phosphorylation of PKB-Ser473 and eNOS-Ser1177 in a concentration-dependent manner, with no alteration in the expression of PKB and eNOS in cultured HUVECs.	Rosiglitazone	9-22	nitric oxide synthase 3	Homo sapiens	209-213
18007078-4	2007	RESULTS: Rosiglitazone increased the endothelial NO production in a dose- and time-dependent manner in cultured HUVECs, and also increased the expression of PI3K mRNA and the phosphorylation of PKB-Ser473 and eNOS-Ser1177 in a concentration-dependent manner, with no alteration in the expression of PKB and eNOS in cultured HUVECs.	Rosiglitazone	9-22	nitric oxide synthase 3	Homo sapiens	307-311
18007078-5	2007	N(w)-nitro-L- arginine methyl ester (L-NAME, eNOS synthase inhibitor) blocked the rosiglitazone-induced NO formation; LY294002 (a PI3K inhibitor) prevented the NO production; and the phosphorylation of eNOS and PKB was induced by rosiglitazone.	n(w)-nitro-l- arginine methyl ester	0-35	nitric oxide synthase 3	Homo sapiens	45-49
18007078-5	2007	N(w)-nitro-L- arginine methyl ester (L-NAME, eNOS synthase inhibitor) blocked the rosiglitazone-induced NO formation; LY294002 (a PI3K inhibitor) prevented the NO production; and the phosphorylation of eNOS and PKB was induced by rosiglitazone.	n(w)-nitro-l- arginine methyl ester	0-35	nitric oxide synthase 3	Homo sapiens	202-206
18007078-5	2007	N(w)-nitro-L- arginine methyl ester (L-NAME, eNOS synthase inhibitor) blocked the rosiglitazone-induced NO formation; LY294002 (a PI3K inhibitor) prevented the NO production; and the phosphorylation of eNOS and PKB was induced by rosiglitazone.	NG-Nitroarginine Methyl Ester	37-43	nitric oxide synthase 3	Homo sapiens	202-206
18007078-5	2007	N(w)-nitro-L- arginine methyl ester (L-NAME, eNOS synthase inhibitor) blocked the rosiglitazone-induced NO formation; LY294002 (a PI3K inhibitor) prevented the NO production; and the phosphorylation of eNOS and PKB was induced by rosiglitazone.	Rosiglitazone	82-95	nitric oxide synthase 3	Homo sapiens	45-49
18007078-5	2007	N(w)-nitro-L- arginine methyl ester (L-NAME, eNOS synthase inhibitor) blocked the rosiglitazone-induced NO formation; LY294002 (a PI3K inhibitor) prevented the NO production; and the phosphorylation of eNOS and PKB was induced by rosiglitazone.	Rosiglitazone	82-95	nitric oxide synthase 3	Homo sapiens	202-206
18007078-5	2007	N(w)-nitro-L- arginine methyl ester (L-NAME, eNOS synthase inhibitor) blocked the rosiglitazone-induced NO formation; LY294002 (a PI3K inhibitor) prevented the NO production; and the phosphorylation of eNOS and PKB was induced by rosiglitazone.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	118-126	nitric oxide synthase 3	Homo sapiens	202-206
18007078-6	2007	CONCLUSION: Treatment with rosiglitazone can increase the NO production and improve the endothelial function through up-regulating the PI3K/PKB/eNOS signal pathways in cultured HUVECs.	Rosiglitazone	27-40	nitric oxide synthase 3	Homo sapiens	144-148
17658478-1	2007	Nitric oxide (NO) plays critical role in endothelial dysfunction and oxidative stress in COPD, pointing to the significance of endothelial nitric oxide synthase gene (eNOS) variants.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	127-160
17697943-0	2007	Modulation of nitric oxide formation by endothelial nitric oxide synthase gene haplotypes.	Nitric Oxide	14-26	nitric oxide synthase 3	Homo sapiens	40-73
17697943-2	2007	However, the effects of endothelial nitric oxide synthase (eNOS) gene polymorphisms or haplotypes on the circulating concentrations of nitrite (a sensitive marker of NO formation) and cGMP are unknown.	Nitrites	135-142	nitric oxide synthase 3	Homo sapiens	59-63
17658478-1	2007	Nitric oxide (NO) plays critical role in endothelial dysfunction and oxidative stress in COPD, pointing to the significance of endothelial nitric oxide synthase gene (eNOS) variants.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	167-171
17658478-2	2007	We investigated the association of -786T/C, -922A/G, 4B/4A, and 894G/T polymorphisms of eNOS with the disease and its impact on nitrite and malonaldehyde levels in 190 COPD patients and 134 healthy controls, all smokers.	Nitrites	128-135	nitric oxide synthase 3	Homo sapiens	88-92
17658478-2	2007	We investigated the association of -786T/C, -922A/G, 4B/4A, and 894G/T polymorphisms of eNOS with the disease and its impact on nitrite and malonaldehyde levels in 190 COPD patients and 134 healthy controls, all smokers.	Malondialdehyde	140-153	nitric oxide synthase 3	Homo sapiens	88-92
17827719-0	2007	Water extract of Korean red ginseng stimulates angiogenesis by activating the PI3K/Akt-dependent ERK1/2 and eNOS pathways in human umbilical vein endothelial cells.	Water	0-5	nitric oxide synthase 3	Homo sapiens	108-112
17827719-5	2007	Inhibition of PI3K activity by wortmannin completely inhibited KRGE-induced angiogenesis and phosphorylation of Akt, ERK1/2, and eNOS, indicating that PI3K/Akt activation is an upstream event of the KRGE-mediated angiogenic pathway.	Wortmannin	31-41	nitric oxide synthase 3	Homo sapiens	129-133
17827719-7	2007	However, the eNOS inhibitor N(G)-monomethyl-L-arginine effectively inhibited tube formation, but partially blocked proliferation and migration as well as ERK phosphorylation, without altering Akt and eNOS activation, revealing that the eNOS/NO pathway is partially involved in ERK1/2 activation.	omega-N-Methylarginine	28-54	nitric oxide synthase 3	Homo sapiens	13-17
17572401-9	2007	Platelet NOS3 expression was similar in both age groups, but NOS3 serine-1177 phosphorylation was greater in younger subjects.	Serine	66-72	nitric oxide synthase 3	Homo sapiens	61-65
17449720-8	2007	Further, immunoprecipitation studies demonstrated that Asp variants had substantially less NOS3/Cav-1 association (approximately 40%) during static conditions.	Aspartic Acid	55-58	nitric oxide synthase 3	Homo sapiens	91-95
17726138-0	2007	Genetic variability in iron-related oxidative stress pathways (Nrf2, NQ01, NOS3, and HO-1), iron intake, and risk of postmenopausal breast cancer.	Iron	23-27	nitric oxide synthase 3	Homo sapiens	75-79
17696958-0	2007	Fatty acid incorporation in endothelial cells and effects on endothelial nitric oxide synthase.	Fatty Acids	0-10	nitric oxide synthase 3	Homo sapiens	61-94
17696958-5	2007	The effects of the FFAs on the endothelial nitric oxide synthase were investigated on mRNA level by quantitative PCR, on protein level and Ser1177 phosphorylation by Western blot and on enzymatic activity on living cells using radiolabelled arginine.	Arginine	241-249	nitric oxide synthase 3	Homo sapiens	31-64
17610838-1	2007	The object of this study was to clarify the mechanism of electron transfer in the human endothelial nitric oxide synthase (eNOS) reductase domain using recombinant eNOS reductase domains; the FAD/NADPH domain containing FAD- and NADPH-binding sites and the FAD/FMN domain containing FAD/NADPH-, FMN-, and a calmodulin-binding sites.	Flavin-Adenine Dinucleotide	192-195	nitric oxide synthase 3	Homo sapiens	88-121
17610838-1	2007	The object of this study was to clarify the mechanism of electron transfer in the human endothelial nitric oxide synthase (eNOS) reductase domain using recombinant eNOS reductase domains; the FAD/NADPH domain containing FAD- and NADPH-binding sites and the FAD/FMN domain containing FAD/NADPH-, FMN-, and a calmodulin-binding sites.	NADP	196-201	nitric oxide synthase 3	Homo sapiens	88-121
17610838-1	2007	The object of this study was to clarify the mechanism of electron transfer in the human endothelial nitric oxide synthase (eNOS) reductase domain using recombinant eNOS reductase domains; the FAD/NADPH domain containing FAD- and NADPH-binding sites and the FAD/FMN domain containing FAD/NADPH-, FMN-, and a calmodulin-binding sites.	Flavin-Adenine Dinucleotide	220-223	nitric oxide synthase 3	Homo sapiens	88-121
17610838-1	2007	The object of this study was to clarify the mechanism of electron transfer in the human endothelial nitric oxide synthase (eNOS) reductase domain using recombinant eNOS reductase domains; the FAD/NADPH domain containing FAD- and NADPH-binding sites and the FAD/FMN domain containing FAD/NADPH-, FMN-, and a calmodulin-binding sites.	NADP	229-234	nitric oxide synthase 3	Homo sapiens	88-121
17610838-1	2007	The object of this study was to clarify the mechanism of electron transfer in the human endothelial nitric oxide synthase (eNOS) reductase domain using recombinant eNOS reductase domains; the FAD/NADPH domain containing FAD- and NADPH-binding sites and the FAD/FMN domain containing FAD/NADPH-, FMN-, and a calmodulin-binding sites.	Flavin-Adenine Dinucleotide	220-223	nitric oxide synthase 3	Homo sapiens	88-121
17610838-1	2007	The object of this study was to clarify the mechanism of electron transfer in the human endothelial nitric oxide synthase (eNOS) reductase domain using recombinant eNOS reductase domains; the FAD/NADPH domain containing FAD- and NADPH-binding sites and the FAD/FMN domain containing FAD/NADPH-, FMN-, and a calmodulin-binding sites.	Flavin-Adenine Dinucleotide	220-223	nitric oxide synthase 3	Homo sapiens	88-121
17610838-1	2007	The object of this study was to clarify the mechanism of electron transfer in the human endothelial nitric oxide synthase (eNOS) reductase domain using recombinant eNOS reductase domains; the FAD/NADPH domain containing FAD- and NADPH-binding sites and the FAD/FMN domain containing FAD/NADPH-, FMN-, and a calmodulin-binding sites.	NADP	229-234	nitric oxide synthase 3	Homo sapiens	88-121
17427197-6	2007	TGF-beta1 and high D-glucose increased hCAT-1 mRNA expression ( approximately 8-fold) and maximal transport velocity (V(max)), L-[(3)H]citrulline formation from L-[(3)H]arginine (index of NO synthesis) and endothelial NO synthase (eNOS) protein abundance, but did not alter eNOS phosphorylation.	Citrulline	135-145	nitric oxide synthase 3	Homo sapiens	231-235
17427197-6	2007	TGF-beta1 and high D-glucose increased hCAT-1 mRNA expression ( approximately 8-fold) and maximal transport velocity (V(max)), L-[(3)H]citrulline formation from L-[(3)H]arginine (index of NO synthesis) and endothelial NO synthase (eNOS) protein abundance, but did not alter eNOS phosphorylation.	Citrulline	135-145	nitric oxide synthase 3	Homo sapiens	274-278
17427197-6	2007	TGF-beta1 and high D-glucose increased hCAT-1 mRNA expression ( approximately 8-fold) and maximal transport velocity (V(max)), L-[(3)H]citrulline formation from L-[(3)H]arginine (index of NO synthesis) and endothelial NO synthase (eNOS) protein abundance, but did not alter eNOS phosphorylation.	Glucose	19-28	nitric oxide synthase 3	Homo sapiens	231-235
17427197-9	2007	High D-glucose increases L-arginine transport and eNOS expression following TbetaRII activation by TGF-beta1 involving p42/44(mapk) and Smad2 in HUVEC.	Glucose	5-14	nitric oxide synthase 3	Homo sapiens	50-54
17427197-6	2007	TGF-beta1 and high D-glucose increased hCAT-1 mRNA expression ( approximately 8-fold) and maximal transport velocity (V(max)), L-[(3)H]citrulline formation from L-[(3)H]arginine (index of NO synthesis) and endothelial NO synthase (eNOS) protein abundance, but did not alter eNOS phosphorylation.	Glucose	19-28	nitric oxide synthase 3	Homo sapiens	274-278
17878755-5	2007	The migration can also be nearly completely blocked by phosphoinositide 3-kinase inhibitors (LY294002 and wortmannin) and eNOS inhibitor (N-nitro-arginine methyl ester), whereas mitogen-activated protein kinase/ERK inhibitor (PD98059) had no significant effect on SDF-1alpha-induced migration.	NG-Nitroarginine Methyl Ester	138-167	nitric oxide synthase 3	Homo sapiens	122-126
16938300-0	2007	Anti-inflammatory effects of atorvastatin: modulation by the T-786C polymorphism in the endothelial nitric oxide synthase gene.	Atorvastatin	29-41	nitric oxide synthase 3	Homo sapiens	88-121
17878755-5	2007	The migration can also be nearly completely blocked by phosphoinositide 3-kinase inhibitors (LY294002 and wortmannin) and eNOS inhibitor (N-nitro-arginine methyl ester), whereas mitogen-activated protein kinase/ERK inhibitor (PD98059) had no significant effect on SDF-1alpha-induced migration.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	226-233	nitric oxide synthase 3	Homo sapiens	122-126
17762636-0	2007	Three endothelial nitric oxide (NOS3) gene polymorphisms in hypertensive and normotensive individuals: meta-analysis of 53 studies reveals evidence of publication bias.	Nitric Oxide	18-30	nitric oxide synthase 3	Homo sapiens	32-36
17762636-1	2007	BACKGROUND: Studies on the relationship between endothelial nitric oxide (NOS3) gene variants and hypertension have been conflicting.	Nitric Oxide	60-72	nitric oxide synthase 3	Homo sapiens	74-78
17350298-1	2007	Molecular dynamics (MD) simulations were carried out for inducible nitric oxide synthase (iNOS) and endothelial nitric oxide synthase (eNOS) isoforms complexed with substrate (L-arginine) and the iNOS specific inhibitor GW 273629, 2 for a time period of 1.2ns.	Arginine	176-186	nitric oxide synthase 3	Homo sapiens	100-133
17350298-1	2007	Molecular dynamics (MD) simulations were carried out for inducible nitric oxide synthase (iNOS) and endothelial nitric oxide synthase (eNOS) isoforms complexed with substrate (L-arginine) and the iNOS specific inhibitor GW 273629, 2 for a time period of 1.2ns.	glycyltryptophan	220-222	nitric oxide synthase 3	Homo sapiens	100-133
17472573-9	2007	Fluvastatin increased eNOS [endothelial NOS (NO synthase)] expression, but NOS inhibitors failed to reverse the effect of fluvastatin on vWF secretion.	Fluvastatin	0-11	nitric oxide synthase 3	Homo sapiens	22-26
20409867-1	2007	Nitric oxide generated by the vascular endothelial nitric oxide synthase (eNOS) plays an important role in the regulation of vascular structure/function and blood pressure.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	39-72
20409867-1	2007	Nitric oxide generated by the vascular endothelial nitric oxide synthase (eNOS) plays an important role in the regulation of vascular structure/function and blood pressure.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	74-78
17928646-2	2007	Based on the differences between hydrophobic and hydrophilic statins in their reduction of cardiac events, we analyzed the effects of rosuvastatin and cerivastatin on eNOS and inducible NO synthase (iNOS) expression and NOS activity in TNF-alpha-stimulated human umbilical vein endothelial cells (HUVEC).	Rosuvastatin Calcium	134-146	nitric oxide synthase 3	Homo sapiens	167-171
17928646-2	2007	Based on the differences between hydrophobic and hydrophilic statins in their reduction of cardiac events, we analyzed the effects of rosuvastatin and cerivastatin on eNOS and inducible NO synthase (iNOS) expression and NOS activity in TNF-alpha-stimulated human umbilical vein endothelial cells (HUVEC).	cerivastatin	151-163	nitric oxide synthase 3	Homo sapiens	167-171
17928646-3	2007	Both statins reversed down-regulation of eNOS mRNA and protein expression by inhibiting HMG-CoA reductase and isoprenoid synthesis.	Terpenes	110-120	nitric oxide synthase 3	Homo sapiens	41-45
17928646-4	2007	Cerivastatin tended to a more pronounced effect on eNOS expression compared to rosuvastatin.	cerivastatin	0-12	nitric oxide synthase 3	Homo sapiens	51-55
17928646-7	2007	Rosuvastatin and cerivastatin reverse the detrimental effects of TNF-alpha-induced down-regulation in eNOS protein expression and increase NO synthase activity by inhibiting HMG-CoA reductase and subsequent blocking of isoprenoid synthesis.	Rosuvastatin Calcium	0-12	nitric oxide synthase 3	Homo sapiens	102-106
17928646-7	2007	Rosuvastatin and cerivastatin reverse the detrimental effects of TNF-alpha-induced down-regulation in eNOS protein expression and increase NO synthase activity by inhibiting HMG-CoA reductase and subsequent blocking of isoprenoid synthesis.	cerivastatin	17-29	nitric oxide synthase 3	Homo sapiens	102-106
17928646-7	2007	Rosuvastatin and cerivastatin reverse the detrimental effects of TNF-alpha-induced down-regulation in eNOS protein expression and increase NO synthase activity by inhibiting HMG-CoA reductase and subsequent blocking of isoprenoid synthesis.	Terpenes	219-229	nitric oxide synthase 3	Homo sapiens	102-106
17827916-2	2007	We investigated how aldosterone regulates endothelial nitric oxide synthase (eNOS) function in human umbilical vein endothelial cells (HUVECs).	Aldosterone	20-31	nitric oxide synthase 3	Homo sapiens	42-75
17496212-2	2007	Cellular NO production depends absolutely on the availability of arginine, substrate of endothelial nitric oxide synthase (eNOS).	Arginine	65-73	nitric oxide synthase 3	Homo sapiens	88-121
17486142-6	2007	Uncoupling of eNOS (one electron transfer to molecular oxygen, the second substrate of eNOS) during ischemia-reperfusion due to diminished availability of L-arginine and/or tetrahydrobiopterin is even discussed as one major source of superoxide formation.	Oxygen	55-61	nitric oxide synthase 3	Homo sapiens	14-18
17486142-6	2007	Uncoupling of eNOS (one electron transfer to molecular oxygen, the second substrate of eNOS) during ischemia-reperfusion due to diminished availability of L-arginine and/or tetrahydrobiopterin is even discussed as one major source of superoxide formation.	Oxygen	55-61	nitric oxide synthase 3	Homo sapiens	87-91
17486142-6	2007	Uncoupling of eNOS (one electron transfer to molecular oxygen, the second substrate of eNOS) during ischemia-reperfusion due to diminished availability of L-arginine and/or tetrahydrobiopterin is even discussed as one major source of superoxide formation.	Arginine	155-165	nitric oxide synthase 3	Homo sapiens	14-18
17486142-6	2007	Uncoupling of eNOS (one electron transfer to molecular oxygen, the second substrate of eNOS) during ischemia-reperfusion due to diminished availability of L-arginine and/or tetrahydrobiopterin is even discussed as one major source of superoxide formation.	Arginine	155-165	nitric oxide synthase 3	Homo sapiens	87-91
17486142-6	2007	Uncoupling of eNOS (one electron transfer to molecular oxygen, the second substrate of eNOS) during ischemia-reperfusion due to diminished availability of L-arginine and/or tetrahydrobiopterin is even discussed as one major source of superoxide formation.	sapropterin	173-192	nitric oxide synthase 3	Homo sapiens	14-18
17486142-6	2007	Uncoupling of eNOS (one electron transfer to molecular oxygen, the second substrate of eNOS) during ischemia-reperfusion due to diminished availability of L-arginine and/or tetrahydrobiopterin is even discussed as one major source of superoxide formation.	sapropterin	173-192	nitric oxide synthase 3	Homo sapiens	87-91
17486142-6	2007	Uncoupling of eNOS (one electron transfer to molecular oxygen, the second substrate of eNOS) during ischemia-reperfusion due to diminished availability of L-arginine and/or tetrahydrobiopterin is even discussed as one major source of superoxide formation.	Superoxides	234-244	nitric oxide synthase 3	Homo sapiens	14-18
17486142-6	2007	Uncoupling of eNOS (one electron transfer to molecular oxygen, the second substrate of eNOS) during ischemia-reperfusion due to diminished availability of L-arginine and/or tetrahydrobiopterin is even discussed as one major source of superoxide formation.	Superoxides	234-244	nitric oxide synthase 3	Homo sapiens	87-91
17045269-4	2007	Cyanidin significantly elevated expression of endothelial nitric oxide synthase (eNOS) and thioredoxin (Trx).	cyanidin	0-8	nitric oxide synthase 3	Homo sapiens	46-79
17545686-8	2007	When the cells are exposed to aldosterone, a reduction of eNOS expression is found that is antagonized by DRSP.	Aldosterone	30-41	nitric oxide synthase 3	Homo sapiens	58-62
17602951-10	2007	The data show that ROS are formed within skeletal muscle during exercise and that oral intake of antioxidants can enhance the exercise-induced adaptive mRNA responses of eNOS and UCP3.	Reactive Oxygen Species	19-22	nitric oxide synthase 3	Homo sapiens	170-174
17496167-8	2007	Interestingly, betulinic acid also attenuated the expression of NADPH oxidase subunits Nox4 and p22phox, thereby reducing oxidative stress and improving eNOS function.	betulinic acid	15-29	nitric oxide synthase 3	Homo sapiens	153-157
17496167-0	2007	Reciprocal regulation of endothelial nitric-oxide synthase and NADPH oxidase by betulinic acid in human endothelial cells.	betulinic acid	80-94	nitric oxide synthase 3	Homo sapiens	25-58
17496167-1	2007	Nitric oxide (NO) produced by endothelial NO synthase (eNOS) is a protective principle in the vasculature.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	55-59
17496167-10	2007	Thus, betulinic acid possesses combined properties of eNOS up-regulation and NADPH oxidase down-regulation.	betulinic acid	6-20	nitric oxide synthase 3	Homo sapiens	54-58
17496167-7	2007	Jujuboside A, jujuboside B, or betulin had no significant effect on eNOS expression, whereas betulinic acid increased eNOS mRNA and protein expression in HUVEC and EA.hy 926 cells.	betulinic acid	93-107	nitric oxide synthase 3	Homo sapiens	118-122
17922342-0	2007	Cigarette smoke-induced alterations in endothelial nitric oxide synthase phosphorylation: role of protein kinase C. Endothelial nitric oxide synthase (eNOS) is regulated by phosphorylation of Ser(1177) and Thr(495), which affects NO bioavailability.	Serine	192-195	nitric oxide synthase 3	Homo sapiens	39-72
17356797-5	2007	In transduced carotid artery, calcium-dependent eNOS activity was minimal and did not differ from control conditions.	Calcium	30-37	nitric oxide synthase 3	Homo sapiens	48-52
17637430-10	2007	All cardioprotective effects of endothelial nitric oxide synthase were blocked by N(omega)-nitro-l-arginine methyl ester administration, indicating a nitric-oxide-mediated event.	NG-Nitroarginine Methyl Ester	82-120	nitric oxide synthase 3	Homo sapiens	32-65
17637430-10	2007	All cardioprotective effects of endothelial nitric oxide synthase were blocked by N(omega)-nitro-l-arginine methyl ester administration, indicating a nitric-oxide-mediated event.	Nitric Oxide	150-162	nitric oxide synthase 3	Homo sapiens	32-65
17449545-7	2007	Apocynin caused significant improvement of increased mRNA and protein levels of endothelial nitric oxide synthase (eNOS) in BAECs given nitroglycerin continuously over the treatment period.	Nitroglycerin	136-149	nitric oxide synthase 3	Homo sapiens	80-113
16842798-1	2007	The nitric oxide produced by endothelial nitric oxide synthase (eNOS) plays a pivotal role in protecting the arterial wall from damages and atherosclerosis.	Nitric Oxide	4-16	nitric oxide synthase 3	Homo sapiens	29-62
16842798-1	2007	The nitric oxide produced by endothelial nitric oxide synthase (eNOS) plays a pivotal role in protecting the arterial wall from damages and atherosclerosis.	Nitric Oxide	4-16	nitric oxide synthase 3	Homo sapiens	64-68
17611397-9	2007	NOS1 and NOS3 isoforms are expressed in MCF-7 cells and its activation by CARB triggers nitric oxide synthesis and vascular endothelial growth factor expression increasing blood vessels formation induced by mammary tumor cells in vivo.	Carbachol	74-78	nitric oxide synthase 3	Homo sapiens	9-13
17611397-9	2007	NOS1 and NOS3 isoforms are expressed in MCF-7 cells and its activation by CARB triggers nitric oxide synthesis and vascular endothelial growth factor expression increasing blood vessels formation induced by mammary tumor cells in vivo.	Nitric Oxide	88-100	nitric oxide synthase 3	Homo sapiens	9-13
17922342-0	2007	Cigarette smoke-induced alterations in endothelial nitric oxide synthase phosphorylation: role of protein kinase C. Endothelial nitric oxide synthase (eNOS) is regulated by phosphorylation of Ser(1177) and Thr(495), which affects NO bioavailability.	Serine	192-195	nitric oxide synthase 3	Homo sapiens	116-149
17922342-0	2007	Cigarette smoke-induced alterations in endothelial nitric oxide synthase phosphorylation: role of protein kinase C. Endothelial nitric oxide synthase (eNOS) is regulated by phosphorylation of Ser(1177) and Thr(495), which affects NO bioavailability.	Threonine	206-209	nitric oxide synthase 3	Homo sapiens	116-149
17563560-1	2007	BACKGROUND: The Glu298Asp, T786C and 4a/4b genetic polymorphisms within the endothelial nitric oxide synthase (e-NOS) gene may predispose to hypertension, ischaemic heart disease and renal damage, possibly by reducing the generation of nitric oxide (NO), a fundamental substance in renal and cardiovascular biology.	Nitric Oxide	88-100	nitric oxide synthase 3	Homo sapiens	111-116
17427956-6	2007	Other signaling molecules like the insulin receptor substrate-1 (IRS-1), the S6 ribosomal subunit kinase, and the endothelial nitric oxide synthase (eNOS) were phosphorylated by PTH, insulin, and PEMF to the same relative extent and within the same time frame.	pemf	196-200	nitric oxide synthase 3	Homo sapiens	114-147
17499557-7	2007	NO production was enhanced in a time- and concentration-dependent manner (P&lt;0.05), which was well matched with the expression of eNOS mRNA (up to 2.4-fold) and protein (up to 2.5-fold) after long-term incubation with icariin in endothelial cells (P&lt;0.05).	icariin	220-227	nitric oxide synthase 3	Homo sapiens	132-136
17717927-3	2007	The nitric oxide (NO) level, the protein and mRNA expression of nitric oxide synthase (cNOS) in PAEC were measured by nitric acid deoxidizing assay, RT-PCR and immunohistochemical assay, respectively.	Nitric Acid	118-129	nitric oxide synthase 3	Homo sapiens	87-91
17499557-9	2007	hy926 cells incubated with icariin for 24 h, in association with an increase in the expression of eNOS gene.	icariin	27-34	nitric oxide synthase 3	Homo sapiens	98-102
17512554-12	2007	Since cardiovascular diseases are often associated with the development of erectile dysfunction, the nebivolol-induced eNOS-activation in corpus cavernosum may be beneficial when treating patients suffering from cardiovascular disease.	Nebivolol	101-110	nitric oxide synthase 3	Homo sapiens	119-123
17966596-6	2007	The relationship between alcohol consumption and incidence of metabolic syndrome is more pronounced among red wine drinkers because polyphenoles contained in red wine increase the activity of endothelial nitric oxide synthase (eNOS), which plays a key role in the pathogenesis of metabolic syndrome.	Alcohols	25-32	nitric oxide synthase 3	Homo sapiens	192-225
17966596-6	2007	The relationship between alcohol consumption and incidence of metabolic syndrome is more pronounced among red wine drinkers because polyphenoles contained in red wine increase the activity of endothelial nitric oxide synthase (eNOS), which plays a key role in the pathogenesis of metabolic syndrome.	polyphenoles	132-144	nitric oxide synthase 3	Homo sapiens	192-225
17966596-9	2007	Endothelial nitric oxide synthase requires the presence of antioxidants, which prevent both inactivation of nitric oxide in the reaction with peroxide anions and the accumulation of peroxynitrates.	peroxide anions	142-157	nitric oxide synthase 3	Homo sapiens	0-33
17966596-9	2007	Endothelial nitric oxide synthase requires the presence of antioxidants, which prevent both inactivation of nitric oxide in the reaction with peroxide anions and the accumulation of peroxynitrates.	Peroxynitrous Acid	182-196	nitric oxide synthase 3	Homo sapiens	0-33
17619801-2	2007	Monomethylarsonous acid (MMA(III)) is a reactive metabolite of inorganic arsenic and a potent inhibitor of endothelial nitric oxide synthase (eNOS).	monomethylarsonous acid	25-33	nitric oxide synthase 3	Homo sapiens	142-146
17413035-1	2007	OBJECTIVE: 6R-5,6,7,8-tetrahydro-L-biopterin (6R-BH4) is a cofactor for endothelial nitric oxide synthase but also has antioxidant properties.	sapropterin	11-44	nitric oxide synthase 3	Homo sapiens	72-105
17413035-1	2007	OBJECTIVE: 6R-5,6,7,8-tetrahydro-L-biopterin (6R-BH4) is a cofactor for endothelial nitric oxide synthase but also has antioxidant properties.	sapropterin	46-52	nitric oxide synthase 3	Homo sapiens	72-105
17413035-3	2007	When endothelial nitric oxide synthase is 6R-BH4-deplete, it synthesizes superoxide rather than nitric oxide.	Superoxides	73-83	nitric oxide synthase 3	Homo sapiens	5-38
17619801-0	2007	Monomethylarsonous acid induced cytotoxicity and endothelial nitric oxide synthase phosphorylation in endothelial cells.	monomethylarsonous acid	0-23	nitric oxide synthase 3	Homo sapiens	49-82
17329403-7	2007	ANG II-dependent activation of MAPK and the increase in endothelial NOS (eNOS) were prevented when PAECs were transfected with Ras DN cDNA or treated with FTI-277, a farnesyl transferase inhibitor.	FTI 277	155-162	nitric oxide synthase 3	Homo sapiens	56-71
17619801-3	2007	Arsenic is also reported to phosphorylate eNOS in cultured keratinocyte and Human T cell leukemia Jurkat cells, respectively.	Arsenic	0-7	nitric oxide synthase 3	Homo sapiens	42-46
17619801-2	2007	Monomethylarsonous acid (MMA(III)) is a reactive metabolite of inorganic arsenic and a potent inhibitor of endothelial nitric oxide synthase (eNOS).	monomethylarsonous acid	0-23	nitric oxide synthase 3	Homo sapiens	107-140
17619801-2	2007	Monomethylarsonous acid (MMA(III)) is a reactive metabolite of inorganic arsenic and a potent inhibitor of endothelial nitric oxide synthase (eNOS).	monomethylarsonous acid	0-23	nitric oxide synthase 3	Homo sapiens	142-146
17619801-10	2007	Our study also suggests that MMA(III) could induce the eNOS phosphorylation through modification to cellular thiols of the eNOS enzyme.	mma(	29-33	nitric oxide synthase 3	Homo sapiens	55-59
17619801-2	2007	Monomethylarsonous acid (MMA(III)) is a reactive metabolite of inorganic arsenic and a potent inhibitor of endothelial nitric oxide synthase (eNOS).	monomethylarsonous acid	25-33	nitric oxide synthase 3	Homo sapiens	107-140
17619801-10	2007	Our study also suggests that MMA(III) could induce the eNOS phosphorylation through modification to cellular thiols of the eNOS enzyme.	mma(	29-33	nitric oxide synthase 3	Homo sapiens	123-127
17619801-10	2007	Our study also suggests that MMA(III) could induce the eNOS phosphorylation through modification to cellular thiols of the eNOS enzyme.	Sulfhydryl Compounds	109-115	nitric oxide synthase 3	Homo sapiens	55-59
17619801-10	2007	Our study also suggests that MMA(III) could induce the eNOS phosphorylation through modification to cellular thiols of the eNOS enzyme.	Sulfhydryl Compounds	109-115	nitric oxide synthase 3	Homo sapiens	123-127
17619801-11	2007	And the initial up-regulation of eNOS phosphorylation by MMA(III )seems to be an adaptive response against disruption of eNOS bioactivity during arsenic exposure.	Arsenic	145-152	nitric oxide synthase 3	Homo sapiens	33-37
17619801-11	2007	And the initial up-regulation of eNOS phosphorylation by MMA(III )seems to be an adaptive response against disruption of eNOS bioactivity during arsenic exposure.	Arsenic	145-152	nitric oxide synthase 3	Homo sapiens	121-125
17476577-1	2007	In order to clarify the developmental regulation of the eNOS activity in intestine by phosphorylation, we examined the immunohistochemical localizations of the eNOS phosphorylation sites at Ser(1177), Ser(116) and at Thr(495) in cells of the mouse enteric mucosa and myenteric plexus at E13.5, E14.5, E16.5, E18.5, E20.5 and P3.	Serine	190-193	nitric oxide synthase 3	Homo sapiens	56-60
17622691-12	2007	Reduced arginine supply may lead to eNOS uncoupling and generation of superoxide, contributing to HCY-induced oxidative stress.	Arginine	8-16	nitric oxide synthase 3	Homo sapiens	36-40
17622691-12	2007	Reduced arginine supply may lead to eNOS uncoupling and generation of superoxide, contributing to HCY-induced oxidative stress.	Homocysteine	98-101	nitric oxide synthase 3	Homo sapiens	36-40
17259657-1	2007	NOS3 and MPO genes encode endothelial nitric oxide synthase and myeloperoxidase (MPO), respectively, which generate nitric oxide and reactive oxygen species.	Nitric Oxide	38-50	nitric oxide synthase 3	Homo sapiens	0-4
17259657-1	2007	NOS3 and MPO genes encode endothelial nitric oxide synthase and myeloperoxidase (MPO), respectively, which generate nitric oxide and reactive oxygen species.	Reactive Oxygen Species	133-156	nitric oxide synthase 3	Homo sapiens	0-4
17476577-1	2007	In order to clarify the developmental regulation of the eNOS activity in intestine by phosphorylation, we examined the immunohistochemical localizations of the eNOS phosphorylation sites at Ser(1177), Ser(116) and at Thr(495) in cells of the mouse enteric mucosa and myenteric plexus at E13.5, E14.5, E16.5, E18.5, E20.5 and P3.	Serine	190-193	nitric oxide synthase 3	Homo sapiens	160-164
17482266-4	2007	L-Arginine is the substrate for the endothelial NO synthase (eNOS) to generate NO.	Arginine	0-10	nitric oxide synthase 3	Homo sapiens	61-65
17482266-9	2007	This could solve the L-arginine paradox namely that L-arginine improves NO-mediated vascular function in vivo, although its baseline plasma concentration is about 25- to 30-fold higher than the Michaelis-Menten constant Km of the isolated, purified eNOS in vitro.	Arginine	52-62	nitric oxide synthase 3	Homo sapiens	249-253
17418102-0	2007	15-deoxy-Delta12,14-prostaglandin J2-induced down-regulation of endothelial nitric oxide synthase in association with HSP70 induction.	14-prostaglandin j2	17-36	nitric oxide synthase 3	Homo sapiens	64-97
17502619-2	2007	Nitric oxide (NO) is an important paracrine mediator of vascular and platelet function and is produced in the vasculature by the enzyme NO synthase type 3 (NOS-3).	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	136-161
17502619-5	2007	Formation of this ternary complex among NOS-3, globular beta-actin, and Hsp90, in turn, results in an increase in both NOS activity and cyclic guanosine-3",5"-monophosphate, an index of bioactive NO, as well as an increased rate of Hsp90 degradation, thus limiting the duration for which NOS-3 remains activated.	Cyclic GMP	136-172	nitric oxide synthase 3	Homo sapiens	40-45
17418102-1	2007	A natural ligand of peroxisome proliferator-activated receptor gamma (PPARgamma), 15-deoxy-Delta(12,14)-prostaglandin J(2) (15d-PGJ(2)), decreases endothelial nitric oxide synthase (eNOS) expression by an unknown mechanism.	prostaglandin j	104-119	nitric oxide synthase 3	Homo sapiens	147-180
17418102-1	2007	A natural ligand of peroxisome proliferator-activated receptor gamma (PPARgamma), 15-deoxy-Delta(12,14)-prostaglandin J(2) (15d-PGJ(2)), decreases endothelial nitric oxide synthase (eNOS) expression by an unknown mechanism.	prostaglandin j	104-119	nitric oxide synthase 3	Homo sapiens	182-186
17418102-2	2007	Here we found that 15d-PGJ(2)-induced eNOS reduction is inversely associated with heat shock protein 70 (HSP70) induction in endothelial cells.	15d-pgj	19-26	nitric oxide synthase 3	Homo sapiens	38-42
17418102-7	2007	Cellular fractionation revealed that treatment with 15d-PGJ(2) increased eNOS distribution 2.5-fold from soluble to insoluble fractions.	15d-pgj	52-59	nitric oxide synthase 3	Homo sapiens	73-77
17237240-2	2007	Several enzymatic systems contribute to ROS production in vascular endothelial cells, including NA(D)PH oxidase, xanthine oxidase, uncoupled endothelial nitric oxide synthase, and the mitochondrial electron transport chain.	Reactive Oxygen Species	40-43	nitric oxide synthase 3	Homo sapiens	141-174
17438380-4	2007	NO, generated by catalytic activity of endothelial NO synthase (eNOS) on l-arginine, modulates vascular function and structure.	Arginine	73-83	nitric oxide synthase 3	Homo sapiens	39-62
17223008-5	2007	OPC-28326 markedly induced phosphorylation of endothelial nitric oxide synthase (eNOS) in HAECs via phosphatidylinositol-3 kinase PI3K/Akt (PI3K/Akt) pathway.	OPC 28326	0-9	nitric oxide synthase 3	Homo sapiens	46-79
17438380-4	2007	NO, generated by catalytic activity of endothelial NO synthase (eNOS) on l-arginine, modulates vascular function and structure.	Arginine	73-83	nitric oxide synthase 3	Homo sapiens	64-68
17264164-5	2007	Coexpression of full-length eNOS with eNOS13A diminished eNOS enzyme activity in COS-7 cells by formation of heterodimers.	carbonyl sulfide	81-84	nitric oxide synthase 3	Homo sapiens	28-32
17420345-7	2007	Low-dose folic acid increased nitric oxide-mediated endothelium-dependent vasomotor responses, reduced vascular superoxide production, and improved enzymatic coupling of endothelial nitric oxide synthase through availability of the cofactor tetrahydrobiopterin.	Folic Acid	9-19	nitric oxide synthase 3	Homo sapiens	170-203
17420345-7	2007	Low-dose folic acid increased nitric oxide-mediated endothelium-dependent vasomotor responses, reduced vascular superoxide production, and improved enzymatic coupling of endothelial nitric oxide synthase through availability of the cofactor tetrahydrobiopterin.	sapropterin	241-260	nitric oxide synthase 3	Homo sapiens	170-203
17420345-10	2007	CONCLUSIONS: Low-dose folic acid treatment, comparable to daily intake and dietary fortification, improves vascular function through effects on endothelial nitric oxide synthase and vascular oxidative stress.	Folic Acid	22-32	nitric oxide synthase 3	Homo sapiens	144-177
18690862-7	2007	On the other hand, it is clear that acute low doses of EtOH increase both the release of NO and endothelial NOS (eNOS) expression, and augment endothelium-mediated vasodilatation, whereas higher doses impair endothelial functions.	Ethanol	55-59	nitric oxide synthase 3	Homo sapiens	96-111
17264164-5	2007	Coexpression of full-length eNOS with eNOS13A diminished eNOS enzyme activity in COS-7 cells by formation of heterodimers.	carbonyl sulfide	81-84	nitric oxide synthase 3	Homo sapiens	38-42
17413318-4	2007	Overexpression of NOS3 in the brain increased the levels of APP, APP-Abeta, p53, Tau, glial fibrillary acidic protein, and peroxisome proliferator activated receptors (PPAR) delta and gamma and decreased the levels of Hu (neuronal marker) mRNA, phosphorylated glycogen synthase kinase 3beta, ATP synthase, and choline acetyltransferase expression as demonstrated by real-time quantitative reverse-transcribed polymerase chain reaction, Western blot analysis, or immunohistochemical staining.	Choline	310-317	nitric oxide synthase 3	Homo sapiens	18-22
17457350-3	2007	Endothelial production of nitric oxide by endothelial nitric oxide synthase in the corpus cavernosum is involved in the maintenance of penile erection.	Nitric Oxide	26-38	nitric oxide synthase 3	Homo sapiens	42-75
17457351-1	2007	L-arginine is the substrate of endothelial nitric oxide synthase and the main precursor of nitric oxide in the vascular endothelium, thus its effects are mediated largely by increases in nitric oxide production.	Arginine	0-10	nitric oxide synthase 3	Homo sapiens	31-64
16860889-1	2007	L-Arginine is the substrate of endothelial nitric oxide synthase (eNOS) and the main precursor of nitric oxide (NO) in the vascular endothelium.	Arginine	0-10	nitric oxide synthase 3	Homo sapiens	31-64
16860889-1	2007	L-Arginine is the substrate of endothelial nitric oxide synthase (eNOS) and the main precursor of nitric oxide (NO) in the vascular endothelium.	Arginine	0-10	nitric oxide synthase 3	Homo sapiens	66-70
16860889-1	2007	L-Arginine is the substrate of endothelial nitric oxide synthase (eNOS) and the main precursor of nitric oxide (NO) in the vascular endothelium.	Nitric Oxide	43-55	nitric oxide synthase 3	Homo sapiens	66-70
17306574-0	2007	Influence of eNOS haplotypes on the plasma nitric oxide products concentrations in hypertensive and type 2 diabetes mellitus patients.	Nitric Oxide	43-55	nitric oxide synthase 3	Homo sapiens	13-17
17306574-2	2007	We evaluated the association of eNOS genotypes/haplotypes with the plasma concentrations of nitrite/nitrate (NO(x)), which are products of nitric oxide in HT, T2DM, and T2DM+HT patients.	Nitrites	92-99	nitric oxide synthase 3	Homo sapiens	32-36
17306574-2	2007	We evaluated the association of eNOS genotypes/haplotypes with the plasma concentrations of nitrite/nitrate (NO(x)), which are products of nitric oxide in HT, T2DM, and T2DM+HT patients.	Nitrates	100-107	nitric oxide synthase 3	Homo sapiens	32-36
17306574-2	2007	We evaluated the association of eNOS genotypes/haplotypes with the plasma concentrations of nitrite/nitrate (NO(x)), which are products of nitric oxide in HT, T2DM, and T2DM+HT patients.	Nitric Oxide	139-151	nitric oxide synthase 3	Homo sapiens	32-36
17413318-6	2007	The results suggest that increased cerebral expression of NOS3 causes several molecular abnormalities related to AD-type neurodegeneration, including oxidative stress, mitochondrial dysfunction, and impaired acetylcholine homeostasis.	Acetylcholine	208-221	nitric oxide synthase 3	Homo sapiens	58-62
17505150-2	2007	Asymmetric dimethylarginine (ADMA), a novel inhibitor of endothelial nitric oxide synthase (eNOS), blocks nitric oxide (NO) synthesis from L-arginine.	dimethylarginine	11-27	nitric oxide synthase 3	Homo sapiens	57-90
17320763-0	2007	Vascular and perivascular nitric oxide release and transport: biochemical pathways of neuronal nitric oxide synthase (NOS1) and endothelial nitric oxide synthase (NOS3).	Nitric Oxide	26-38	nitric oxide synthase 3	Homo sapiens	128-161
17293684-3	2007	In models of hypertension, and chronic and acute renal disease, the loss of nitric oxide bioavailability may occur due to inactivation of endothelial nitric oxide synthase, synthesis of endogenous inhibitors or oxidative inactivation of nitric oxide.	Nitric Oxide	76-88	nitric oxide synthase 3	Homo sapiens	138-171
16871271-0	2007	The association between intron 4 VNTR, E298A and IVF 23+10 G/T polymorphisms of ecNOS gene and sildenafil responsiveness in patients with erectile dysfunction.	Sildenafil Citrate	95-105	nitric oxide synthase 3	Homo sapiens	80-85
16871271-1	2007	The objective of the study was to determine the association between intron 4 variable number of tandem repeats (VNTR), E298A and IVF 23+10 G/T polymorphisms of ec-NOS gene and sildenafil responsiveness in patients with erectile dysfunction (ED).	Sildenafil Citrate	176-186	nitric oxide synthase 3	Homo sapiens	160-166
16871271-7	2007	The frequency of the ec-NOS gene intron 4 genotype were found as bb=41.7%, ab=50% and aa=8.3% in the sildenafil responders and bb=93.5% and ba=6.5% in the sildenafil non-responders.	boeravinone B	65-67	nitric oxide synthase 3	Homo sapiens	21-27
16871271-7	2007	The frequency of the ec-NOS gene intron 4 genotype were found as bb=41.7%, ab=50% and aa=8.3% in the sildenafil responders and bb=93.5% and ba=6.5% in the sildenafil non-responders.	Sildenafil Citrate	101-111	nitric oxide synthase 3	Homo sapiens	21-27
16871271-7	2007	The frequency of the ec-NOS gene intron 4 genotype were found as bb=41.7%, ab=50% and aa=8.3% in the sildenafil responders and bb=93.5% and ba=6.5% in the sildenafil non-responders.	boeravinone B	127-129	nitric oxide synthase 3	Homo sapiens	21-27
16871271-7	2007	The frequency of the ec-NOS gene intron 4 genotype were found as bb=41.7%, ab=50% and aa=8.3% in the sildenafil responders and bb=93.5% and ba=6.5% in the sildenafil non-responders.	Barium	140-142	nitric oxide synthase 3	Homo sapiens	21-27
16871271-7	2007	The frequency of the ec-NOS gene intron 4 genotype were found as bb=41.7%, ab=50% and aa=8.3% in the sildenafil responders and bb=93.5% and ba=6.5% in the sildenafil non-responders.	Sildenafil Citrate	155-165	nitric oxide synthase 3	Homo sapiens	21-27
16871271-10	2007	These findings may indicate that "a" allele of ec-NOS gene intron 4 VNTR polymorphism associates with a better sildenafil response.	Sildenafil Citrate	111-121	nitric oxide synthase 3	Homo sapiens	47-53
17381681-0	2007	Direct measurements of nitric oxide release in relation to expression of endothelial nitric oxide synthase in isolated porcine mitral valves.	Nitric Oxide	23-35	nitric oxide synthase 3	Homo sapiens	73-106
17409706-3	2007	In vascular endothelial cells, microsphere embolism-induced eNOS expression was associated with protein tyrosine nitration, which is a marker of generation of peroxynitrite.	Tyrosine	104-112	nitric oxide synthase 3	Homo sapiens	60-64
17409706-3	2007	In vascular endothelial cells, microsphere embolism-induced eNOS expression was associated with protein tyrosine nitration, which is a marker of generation of peroxynitrite.	Peroxynitrous Acid	159-172	nitric oxide synthase 3	Homo sapiens	60-64
17327434-1	2007	Uncoupling of the endothelial nitric oxide synthase (eNOS) resulting in superoxide anion (O(2)(-)) formation instead of nitric oxide (NO) causes diabetic endothelial dysfunction.	Superoxides	72-88	nitric oxide synthase 3	Homo sapiens	18-51
17327434-1	2007	Uncoupling of the endothelial nitric oxide synthase (eNOS) resulting in superoxide anion (O(2)(-)) formation instead of nitric oxide (NO) causes diabetic endothelial dysfunction.	Superoxides	90-95	nitric oxide synthase 3	Homo sapiens	18-51
17278969-0	2007	Activation of endothelial nitric oxide synthase by red wine polyphenols: impact of grape cultivars, growing area and the vinification process.	Polyphenols	60-71	nitric oxide synthase 3	Homo sapiens	14-47
17278969-3	2007	The aim of the present study was to elucidate the impact of grape cultivars, growing area and the vinification/fermentation process on the ability of red wine polyphenol extracts to increase human endothelial nitric oxide synthase (eNOS) promotor and enzyme activity.	Polyphenols	159-169	nitric oxide synthase 3	Homo sapiens	197-230
17278969-3	2007	The aim of the present study was to elucidate the impact of grape cultivars, growing area and the vinification/fermentation process on the ability of red wine polyphenol extracts to increase human endothelial nitric oxide synthase (eNOS) promotor and enzyme activity.	Polyphenols	159-169	nitric oxide synthase 3	Homo sapiens	232-236
17278969-4	2007	METHODS: We produced polyphenol extracts from a variety of red wines from all over the world and tested their influence on eNOS promotor activity by a luciferase reporter gene assay.	Polyphenols	21-31	nitric oxide synthase 3	Homo sapiens	123-127
17278969-8	2007	Resveratrol alone significantly enhanced eNOS promotor and enzyme activity, although at concentrations higher than those available in effective concentrations of red wine polyphenol extracts.	Resveratrol	0-11	nitric oxide synthase 3	Homo sapiens	41-45
17505150-2	2007	Asymmetric dimethylarginine (ADMA), a novel inhibitor of endothelial nitric oxide synthase (eNOS), blocks nitric oxide (NO) synthesis from L-arginine.	N,N-dimethylarginine	29-33	nitric oxide synthase 3	Homo sapiens	57-90
17505150-2	2007	Asymmetric dimethylarginine (ADMA), a novel inhibitor of endothelial nitric oxide synthase (eNOS), blocks nitric oxide (NO) synthesis from L-arginine.	Arginine	139-149	nitric oxide synthase 3	Homo sapiens	57-90
17138963-5	2007	In OT-induced cells, L-NAME significantly decreased transcripts of the cardiac markers Nkx2.5, MEF2c, alpha-myosin heavy chain, and less, GATA4, endothelial NOS, and atrial natriuretic peptide, as well as the skeletal myocyte (SM) marker myogenin.	NG-Nitroarginine Methyl Ester	21-27	nitric oxide synthase 3	Homo sapiens	145-160
17229561-1	2007	The aim of this study was to evaluate the effects of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) on NO synthase (eNOS) activation in Ea hy 926 endothelial cells.	Eicosapentaenoic Acid	53-74	nitric oxide synthase 3	Homo sapiens	128-132
17229561-1	2007	The aim of this study was to evaluate the effects of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) on NO synthase (eNOS) activation in Ea hy 926 endothelial cells.	Eicosapentaenoic Acid	76-79	nitric oxide synthase 3	Homo sapiens	128-132
17229561-1	2007	The aim of this study was to evaluate the effects of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) on NO synthase (eNOS) activation in Ea hy 926 endothelial cells.	Docosahexaenoic Acids	85-105	nitric oxide synthase 3	Homo sapiens	128-132
17229561-1	2007	The aim of this study was to evaluate the effects of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) on NO synthase (eNOS) activation in Ea hy 926 endothelial cells.	Docosahexaenoic Acids	107-110	nitric oxide synthase 3	Homo sapiens	128-132
17229561-3	2007	In control medium, eNOS activity (evaluated by the citrulline assay) and eNOS phosphorylation on Ser 1177 were correlated.	Citrulline	51-61	nitric oxide synthase 3	Homo sapiens	19-23
17229561-3	2007	In control medium, eNOS activity (evaluated by the citrulline assay) and eNOS phosphorylation on Ser 1177 were correlated.	Serine	97-100	nitric oxide synthase 3	Homo sapiens	73-77
17229561-7	2007	In conclusion, incorporation of EPA and DHA could be deleterious for endothelial cells by deregulating the activation of eNOS and preventing NO liberation.	Eicosapentaenoic Acid	32-35	nitric oxide synthase 3	Homo sapiens	121-125
17229561-7	2007	In conclusion, incorporation of EPA and DHA could be deleterious for endothelial cells by deregulating the activation of eNOS and preventing NO liberation.	Docosahexaenoic Acids	40-43	nitric oxide synthase 3	Homo sapiens	121-125
16616146-0	2007	Effects of homocysteine on the levels of caveolin-1 and eNOS in caveolae of human coronary artery endothelial cells.	Homocysteine	11-23	nitric oxide synthase 3	Homo sapiens	56-60
17274989-5	2007	In this paper we demonstrate that BH4 domain of Bcl-xl administrated to endothelial cells as the conjugated form with TAT peptide, reverts Abeta-induced apoptotic cell death by activating a survival programme which is Akt/endothelial nitric oxide synthase dependent.	sapropterin	34-37	nitric oxide synthase 3	Homo sapiens	222-255
16678833-2	2007	In parallel studies, we found that statin induces the nuclear translocation of HSF1 and that a decoy oligonucleotide encoding the heat shock element inhibits the statin-induced expression of heat shock protein 70, endothelial nitric oxide synthase (eNOS) and thrombomodulin.	Oligonucleotides	101-116	nitric oxide synthase 3	Homo sapiens	214-247
17263536-3	2007	Specific binding of the nanotrigger to the reductase domain of the endothelial nitric oxide synthase (eNOSred) was demonstrated by competition between NADPH and the nanotrigger on the reduction of eNOSred flavin.	NADP	151-156	nitric oxide synthase 3	Homo sapiens	67-100
17263536-3	2007	Specific binding of the nanotrigger to the reductase domain of the endothelial nitric oxide synthase (eNOSred) was demonstrated by competition between NADPH and the nanotrigger on the reduction of eNOSred flavin.	4,6-dinitro-o-cresol	205-211	nitric oxide synthase 3	Homo sapiens	67-100
16616146-3	2007	The aim of this study was to determine whether Hcy may alter the levels of Cav-1 and eNOS in endothelial caveolae.	Homocysteine	47-50	nitric oxide synthase 3	Homo sapiens	85-89
16616146-5	2007	We found that treatment with 500 microM Hcy for 6h significantly reduced the levels of Cav-1 and eNOS in caveolae compared to untreated control by 47+/-7% and by 38+/-14%, respectively.	Homocysteine	40-43	nitric oxide synthase 3	Homo sapiens	97-101
16616146-10	2007	These results suggest that Hcy induced impairment of NO production through a modulation of Cav-1 expression associated with a loss of eNOS in caveolae.	Homocysteine	27-30	nitric oxide synthase 3	Homo sapiens	134-138
17126309-9	2007	NOS3 intron 4A/B STR was associated with increased concentrations of total cholesterol and apo B.	Cholesterol	75-86	nitric oxide synthase 3	Homo sapiens	0-4
17126309-12	2007	NOS3 is also related to hypertension, endothelial dysfunction and variation on serum cholesterol in young adults with AMI.	Cholesterol	85-96	nitric oxide synthase 3	Homo sapiens	0-4
16633797-8	2007	Our data suggest that the T(-786)C polymorphism of the eNOS gene may be an important risk factor in the development of NAION in Japanese subjects.	naion	119-124	nitric oxide synthase 3	Homo sapiens	55-59
17357445-0	2007	[The pathogenic mechanism of homocysteine -induced endothelial nitric oxide synthase dysfunction and the antagonistic effects by folic acid].	Homocysteine	29-41	nitric oxide synthase 3	Homo sapiens	51-84
16839566-1	2007	The controlled regulation of nitric oxide (NO) synthesis in endothelial cells and cardiomyocytes by the endothelial form of nitric oxide synthase (eNOS or NOS3) is essential for cardiovascular health.	Nitric Oxide	29-41	nitric oxide synthase 3	Homo sapiens	155-159
17357445-1	2007	To investigate the pathogenic mechanism of homocysteine-induced endothelial nitric oxide synthase dysfunction and the antagonistic effects by folic acid (FA).	Homocysteine	43-55	nitric oxide synthase 3	Homo sapiens	64-97
17357445-7	2007	After HUVEC were exposed to Hcy at different concentrations for 72 hours, the level of eNOS mRNA and the content of eNOS protein, the eNOS activity, and the production of nitric oxide (NO) were all significantly and dose-dependently reduced compared with the control group (P&lt; 0.05).	Homocysteine	28-31	nitric oxide synthase 3	Homo sapiens	87-91
17082313-0	2007	17beta-estradiol antagonizes the down-regulation of endothelial nitric-oxide synthase and GTP cyclohydrolase I by high glucose: relevance to postmenopausal diabetic cardiovascular disease.	Estradiol	0-16	nitric oxide synthase 3	Homo sapiens	52-85
17357445-7	2007	After HUVEC were exposed to Hcy at different concentrations for 72 hours, the level of eNOS mRNA and the content of eNOS protein, the eNOS activity, and the production of nitric oxide (NO) were all significantly and dose-dependently reduced compared with the control group (P&lt; 0.05).	Homocysteine	28-31	nitric oxide synthase 3	Homo sapiens	116-120
17082313-0	2007	17beta-estradiol antagonizes the down-regulation of endothelial nitric-oxide synthase and GTP cyclohydrolase I by high glucose: relevance to postmenopausal diabetic cardiovascular disease.	Glucose	119-126	nitric oxide synthase 3	Homo sapiens	52-85
17082313-9	2007	These results suggest that the activation of ERalpha with 17beta-E2 can counteract high-glucose-induced down-regulation of eNOS and GTPCH-I in endothelial cells.	Glucose	88-95	nitric oxide synthase 3	Homo sapiens	123-127
17357445-7	2007	After HUVEC were exposed to Hcy at different concentrations for 72 hours, the level of eNOS mRNA and the content of eNOS protein, the eNOS activity, and the production of nitric oxide (NO) were all significantly and dose-dependently reduced compared with the control group (P&lt; 0.05).	Homocysteine	28-31	nitric oxide synthase 3	Homo sapiens	116-120
17082313-8	2007	Transfection of small-interfering RNA targeting eNOS resulted in a marked reduction in GTPCH-I mRNA under both normal and high-glucose conditions, but this reduction was strongly reversed by 17beta-E2.	Glucose	127-134	nitric oxide synthase 3	Homo sapiens	48-52
17357445-9	2007	The addition of folic acid (100 micromol/L)resulted in partial antagonistic effects against the injury of Hcy on NOS system of endothelial cells, the eNOS protein level and eNOS activity, and NO production increased,and so does the DDAH activity,and the ADMA concentration reduced.	Folic Acid	16-26	nitric oxide synthase 3	Homo sapiens	150-154
17357445-9	2007	The addition of folic acid (100 micromol/L)resulted in partial antagonistic effects against the injury of Hcy on NOS system of endothelial cells, the eNOS protein level and eNOS activity, and NO production increased,and so does the DDAH activity,and the ADMA concentration reduced.	Folic Acid	16-26	nitric oxide synthase 3	Homo sapiens	173-177
17357445-9	2007	The addition of folic acid (100 micromol/L)resulted in partial antagonistic effects against the injury of Hcy on NOS system of endothelial cells, the eNOS protein level and eNOS activity, and NO production increased,and so does the DDAH activity,and the ADMA concentration reduced.	Homocysteine	106-109	nitric oxide synthase 3	Homo sapiens	150-154
17357445-9	2007	The addition of folic acid (100 micromol/L)resulted in partial antagonistic effects against the injury of Hcy on NOS system of endothelial cells, the eNOS protein level and eNOS activity, and NO production increased,and so does the DDAH activity,and the ADMA concentration reduced.	Homocysteine	106-109	nitric oxide synthase 3	Homo sapiens	173-177
17357445-11	2007	The pathogenic mechanism of homocysteine-induced eNOS dysfunction may involve two levels,the level of eNOS protein and eNOS activity,and the level of the expression of eNOS gene.	Homocysteine	28-40	nitric oxide synthase 3	Homo sapiens	49-53
17357445-11	2007	The pathogenic mechanism of homocysteine-induced eNOS dysfunction may involve two levels,the level of eNOS protein and eNOS activity,and the level of the expression of eNOS gene.	Homocysteine	28-40	nitric oxide synthase 3	Homo sapiens	102-106
17357445-11	2007	The pathogenic mechanism of homocysteine-induced eNOS dysfunction may involve two levels,the level of eNOS protein and eNOS activity,and the level of the expression of eNOS gene.	Homocysteine	28-40	nitric oxide synthase 3	Homo sapiens	102-106
17357445-12	2007	The injury on the level of eNOS protein and eNOS activity may go through the DDAH-ADMA pathway.	N,N-dimethylarginine	82-86	nitric oxide synthase 3	Homo sapiens	27-31
17357445-12	2007	The injury on the level of eNOS protein and eNOS activity may go through the DDAH-ADMA pathway.	N,N-dimethylarginine	82-86	nitric oxide synthase 3	Homo sapiens	44-48
17357445-13	2007	Folic acid can exert partial protective roles against the Hcy in the level of eNOS protein and eNOS activity,but without impact on the expression of eNOS gene.	Folic Acid	0-10	nitric oxide synthase 3	Homo sapiens	78-82
17357445-13	2007	Folic acid can exert partial protective roles against the Hcy in the level of eNOS protein and eNOS activity,but without impact on the expression of eNOS gene.	Folic Acid	0-10	nitric oxide synthase 3	Homo sapiens	95-99
17357445-13	2007	Folic acid can exert partial protective roles against the Hcy in the level of eNOS protein and eNOS activity,but without impact on the expression of eNOS gene.	Folic Acid	0-10	nitric oxide synthase 3	Homo sapiens	95-99
17357445-13	2007	Folic acid can exert partial protective roles against the Hcy in the level of eNOS protein and eNOS activity,but without impact on the expression of eNOS gene.	Homocysteine	58-61	nitric oxide synthase 3	Homo sapiens	78-82
17357445-13	2007	Folic acid can exert partial protective roles against the Hcy in the level of eNOS protein and eNOS activity,but without impact on the expression of eNOS gene.	Homocysteine	58-61	nitric oxide synthase 3	Homo sapiens	95-99
17357445-13	2007	Folic acid can exert partial protective roles against the Hcy in the level of eNOS protein and eNOS activity,but without impact on the expression of eNOS gene.	Homocysteine	58-61	nitric oxide synthase 3	Homo sapiens	95-99
16889995-1	2007	Cytokines generate nitric oxide (NO) in osteoblasts and neutrophils through the induction of NO synthase isoforms, endothelial (NOS3) and inducible (NOS2), thereby producing bone loss.	Nitric Oxide	19-31	nitric oxide synthase 3	Homo sapiens	115-132
17105827-7	2007	Clofibrate increased PPARalpha expression, accompanied by increased NO production and eNOS expression.	Clofibrate	0-10	nitric oxide synthase 3	Homo sapiens	86-90
17125900-0	2007	Eicosapentaenoic acid modifies lipid composition in caveolae and induces translocation of endothelial nitric oxide synthase.	Eicosapentaenoic Acid	0-21	nitric oxide synthase 3	Homo sapiens	90-123
17285538-3	2007	The genotypes of NOS3 gene VNTR polymorphism were determined by polymerase chain reaction and agarose gel electrophoresis.	Sepharose	94-101	nitric oxide synthase 3	Homo sapiens	17-21
17974175-5	2007	There was applied a new method for treatment with mechanism of action stimulation the production cGMP of spermatozoa endothelial nitric oxide synthase (eNOS).	Cyclic GMP	97-101	nitric oxide synthase 3	Homo sapiens	117-150
17184584-5	2007	eNOS activity was assayed by L- [3H]citrulline production from L-[3H]arginine.	l- [3h]citrulline	29-46	nitric oxide synthase 3	Homo sapiens	0-4
17184584-5	2007	eNOS activity was assayed by L- [3H]citrulline production from L-[3H]arginine.	l-[3h]arginine	63-77	nitric oxide synthase 3	Homo sapiens	0-4
17184584-6	2007	The involvement of eNOS was explored using an eNOS inhibitor (L-NAME) and the effects in the process were observed.	NG-Nitroarginine Methyl Ester	62-68	nitric oxide synthase 3	Homo sapiens	19-23
17184584-6	2007	The involvement of eNOS was explored using an eNOS inhibitor (L-NAME) and the effects in the process were observed.	NG-Nitroarginine Methyl Ester	62-68	nitric oxide synthase 3	Homo sapiens	46-50
17184584-9	2007	Moreover, cell migration, proliferation and tube formation induced by CD151 are inhibited when L-NAME is used, which indicates that there is an involvement of eNOS in CD151-induced cell migration, cell proliferation and tube formation.	NG-Nitroarginine Methyl Ester	95-101	nitric oxide synthase 3	Homo sapiens	159-163
17125900-8	2007	EPA treatment induced the translocation of eNOS from caveolae fractions to soluble fractions.	Eicosapentaenoic Acid	0-3	nitric oxide synthase 3	Homo sapiens	43-47
17125900-10	2007	After EPA treatment, the level of p-eNOS in each fraction was increased but the distribution of which was unaffected.	Eicosapentaenoic Acid	6-9	nitric oxide synthase 3	Homo sapiens	36-40
17125900-4	2007	In the present study we investigated the effects of eicosapentaenoic acid (EPA, 20:5 n-3) on subcellular distribution of eNOS and lipid composition of caveolae.	Eicosapentaenoic Acid	52-73	nitric oxide synthase 3	Homo sapiens	121-125
17125900-12	2007	eNOS activity in HUVEC cells was increased after EPA treatment, which was in a dose dependent manner.	Eicosapentaenoic Acid	49-52	nitric oxide synthase 3	Homo sapiens	0-4
17125900-13	2007	And incubation with 50 microM EPA had the maximum effect on eNOS activity.	Eicosapentaenoic Acid	30-33	nitric oxide synthase 3	Homo sapiens	60-64
17125900-4	2007	In the present study we investigated the effects of eicosapentaenoic acid (EPA, 20:5 n-3) on subcellular distribution of eNOS and lipid composition of caveolae.	Eicosapentaenoic Acid	75-78	nitric oxide synthase 3	Homo sapiens	121-125
17406107-1	2007	BACKGROUND: Asymmetric dimethylarginine (ADMA) assumes a significant role in atherosclerosis by inhibiting the endothelial nitric oxide synthase (eNOS).	dimethylarginine	23-39	nitric oxide synthase 3	Homo sapiens	111-144
17140552-8	2007	Perindopril upregulated 19% and 27% protein expression/activity of endothelial nitric oxide synthase (P &lt; 0.05) as well as reduced the rate of apoptosis by 31% (P &lt; 0.05).	Perindopril	0-11	nitric oxide synthase 3	Homo sapiens	67-100
17406107-1	2007	BACKGROUND: Asymmetric dimethylarginine (ADMA) assumes a significant role in atherosclerosis by inhibiting the endothelial nitric oxide synthase (eNOS).	N,N-dimethylarginine	41-45	nitric oxide synthase 3	Homo sapiens	111-144
16946027-2	2007	Impaired FMD may be mediated in part by a decrease in synthesis of nitric oxide by endothelial nitric oxide synthase, and in clinical populations this has been attributed to competitive inhibition of l-arginine binding sites by asymmetric dimethylarginine (ADMA).	Nitric Oxide	67-79	nitric oxide synthase 3	Homo sapiens	83-116
17110473-8	2007	CONCLUSIONS: Our results suggest that genetic variation at the eNOS locus is associated with features of metabolic syndrome, and might represent a new genetic susceptibility component for insulin resistance, hypertriglyceridemia, and low HDL-cholesterol concentrations.	Cholesterol	242-253	nitric oxide synthase 3	Homo sapiens	63-67
17116740-5	2007	Medroxyprogesterone acetate (MPA) and progesterone markedly decreased the eNOS mRNA and protein levels, whereas levonorgestrel and nomegestrol acetate had only small effects.	Medroxyprogesterone Acetate	0-27	nitric oxide synthase 3	Homo sapiens	74-78
17116740-5	2007	Medroxyprogesterone acetate (MPA) and progesterone markedly decreased the eNOS mRNA and protein levels, whereas levonorgestrel and nomegestrol acetate had only small effects.	Progesterone	7-19	nitric oxide synthase 3	Homo sapiens	74-78
17970703-1	2007	BACKGROUND: Nitric oxide (NO) produced by endothelial nitric oxide synthase (eNOS) mediates endothelium-dependent vasodilatation and antithrombotic action.	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	42-75
17970703-1	2007	BACKGROUND: Nitric oxide (NO) produced by endothelial nitric oxide synthase (eNOS) mediates endothelium-dependent vasodilatation and antithrombotic action.	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	77-81
16946027-10	2007	Together with the finding that endothelial cell ADMA protein expression was not increased in older adults, these findings suggest that competitive inhibition of l-arginine binding sites on endothelial nitric oxide synthase by ADMA is not an important mechanism contributing to impaired conduit artery endothelium-dependent dilation with aging in healthy humans.	Arginine	161-171	nitric oxide synthase 3	Homo sapiens	189-222
17365407-3	2007	We conducted a study to investigate for possible associations between ecNOS gene intron 4 variable-number tandem repeat (VNTR) polymorphism and thrombosis of polytetrafluoroethylene hemodialysis arteriovenous access grafts (AVG) in Turkish patients.	Polytetrafluoroethylene	158-181	nitric oxide synthase 3	Homo sapiens	70-75
17293058-4	2007	Superoxide can directly quench NO; moreover, by giving rise to peroxynitrite, it can oxidize the cNOS cofactor tetrahydrobiopterin (BH4), thereby suppressing cNOS activity and converting it to superoxide generator.	Superoxides	0-10	nitric oxide synthase 3	Homo sapiens	97-101
17982927-1	2007	BACKGROUND: Vasoconstrictor drugs reduce nitric oxide (NO) production in vitro by inhibiting the enzyme involved in the regulation of inducible and constitutive NO synthases (iNOS and cNOS).	Nitric Oxide	41-53	nitric oxide synthase 3	Homo sapiens	184-188
17825498-1	2007	Oxidation of tetrahydrobiopterin by peroxynitrite in oxidant-stressed endothelium compromises nitric oxide synthase (eNOS) activity while amplifying superoxide production; this mechanism contributes prominently to the endothelial dysfunction that characterizes many common clinical disorders.	sapropterin	13-32	nitric oxide synthase 3	Homo sapiens	70-115
17825498-1	2007	Oxidation of tetrahydrobiopterin by peroxynitrite in oxidant-stressed endothelium compromises nitric oxide synthase (eNOS) activity while amplifying superoxide production; this mechanism contributes prominently to the endothelial dysfunction that characterizes many common clinical disorders.	sapropterin	13-32	nitric oxide synthase 3	Homo sapiens	117-121
17825498-1	2007	Oxidation of tetrahydrobiopterin by peroxynitrite in oxidant-stressed endothelium compromises nitric oxide synthase (eNOS) activity while amplifying superoxide production; this mechanism contributes prominently to the endothelial dysfunction that characterizes many common clinical disorders.	Peroxynitrous Acid	36-49	nitric oxide synthase 3	Homo sapiens	70-115
17825498-1	2007	Oxidation of tetrahydrobiopterin by peroxynitrite in oxidant-stressed endothelium compromises nitric oxide synthase (eNOS) activity while amplifying superoxide production; this mechanism contributes prominently to the endothelial dysfunction that characterizes many common clinical disorders.	Peroxynitrous Acid	36-49	nitric oxide synthase 3	Homo sapiens	117-121
17825498-2	2007	As a physiological peroxynitrite scavenger, gamma-tocopherol may have the potential to protect tetrahydrobiopterin and thus preserve effective eNOS activity.	gamma-Tocopherol	44-60	nitric oxide synthase 3	Homo sapiens	143-147
17825498-3	2007	Indeed, in clinical studies, supplemental gamma-tocopherol has enhanced platelet eNOS activity, and a diet high in gamma-tocopherol-rich walnuts has improved endothelium-dependent vasodilation in hypercholesterolemia.	gamma-Tocopherol	42-58	nitric oxide synthase 3	Homo sapiens	81-85
17825498-4	2007	In rodents, gamma-tocopherol is reported to increase arterial expression of eNOS while up-regulating an activating phosphorylation of this enzyme.	gamma-Tocopherol	12-28	nitric oxide synthase 3	Homo sapiens	76-80
17293058-4	2007	Superoxide can directly quench NO; moreover, by giving rise to peroxynitrite, it can oxidize the cNOS cofactor tetrahydrobiopterin (BH4), thereby suppressing cNOS activity and converting it to superoxide generator.	Superoxides	0-10	nitric oxide synthase 3	Homo sapiens	158-162
17293058-4	2007	Superoxide can directly quench NO; moreover, by giving rise to peroxynitrite, it can oxidize the cNOS cofactor tetrahydrobiopterin (BH4), thereby suppressing cNOS activity and converting it to superoxide generator.	Peroxynitrous Acid	63-76	nitric oxide synthase 3	Homo sapiens	97-101
17293058-4	2007	Superoxide can directly quench NO; moreover, by giving rise to peroxynitrite, it can oxidize the cNOS cofactor tetrahydrobiopterin (BH4), thereby suppressing cNOS activity and converting it to superoxide generator.	Peroxynitrous Acid	63-76	nitric oxide synthase 3	Homo sapiens	158-162
17293058-4	2007	Superoxide can directly quench NO; moreover, by giving rise to peroxynitrite, it can oxidize the cNOS cofactor tetrahydrobiopterin (BH4), thereby suppressing cNOS activity and converting it to superoxide generator.	sapropterin	111-130	nitric oxide synthase 3	Homo sapiens	97-101
17293058-4	2007	Superoxide can directly quench NO; moreover, by giving rise to peroxynitrite, it can oxidize the cNOS cofactor tetrahydrobiopterin (BH4), thereby suppressing cNOS activity and converting it to superoxide generator.	sapropterin	111-130	nitric oxide synthase 3	Homo sapiens	158-162
17293058-4	2007	Superoxide can directly quench NO; moreover, by giving rise to peroxynitrite, it can oxidize the cNOS cofactor tetrahydrobiopterin (BH4), thereby suppressing cNOS activity and converting it to superoxide generator.	sapropterin	132-135	nitric oxide synthase 3	Homo sapiens	97-101
17293058-4	2007	Superoxide can directly quench NO; moreover, by giving rise to peroxynitrite, it can oxidize the cNOS cofactor tetrahydrobiopterin (BH4), thereby suppressing cNOS activity and converting it to superoxide generator.	sapropterin	132-135	nitric oxide synthase 3	Homo sapiens	158-162
17293058-4	2007	Superoxide can directly quench NO; moreover, by giving rise to peroxynitrite, it can oxidize the cNOS cofactor tetrahydrobiopterin (BH4), thereby suppressing cNOS activity and converting it to superoxide generator.	Superoxides	193-203	nitric oxide synthase 3	Homo sapiens	97-101
16842840-1	2007	INTRODUCTION: Endothelium-derived nitric oxide (NO) is synthesized from l-arginine by endothelial nitric oxide synthase (eNOS) encoded by the eNOS3 gene on chromosome 7.	Nitric Oxide	34-46	nitric oxide synthase 3	Homo sapiens	86-119
16925467-0	2007	A preliminary study on T-786C endothelial nitric oxide synthase gene and renal hemodynamic and blood pressure responses to dietary sodium.	Sodium	131-137	nitric oxide synthase 3	Homo sapiens	30-63
16951945-1	2007	The objective of this study was to analyze the genotype distributions and allele frequencies for the Glu298Asp (G894T) polymorphism of the eNOS gene and the serum nitric oxide level among the patients with fibromyalgia syndrome (FS).	Nitric Oxide	163-175	nitric oxide synthase 3	Homo sapiens	139-143
17365914-6	2007	RESULTS: The distribution of GG, TG, and TT genotypes for eNOS gene was 48%, 33%, and 19% in PNE, compared with 61%, 26%, and 13% in the controls (p &gt; 0.05).	Thioguanine	33-35	nitric oxide synthase 3	Homo sapiens	58-62
18473989-1	2007	Nitric oxide (NO) is produced by the endothelial NOS (eNOS) in the intima and by the neuronal NOS (nNOS) in the adventitia of cerebral vessels.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	37-52
16842840-1	2007	INTRODUCTION: Endothelium-derived nitric oxide (NO) is synthesized from l-arginine by endothelial nitric oxide synthase (eNOS) encoded by the eNOS3 gene on chromosome 7.	Nitric Oxide	34-46	nitric oxide synthase 3	Homo sapiens	121-125
16842840-1	2007	INTRODUCTION: Endothelium-derived nitric oxide (NO) is synthesized from l-arginine by endothelial nitric oxide synthase (eNOS) encoded by the eNOS3 gene on chromosome 7.	Arginine	72-82	nitric oxide synthase 3	Homo sapiens	86-119
16842840-1	2007	INTRODUCTION: Endothelium-derived nitric oxide (NO) is synthesized from l-arginine by endothelial nitric oxide synthase (eNOS) encoded by the eNOS3 gene on chromosome 7.	Arginine	72-82	nitric oxide synthase 3	Homo sapiens	121-125
16169754-0	2007	L-arginine prevents reduced expression of endothelial nitric oxide synthase (NOS) in pulmonary arterioles of broilers exposed to cool temperatures.	Arginine	0-10	nitric oxide synthase 3	Homo sapiens	42-75
16684613-3	2006	Endothelium damage induced by atherosclerosis leads to the reduction in bioactivity of endothelial NO synthase (eNOS) with subsequent impaired release of NO together with a local enhanced degradation of NO by increased generation of reactive oxygen species with subsequent cascade of oxidation-sensitive mechanisms in the arterial wall.	Reactive Oxygen Species	233-256	nitric oxide synthase 3	Homo sapiens	112-116
19618598-0	2007	PICSO in progress: lactate, oxygen, eNOS, iNOS, MMP and TIMP in the PICSO treated myocardium--a preview.	picso	0-5	nitric oxide synthase 3	Homo sapiens	36-40
16822949-3	2006	Cultured eNOS knockout (eNOS(-/-)) cardiomyocytes displayed fewer cells and lower bromodeoxyuridine (BrdU) incorporation in vitro compared with wild-type (WT) cardiomyocytes (P &lt; 0.05).	Bromodeoxyuridine	82-99	nitric oxide synthase 3	Homo sapiens	9-13
16822949-3	2006	Cultured eNOS knockout (eNOS(-/-)) cardiomyocytes displayed fewer cells and lower bromodeoxyuridine (BrdU) incorporation in vitro compared with wild-type (WT) cardiomyocytes (P &lt; 0.05).	Bromodeoxyuridine	101-105	nitric oxide synthase 3	Homo sapiens	9-13
16822949-4	2006	Treatment with the nitric oxide (NO) donor diethylenetriamine NONOate increased BrdU incorporation and cell counts in eNOS(-/-) cardiomyocytes (P &lt; 0.05).	Nitric Oxide	19-31	nitric oxide synthase 3	Homo sapiens	118-122
16822949-4	2006	Treatment with the nitric oxide (NO) donor diethylenetriamine NONOate increased BrdU incorporation and cell counts in eNOS(-/-) cardiomyocytes (P &lt; 0.05).	2,2'-(hydroxynitrosohydrazono)bis-ethanamine	43-69	nitric oxide synthase 3	Homo sapiens	118-122
16822949-8	2006	Furthermore, deficiency in eNOS significantly decreased BrdU labeling indexes in neonatal hearts in vivo.	Bromodeoxyuridine	56-60	nitric oxide synthase 3	Homo sapiens	27-31
17023679-1	2006	OBJECTIVE: The aim of the present study is to determine whether hypochlorous acid (HOCl), the major oxidant of leukocyte-derived myeloperoxidase (MPO), oxidizes the zinc-thiolate center of endothelial nitric oxide synthase (eNOS) and uncouples the enzyme.	Hypochlorous Acid	64-81	nitric oxide synthase 3	Homo sapiens	189-222
17023679-1	2006	OBJECTIVE: The aim of the present study is to determine whether hypochlorous acid (HOCl), the major oxidant of leukocyte-derived myeloperoxidase (MPO), oxidizes the zinc-thiolate center of endothelial nitric oxide synthase (eNOS) and uncouples the enzyme.	Hypochlorous Acid	83-87	nitric oxide synthase 3	Homo sapiens	189-222
17023679-1	2006	OBJECTIVE: The aim of the present study is to determine whether hypochlorous acid (HOCl), the major oxidant of leukocyte-derived myeloperoxidase (MPO), oxidizes the zinc-thiolate center of endothelial nitric oxide synthase (eNOS) and uncouples the enzyme.	zinc-thiolate	165-178	nitric oxide synthase 3	Homo sapiens	189-222
16824503-8	2006	Nicorandil also increased the cNOS activity and decreased iNOS activity (P&lt;0.05).	Nicorandil	0-10	nitric oxide synthase 3	Homo sapiens	30-34
16824503-9	2006	L-NMMA and glibenclamide abrogated the effects of nicorandil on ventricular function, coronary blood flow volume, area of no-reflow, necrosis area and cNOS activity, but not iNOS activity.	omega-N-Methylarginine	0-6	nitric oxide synthase 3	Homo sapiens	151-155
16824503-9	2006	L-NMMA and glibenclamide abrogated the effects of nicorandil on ventricular function, coronary blood flow volume, area of no-reflow, necrosis area and cNOS activity, but not iNOS activity.	Glyburide	11-24	nitric oxide synthase 3	Homo sapiens	151-155
17070516-4	2006	It has been demonstrated that a small GTP-binding protein, Rho, and its downstream effecter, Rho kinase (ROCK), negatively regulate endothelial nitric oxide synthase (eNOS) production.	Guanosine Triphosphate	38-41	nitric oxide synthase 3	Homo sapiens	132-165
17535737-4	2006	While ouabain-induced ET-1 release seems to be accomplished within 10 min, ouabain also stimulates a second signaling cascade that involves activation of Akt (also known as protein kinase B, or PKB), activation of endothelial nitric oxide synthase (eNOS) and increased NO production in HUAECs.	Ouabain	75-82	nitric oxide synthase 3	Homo sapiens	214-247
16545819-0	2006	Activation of endothelial nitric oxide synthase by cilostazol via a cAMP/protein kinase A- and phosphatidylinositol 3-kinase/Akt-dependent mechanism.	Cilostazol	51-61	nitric oxide synthase 3	Homo sapiens	14-47
16545819-0	2006	Activation of endothelial nitric oxide synthase by cilostazol via a cAMP/protein kinase A- and phosphatidylinositol 3-kinase/Akt-dependent mechanism.	Cyclic AMP	68-72	nitric oxide synthase 3	Homo sapiens	14-47
16545819-4	2006	In Western blot analysis, cilostazol increased phosphorylation of endothelial nitric oxide synthase (eNOS) at Ser(1177) and of Akt at Ser(473) and dephosphorylation of eNOS at Thr(495).	Cilostazol	26-36	nitric oxide synthase 3	Homo sapiens	66-99
16545819-4	2006	In Western blot analysis, cilostazol increased phosphorylation of endothelial nitric oxide synthase (eNOS) at Ser(1177) and of Akt at Ser(473) and dephosphorylation of eNOS at Thr(495).	Serine	110-113	nitric oxide synthase 3	Homo sapiens	66-99
17145829-6	2006	However, relationships between overweight/obesity [body mass index (BMI), &gt;25] and radiotoxicity risk seemed to be modified by eNOS and MPO genotypes associated with higher generation of nitric oxide and ROS, respectively.	Nitric Oxide	190-202	nitric oxide synthase 3	Homo sapiens	130-134
17145829-6	2006	However, relationships between overweight/obesity [body mass index (BMI), &gt;25] and radiotoxicity risk seemed to be modified by eNOS and MPO genotypes associated with higher generation of nitric oxide and ROS, respectively.	Reactive Oxygen Species	207-210	nitric oxide synthase 3	Homo sapiens	130-134
17287556-1	2006	BACKGROUND &amp; OBJECTIVES: Endo-derived nitric oxide (NO) is synthesized from L-arginine by endothelium nitric oxide synthase (eNOS) encoded by the NOS3 gene on chromosome7.	Adenosine Monophosphate	12-15	nitric oxide synthase 3	Homo sapiens	129-133
17287556-1	2006	BACKGROUND &amp; OBJECTIVES: Endo-derived nitric oxide (NO) is synthesized from L-arginine by endothelium nitric oxide synthase (eNOS) encoded by the NOS3 gene on chromosome7.	Nitric Oxide	42-54	nitric oxide synthase 3	Homo sapiens	129-133
17287556-1	2006	BACKGROUND &amp; OBJECTIVES: Endo-derived nitric oxide (NO) is synthesized from L-arginine by endothelium nitric oxide synthase (eNOS) encoded by the NOS3 gene on chromosome7.	Nitric Oxide	42-54	nitric oxide synthase 3	Homo sapiens	150-154
17287556-1	2006	BACKGROUND &amp; OBJECTIVES: Endo-derived nitric oxide (NO) is synthesized from L-arginine by endothelium nitric oxide synthase (eNOS) encoded by the NOS3 gene on chromosome7.	Arginine	80-90	nitric oxide synthase 3	Homo sapiens	129-133
17287556-1	2006	BACKGROUND &amp; OBJECTIVES: Endo-derived nitric oxide (NO) is synthesized from L-arginine by endothelium nitric oxide synthase (eNOS) encoded by the NOS3 gene on chromosome7.	Arginine	80-90	nitric oxide synthase 3	Homo sapiens	150-154
17116549-6	2006	Endothelial nitric oxide synthase (eNOS) activity was assayed by measuring conversion of L-arginine to L-citrulline.	Arginine	89-99	nitric oxide synthase 3	Homo sapiens	0-33
17116549-6	2006	Endothelial nitric oxide synthase (eNOS) activity was assayed by measuring conversion of L-arginine to L-citrulline.	Citrulline	103-115	nitric oxide synthase 3	Homo sapiens	0-33
17026986-0	2006	N-acetylcysteine attenuates TNF-alpha-induced human vascular endothelial cell apoptosis and restores eNOS expression.	Acetylcysteine	0-16	nitric oxide synthase 3	Homo sapiens	101-105
17026986-11	2006	N-acetylcysteine attenuation of TNF-alpha-induced human vascular endothelial cell apoptosis is associated with the restoration of eNOS expression.	Acetylcysteine	0-16	nitric oxide synthase 3	Homo sapiens	130-134
17062240-7	2006	Gray unit values for cGMP, a downstream NO-signal-pathway molecule, showed results grossly corresponding to NOS-III activation.	Cyclic GMP	21-25	nitric oxide synthase 3	Homo sapiens	108-115
16966328-3	2006	In the present study, the homologous serines of both nNOS (Ser-1176) and endothelial nitric-oxide synthase (eNOS) (Ser-942) were mutated to threonine and alanine.	Serine	37-44	nitric oxide synthase 3	Homo sapiens	73-106
16966328-3	2006	In the present study, the homologous serines of both nNOS (Ser-1176) and endothelial nitric-oxide synthase (eNOS) (Ser-942) were mutated to threonine and alanine.	Serine	115-118	nitric oxide synthase 3	Homo sapiens	73-106
16966328-3	2006	In the present study, the homologous serines of both nNOS (Ser-1176) and endothelial nitric-oxide synthase (eNOS) (Ser-942) were mutated to threonine and alanine.	Threonine	140-149	nitric oxide synthase 3	Homo sapiens	73-106
16966328-3	2006	In the present study, the homologous serines of both nNOS (Ser-1176) and endothelial nitric-oxide synthase (eNOS) (Ser-942) were mutated to threonine and alanine.	Alanine	154-161	nitric oxide synthase 3	Homo sapiens	73-106
16996686-2	2006	Nitric oxide (NO) produced by endothelial NO synthase (eNOS) is an important mediator of vascular homeostasis and cerebral blood flow.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	55-59
16996686-6	2006	On the other hand, endothelial eNOS expression was similar after 3h of hypoxia, but was significantly decreased after 5h.	Tritium	65-67	nitric oxide synthase 3	Homo sapiens	31-35
16997880-1	2006	We determined the effect of oxygen [approximately 100 Torr (normoxia) and approximately 30-40 Torr (hypoxia)] on functions of endothelial nitric oxide (NO) synthase (NOS-3) and its negative regulator caveolin-1 in ovine fetal and neonatal lung microvascular endothelial cells (MVECs).	Oxygen	28-34	nitric oxide synthase 3	Homo sapiens	166-171
16997880-2	2006	Fetal NOS-3 activity, measured as NO production with 0.5-0.9 microM 4-amino-5-methylamino-2,7-difluorofluorescein, was decreased in hypoxia by 14.4% (P &lt; 0.01), inhibitable by the NOS inhibitor N-nitro-L-arginine, and dependent on extracellular arginine.	4-amino-5-methylamino-2,7-difluorofluorescein	68-113	nitric oxide synthase 3	Homo sapiens	6-11
16997880-2	2006	Fetal NOS-3 activity, measured as NO production with 0.5-0.9 microM 4-amino-5-methylamino-2,7-difluorofluorescein, was decreased in hypoxia by 14.4% (P &lt; 0.01), inhibitable by the NOS inhibitor N-nitro-L-arginine, and dependent on extracellular arginine.	Nitroarginine	197-215	nitric oxide synthase 3	Homo sapiens	6-11
16997880-2	2006	Fetal NOS-3 activity, measured as NO production with 0.5-0.9 microM 4-amino-5-methylamino-2,7-difluorofluorescein, was decreased in hypoxia by 14.4% (P &lt; 0.01), inhibitable by the NOS inhibitor N-nitro-L-arginine, and dependent on extracellular arginine.	Arginine	207-215	nitric oxide synthase 3	Homo sapiens	6-11
16997880-9	2006	These data support our hypothesis that increased Po(2) at birth promotes dissociation of caveolin-1 and NOS-3, with an increase in their activities, and that PKC and an oxygen-sensitive cell surface G protein-coupled receptor regulate caveolin-1 and NOS-3 interactions in fetal and neonatal lung MVECs.	Oxygen	169-175	nitric oxide synthase 3	Homo sapiens	250-255
16738003-6	2006	In contrast, tumor necrosis factor-alpha, hypoxia, lipopolysaccaride, thrombin, and oxidized LDL can decrease eNOS mRNA levels.	lipopolysaccaride	51-68	nitric oxide synthase 3	Homo sapiens	110-114
17062240-9	2006	CONCLUSIONS: Significant activation of NOS-III and subsequent NO-cGMP signal pathway occurs in human cryopreserved allografts during the thawing process and can be significantly reduced by a NOS-III inhibitor administered during thawing.	Cyclic GMP	65-69	nitric oxide synthase 3	Homo sapiens	191-198
17016497-9	2006	Furthermore, tamoxifen increased endothelial nitric oxide synthase (eNOS) phosphorylation at Ser-1177 and ICI 182,780 prevented this effect.	Tamoxifen	13-22	nitric oxide synthase 3	Homo sapiens	33-66
17016497-9	2006	Furthermore, tamoxifen increased endothelial nitric oxide synthase (eNOS) phosphorylation at Ser-1177 and ICI 182,780 prevented this effect.	Serine	93-96	nitric oxide synthase 3	Homo sapiens	33-66
17063466-1	2006	BACKGROUND: Nitric oxide (NO) is constitutively synthesized in the endothelium by endothelial nitric oxide synthase (eNOS) and acts as a pleiotropic regulator involved in carcinogenesis.	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	82-115
17063466-1	2006	BACKGROUND: Nitric oxide (NO) is constitutively synthesized in the endothelium by endothelial nitric oxide synthase (eNOS) and acts as a pleiotropic regulator involved in carcinogenesis.	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	117-121
16898954-1	2006	BACKGROUND: Endothelial nitric oxide synthase (eNOS) activity in endothelial cells is regulated by post-translational phosphorylation of critical serine, threonine and tyrosine residues in response to a variety of stimuli.	Serine	146-152	nitric oxide synthase 3	Homo sapiens	12-45
17099031-0	2006	Heterozygotes of NOS3 polymorphisms contribute to reduced nitrogen oxides in high-altitude pulmonary edema.	Nitrogen Oxides	58-73	nitric oxide synthase 3	Homo sapiens	17-21
16898954-1	2006	BACKGROUND: Endothelial nitric oxide synthase (eNOS) activity in endothelial cells is regulated by post-translational phosphorylation of critical serine, threonine and tyrosine residues in response to a variety of stimuli.	Serine	146-152	nitric oxide synthase 3	Homo sapiens	47-51
16898954-1	2006	BACKGROUND: Endothelial nitric oxide synthase (eNOS) activity in endothelial cells is regulated by post-translational phosphorylation of critical serine, threonine and tyrosine residues in response to a variety of stimuli.	Threonine	154-163	nitric oxide synthase 3	Homo sapiens	12-45
16898954-1	2006	BACKGROUND: Endothelial nitric oxide synthase (eNOS) activity in endothelial cells is regulated by post-translational phosphorylation of critical serine, threonine and tyrosine residues in response to a variety of stimuli.	Threonine	154-163	nitric oxide synthase 3	Homo sapiens	47-51
16898954-1	2006	BACKGROUND: Endothelial nitric oxide synthase (eNOS) activity in endothelial cells is regulated by post-translational phosphorylation of critical serine, threonine and tyrosine residues in response to a variety of stimuli.	Tyrosine	168-176	nitric oxide synthase 3	Homo sapiens	12-45
16898954-1	2006	BACKGROUND: Endothelial nitric oxide synthase (eNOS) activity in endothelial cells is regulated by post-translational phosphorylation of critical serine, threonine and tyrosine residues in response to a variety of stimuli.	Tyrosine	168-176	nitric oxide synthase 3	Homo sapiens	47-51
16898954-3	2006	OBJECTIVES: We investigated the role of tyrosine phosphorylation in the regulation of platelet eNOS activity.	Tyrosine	40-48	nitric oxide synthase 3	Homo sapiens	95-99
16898954-4	2006	METHODS: Tyrosine phosphorylation of eNOS and interaction with the tyrosine phosphatase SHP-1 were investigated by coimmunoprecipitation and immunoblotting.	Tyrosine	9-17	nitric oxide synthase 3	Homo sapiens	37-41
16898954-6	2006	RESULTS: We found platelet eNOS was tyrosine phosphorylated under basal conditions.	Tyrosine	36-44	nitric oxide synthase 3	Homo sapiens	27-31
16898954-8	2006	In vitro tyrosine dephosphorylation of platelet eNOS using a recombinant protein tyrosine phosphatase enhanced thrombin-induced activity compared to thrombin alone, but had no effect on endothelial eNOS activity either at basal or after stimulation with bradykinin.	Tyrosine	9-17	nitric oxide synthase 3	Homo sapiens	48-52
16898954-12	2006	CONCLUSIONS: Our data suggest a novel role for tyrosine dephosphorylation in platelet eNOS activation, which may be mediated by SHP-1.	Tyrosine	47-55	nitric oxide synthase 3	Homo sapiens	86-90
16413211-2	2006	Western blot and Northern blot analyses showed a significant decrease of NOSIII expression after a 24-h treatment with oxLDL.	oxldl	119-124	nitric oxide synthase 3	Homo sapiens	73-79
16868034-8	2006	The overexpression of eNOS/FGF-2 produced, at the functional level, enhanced cell proliferation and migration, the latter effect being dose-dependent and maximal at 0.1 microM zofenoprilat.	zofenoprilate	176-188	nitric oxide synthase 3	Homo sapiens	22-26
17040412-9	2006	Activation of the cGMP-pathway by sodium nitroprusside or its inhibition by guanylate cyclase (LY83583) or kinase (KT5823) inhibitors had more effects on fundus SMC, on which a higher expression of endothelial nitric oxide synthase was found.	Cyclic GMP	18-22	nitric oxide synthase 3	Homo sapiens	198-231
17040412-9	2006	Activation of the cGMP-pathway by sodium nitroprusside or its inhibition by guanylate cyclase (LY83583) or kinase (KT5823) inhibitors had more effects on fundus SMC, on which a higher expression of endothelial nitric oxide synthase was found.	Nitroprusside	34-54	nitric oxide synthase 3	Homo sapiens	198-231
16873402-7	2006	beta(2)AR activation also increased NOS activity and phosphorylation of NOS-3 on serine-1177, and these increases were attenuated by inhibition of protein kinase A (PKA), phosphatidylinositol 3-kinase (PI3K) or Akt, and abolished by coinhibition of PKA and Akt.	Serine	81-87	nitric oxide synthase 3	Homo sapiens	72-77
16873402-8	2006	These findings suggest that beta(2)AR-mediated NOS-3 activation in HUVEC is mediated through phosphorylation of NOS-3 on serine-1177 through both the PKA and the PI3K/Akt systems, and is sustained by an increase in l-arginine uptake resulting from NO-mediated membrane hyperpolarization.	Serine	121-127	nitric oxide synthase 3	Homo sapiens	47-52
16873402-8	2006	These findings suggest that beta(2)AR-mediated NOS-3 activation in HUVEC is mediated through phosphorylation of NOS-3 on serine-1177 through both the PKA and the PI3K/Akt systems, and is sustained by an increase in l-arginine uptake resulting from NO-mediated membrane hyperpolarization.	Serine	121-127	nitric oxide synthase 3	Homo sapiens	112-117
16873402-8	2006	These findings suggest that beta(2)AR-mediated NOS-3 activation in HUVEC is mediated through phosphorylation of NOS-3 on serine-1177 through both the PKA and the PI3K/Akt systems, and is sustained by an increase in l-arginine uptake resulting from NO-mediated membrane hyperpolarization.	Arginine	215-225	nitric oxide synthase 3	Homo sapiens	47-52
16873402-8	2006	These findings suggest that beta(2)AR-mediated NOS-3 activation in HUVEC is mediated through phosphorylation of NOS-3 on serine-1177 through both the PKA and the PI3K/Akt systems, and is sustained by an increase in l-arginine uptake resulting from NO-mediated membrane hyperpolarization.	Arginine	215-225	nitric oxide synthase 3	Homo sapiens	112-117
16963021-9	2006	Isorhamnetin pretreatment inhibited the ox-LDL-induced downregulation of eNOS, upregulation of lectin-like ox-LDL receptor-1, phosphorylation of the p38MAPK and translocation of NF-kappaB.	3-methylquercetin	0-12	nitric oxide synthase 3	Homo sapiens	73-77
16375908-5	2006	A decoy oligonucleotide encoding the heat shock element inhibited statin-induced expression of heat shock protein 70, endothelial nitric oxide synthase, and thrombomodulin.	Oligonucleotides	8-23	nitric oxide synthase 3	Homo sapiens	118-151
17038647-0	2006	A new paradigm: calcium independent and caveolae internalization dependent release of nitric oxide by the endothelial nitric oxide synthase.	Nitric Oxide	86-98	nitric oxide synthase 3	Homo sapiens	106-139
16963030-10	2006	20-Alpha-dihydrodydrogesterone and P also potentiate eNOS induction by E2.	20-alpha-dihydrodydrogesterone	0-30	nitric oxide synthase 3	Homo sapiens	53-57
16962929-0	2006	eNOS gene T-786C polymorphism modulates atorvastatin-induced increase in blood nitrite.	Atorvastatin	40-52	nitric oxide synthase 3	Homo sapiens	0-4
17000306-9	2006	The downregulated endothelial nitric oxide synthase level in the distended grafts was accompanied by a 45.2% +/- 3.1% reduction of phospho-endothelial nitric oxide synthase Ser1177 levels and by a significant reduction in nitric oxide synthase activity (12.1% +/- 1.2%) and nitrate production (48.9% +/- 5.6%) in comparison with that seen in drug-treated grafts.	Nitrates	274-281	nitric oxide synthase 3	Homo sapiens	18-51
16962929-0	2006	eNOS gene T-786C polymorphism modulates atorvastatin-induced increase in blood nitrite.	Nitrites	79-86	nitric oxide synthase 3	Homo sapiens	0-4
16716148-5	2006	U0126 pretreatment of HUVEC-CS potentiated ATP-stimulated eNOS activity, independent of changes in intracellular Ca2+ concentration ([Ca2+]i).	U 0126	0-5	nitric oxide synthase 3	Homo sapiens	58-62
17164036-1	2006	Nitric oxide (NO), also known as endothelium-derived relaxing factor, is produced by endothelial nitric oxide synthase (eNOS) in the intima and by neuronal nitric oxide synthase (nNOS) in the adventitia of cerebral vessels.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	85-118
16983080-4	2006	Ex vivo pretreatment of BMC from patients with ICMP with AVE significantly increased eNOS mRNA expression by 2.1-fold (P &lt; 0.05) and eNOS activity as assessed by ESR by &gt;3-fold (P &lt; 0.05).	bmc	24-27	nitric oxide synthase 3	Homo sapiens	85-89
16983080-4	2006	Ex vivo pretreatment of BMC from patients with ICMP with AVE significantly increased eNOS mRNA expression by 2.1-fold (P &lt; 0.05) and eNOS activity as assessed by ESR by &gt;3-fold (P &lt; 0.05).	bmc	24-27	nitric oxide synthase 3	Homo sapiens	136-140
16983080-5	2006	The increased eNOS expression was associated with an enhanced migratory capacity in vitro (P &lt; 0.01) and improved neovascularization capacity of the infused BMC in an ischemic hind limb model in vivo (P &lt; 0.001).	bmc	160-163	nitric oxide synthase 3	Homo sapiens	14-18
16940192-0	2006	5-methyltetrahydrofolate rapidly improves endothelial function and decreases superoxide production in human vessels: effects on vascular tetrahydrobiopterin availability and endothelial nitric oxide synthase coupling.	5-methyltetrahydrofolate	0-24	nitric oxide synthase 3	Homo sapiens	174-207
16983080-7	2006	The enhancement of limb perfusion by AVE-treated BMC was abrogated by ex vivo pretreatment with the eNOS inhibitor N(G)-nitro-l-arginine methyl ester.	bmc	49-52	nitric oxide synthase 3	Homo sapiens	100-104
16983080-7	2006	The enhancement of limb perfusion by AVE-treated BMC was abrogated by ex vivo pretreatment with the eNOS inhibitor N(G)-nitro-l-arginine methyl ester.	NG-Nitroarginine Methyl Ester	115-149	nitric oxide synthase 3	Homo sapiens	100-104
16983080-10	2006	Here, we show that pharmacological enhancement of eNOS expression with AVE at least partially reverses the impaired functional activity of BMC from ICMP patients, highlighting the critical role of NO for progenitor cell function.	bmc	139-142	nitric oxide synthase 3	Homo sapiens	50-54
16840783-0	2006	The isoflavone Equol mediates rapid vascular relaxation: Ca2+-independent activation of endothelial nitric-oxide synthase/Hsp90 involving ERK1/2 and Akt phosphorylation in human endothelial cells.	Isoflavones	4-14	nitric oxide synthase 3	Homo sapiens	88-121
16840783-1	2006	We recently reported that soy isoflavones increase gene expression of endothelial nitric-oxide synthase (eNOS) and antioxidant defense enzymes, resulting in improved endothelial function and lower blood pressure in vivo.	Isoflavones	30-41	nitric oxide synthase 3	Homo sapiens	70-103
16840783-1	2006	We recently reported that soy isoflavones increase gene expression of endothelial nitric-oxide synthase (eNOS) and antioxidant defense enzymes, resulting in improved endothelial function and lower blood pressure in vivo.	Isoflavones	30-41	nitric oxide synthase 3	Homo sapiens	105-109
16840783-4	2006	Rapid phosphorylation of ERK1/2, protein kinase B/Akt, and eNOS serine 1177 by equol was paralleled by association of eNOS with heat shock protein 90 (Hsp90) and NO synthesis in human umbilical vein endothelial cells, expressing estrogen receptors (ER)alpha and ERbeta.	Serine	64-70	nitric oxide synthase 3	Homo sapiens	59-63
16716148-5	2006	U0126 pretreatment of HUVEC-CS potentiated ATP-stimulated eNOS activity, independent of changes in intracellular Ca2+ concentration ([Ca2+]i).	Cesium	28-30	nitric oxide synthase 3	Homo sapiens	58-62
16716148-5	2006	U0126 pretreatment of HUVEC-CS potentiated ATP-stimulated eNOS activity, independent of changes in intracellular Ca2+ concentration ([Ca2+]i).	Adenosine Triphosphate	43-46	nitric oxide synthase 3	Homo sapiens	58-62
16716148-6	2006	In COS-7 cells transiently expressing ovine eNOS, U0126 potentiated A23187-stimulated eNOS activity, but inhibited ATP-stimulated activity.	U 0126	50-55	nitric oxide synthase 3	Homo sapiens	44-48
16716148-6	2006	In COS-7 cells transiently expressing ovine eNOS, U0126 potentiated A23187-stimulated eNOS activity, but inhibited ATP-stimulated activity.	U 0126	50-55	nitric oxide synthase 3	Homo sapiens	86-90
16716148-6	2006	In COS-7 cells transiently expressing ovine eNOS, U0126 potentiated A23187-stimulated eNOS activity, but inhibited ATP-stimulated activity.	Calcimycin	68-74	nitric oxide synthase 3	Homo sapiens	44-48
16716148-6	2006	In COS-7 cells transiently expressing ovine eNOS, U0126 potentiated A23187-stimulated eNOS activity, but inhibited ATP-stimulated activity.	Calcimycin	68-74	nitric oxide synthase 3	Homo sapiens	86-90
16716148-9	2006	Finally, seven eNOS alanine mutants of putative ERK1/2 targets were generated and the effects of U0126 pretreatment on eNOS activity were gauged with A23187 and ATP treatment.	U 0126	97-102	nitric oxide synthase 3	Homo sapiens	119-123
16716148-10	2006	T97A-eNOS was the only construct significantly different from wild-type after U0126 pretreatment and ATP stimulation of eNOS activation.	U 0126	78-83	nitric oxide synthase 3	Homo sapiens	5-9
16716148-10	2006	T97A-eNOS was the only construct significantly different from wild-type after U0126 pretreatment and ATP stimulation of eNOS activation.	Adenosine Triphosphate	101-104	nitric oxide synthase 3	Homo sapiens	5-9
16716148-10	2006	T97A-eNOS was the only construct significantly different from wild-type after U0126 pretreatment and ATP stimulation of eNOS activation.	Adenosine Triphosphate	101-104	nitric oxide synthase 3	Homo sapiens	120-124
16716148-11	2006	In the present study, eNOS activity was either potentiated or inhibited in COS-7 cells, suggesting agonist dependence for MEK/ERK1/2 signalling [where MEK is MAPK (mitogen-activated protein kinase)/ERK kinase] to eNOS and a complex mechanism including [Ca2+]i, phosphorylation and, possibly, intracellular trafficking.	carbonyl sulfide	75-78	nitric oxide synthase 3	Homo sapiens	22-26
16895801-1	2006	Reactive oxygen species (ROS) can stimulate nitric oxide (NO(*)) production from the endothelium by transient activation of endothelial nitric oxide synthase (eNOS).	Reactive Oxygen Species	0-23	nitric oxide synthase 3	Homo sapiens	124-157
16616056-1	2006	BACKGROUND: Nitric oxide (NO) from the endothelium, produced by oxidation of l-arginine to L-citruline for the action at the endothelial nitric oxide synthase (eNOS), is considered an important atheroprotective factor.	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	125-158
16616056-1	2006	BACKGROUND: Nitric oxide (NO) from the endothelium, produced by oxidation of l-arginine to L-citruline for the action at the endothelial nitric oxide synthase (eNOS), is considered an important atheroprotective factor.	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	160-164
16616056-1	2006	BACKGROUND: Nitric oxide (NO) from the endothelium, produced by oxidation of l-arginine to L-citruline for the action at the endothelial nitric oxide synthase (eNOS), is considered an important atheroprotective factor.	Arginine	77-87	nitric oxide synthase 3	Homo sapiens	125-158
16616056-1	2006	BACKGROUND: Nitric oxide (NO) from the endothelium, produced by oxidation of l-arginine to L-citruline for the action at the endothelial nitric oxide synthase (eNOS), is considered an important atheroprotective factor.	Arginine	77-87	nitric oxide synthase 3	Homo sapiens	160-164
16616056-1	2006	BACKGROUND: Nitric oxide (NO) from the endothelium, produced by oxidation of l-arginine to L-citruline for the action at the endothelial nitric oxide synthase (eNOS), is considered an important atheroprotective factor.	DL-Citrulline	91-102	nitric oxide synthase 3	Homo sapiens	125-158
16616056-1	2006	BACKGROUND: Nitric oxide (NO) from the endothelium, produced by oxidation of l-arginine to L-citruline for the action at the endothelial nitric oxide synthase (eNOS), is considered an important atheroprotective factor.	DL-Citrulline	91-102	nitric oxide synthase 3	Homo sapiens	160-164
16895801-1	2006	Reactive oxygen species (ROS) can stimulate nitric oxide (NO(*)) production from the endothelium by transient activation of endothelial nitric oxide synthase (eNOS).	Reactive Oxygen Species	25-28	nitric oxide synthase 3	Homo sapiens	124-157
16895801-1	2006	Reactive oxygen species (ROS) can stimulate nitric oxide (NO(*)) production from the endothelium by transient activation of endothelial nitric oxide synthase (eNOS).	Nitric Oxide	44-56	nitric oxide synthase 3	Homo sapiens	124-157
16716362-1	2006	Nebivolol is a highly selective beta(1)-adrenoceptor blocker with additional vasodilatory properties, which may be due to an endothelial-dependent beta(3)-adrenergic activation of the endothelial nitric oxide synthase (eNOS).	Nebivolol	0-9	nitric oxide synthase 3	Homo sapiens	184-217
16949522-3	2006	In the present study, we evaluated the effects of thiazolidinediones (TZDs), antidiabetic drugs known to improve insulin resistance and to have vasodilating properties, on endothelial NO synthase (eNOS) expression in cultured vascular endothelial cells.	Thiazolidinediones	50-68	nitric oxide synthase 3	Homo sapiens	197-201
16949522-7	2006	Troglitazone up-regulated eNOS protein and its mRNA levels, whereas pioglitazone and 15-dPGJ2 failed to increase their levels.	Troglitazone	0-12	nitric oxide synthase 3	Homo sapiens	26-30
16949522-8	2006	By contrast, alpha-tocopherol also increased in eNOS protein and mRNA.	alpha-Tocopherol	13-29	nitric oxide synthase 3	Homo sapiens	48-52
16949522-9	2006	These results suggest that troglitazone up-regulates eNOS expression probably through its 6-hydroxychromanes structure but not activating PPARgamma.	Troglitazone	27-39	nitric oxide synthase 3	Homo sapiens	53-57
16949522-9	2006	These results suggest that troglitazone up-regulates eNOS expression probably through its 6-hydroxychromanes structure but not activating PPARgamma.	6-hydroxychromanes	90-108	nitric oxide synthase 3	Homo sapiens	53-57
16717106-4	2006	It is unknown whether cl-L-Arg has a direct inhibitory effect on endothelial NOS (eNOS).	cl-l-arg	22-30	nitric oxide synthase 3	Homo sapiens	65-80
16915032-2	2006	An inadequate nitric oxide availability related to polymorphisms in the endothelial nitric oxide synthase gene (eNOS) might predispose to the disease.	Nitric Oxide	14-26	nitric oxide synthase 3	Homo sapiens	72-105
16814758-6	2006	Interestingly, we also documented that the dissociation of the caveolin/eNOS heterocomplex induced by amlodipine was not mediated by the traditional calcium-dependent calmodulin binding to eNOS and that recombinant caveolin expression could compete with the stimulatory effects of amlodipine on eNOS activity.	Amlodipine	281-291	nitric oxide synthase 3	Homo sapiens	72-76
17009539-6	2006	On animal models, sildenafil could resume the cavernous epithelial function, up-regulate the protein expression of phosphorylated endothelial NO synthase (eNOS), reverse the decreased intracavernosal pressure (ICP) induced by pudendal artery blood flow restriction or hypoxia.	Sildenafil Citrate	18-28	nitric oxide synthase 3	Homo sapiens	155-159
16912198-5	2006	Taxotere prevented the VEGF-induced phosphorylation of focal adhesion kinase, Akt, and endothelial nitric oxide synthase (eNOS), all of which are Hsp90 client proteins.	Docetaxel	0-8	nitric oxide synthase 3	Homo sapiens	87-120
16864000-1	2006	Vascular endothelium expressing endothelial nitric oxide synthase (eNOS) produces nitric oxide (NO), which has a number of important physiological functions in the microvasculature.	Nitric Oxide	44-56	nitric oxide synthase 3	Homo sapiens	67-71
16737962-2	2006	In particular, phosphorylation of serine 1179 (bovine)/1177 (human) by Akt has been shown to be the central mechanism of eNOS regulation.	Serine	34-40	nitric oxide synthase 3	Homo sapiens	121-125
16737962-3	2006	Here we revealed a novel role of proteasome in controlling eNOS serine 1179 phosphorylation and function.	Serine	64-70	nitric oxide synthase 3	Homo sapiens	59-63
16737962-4	2006	Rather than affecting eNOS turnover, proteasomal inhibition specifically dephosphorylated eNOS serine 1179, leading to decreased enzymatic activity.	Serine	95-101	nitric oxide synthase 3	Homo sapiens	90-94
16737962-5	2006	Blocking protein phosphatase 2A (PP2A) by okadaic acid or PP2A knockdown restored eNOS serine 1179 phosphorylation and activity in proteasome-inhibited cells.	Okadaic Acid	42-54	nitric oxide synthase 3	Homo sapiens	82-86
16737962-5	2006	Blocking protein phosphatase 2A (PP2A) by okadaic acid or PP2A knockdown restored eNOS serine 1179 phosphorylation and activity in proteasome-inhibited cells.	Serine	87-93	nitric oxide synthase 3	Homo sapiens	82-86
16814758-0	2006	The calcium channel blocker amlodipine promotes the unclamping of eNOS from caveolin in endothelial cells.	Amlodipine	28-38	nitric oxide synthase 3	Homo sapiens	66-70
16814758-7	2006	Finally, we showed that the amlodipine-triggered, caveolin-dependent mechanism of eNOS activation was independent of other pleiotropic effects of the CCB such as superoxide anion scavenging and angiotensin-converting enzyme (ACE) inhibition.	Amlodipine	28-38	nitric oxide synthase 3	Homo sapiens	82-86
16814758-3	2006	Here, we reasoned that since the endothelial nitric oxide synthase is, in part, expressed in cholesterol-rich plasmalemmal microdomains (e.g., caveolae and rafts), amlodipine could interfere with this specific locale of the enzyme and thereby modulate NO production in endothelial cells.	Cholesterol	93-104	nitric oxide synthase 3	Homo sapiens	33-66
16820143-0	2006	Translocation of endothelial nitric oxide synthase: another feat of amlodipine, a cardiovascular jack-of-all-trades.	Amlodipine	68-78	nitric oxide synthase 3	Homo sapiens	17-50
16814758-3	2006	Here, we reasoned that since the endothelial nitric oxide synthase is, in part, expressed in cholesterol-rich plasmalemmal microdomains (e.g., caveolae and rafts), amlodipine could interfere with this specific locale of the enzyme and thereby modulate NO production in endothelial cells.	Amlodipine	164-174	nitric oxide synthase 3	Homo sapiens	33-66
16814758-4	2006	METHODS AND RESULTS: Using a method combining lubrol-based extraction and subcellular fractionation on sucrose gradient, we found that amlodipine, but not verapamil or nifedipine, induced the segregation of endothelial NO synthase (eNOS) from caveolin-enriched low-density membranes (8+/-2% vs. 42+/-3% in untreated condition; P&lt;0.01).	Amlodipine	135-145	nitric oxide synthase 3	Homo sapiens	232-236
16814758-5	2006	We then performed co-immunoprecipitation experiments and found that amlodipine dose-dependently disrupted the caveolin/eNOS interaction contrary to other calcium channel blockers, and potentiated the stimulation of NO production by agonists such as bradykinin and vascular endothelial growth factor (VEGF) (+138+/-28% and +183+/-27% over values obtained with the agonist alone, respectively; P&lt;0.01).	Amlodipine	68-78	nitric oxide synthase 3	Homo sapiens	119-123
16775727-6	2006	However, it has to be taken into account that ketamine inhibits endothelial nitric oxide synthase, thereby potentially aggravating impaired (micro) regional blood flow in sepsis.	Ketamine	46-54	nitric oxide synthase 3	Homo sapiens	64-97
16814758-6	2006	Interestingly, we also documented that the dissociation of the caveolin/eNOS heterocomplex induced by amlodipine was not mediated by the traditional calcium-dependent calmodulin binding to eNOS and that recombinant caveolin expression could compete with the stimulatory effects of amlodipine on eNOS activity.	Amlodipine	102-112	nitric oxide synthase 3	Homo sapiens	72-76
16895546-0	2006	Mechanisms underlying nebivolol-induced endothelial nitric oxide synthase activation in human umbilical vein endothelial cells.	Nebivolol	22-31	nitric oxide synthase 3	Homo sapiens	40-73
16764826-1	2006	Nitric oxide (NO) is a small, uncharged molecule, which is primarily generated by the nitric oxide synthase (NOS) family of proteins, including neuronal nitric oxide synthase (nNOS), inducible NOS (iNOS), and endothelial NOS (eNOS).	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	209-224
16779830-9	2006	Because 4a allele is associated with lower synthesis of eNOS, these results suggest that carrier state of 4a allele in intron 4 might be a genetic risk factor of FHON and could provide insight into the protective role of nitric oxide in the pathogenesis of FHON.	Nitric Oxide	221-233	nitric oxide synthase 3	Homo sapiens	56-60
17144095-15	2006	Decrease of proteinuria during treatment is, among others, related to decrease of metabolic disorders, while the initial results of analysis of polymorphism of the human angiotensin converting enzyme gene and endothelial nitric oxide synthase gene suggest that it may affect the decrease of proteinuria and concentration of homocysteine in the blood.	Homocysteine	324-336	nitric oxide synthase 3	Homo sapiens	209-242
16864653-3	2006	Palmitoylation-deficient mutants of eNOS release less nitric oxide (NO).	Nitric Oxide	54-66	nitric oxide synthase 3	Homo sapiens	36-40
16847153-3	2006	METHODS AND RESULTS: BMC- and CD34+-derived progenitor cells interacted with ischemic femoral arteries through SDF-1 and CXCR4 signaling and released nitric oxide (NO) via an endothelial nitric oxide synthase (eNOS)-dependent pathway.	bmc	21-24	nitric oxide synthase 3	Homo sapiens	175-208
16764985-6	2006	LY294002, a PI3K-inhibitor, blocked SST-induced p-Akt-Ser473 and partially p-eNOS-Ser617, however, it did not reverse SST-induced NHE attenuation.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	0-8	nitric oxide synthase 3	Homo sapiens	77-81
16725109-4	2006	Inhibition of endothelial nitric oxide synthase (eNOS) using l-NNA blocked VEGF-E-induced NO release and angiogenesis.	Nitroarginine	61-66	nitric oxide synthase 3	Homo sapiens	14-47
16725109-0	2006	VEGF-E activates endothelial nitric oxide synthase to induce angiogenesis via cGMP and PKG-independent pathways.	Cyclic GMP	78-82	nitric oxide synthase 3	Homo sapiens	17-50
16620829-0	2006	Atorvastatin prevents hypoxia-induced inhibition of endothelial nitric oxide synthase expression but does not affect heme oxygenase-1 in human microvascular endothelial cells.	Atorvastatin	0-12	nitric oxide synthase 3	Homo sapiens	52-85
16834924-1	2006	BACKGROUND: Nitric oxide (NO) synthesized by endothelial nitric oxide synthase (eNOS) plays an important role in both the regulation of endothelial function and the control of blood pressure.	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	45-78
16834924-1	2006	BACKGROUND: Nitric oxide (NO) synthesized by endothelial nitric oxide synthase (eNOS) plays an important role in both the regulation of endothelial function and the control of blood pressure.	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	80-84
16620829-3	2006	Here we show that atorvastatin at pharmacologically relevant concentration (0.1 microM) enhanced the expression of eNOS in human microvascular endothelial cells (HMEC-1).	Atorvastatin	18-30	nitric oxide synthase 3	Homo sapiens	115-119
16620829-4	2006	Moreover, atorvastatin prevented hypoxia-induced decrease in eNOS expression.	Atorvastatin	10-22	nitric oxide synthase 3	Homo sapiens	61-65
16503213-8	2006	The frequencies of the NOS3 Glu298Asp genotypes were Glu/Glu=46.2%, Glu/Asp=42.7%, and Asp/Asp=11.1%.	Glutamic Acid	28-31	nitric oxide synthase 3	Homo sapiens	23-27
16503213-8	2006	The frequencies of the NOS3 Glu298Asp genotypes were Glu/Glu=46.2%, Glu/Asp=42.7%, and Asp/Asp=11.1%.	Glutamic Acid	53-56	nitric oxide synthase 3	Homo sapiens	23-27
16503213-8	2006	The frequencies of the NOS3 Glu298Asp genotypes were Glu/Glu=46.2%, Glu/Asp=42.7%, and Asp/Asp=11.1%.	Glutamic Acid	53-56	nitric oxide synthase 3	Homo sapiens	23-27
16503213-8	2006	The frequencies of the NOS3 Glu298Asp genotypes were Glu/Glu=46.2%, Glu/Asp=42.7%, and Asp/Asp=11.1%.	Aspartic Acid	34-37	nitric oxide synthase 3	Homo sapiens	23-27
16715118-10	2006	Activation of eNOS by myristoylated peptides was dependent on the PI3K/Akt pathway and the rise of intracellular calcium and was associated with an elevation of cGMP levels in PAEC and with relaxation of precontracted isolated pulmonary artery segments.	Cyclic GMP	161-165	nitric oxide synthase 3	Homo sapiens	14-18
16802365-3	2006	An impaired availability of nitric oxide, related to polymorphisms in NOS3, the gene for endothelial cell nitric oxide synthase, might influence erythrocyte deformability.	Nitric Oxide	28-40	nitric oxide synthase 3	Homo sapiens	70-74
16715118-10	2006	Activation of eNOS by myristoylated peptides was dependent on the PI3K/Akt pathway and the rise of intracellular calcium and was associated with an elevation of cGMP levels in PAEC and with relaxation of precontracted isolated pulmonary artery segments.	Calcium	113-120	nitric oxide synthase 3	Homo sapiens	14-18
16497478-7	2006	An in situ hybridisation (ISH) study showed clearly that L-NAME down-regulated eNOS and iNOS mRNA expression and this was followed by a decrease in NO production.	NG-Nitroarginine Methyl Ester	57-63	nitric oxide synthase 3	Homo sapiens	79-83
16813604-2	2006	The Glu/Glu genotype at the Glu298Asp variant of the endothelial nitric oxide synthase (NOS3) gene has been tested for association with AD in several Caucasian and Asian populations, with conflicting results.	Glutamic Acid	4-7	nitric oxide synthase 3	Homo sapiens	53-86
16813604-2	2006	The Glu/Glu genotype at the Glu298Asp variant of the endothelial nitric oxide synthase (NOS3) gene has been tested for association with AD in several Caucasian and Asian populations, with conflicting results.	Glutamic Acid	4-7	nitric oxide synthase 3	Homo sapiens	88-92
16813604-2	2006	The Glu/Glu genotype at the Glu298Asp variant of the endothelial nitric oxide synthase (NOS3) gene has been tested for association with AD in several Caucasian and Asian populations, with conflicting results.	Glutamic Acid	8-11	nitric oxide synthase 3	Homo sapiens	53-86
16813604-2	2006	The Glu/Glu genotype at the Glu298Asp variant of the endothelial nitric oxide synthase (NOS3) gene has been tested for association with AD in several Caucasian and Asian populations, with conflicting results.	Glutamic Acid	8-11	nitric oxide synthase 3	Homo sapiens	88-92
16891912-0	2006	Flavonoids from seabuckthorn protect endothelial cells (EA.hy926) from oxidized low-density lipoprotein induced injuries via regulation of LOX-1 and eNOS expression.	Flavonoids	0-10	nitric oxide synthase 3	Homo sapiens	149-153
16732295-5	2006	We detected NO produced by both constitutive and inducible NO synthases (cNOS and iNOS, respectively) in live neurons and macrophages in a concentration- and time-dependent manner by using the Cu(II)-based imaging agent.	cu(ii)	193-199	nitric oxide synthase 3	Homo sapiens	73-77
16453281-0	2006	Role of AP1 element in the activation of human eNOS promoter by lysophosphatidylcholine.	Lysophosphatidylcholines	64-87	nitric oxide synthase 3	Homo sapiens	47-51
16111867-3	2006	S1P also stimulated endothelial nitric oxide synthase (eNOS) and its activation was markedly inhibited by the antisense oligonucleotide for the S1P(1) receptor rather than that for the S1P(3) receptor.	Oligonucleotides	120-135	nitric oxide synthase 3	Homo sapiens	20-53
16755443-3	2006	Thus, we hypothesized that eNOS gene polymorphism could influence perioperative hemodynamics and catecholamine support in patients undergoing cardiac surgery with CPB.	Catecholamines	97-110	nitric oxide synthase 3	Homo sapiens	27-31
16696853-8	2006	Although the physiological relevance of the Aha1-GCH1 interaction requires further study, Aha1 may recruit GCH1 into the endothelial nitric oxide synthase/heat shock protein (eNOS/Hsp90) complex to support changes in endothelial nitric oxide production through the local synthesis of BH4.	sapropterin	284-287	nitric oxide synthase 3	Homo sapiens	121-154
16696853-8	2006	Although the physiological relevance of the Aha1-GCH1 interaction requires further study, Aha1 may recruit GCH1 into the endothelial nitric oxide synthase/heat shock protein (eNOS/Hsp90) complex to support changes in endothelial nitric oxide production through the local synthesis of BH4.	sapropterin	284-287	nitric oxide synthase 3	Homo sapiens	175-179
16696853-8	2006	Although the physiological relevance of the Aha1-GCH1 interaction requires further study, Aha1 may recruit GCH1 into the endothelial nitric oxide synthase/heat shock protein (eNOS/Hsp90) complex to support changes in endothelial nitric oxide production through the local synthesis of BH4.	Nitric Oxide	133-145	nitric oxide synthase 3	Homo sapiens	175-179
16755443-3	2006	Thus, we hypothesized that eNOS gene polymorphism could influence perioperative hemodynamics and catecholamine support in patients undergoing cardiac surgery with CPB.	cpb	163-166	nitric oxide synthase 3	Homo sapiens	27-31
16859127-1	2006	OBJECTIVE: To investigate the effects of fenofibrate on the proliferation and apoptosis and endothelial nitric oxide synthase (eNOS) mRNA expression of cultured human umbilical vein endothelial cells (HUVECs) induced by lysophosphatidylcholine (LPC).	Lysophosphatidylcholines	220-243	nitric oxide synthase 3	Homo sapiens	92-125
16859127-6	2006	RESULTS: Compared with the control group, LPC could inhibit the proliferation and induce apoptosis, and downregulate eNOS mRNA expression and decrease NO production of HUVECs.	Lysophosphatidylcholines	42-45	nitric oxide synthase 3	Homo sapiens	117-121
16859127-7	2006	Fenofibrate could increase the proliferation and decrease the apoptosis, and up-regulate eNOS mRNA expression and enhance NO production in HUVECs.	Fenofibrate	0-11	nitric oxide synthase 3	Homo sapiens	89-93
16859127-8	2006	CONCLUSION: Fenofibrate could improve the proliferation and inhibit the apoptosis, and up-regulate eNOS mRNA expression of HUVECs induced by LPC, which may be responsible for fenofibrate to prevent and treat atherosclerosis.	Fenofibrate	12-23	nitric oxide synthase 3	Homo sapiens	99-103
16842672-5	2006	Then luciferase reporter gene driven by human eNOS promoter were cloned and transfected endothelial cells to see the effects of bezafibrate on eNOS promoter-driven luciferase activity.	Bezafibrate	128-139	nitric oxide synthase 3	Homo sapiens	143-147
16859127-8	2006	CONCLUSION: Fenofibrate could improve the proliferation and inhibit the apoptosis, and up-regulate eNOS mRNA expression of HUVECs induced by LPC, which may be responsible for fenofibrate to prevent and treat atherosclerosis.	Fenofibrate	175-186	nitric oxide synthase 3	Homo sapiens	99-103
16771686-7	2006	If confirmed in vivo, this finding suggests that constitutive NOS-3 expression may play a key role in OLG injury due to its activation by calcium, in interaction with pathways mediating glutamate toxicity.	Calcium	138-145	nitric oxide synthase 3	Homo sapiens	62-67
16813971-7	2006	We hereby present evidence that prolonged exposure to CO(2) impairs developmental retinal neovascularization through a mechanism involving increased endothelial nitric oxide synthase and induction of a nitrative stress; effects of hypercapnia are independent of its hyperaemic effects.	Carbon Dioxide	54-59	nitric oxide synthase 3	Homo sapiens	149-182
16650388-1	2006	The enzyme nitric oxide synthase (NOS) which is necessary for the production of nitric oxide from L-arginine exists in three isoforms: neuronal NOS (nNOS), endothelial NOS (eNOS), and inducible NOS (iNOS).	Nitric Oxide	11-23	nitric oxide synthase 3	Homo sapiens	156-171
16771686-7	2006	If confirmed in vivo, this finding suggests that constitutive NOS-3 expression may play a key role in OLG injury due to its activation by calcium, in interaction with pathways mediating glutamate toxicity.	Glutamic Acid	186-195	nitric oxide synthase 3	Homo sapiens	62-67
16431112-2	2006	The most potent and selective compound was the methylthio amidine analogue 9, which was more potent than L-nitroarginine with 185-fold selectivity for inhibition of neuronal NOS over endothelial NOS.	methylthio amidine	47-65	nitric oxide synthase 3	Homo sapiens	183-198
16431112-2	2006	The most potent and selective compound was the methylthio amidine analogue 9, which was more potent than L-nitroarginine with 185-fold selectivity for inhibition of neuronal NOS over endothelial NOS.	H-Arg(NO2)-OH	105-120	nitric oxide synthase 3	Homo sapiens	183-198
16616865-8	2006	Cadmium was also found to inhibit nitric oxide production in endothelial cells in a calcium free medium, which further hints that cadmium might impair endothelial functions by inhibiting endothelial nitric oxide synthase.	Cadmium	0-7	nitric oxide synthase 3	Homo sapiens	187-220
16497991-7	2006	BPS attenuated the IL-1beta-mediated decrease in eNOS promoter activity and the expression of eNOS gene through PKA pathway.	beraprost	0-3	nitric oxide synthase 3	Homo sapiens	49-53
16497991-7	2006	BPS attenuated the IL-1beta-mediated decrease in eNOS promoter activity and the expression of eNOS gene through PKA pathway.	beraprost	0-3	nitric oxide synthase 3	Homo sapiens	94-98
16497991-10	2006	CONCLUSIONS: These results indicate that IL-1beta and BPS antagonistically regulates the eNOS expression through the activation of p38 and PKA, respectively.	beraprost	54-57	nitric oxide synthase 3	Homo sapiens	89-93
16497991-2	2006	We examined the effects of Beraprost sodium (BPS), a stable analogue of prostacyclin, on the eNOS gene expression in the presence of inflammatory cytokine interleukin (IL)-1beta in cultured endothelial cells.	beraprost	27-43	nitric oxide synthase 3	Homo sapiens	93-97
16497991-2	2006	We examined the effects of Beraprost sodium (BPS), a stable analogue of prostacyclin, on the eNOS gene expression in the presence of inflammatory cytokine interleukin (IL)-1beta in cultured endothelial cells.	beraprost	45-48	nitric oxide synthase 3	Homo sapiens	93-97
16616865-8	2006	Cadmium was also found to inhibit nitric oxide production in endothelial cells in a calcium free medium, which further hints that cadmium might impair endothelial functions by inhibiting endothelial nitric oxide synthase.	Nitric Oxide	34-46	nitric oxide synthase 3	Homo sapiens	187-220
16616865-8	2006	Cadmium was also found to inhibit nitric oxide production in endothelial cells in a calcium free medium, which further hints that cadmium might impair endothelial functions by inhibiting endothelial nitric oxide synthase.	Cadmium	130-137	nitric oxide synthase 3	Homo sapiens	187-220
16681591-3	2006	To investigate the correlation between eNOS and VEGF and the role of nitric oxide (NO) generated by eNOS in the process of mediating angiogenesis by VEGF.	Nitric Oxide	69-81	nitric oxide synthase 3	Homo sapiens	100-104
16689381-3	2006	In addition, ischemia will also be controlled by decreasing oxygen demand related to BP and HR, and with increasing oxygen supply by increased ECNOS gene expression, collateral formation and regression of coronary stenosis.	Oxygen	116-122	nitric oxide synthase 3	Homo sapiens	143-148
16640954-5	2006	In this review, we discuss polymorphisms in genes that are main sources of reactive oxygen species generation (NADH oxidase, endothelial nitric oxide synthase, and myeloperoxidase) in mitochondria and the antioxidant enzymes paraoxonase, glutathione reductase, and heme oxygenase.	Reactive Oxygen Species	75-98	nitric oxide synthase 3	Homo sapiens	125-158
16455784-0	2006	Pregnancy-enhanced endothelial nitric oxide synthase (eNOS) activation in uterine artery endothelial cells shows altered sensitivity to Ca2+, U0126, and wortmannin but not LY294002--evidence that pregnancy adaptation of eNOS activation occurs at multiple levels of cell signaling.	U 0126	142-147	nitric oxide synthase 3	Homo sapiens	19-52
16455784-0	2006	Pregnancy-enhanced endothelial nitric oxide synthase (eNOS) activation in uterine artery endothelial cells shows altered sensitivity to Ca2+, U0126, and wortmannin but not LY294002--evidence that pregnancy adaptation of eNOS activation occurs at multiple levels of cell signaling.	U 0126	142-147	nitric oxide synthase 3	Homo sapiens	54-58
16455784-0	2006	Pregnancy-enhanced endothelial nitric oxide synthase (eNOS) activation in uterine artery endothelial cells shows altered sensitivity to Ca2+, U0126, and wortmannin but not LY294002--evidence that pregnancy adaptation of eNOS activation occurs at multiple levels of cell signaling.	Wortmannin	153-163	nitric oxide synthase 3	Homo sapiens	19-52
16455784-0	2006	Pregnancy-enhanced endothelial nitric oxide synthase (eNOS) activation in uterine artery endothelial cells shows altered sensitivity to Ca2+, U0126, and wortmannin but not LY294002--evidence that pregnancy adaptation of eNOS activation occurs at multiple levels of cell signaling.	Wortmannin	153-163	nitric oxide synthase 3	Homo sapiens	54-58
16455784-7	2006	Expression of constitutively active Akt (ca-Akt) in UAEC resulted in slight elevation of basal eNOS activity, but relative ATP-stimulated eNOS activation was not altered by ca-Akt.	Adenosine Triphosphate	123-126	nitric oxide synthase 3	Homo sapiens	138-142
16455784-8	2006	Wortmannin continued to inhibit eNOS activation by ATP in the presence of ca-Akt; LY294002 still had no inhibitory effect.	Wortmannin	0-10	nitric oxide synthase 3	Homo sapiens	32-36
16455784-8	2006	Wortmannin continued to inhibit eNOS activation by ATP in the presence of ca-Akt; LY294002 still had no inhibitory effect.	Adenosine Triphosphate	51-54	nitric oxide synthase 3	Homo sapiens	32-36
16455784-10	2006	We report that pregnancy adaptation of eNOS activation includes the reduced sensitivity to ERK-mediated attenuation of eNOS activity and enhanced stimulation of eNOS activity through a wortmannin-sensitive, LY294002-insensitive, Akt-independent mechanism.	Wortmannin	185-195	nitric oxide synthase 3	Homo sapiens	39-43
16455784-10	2006	We report that pregnancy adaptation of eNOS activation includes the reduced sensitivity to ERK-mediated attenuation of eNOS activity and enhanced stimulation of eNOS activity through a wortmannin-sensitive, LY294002-insensitive, Akt-independent mechanism.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	207-215	nitric oxide synthase 3	Homo sapiens	39-43
16609365-0	2006	A -786T&gt;C polymorphism in the endothelial nitric oxide synthase gene reduces serum nitrite/nitrate levels from the heart due to an intracoronary injection of acetylcholine.	Nitrites	86-93	nitric oxide synthase 3	Homo sapiens	33-66
16609365-0	2006	A -786T&gt;C polymorphism in the endothelial nitric oxide synthase gene reduces serum nitrite/nitrate levels from the heart due to an intracoronary injection of acetylcholine.	Nitrates	94-101	nitric oxide synthase 3	Homo sapiens	33-66
16609365-0	2006	A -786T&gt;C polymorphism in the endothelial nitric oxide synthase gene reduces serum nitrite/nitrate levels from the heart due to an intracoronary injection of acetylcholine.	Acetylcholine	161-174	nitric oxide synthase 3	Homo sapiens	33-66
16585403-2	2006	A functional eNOS oxidizes its substrate L-arginine to L-citrulline and NO*.	Arginine	41-51	nitric oxide synthase 3	Homo sapiens	13-17
16585403-2	2006	A functional eNOS oxidizes its substrate L-arginine to L-citrulline and NO*.	Citrulline	55-67	nitric oxide synthase 3	Homo sapiens	13-17
16585403-3	2006	This normal function of eNOS requires dimerization of the enzyme, the presence of the substrate L-arginine, and the essential cofactor (6R)-5,6,7,8-tetrahydro-L-biopterin (BH4), one of the most potent naturally occurring reducing agents.	Arginine	96-106	nitric oxide synthase 3	Homo sapiens	24-28
16585403-3	2006	This normal function of eNOS requires dimerization of the enzyme, the presence of the substrate L-arginine, and the essential cofactor (6R)-5,6,7,8-tetrahydro-L-biopterin (BH4), one of the most potent naturally occurring reducing agents.	sapropterin	135-170	nitric oxide synthase 3	Homo sapiens	24-28
16585403-3	2006	This normal function of eNOS requires dimerization of the enzyme, the presence of the substrate L-arginine, and the essential cofactor (6R)-5,6,7,8-tetrahydro-L-biopterin (BH4), one of the most potent naturally occurring reducing agents.	sapropterin	172-175	nitric oxide synthase 3	Homo sapiens	24-28
16585403-8	2006	Diminished levels of BH4 promote O2*- production by eNOS (referred to as eNOS uncoupling).	sapropterin	21-24	nitric oxide synthase 3	Homo sapiens	52-56
16585403-8	2006	Diminished levels of BH4 promote O2*- production by eNOS (referred to as eNOS uncoupling).	sapropterin	21-24	nitric oxide synthase 3	Homo sapiens	73-77
16585403-8	2006	Diminished levels of BH4 promote O2*- production by eNOS (referred to as eNOS uncoupling).	Superoxides	33-35	nitric oxide synthase 3	Homo sapiens	52-56
16585403-8	2006	Diminished levels of BH4 promote O2*- production by eNOS (referred to as eNOS uncoupling).	Superoxides	33-35	nitric oxide synthase 3	Homo sapiens	73-77
16585403-10	2006	In many cases, supplementation with BH4 has been shown to correct eNOS dysfunction in animal models and patients.	sapropterin	36-39	nitric oxide synthase 3	Homo sapiens	66-70
16585403-11	2006	In addition, folic acid and infusions of vitamin C are able to restore eNOS functionality, most probably by enhancing BH4 levels as well.	Folic Acid	13-23	nitric oxide synthase 3	Homo sapiens	71-75
16585403-11	2006	In addition, folic acid and infusions of vitamin C are able to restore eNOS functionality, most probably by enhancing BH4 levels as well.	Ascorbic Acid	41-50	nitric oxide synthase 3	Homo sapiens	71-75
16585403-11	2006	In addition, folic acid and infusions of vitamin C are able to restore eNOS functionality, most probably by enhancing BH4 levels as well.	sapropterin	118-121	nitric oxide synthase 3	Homo sapiens	71-75
16463158-2	2006	This study investigated the relationship of the eNOS Glu298 --&gt; Asp polymorphism with the presence and severity of BD in the Turkish population.	Aspartic Acid	67-70	nitric oxide synthase 3	Homo sapiens	48-52
16463158-7	2006	Glu298 --&gt; Asp polymorphism of the eNOS gene does not appear to be associated with the presence of BD in the Turkish population.	Aspartic Acid	14-17	nitric oxide synthase 3	Homo sapiens	38-42
16600160-4	2006	Emerging evidence demonstrates that L-arginine is not only converted to NO via eNOS, but also metabolized to urea and l-ornithine via arginase in endothelial cells.	Arginine	36-46	nitric oxide synthase 3	Homo sapiens	79-83
16565556-2	2006	Endothelial nitric oxide synthase (ecNOS) catalyzes the synthesis of nitric oxide, which regulates vascular tone, and may be related to coronary vasospasm.	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	35-40
16600160-5	2006	Hence, arginase competes with eNOS for the substrate L-arginine, resulting in deceased NO production.	Arginine	53-63	nitric oxide synthase 3	Homo sapiens	30-34
16600162-3	2006	Multiple enzymes are expressed in vascular cells that are involved in the elimination and production of reactive oxygen species, including the superoxide dismutases, catalase, thioredoxin reductase, glutathione peroxidase, NAD(P)H oxidase, xanthine oxidase, myeloperoxidase, and endothelial nitric oxide synthase.	Reactive Oxygen Species	104-127	nitric oxide synthase 3	Homo sapiens	279-312
16528409-0	2006	Insulin resistance reduces arterial prostacyclin synthase and eNOS activities by increasing endothelial fatty acid oxidation.	Fatty Acids	104-114	nitric oxide synthase 3	Homo sapiens	62-66
17318973-1	2006	PURPOSE: Many characteristics of malignant brain tumors (increased vascular permeability, vasodilatation, neovascularisation and free radical injury to the tumor and adjacent normal tissues) are believed to be mediated by nitric oxide (NO) synthetized by endothelial NO synthase (eNOS).	Nitric Oxide	222-234	nitric oxide synthase 3	Homo sapiens	280-284
16528409-3	2006	FFA-induced overproduction of superoxide activated a variety of proinflammatory signals previously implicated in hyperglycemia-induced vascular damage and inactivated 2 important antiatherogenic enzymes, prostacyclin synthase and eNOS.	Flufenamic Acid	0-3	nitric oxide synthase 3	Homo sapiens	230-234
16528409-3	2006	FFA-induced overproduction of superoxide activated a variety of proinflammatory signals previously implicated in hyperglycemia-induced vascular damage and inactivated 2 important antiatherogenic enzymes, prostacyclin synthase and eNOS.	Superoxides	30-40	nitric oxide synthase 3	Homo sapiens	230-234
16009421-2	2006	Moreover, it has been reported that asymmetric dimethylarginine (ADMA) acts as is an endogenous inhibitor of endothelial NOS (eNOS) by competing with the enzyme for L-arginine.	dimethylarginine	47-63	nitric oxide synthase 3	Homo sapiens	109-124
16009421-2	2006	Moreover, it has been reported that asymmetric dimethylarginine (ADMA) acts as is an endogenous inhibitor of endothelial NOS (eNOS) by competing with the enzyme for L-arginine.	dimethylarginine	47-63	nitric oxide synthase 3	Homo sapiens	126-130
16009421-2	2006	Moreover, it has been reported that asymmetric dimethylarginine (ADMA) acts as is an endogenous inhibitor of endothelial NOS (eNOS) by competing with the enzyme for L-arginine.	N,N-dimethylarginine	65-69	nitric oxide synthase 3	Homo sapiens	109-124
16009421-2	2006	Moreover, it has been reported that asymmetric dimethylarginine (ADMA) acts as is an endogenous inhibitor of endothelial NOS (eNOS) by competing with the enzyme for L-arginine.	N,N-dimethylarginine	65-69	nitric oxide synthase 3	Homo sapiens	126-130
16009421-2	2006	Moreover, it has been reported that asymmetric dimethylarginine (ADMA) acts as is an endogenous inhibitor of endothelial NOS (eNOS) by competing with the enzyme for L-arginine.	Arginine	165-175	nitric oxide synthase 3	Homo sapiens	109-124
16009421-2	2006	Moreover, it has been reported that asymmetric dimethylarginine (ADMA) acts as is an endogenous inhibitor of endothelial NOS (eNOS) by competing with the enzyme for L-arginine.	Arginine	165-175	nitric oxide synthase 3	Homo sapiens	126-130
16497987-0	2006	Role of endothelial nitric oxide synthase in the regulation of SREBP activation by oxidized phospholipids.	Phospholipids	92-105	nitric oxide synthase 3	Homo sapiens	8-41
16497987-4	2006	Ox-PAPC treatment of EC induced a dose- and time-dependent activation of eNOS, as measured by phosphorylation of serine 1177, dephosphorylation of threonine 495, and the conversion of L-arginine to L-citrulline.	Serine	113-119	nitric oxide synthase 3	Homo sapiens	73-77
16497987-4	2006	Ox-PAPC treatment of EC induced a dose- and time-dependent activation of eNOS, as measured by phosphorylation of serine 1177, dephosphorylation of threonine 495, and the conversion of L-arginine to L-citrulline.	Threonine	147-156	nitric oxide synthase 3	Homo sapiens	73-77
16497987-4	2006	Ox-PAPC treatment of EC induced a dose- and time-dependent activation of eNOS, as measured by phosphorylation of serine 1177, dephosphorylation of threonine 495, and the conversion of L-arginine to L-citrulline.	Arginine	184-194	nitric oxide synthase 3	Homo sapiens	73-77
16497987-4	2006	Ox-PAPC treatment of EC induced a dose- and time-dependent activation of eNOS, as measured by phosphorylation of serine 1177, dephosphorylation of threonine 495, and the conversion of L-arginine to L-citrulline.	Citrulline	198-210	nitric oxide synthase 3	Homo sapiens	73-77
16442496-2	2006	Additionally, fenofibrate has been demonstrated to upregulate endothelial nitric oxide synthase (eNOS).	Fenofibrate	14-25	nitric oxide synthase 3	Homo sapiens	62-95
16407220-5	2006	Further, inhibition of PKCzeta abrogated ONOO- -induced AMPK-Thr172 phosphorylation as that of endothelial nitric-oxide synthase.	onoo	41-45	nitric oxide synthase 3	Homo sapiens	95-128
16442076-1	2006	In this work, we demonstrate that endothelial nitric oxide synthase is capable of anoxic reduction of nitrite anions to nitric oxide at physiological pH by absorption and EPR spectroscopy and electrochemical measurements.	Nitrites	102-109	nitric oxide synthase 3	Homo sapiens	34-67
16384887-1	2006	BACKGROUND: Nitric oxide is synthesized from the amino acid Arg by the enzyme endothelial nitric oxide synthase, which is competitively inhibited by the arginine metabolite asymmetric dimethylarginine (ADMA).	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	78-111
16384887-1	2006	BACKGROUND: Nitric oxide is synthesized from the amino acid Arg by the enzyme endothelial nitric oxide synthase, which is competitively inhibited by the arginine metabolite asymmetric dimethylarginine (ADMA).	Arginine	60-63	nitric oxide synthase 3	Homo sapiens	78-111
16384887-1	2006	BACKGROUND: Nitric oxide is synthesized from the amino acid Arg by the enzyme endothelial nitric oxide synthase, which is competitively inhibited by the arginine metabolite asymmetric dimethylarginine (ADMA).	Arginine	153-161	nitric oxide synthase 3	Homo sapiens	78-111
16384887-1	2006	BACKGROUND: Nitric oxide is synthesized from the amino acid Arg by the enzyme endothelial nitric oxide synthase, which is competitively inhibited by the arginine metabolite asymmetric dimethylarginine (ADMA).	dimethylarginine	184-200	nitric oxide synthase 3	Homo sapiens	78-111
16384887-1	2006	BACKGROUND: Nitric oxide is synthesized from the amino acid Arg by the enzyme endothelial nitric oxide synthase, which is competitively inhibited by the arginine metabolite asymmetric dimethylarginine (ADMA).	N,N-dimethylarginine	202-206	nitric oxide synthase 3	Homo sapiens	78-111
16595793-1	2006	Over the last two decades, it has become evident that decreased bioavailability of endothelial nitric oxide (NO) produced from endothelial NO synthase (eNOS), referred to as endothelial dysfunction, plays a crucial role in the development and progression of atherosclerosis.	Nitric Oxide	95-107	nitric oxide synthase 3	Homo sapiens	127-150
16595793-1	2006	Over the last two decades, it has become evident that decreased bioavailability of endothelial nitric oxide (NO) produced from endothelial NO synthase (eNOS), referred to as endothelial dysfunction, plays a crucial role in the development and progression of atherosclerosis.	Nitric Oxide	95-107	nitric oxide synthase 3	Homo sapiens	152-156
16337498-4	2006	RESULTS: HO-1 as well as ecNOS gene and protein expression significantly increased upon Carnitines incubation.	Carnitine	88-98	nitric oxide synthase 3	Homo sapiens	25-30
16157324-1	2006	BACKGROUND: Nitric oxide (NO) produced by endothelial nitric oxide synthase (eNOS) mediates endothelium-dependent vasodilation and antithrombotic action.	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	42-75
16157324-1	2006	BACKGROUND: Nitric oxide (NO) produced by endothelial nitric oxide synthase (eNOS) mediates endothelium-dependent vasodilation and antithrombotic action.	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	77-81
16326932-2	2006	Multiple signaling inputs, including calcium, caveolin-1, phosphorylation by several kinases, and binding to the 90-kDa heat shock protein (Hsp90), regulate eNOS activity.	Calcium	37-44	nitric oxide synthase 3	Homo sapiens	157-161
16489746-2	2006	Correlating with a Val-to-Ile residue substitution in the bsNOS heme pocket, the Fe(II)-NO complex with both l-Arg and NOHA is more bent than the Fe(II)-NO, l-Arg complex of mammalian eNOS [Li, H., Raman, C. S., Martasek, P., Masters, B. S. S., and Poulos, T. L. (2001) Biochemistry 40, 5399-5406].	Valine	19-22	nitric oxide synthase 3	Homo sapiens	184-188
16489746-2	2006	Correlating with a Val-to-Ile residue substitution in the bsNOS heme pocket, the Fe(II)-NO complex with both l-Arg and NOHA is more bent than the Fe(II)-NO, l-Arg complex of mammalian eNOS [Li, H., Raman, C. S., Martasek, P., Masters, B. S. S., and Poulos, T. L. (2001) Biochemistry 40, 5399-5406].	Isoleucine	26-29	nitric oxide synthase 3	Homo sapiens	184-188
16489746-2	2006	Correlating with a Val-to-Ile residue substitution in the bsNOS heme pocket, the Fe(II)-NO complex with both l-Arg and NOHA is more bent than the Fe(II)-NO, l-Arg complex of mammalian eNOS [Li, H., Raman, C. S., Martasek, P., Masters, B. S. S., and Poulos, T. L. (2001) Biochemistry 40, 5399-5406].	bsnos	58-63	nitric oxide synthase 3	Homo sapiens	184-188
16489746-2	2006	Correlating with a Val-to-Ile residue substitution in the bsNOS heme pocket, the Fe(II)-NO complex with both l-Arg and NOHA is more bent than the Fe(II)-NO, l-Arg complex of mammalian eNOS [Li, H., Raman, C. S., Martasek, P., Masters, B. S. S., and Poulos, T. L. (2001) Biochemistry 40, 5399-5406].	Heme	64-68	nitric oxide synthase 3	Homo sapiens	184-188
16489746-2	2006	Correlating with a Val-to-Ile residue substitution in the bsNOS heme pocket, the Fe(II)-NO complex with both l-Arg and NOHA is more bent than the Fe(II)-NO, l-Arg complex of mammalian eNOS [Li, H., Raman, C. S., Martasek, P., Masters, B. S. S., and Poulos, T. L. (2001) Biochemistry 40, 5399-5406].	fe(ii)-no	81-90	nitric oxide synthase 3	Homo sapiens	184-188
16489746-2	2006	Correlating with a Val-to-Ile residue substitution in the bsNOS heme pocket, the Fe(II)-NO complex with both l-Arg and NOHA is more bent than the Fe(II)-NO, l-Arg complex of mammalian eNOS [Li, H., Raman, C. S., Martasek, P., Masters, B. S. S., and Poulos, T. L. (2001) Biochemistry 40, 5399-5406].	Arginine	109-114	nitric oxide synthase 3	Homo sapiens	184-188
16489746-2	2006	Correlating with a Val-to-Ile residue substitution in the bsNOS heme pocket, the Fe(II)-NO complex with both l-Arg and NOHA is more bent than the Fe(II)-NO, l-Arg complex of mammalian eNOS [Li, H., Raman, C. S., Martasek, P., Masters, B. S. S., and Poulos, T. L. (2001) Biochemistry 40, 5399-5406].	N(omega)-hydroxyarginine	119-123	nitric oxide synthase 3	Homo sapiens	184-188
15970429-0	2006	High glucose-induced apoptosis in human vascular endothelial cells is mediated through NF-kappaB and c-Jun NH2-terminal kinase pathway and prevented by PI3K/Akt/eNOS pathway.	Glucose	5-12	nitric oxide synthase 3	Homo sapiens	161-165
15970429-3	2006	The results showed that high glucose-induced apoptosis was significantly enhanced by PI3K inhibitors (wortmannin and LY294002), NOS inhibitor (NG-nitro-arginine methyl ester) and eNOS antisense oligonucleotide.	Glucose	29-36	nitric oxide synthase 3	Homo sapiens	179-183
15970429-3	2006	The results showed that high glucose-induced apoptosis was significantly enhanced by PI3K inhibitors (wortmannin and LY294002), NOS inhibitor (NG-nitro-arginine methyl ester) and eNOS antisense oligonucleotide.	Oligonucleotides	194-209	nitric oxide synthase 3	Homo sapiens	179-183
15970429-6	2006	Moreover, high glucose-induced increase in eNOS expression was attenuated by PI3K inhibitors and the negative mutant of PI3K.	Glucose	15-22	nitric oxide synthase 3	Homo sapiens	43-47
15970429-9	2006	Activation of the ROS/PI3K/Akt/eNOS signaling pathway in early phase exerts protective effects against the induction of apoptosis by high glucose.	Reactive Oxygen Species	18-21	nitric oxide synthase 3	Homo sapiens	31-35
15970429-9	2006	Activation of the ROS/PI3K/Akt/eNOS signaling pathway in early phase exerts protective effects against the induction of apoptosis by high glucose.	Glucose	138-145	nitric oxide synthase 3	Homo sapiens	31-35
16229016-1	2006	We have recently demonstrated that tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) increases endothelial nitric oxide synthase (eNOS) phosphorylation, NOS activity, and nitric oxide (NO) synthesis in cultured human umbilical vein endothelial cells (HUVEC), without inducing apoptotic cell death.	Nitric Oxide	121-133	nitric oxide synthase 3	Homo sapiens	144-148
16229016-8	2006	Conversely, microtubule disruption and Golgi scattering induced with Nocodazole treatment inhibited TRAIL-increased NOS activity, indicating that, on cultured HUVEC, TRAIL ability to affect NO production by regulating eNOS sub-cellular distribution is mediated by cytoskeleton and Golgi complex modifications.	Nocodazole	69-79	nitric oxide synthase 3	Homo sapiens	218-222
16553284-2	2006	The L-NAME prevents the synthesis of the potent vasodilator nitric oxide (NO) by inhibiting both the constitutive [endothelial NO synthase (eNOS or NOS-3)] and inducible [inducible NO synthase (iNOS or NOS-2)] forms of NO synthase.	NG-Nitroarginine Methyl Ester	4-10	nitric oxide synthase 3	Homo sapiens	148-153
16553284-2	2006	The L-NAME prevents the synthesis of the potent vasodilator nitric oxide (NO) by inhibiting both the constitutive [endothelial NO synthase (eNOS or NOS-3)] and inducible [inducible NO synthase (iNOS or NOS-2)] forms of NO synthase.	Nitric Oxide	60-72	nitric oxide synthase 3	Homo sapiens	148-153
16337498-7	2006	Coincubation of C (0.5-1.0-2.0 mM), AC (0.1-0.2-0.4 mM) and PC (0.05-0.1-0.2 mM) with H2O2 further increased HO-1 gene expression and not only normalized vs. H2O2 but even increased vs. basal ecNOS mRNA.	Hydrogen Peroxide	86-90	nitric oxide synthase 3	Homo sapiens	192-197
16337498-9	2006	CONCLUSION: This is the first report that has utilized a molecular biological approach to demonstrate a direct stimulatory effect of Carnitines on gene and protein expression of the oxidative stress related markers HO-1 and ecNOS.	Carnitine	133-143	nitric oxide synthase 3	Homo sapiens	224-229
15979078-8	2006	Over-expression of SR-BI in human endothelial cells activated endothelial nitric oxide synthase (eNOS) activity by phosphorylation of eNOS at residue Ser-1177 in the presence of HDL, leading to increased production of the anti-atherogenic molecule nitric oxide (NO).	Serine	150-153	nitric oxide synthase 3	Homo sapiens	62-95
16472125-6	2006	Data obtained in the present study show that the exposure for 5 days to high glucose increases oxidative stress, reduces DDAH-2 and eNOS expression and increases iNOS expression.	Glucose	77-84	nitric oxide synthase 3	Homo sapiens	132-136
16293798-1	2006	This article explores the physiology of superoxide generation by endothelial nitric oxide synthase (eNOS), the so-called "uncoupled" state of the enzyme.	Superoxides	40-50	nitric oxide synthase 3	Homo sapiens	65-98
16293798-1	2006	This article explores the physiology of superoxide generation by endothelial nitric oxide synthase (eNOS), the so-called "uncoupled" state of the enzyme.	Superoxides	40-50	nitric oxide synthase 3	Homo sapiens	100-104
16293798-4	2006	As the switch from NO production to reactive oxygen species by eNOS is also the final common pathway in atherogenesis, the uncoupling of eNOS further builds on the hypothesis that atherogenesis is driven by cellular mechanisms that originally serve host defense.	Reactive Oxygen Species	36-59	nitric oxide synthase 3	Homo sapiens	63-67
16472125-7	2006	These results indicate that DDAH-2 and iNOS/eNOS dysregulation may play a key role in high glucose-mediated oxidative stress, suggesting that selective modulation of DDAH isoforms may result in selective inhibition/activation of NOS isoforms, thereby providing a novel strategy of approach in vascular complications of several pathologies.	Glucose	91-98	nitric oxide synthase 3	Homo sapiens	44-48
16234413-0	2006	Sphingosine 1-phosphate induces endothelial nitric-oxide synthase activation through phosphorylation in human corpus cavernosum.	sphingosine 1-phosphate	0-23	nitric oxide synthase 3	Homo sapiens	32-65
16443786-6	2006	Finally, incubation of BAECs with clinically relevant concentrations of metformin dramatically attenuated high-glucose (30 mmol/l)-induced reduction in the association of hsp90 with eNOS, which resulted in increased NO bioactivity with a reduction in overexpression of adhesion molecules and endothelial apoptosis caused by high-glucose exposure.	Metformin	72-81	nitric oxide synthase 3	Homo sapiens	182-186
16443786-6	2006	Finally, incubation of BAECs with clinically relevant concentrations of metformin dramatically attenuated high-glucose (30 mmol/l)-induced reduction in the association of hsp90 with eNOS, which resulted in increased NO bioactivity with a reduction in overexpression of adhesion molecules and endothelial apoptosis caused by high-glucose exposure.	Glucose	111-118	nitric oxide synthase 3	Homo sapiens	182-186
16443786-6	2006	Finally, incubation of BAECs with clinically relevant concentrations of metformin dramatically attenuated high-glucose (30 mmol/l)-induced reduction in the association of hsp90 with eNOS, which resulted in increased NO bioactivity with a reduction in overexpression of adhesion molecules and endothelial apoptosis caused by high-glucose exposure.	Glucose	329-336	nitric oxide synthase 3	Homo sapiens	182-186
16443786-7	2006	Taken together, our results indicate that metformin might improve vascular endothelial functions in diabetes by increasing AMPK-dependent, hsp90-mediated eNOS activation.	Metformin	42-51	nitric oxide synthase 3	Homo sapiens	154-158
16495772-7	2006	In human umbilical vein endothelial cells, azelnidipine enhanced basal nitric oxide production by endothelial nitric oxide synthase.	azelnidipine	43-55	nitric oxide synthase 3	Homo sapiens	98-131
16495772-7	2006	In human umbilical vein endothelial cells, azelnidipine enhanced basal nitric oxide production by endothelial nitric oxide synthase.	Nitric Oxide	71-83	nitric oxide synthase 3	Homo sapiens	98-131
16443786-0	2006	Activation of the AMP-activated kinase by antidiabetes drug metformin stimulates nitric oxide synthesis in vivo by promoting the association of heat shock protein 90 and endothelial nitric oxide synthase.	Metformin	60-69	nitric oxide synthase 3	Homo sapiens	170-203
16443786-0	2006	Activation of the AMP-activated kinase by antidiabetes drug metformin stimulates nitric oxide synthesis in vivo by promoting the association of heat shock protein 90 and endothelial nitric oxide synthase.	Nitric Oxide	81-93	nitric oxide synthase 3	Homo sapiens	170-203
16443786-3	2006	Exposure of cultured bovine aortic endothelial cells (BAECs) to clinically relevant concentrations of metformin (50-500 micromol/l) dose-dependently increased serine-1179 (Ser1179) phosphorylation (equal to human Ser1179) of endothelial nitric oxide (NO) synthase (eNOS) as well as its association with heat shock protein (hsp)-90, resulting in increased activation of eNOS and NO bioactivity (cyclic GMP).	Metformin	102-111	nitric oxide synthase 3	Homo sapiens	265-269
16443786-3	2006	Exposure of cultured bovine aortic endothelial cells (BAECs) to clinically relevant concentrations of metformin (50-500 micromol/l) dose-dependently increased serine-1179 (Ser1179) phosphorylation (equal to human Ser1179) of endothelial nitric oxide (NO) synthase (eNOS) as well as its association with heat shock protein (hsp)-90, resulting in increased activation of eNOS and NO bioactivity (cyclic GMP).	Metformin	102-111	nitric oxide synthase 3	Homo sapiens	369-373
16443786-3	2006	Exposure of cultured bovine aortic endothelial cells (BAECs) to clinically relevant concentrations of metformin (50-500 micromol/l) dose-dependently increased serine-1179 (Ser1179) phosphorylation (equal to human Ser1179) of endothelial nitric oxide (NO) synthase (eNOS) as well as its association with heat shock protein (hsp)-90, resulting in increased activation of eNOS and NO bioactivity (cyclic GMP).	Serine	159-165	nitric oxide synthase 3	Homo sapiens	265-269
16443786-3	2006	Exposure of cultured bovine aortic endothelial cells (BAECs) to clinically relevant concentrations of metformin (50-500 micromol/l) dose-dependently increased serine-1179 (Ser1179) phosphorylation (equal to human Ser1179) of endothelial nitric oxide (NO) synthase (eNOS) as well as its association with heat shock protein (hsp)-90, resulting in increased activation of eNOS and NO bioactivity (cyclic GMP).	Serine	159-165	nitric oxide synthase 3	Homo sapiens	369-373
16502366-1	2006	BACKGROUND: Nitric oxide (NO) generated by endothelial nitric oxide synthase (eNOS) plays a crucial role in vascular function and homeostasis.	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	43-76
16502366-1	2006	BACKGROUND: Nitric oxide (NO) generated by endothelial nitric oxide synthase (eNOS) plays a crucial role in vascular function and homeostasis.	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	78-82
16430222-2	2006	Endothelial nitric oxide synthase (eNOS) is dually acylated by the fatty acids myristate and palmitate.	fatty acids myristate	67-88	nitric oxide synthase 3	Homo sapiens	0-33
16430222-2	2006	Endothelial nitric oxide synthase (eNOS) is dually acylated by the fatty acids myristate and palmitate.	fatty acids myristate	67-88	nitric oxide synthase 3	Homo sapiens	35-39
16430222-2	2006	Endothelial nitric oxide synthase (eNOS) is dually acylated by the fatty acids myristate and palmitate.	Palmitates	93-102	nitric oxide synthase 3	Homo sapiens	0-33
16430222-2	2006	Endothelial nitric oxide synthase (eNOS) is dually acylated by the fatty acids myristate and palmitate.	Palmitates	93-102	nitric oxide synthase 3	Homo sapiens	35-39
17101543-13	2006	CONCLUSIONS: The Glu/Glu-genotype of the NOS3 Glu298Asp polymorphism may increase the risk of developing DN independently of other known risk factors.	Glutamic Acid	17-20	nitric oxide synthase 3	Homo sapiens	41-45
16257964-1	2006	Nitric oxide (NO) produced in the endothelium via the enzyme endothelial nitric-oxide synthase (eNOS) is an important vasoactive compound.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	61-94
16413411-2	2006	Recently, we have shown that plasma nitrite mirrors acute changes in endothelial nitric oxide synthase activity in various mammals, including humans.	Nitrites	36-43	nitric oxide synthase 3	Homo sapiens	69-102
16113046-7	2006	There was more beta-actin coimmunoprecipitated with eNOS in Triton X-100-soluble fraction in confluent cells in later growth phase and in high density.	Octoxynol	60-72	nitric oxide synthase 3	Homo sapiens	52-56
16113046-9	2006	Moreover, PAEC incubation with cytochalasin D and jasplakinolide resulted in increases in eNOS/actin association and in eNOS activity without changes in eNOS protein content.	Cytochalasin D	31-45	nitric oxide synthase 3	Homo sapiens	90-94
16113046-9	2006	Moreover, PAEC incubation with cytochalasin D and jasplakinolide resulted in increases in eNOS/actin association and in eNOS activity without changes in eNOS protein content.	Cytochalasin D	31-45	nitric oxide synthase 3	Homo sapiens	120-124
16113046-9	2006	Moreover, PAEC incubation with cytochalasin D and jasplakinolide resulted in increases in eNOS/actin association and in eNOS activity without changes in eNOS protein content.	Cytochalasin D	31-45	nitric oxide synthase 3	Homo sapiens	120-124
16113046-9	2006	Moreover, PAEC incubation with cytochalasin D and jasplakinolide resulted in increases in eNOS/actin association and in eNOS activity without changes in eNOS protein content.	jasplakinolide	50-64	nitric oxide synthase 3	Homo sapiens	90-94
16113046-9	2006	Moreover, PAEC incubation with cytochalasin D and jasplakinolide resulted in increases in eNOS/actin association and in eNOS activity without changes in eNOS protein content.	jasplakinolide	50-64	nitric oxide synthase 3	Homo sapiens	120-124
16113046-9	2006	Moreover, PAEC incubation with cytochalasin D and jasplakinolide resulted in increases in eNOS/actin association and in eNOS activity without changes in eNOS protein content.	jasplakinolide	50-64	nitric oxide synthase 3	Homo sapiens	120-124
17101543-13	2006	CONCLUSIONS: The Glu/Glu-genotype of the NOS3 Glu298Asp polymorphism may increase the risk of developing DN independently of other known risk factors.	Glutamic Acid	21-24	nitric oxide synthase 3	Homo sapiens	41-45
16269668-4	2006	eNOS activation was preceded by sequential activation of neutral-sphingomyelinase-2 (N-SMase2) and sphingosine-kinase-1 (SK1) and generation of sphingosine-1-phosphate (Sph1P).	sphingosine 1-phosphate	144-167	nitric oxide synthase 3	Homo sapiens	0-4
16289876-7	2006	Cryptotanshinone induced a concentration-dependent increase in endothelial nitric oxide synthase (eNOS) expression without significantly changing neuronal nitric oxide synthase (nNOS) expression in HUVECs in the presence or absence of TNF-alpha.	cryptotanshinone	0-16	nitric oxide synthase 3	Homo sapiens	63-96
15916766-0	2006	Endothelial nitric oxide synthase gene variant modulates the relationship between serum cholesterol levels and blood pressure in the general population: new evidence for a direct effect of lipids in arterial blood pressure.	Cholesterol	88-99	nitric oxide synthase 3	Homo sapiens	0-33
16269668-4	2006	eNOS activation was preceded by sequential activation of neutral-sphingomyelinase-2 (N-SMase2) and sphingosine-kinase-1 (SK1) and generation of sphingosine-1-phosphate (Sph1P).	sphingosine 1-phosphate	169-174	nitric oxide synthase 3	Homo sapiens	0-4
16579706-11	2006	In conclusion, the high intensity of NOS1, NOS3, and VEGF were mostly expressed in the titanium group, whereas the low intensity of NOS1, NOS3, and VEGF were mostly expressed in the zirconium oxide group.	zirconium oxide	182-197	nitric oxide synthase 3	Homo sapiens	138-142
17144884-1	2006	NO (nitric oxide), formed in the vascular endothelium and derived from a biochemical reaction catalysed by eNOS (endothelial NO synthase), appears to play a role in exercise-induced dilation of blood vessels supplying cardiac and skeletal muscle.	Nitric Oxide	4-16	nitric oxide synthase 3	Homo sapiens	107-111
16344378-1	2006	NO produced by endothelial NO synthase (NOS3) decreases sodium transport by the thick ascending limb (THAL).	Sodium	56-62	nitric oxide synthase 3	Homo sapiens	40-44
16344378-2	2006	We found previously that 7 days of high salt (HS) increased THAL-NOS3 expression but not NO production.	Salts	40-44	nitric oxide synthase 3	Homo sapiens	65-69
16344378-2	2006	We found previously that 7 days of high salt (HS) increased THAL-NOS3 expression but not NO production.	hassio	46-48	nitric oxide synthase 3	Homo sapiens	65-69
16344378-5	2006	NOS3 expression increased by 71+/-13%, 127+/-24%, and 69+/-16% at days 1, 3, and 7 of HS, respectively.	hassio	86-88	nitric oxide synthase 3	Homo sapiens	0-4
17357484-10	2006	Consequently, the mechanisms of rosuvastatin"s neural protection on ischemic brain injury are to enhance expression of eNOS, to inhibit expression of iNOS and activated caspase-3.	Rosuvastatin Calcium	32-44	nitric oxide synthase 3	Homo sapiens	119-123
16288501-2	2006	Since endothelin-1 (ET-1) and nitric oxide (NO) produced by endothelial NO synthase (eNOS) are vascular tension regulators secreted by endothelial cells, we studied the influence of two anthocyanidins, namely cyanidin (CY) and delphinidin (DP), on the regulation of ET-1 and eNOS in cultured human umbilical vein endothelial cells (HUVECs).	Nitric Oxide	30-42	nitric oxide synthase 3	Homo sapiens	85-89
16409219-1	2006	INTRODUCTION: Endothelial-derived nitric oxide (NO), which is produced by endothelial nitric oxide synthase (eNOS) in response to increased blood flow, maintains the tumescence phase of erection.	Nitric Oxide	34-46	nitric oxide synthase 3	Homo sapiens	74-107
16409219-1	2006	INTRODUCTION: Endothelial-derived nitric oxide (NO), which is produced by endothelial nitric oxide synthase (eNOS) in response to increased blood flow, maintains the tumescence phase of erection.	Nitric Oxide	34-46	nitric oxide synthase 3	Homo sapiens	109-113
16288501-5	2006	CY and DP both increased the protein level of eNOS, but DP showed the major effect raising eNOS protein in a dose-dependent manner.	cyanidin	0-2	nitric oxide synthase 3	Homo sapiens	46-50
16288501-5	2006	CY and DP both increased the protein level of eNOS, but DP showed the major effect raising eNOS protein in a dose-dependent manner.	cyanidin	0-2	nitric oxide synthase 3	Homo sapiens	91-95
16288501-5	2006	CY and DP both increased the protein level of eNOS, but DP showed the major effect raising eNOS protein in a dose-dependent manner.	delphinidin	7-9	nitric oxide synthase 3	Homo sapiens	46-50
17117898-1	2006	BACKGROUND: The nitric oxide synthase (NOS3) G894T gene polymorphism seems as a genetic determinant of total homocysteine (tHcy) concentrations through an effect on folate catabolism.	Homocysteine	109-121	nitric oxide synthase 3	Homo sapiens	39-43
17117898-1	2006	BACKGROUND: The nitric oxide synthase (NOS3) G894T gene polymorphism seems as a genetic determinant of total homocysteine (tHcy) concentrations through an effect on folate catabolism.	thcy	123-127	nitric oxide synthase 3	Homo sapiens	39-43
17117898-1	2006	BACKGROUND: The nitric oxide synthase (NOS3) G894T gene polymorphism seems as a genetic determinant of total homocysteine (tHcy) concentrations through an effect on folate catabolism.	Folic Acid	165-171	nitric oxide synthase 3	Homo sapiens	39-43
16288501-5	2006	CY and DP both increased the protein level of eNOS, but DP showed the major effect raising eNOS protein in a dose-dependent manner.	delphinidin	56-58	nitric oxide synthase 3	Homo sapiens	46-50
17117898-9	2006	CONCLUSION: Our results showed a modulating effect of the NOS3 4a/b gene variant on tHcy concentrations that is at least partially provoked by discrete blood pressure increments.	thcy	84-88	nitric oxide synthase 3	Homo sapiens	58-62
16288501-5	2006	CY and DP both increased the protein level of eNOS, but DP showed the major effect raising eNOS protein in a dose-dependent manner.	delphinidin	56-58	nitric oxide synthase 3	Homo sapiens	91-95
17120617-2	2006	In this study, the aim was to determine the regulation of inducible nitric oxide synthase (iNOS) and endothelial nitric oxide synthase (eNOS) expressions on MTS in response to treatment with the commonly used anti-cancer drugs Doxorubicin and Docetaxel.	Docetaxel	243-252	nitric oxide synthase 3	Homo sapiens	101-134
17120617-2	2006	In this study, the aim was to determine the regulation of inducible nitric oxide synthase (iNOS) and endothelial nitric oxide synthase (eNOS) expressions on MTS in response to treatment with the commonly used anti-cancer drugs Doxorubicin and Docetaxel.	Doxorubicin	227-238	nitric oxide synthase 3	Homo sapiens	101-134
17120617-7	2006	An increase in iNOS immunoreactivity and a decrease in eNOS immunoreactivity were observed after doxorubicin treatment, when compared with the other groups.	Doxorubicin	97-108	nitric oxide synthase 3	Homo sapiens	55-59
17120617-2	2006	In this study, the aim was to determine the regulation of inducible nitric oxide synthase (iNOS) and endothelial nitric oxide synthase (eNOS) expressions on MTS in response to treatment with the commonly used anti-cancer drugs Doxorubicin and Docetaxel.	Doxorubicin	227-238	nitric oxide synthase 3	Homo sapiens	136-140
17120617-8	2006	Furthermore, upregulation of iNOS and downregulation of eNOS were detected in doxorubicin-treated cells using Western blotting.	Doxorubicin	78-89	nitric oxide synthase 3	Homo sapiens	56-60
17120617-13	2006	Interestingly, eNOS expression increased after the addition of both docetaxel and the drug combination, and it was found to negatively correlate with the histological grade of the tumor.	Docetaxel	68-77	nitric oxide synthase 3	Homo sapiens	15-19
17236649-1	2006	It is widely recognized that nitric oxide (NO) in mammalian tissues is produced from L-arginine via catalysis by NO synthase (NOS) isoforms such as neuronal NOS (nNOS) and endothelial NOS (eNOS) that are constitutively expressed mainly in the central and peripheral nervous system and vascular endothelial cells, respectively.	Nitric Oxide	29-41	nitric oxide synthase 3	Homo sapiens	172-187
17236649-1	2006	It is widely recognized that nitric oxide (NO) in mammalian tissues is produced from L-arginine via catalysis by NO synthase (NOS) isoforms such as neuronal NOS (nNOS) and endothelial NOS (eNOS) that are constitutively expressed mainly in the central and peripheral nervous system and vascular endothelial cells, respectively.	Arginine	85-95	nitric oxide synthase 3	Homo sapiens	172-187
16269583-5	2005	There was some evidence for higher risk of CL/P with maternal periconceptional smoking in infants with an NOS3 -922G allele (for homozygotes, OR = 2.5, 95% CI: 1.2, 5.6) but not in those with an 894T allele.	Phosphorus	46-47	nitric oxide synthase 3	Homo sapiens	106-110
16391520-4	2005	PGE2 increased phosphorylation of Akt and endothelial nitric oxide synthase (eNOS), eNOS activity, and nitric oxide (NO) production by the activation of cAMP-dependent protein kinase (PKA) and phosphatidylinositol 3-kinase (PI3K).	Dinoprostone	0-4	nitric oxide synthase 3	Homo sapiens	42-75
16849206-2	2005	A recent crystallographic study mapped the interaction of CaM with endothelial NOS (eNOS) using a 20 residue peptide comprising the binding site within eNOS.	Peptides	109-116	nitric oxide synthase 3	Homo sapiens	67-82
16517248-1	2006	Coronary vasorelaxation depends on nitric oxide (NO) bioavailability, which is a function of endothelial nitric oxide synthase-derived NO production and NO inactivation by reactive oxygen species.	Nitric Oxide	35-47	nitric oxide synthase 3	Homo sapiens	93-126
16210567-1	2005	BACKGROUND: Previously, we showed that the 27nt repeat polymorphism in endothelial nitric oxide synthase (eNOS) intron 4 was associated with altered eNOS mRNA and protein levels, nitric oxide (NO) production and vascular disease risk; the 27-nt repeats had a cis-acting role in eNOS promoter function.	Nitric Oxide	83-95	nitric oxide synthase 3	Homo sapiens	106-110
16297993-7	2005	The increased synthesis of nitric oxide is due, at least in part, to an upregulation of endothelial nitric oxide synthase.	Nitric Oxide	27-39	nitric oxide synthase 3	Homo sapiens	88-121
16150460-7	2005	Resveratrol has been shown to induce the activity of endothelial nitric oxide synthase (eNOS) and increase NO production.	Resveratrol	0-11	nitric oxide synthase 3	Homo sapiens	53-86
16364825-0	2005	Salt intake affects the relation between hypertension and the T-786C polymorphism in the endothelial nitric oxide synthase gene.	Salts	0-4	nitric oxide synthase 3	Homo sapiens	89-122
16210567-1	2005	BACKGROUND: Previously, we showed that the 27nt repeat polymorphism in endothelial nitric oxide synthase (eNOS) intron 4 was associated with altered eNOS mRNA and protein levels, nitric oxide (NO) production and vascular disease risk; the 27-nt repeats had a cis-acting role in eNOS promoter function.	Nitric Oxide	83-95	nitric oxide synthase 3	Homo sapiens	149-153
16210567-1	2005	BACKGROUND: Previously, we showed that the 27nt repeat polymorphism in endothelial nitric oxide synthase (eNOS) intron 4 was associated with altered eNOS mRNA and protein levels, nitric oxide (NO) production and vascular disease risk; the 27-nt repeats had a cis-acting role in eNOS promoter function.	Nitric Oxide	83-95	nitric oxide synthase 3	Homo sapiens	149-153
16317391-10	2005	Further, GLN abrogated increases in lung iNOS expression and enhanced lung eNOS postsepsis.	Glutamine	9-12	nitric oxide synthase 3	Homo sapiens	75-79
16246326-5	2005	As NOS contributes to angiogenesis and is reduced in the hypertensive pulmonary microcirculation, we examined the expression of NOS-III protein in situ in the lungs of patients with PCH.	poly(ethylene oxide)-b-poly(alpha-cholesteryl carboxylate-epsilon-caprolactone) block copolymer	182-185	nitric oxide synthase 3	Homo sapiens	128-135
16246326-6	2005	Reduced microvascular expression of NOS-III protein by endothelial cells was observed in 4/6 (67%) cases of PCH, and all of these showed concomitant pulmonary vascular hypertensive remodeling.	poly(ethylene oxide)-b-poly(alpha-cholesteryl carboxylate-epsilon-caprolactone) block copolymer	108-111	nitric oxide synthase 3	Homo sapiens	36-43
16340449-7	2005	EtOH stimulation also increased eNOS interaction with heat shock protein (hsp90), a molecular chaperone known to enhance eNOS activity.	Ethanol	0-4	nitric oxide synthase 3	Homo sapiens	32-36
16165089-0	2005	Blockade of geranylgeranylation by rosuvastatin upregulates eNOS expression in human venous endothelial cells.	Rosuvastatin Calcium	35-47	nitric oxide synthase 3	Homo sapiens	60-64
16165089-4	2005	In a concentration-dependent manner, rosuvastatin upregulated eNOS mRNA and protein expression.	Rosuvastatin Calcium	37-49	nitric oxide synthase 3	Homo sapiens	62-66
16165089-5	2005	The effects on eNOS expression mediated through rosuvastatin could be reversed by treatment with mevalonate indicating inhibition of HMG-CoA reductase as the underlying mechanism.	Rosuvastatin Calcium	48-60	nitric oxide synthase 3	Homo sapiens	15-19
16165089-5	2005	The effects on eNOS expression mediated through rosuvastatin could be reversed by treatment with mevalonate indicating inhibition of HMG-CoA reductase as the underlying mechanism.	Mevalonic Acid	97-107	nitric oxide synthase 3	Homo sapiens	15-19
16165089-6	2005	Treatment with geranylgeranylpyrophosphate, but not farnesylpyrophosphate, reversed the increase of eNOS expression induced by rosuvastatin.	geranylgeranyl pyrophosphate	15-42	nitric oxide synthase 3	Homo sapiens	100-104
16165089-6	2005	Treatment with geranylgeranylpyrophosphate, but not farnesylpyrophosphate, reversed the increase of eNOS expression induced by rosuvastatin.	Rosuvastatin Calcium	127-139	nitric oxide synthase 3	Homo sapiens	100-104
15951350-0	2005	PGE1 analog alprostadil induces VEGF and eNOS expression in endothelial cells.	Alprostadil	0-4	nitric oxide synthase 3	Homo sapiens	41-45
15951350-0	2005	PGE1 analog alprostadil induces VEGF and eNOS expression in endothelial cells.	Alprostadil	12-23	nitric oxide synthase 3	Homo sapiens	41-45
15951350-3	2005	We have investigated the effects of the PGE1 analog alprostadil on eNOS, VEGF, and HIF-1alpha expression in human umbilical vein endothelial cells (HUVEC) using RT-PCR and immunoblotting under normoxic and hypoxic conditions.	Alprostadil	52-63	nitric oxide synthase 3	Homo sapiens	67-71
15951350-5	2005	Alprostadil causes an upregulation of eNOS and VEGF protein and mRNA expression in HUVEC and decreases HIF-1alpha.	Alprostadil	0-11	nitric oxide synthase 3	Homo sapiens	38-42
15951350-7	2005	The alprostadil-induced upregulation of eNOS and VEGF was prevented by inhibition of MAPKs with PD-98056 or U-0126.	Alprostadil	4-15	nitric oxide synthase 3	Homo sapiens	40-44
15951350-7	2005	The alprostadil-induced upregulation of eNOS and VEGF was prevented by inhibition of MAPKs with PD-98056 or U-0126.	pd-98056	96-104	nitric oxide synthase 3	Homo sapiens	40-44
15951350-7	2005	The alprostadil-induced upregulation of eNOS and VEGF was prevented by inhibition of MAPKs with PD-98056 or U-0126.	U 0126	108-114	nitric oxide synthase 3	Homo sapiens	40-44
15951350-8	2005	Consistently, the expression of eNOS and VEGF was increased, and HIF-1alpha was reduced in failing hearts treated with alprostadil.	Alprostadil	119-130	nitric oxide synthase 3	Homo sapiens	32-36
15951350-9	2005	The potent effects of alprostadil on endothelial VEGF and eNOS synthesis may be useful for patients with HF where endothelial dysfunction is involved in the disease process.	Alprostadil	22-33	nitric oxide synthase 3	Homo sapiens	58-62
16100081-10	2005	Incubation of PAEC with an antisense oligodeoxyribonucleotide of calpastatin prevented CSE-induced increases in calpastatin protein and CSE-induced decreases in calpain activity, eNOS gene transcription, activity and protein content of eNOS, and NO release.	Oligodeoxyribonucleotides	37-61	nitric oxide synthase 3	Homo sapiens	236-240
16340449-3	2005	Although previous reports examined the impact of acute EtOH stimulation on endothelial NO production, this study extends those observations to clarify mechanisms of chronic EtOH-mediated alterations in endothelial nitric oxide synthase (eNOS) expression and NO production.	Ethanol	173-177	nitric oxide synthase 3	Homo sapiens	202-235
16340449-3	2005	Although previous reports examined the impact of acute EtOH stimulation on endothelial NO production, this study extends those observations to clarify mechanisms of chronic EtOH-mediated alterations in endothelial nitric oxide synthase (eNOS) expression and NO production.	Ethanol	173-177	nitric oxide synthase 3	Homo sapiens	237-241
16340449-6	2005	RESULTS: While there was no change in the extent of phosphorylated eNOS at ser, chronic EtOH stimulation caused dose-dependent increases in NO production and increased eNOS expression, effects that were attenuated by the transcriptional inhibitor, alpha-amanitin (AA), and wortmannin, a specific phosphatidylinositol 3 kinase (PI3 K) inhibitor.	Ethanol	88-92	nitric oxide synthase 3	Homo sapiens	168-172
16340449-7	2005	EtOH stimulation also increased eNOS interaction with heat shock protein (hsp90), a molecular chaperone known to enhance eNOS activity.	Ethanol	0-4	nitric oxide synthase 3	Homo sapiens	121-125
16340449-9	2005	CONCLUSIONS: These results indicate that chronic EtOH exposure increases endothelial NO production by increasing eNOS protein levels through PI3 K-dependent up regulation of eNOS gene transcription and by increasing interactions between eNOS and hsp90.	Ethanol	49-53	nitric oxide synthase 3	Homo sapiens	113-117
16340449-9	2005	CONCLUSIONS: These results indicate that chronic EtOH exposure increases endothelial NO production by increasing eNOS protein levels through PI3 K-dependent up regulation of eNOS gene transcription and by increasing interactions between eNOS and hsp90.	Ethanol	49-53	nitric oxide synthase 3	Homo sapiens	174-178
16340449-9	2005	CONCLUSIONS: These results indicate that chronic EtOH exposure increases endothelial NO production by increasing eNOS protein levels through PI3 K-dependent up regulation of eNOS gene transcription and by increasing interactions between eNOS and hsp90.	Ethanol	49-53	nitric oxide synthase 3	Homo sapiens	174-178
16022682-6	2005	By contrast, AGE-modified albumin exerted a concentration- and time-dependent suppression of NOS-3 expression in HUVECs at a range of concentrations (0-200 mg/l) found in diabetic plasma; this was evident after 24 h, whereas inhibition of NOS activity was seen after only 3 h incubation with AGE-modified albumin, consistent with our previous observations of rapid suppression of NOS-3 serine phosphorylation and NOS-3 activity by AGE-modified albumin.	Serine	386-392	nitric oxide synthase 3	Homo sapiens	93-98
16060860-0	2005	Endothelial nitric oxide synthase Glu(298)--&gt;Asp polymorphism, carotid atherosclerosis and intima-media thickness in a general population sample.	Glutamic Acid	34-37	nitric oxide synthase 3	Homo sapiens	0-33
16060860-0	2005	Endothelial nitric oxide synthase Glu(298)--&gt;Asp polymorphism, carotid atherosclerosis and intima-media thickness in a general population sample.	Aspartic Acid	48-51	nitric oxide synthase 3	Homo sapiens	0-33
16022682-2	2005	The aim of the present study was to determine the relative contributions of glucose and AGE (advanced glycation end-product) accumulation in suppressing NOS-3 (the endothelial isoform of NO synthase).	Glucose	76-83	nitric oxide synthase 3	Homo sapiens	153-158
16022682-7	2005	In conclusion, AGE-modified albumin suppresses NOS-3 activity in HUVECs through two mechanisms: one rapid, involving suppression of its serine phosphorylation, and another slower, involving a decrease in its expression.	Serine	136-142	nitric oxide synthase 3	Homo sapiens	47-52
16060860-1	2005	The Glu(298)--&gt;Asp (E298D; 894G--&gt;T) polymorphism of eNOS (endothelial nitric oxide synthase) has been related with cardiovascular disease.	Glutamic Acid	4-7	nitric oxide synthase 3	Homo sapiens	65-98
16060860-1	2005	The Glu(298)--&gt;Asp (E298D; 894G--&gt;T) polymorphism of eNOS (endothelial nitric oxide synthase) has been related with cardiovascular disease.	Aspartic Acid	18-21	nitric oxide synthase 3	Homo sapiens	65-98
16239170-0	2005	Arsenite induces endothelial cytotoxicity by down-regulation of vascular endothelial nitric oxide synthase.	arsenite	0-8	nitric oxide synthase 3	Homo sapiens	73-106
16234629-5	2005	Understanding of the mechanisms leading to endothelial dysfunction has improved, including the notion that dysfunctional endothelial nitric oxide synthase, in part due to deficiency of the endothelial nitric oxide synthase cofactor tetrahydrobiopterin, likely plays an important role.	sapropterin	232-251	nitric oxide synthase 3	Homo sapiens	121-154
16234629-5	2005	Understanding of the mechanisms leading to endothelial dysfunction has improved, including the notion that dysfunctional endothelial nitric oxide synthase, in part due to deficiency of the endothelial nitric oxide synthase cofactor tetrahydrobiopterin, likely plays an important role.	sapropterin	232-251	nitric oxide synthase 3	Homo sapiens	189-222
16260352-9	2005	eNOS down-regulation and apoptosis were seen in HUVECs incubated with serum from CD for 24 h, but those observations were completely counteracted in the incubation by the addition of the antihuman TNF-alpha antibody.	Cadmium	81-83	nitric oxide synthase 3	Homo sapiens	0-4
16260352-10	2005	These results imply that eNOS down-regulation in CD is associated with high serum TNF-alpha levels despite of high serum of VEGF levels.	Cadmium	49-51	nitric oxide synthase 3	Homo sapiens	25-29
16239170-2	2005	Recent research has also linked this vascular damage to impairment of endothelial nitric oxide synthase (eNOS) function by arsenic exposure.	Arsenic	123-130	nitric oxide synthase 3	Homo sapiens	70-103
16239170-2	2005	Recent research has also linked this vascular damage to impairment of endothelial nitric oxide synthase (eNOS) function by arsenic exposure.	Arsenic	123-130	nitric oxide synthase 3	Homo sapiens	105-109
16239170-3	2005	However, the role of eNOS in regulating the arsenite-induced vascular dysfunction still remains to be clarified.	arsenite	44-52	nitric oxide synthase 3	Homo sapiens	21-25
16239170-4	2005	In our present study, we investigated the effect of arsenite on Akt1 and eNOS and its involvement in cytotoxicity of vascular endothelial cells.	arsenite	52-60	nitric oxide synthase 3	Homo sapiens	73-77
16239170-5	2005	Our study demonstrated that arsenite decreased the protein levels of both Akt1 and eNOS accompanied with increased levels of ubiquitination of total cell lysates.	arsenite	28-36	nitric oxide synthase 3	Homo sapiens	83-87
16239170-6	2005	We found that inhibition of the ubiquitin-proteasome pathway by MG-132 could partially protect Akt1 and eNOS from degradation by arsenite together with a proportional protection from the arsenite-induced cytoxicity.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	64-70	nitric oxide synthase 3	Homo sapiens	104-108
16239170-6	2005	We found that inhibition of the ubiquitin-proteasome pathway by MG-132 could partially protect Akt1 and eNOS from degradation by arsenite together with a proportional protection from the arsenite-induced cytoxicity.	arsenite	129-137	nitric oxide synthase 3	Homo sapiens	104-108
16239170-7	2005	Moreover, up-regulation of eNOS protein expression significantly attenuated the arsenite-induced cytotoxicity and eNOS activity could be significantly inhibited after incubation with arsenite for 24 h in a cell-free system.	arsenite	80-88	nitric oxide synthase 3	Homo sapiens	27-31
16239170-7	2005	Moreover, up-regulation of eNOS protein expression significantly attenuated the arsenite-induced cytotoxicity and eNOS activity could be significantly inhibited after incubation with arsenite for 24 h in a cell-free system.	arsenite	183-191	nitric oxide synthase 3	Homo sapiens	27-31
16239170-7	2005	Moreover, up-regulation of eNOS protein expression significantly attenuated the arsenite-induced cytotoxicity and eNOS activity could be significantly inhibited after incubation with arsenite for 24 h in a cell-free system.	arsenite	183-191	nitric oxide synthase 3	Homo sapiens	114-118
16239170-8	2005	Our study indicated that endothelial eNOS activity could be attenuated by arsenite via the ubiquitin-proteasome-mediated degradation of Akt1/eNOS as well as via direct inhibition of eNOS activity.	arsenite	74-82	nitric oxide synthase 3	Homo sapiens	37-41
16239170-8	2005	Our study indicated that endothelial eNOS activity could be attenuated by arsenite via the ubiquitin-proteasome-mediated degradation of Akt1/eNOS as well as via direct inhibition of eNOS activity.	arsenite	74-82	nitric oxide synthase 3	Homo sapiens	141-145
16239170-8	2005	Our study indicated that endothelial eNOS activity could be attenuated by arsenite via the ubiquitin-proteasome-mediated degradation of Akt1/eNOS as well as via direct inhibition of eNOS activity.	arsenite	74-82	nitric oxide synthase 3	Homo sapiens	141-145
16126727-7	2005	Thrombin receptor-activating peptide that only activates PAR-1 and high thrombin concentration induced marked biphasic Ca2+ signals with rapid phosphorylation of PLC(beta3) and NOS3 at both serine 1177 and threonine 495.	Serine	190-196	nitric oxide synthase 3	Homo sapiens	177-181
16239170-9	2005	Our study also demonstrated that eNOS actually played a protective role in arsenite-induced cytoxicity.	arsenite	75-83	nitric oxide synthase 3	Homo sapiens	33-37
16126727-8	2005	The mutant thrombin evoked a Ca2+ spark and progressive phosphorylation of Src family kinases at tyrosine 416 and NOS3 only at threonine 495.	Threonine	127-136	nitric oxide synthase 3	Homo sapiens	114-118
16239170-10	2005	These observations supported the hypothesis that the impairment of eNOS function by arsenite is one of the mechanisms leading to vascular changes and diseases.	arsenite	84-92	nitric oxide synthase 3	Homo sapiens	67-71
16207548-1	2005	OBJECTIVE: To analyze the short-term effects of estradiol (E2) on the expression of nitric oxide synthase (NOS III) and estrogen receptors (ER) alpha and beta.	Estradiol	48-57	nitric oxide synthase 3	Homo sapiens	107-114
16002570-7	2005	Simvastatin additionally prevented pulmonary vascular remodeling and the changes in endothelial nitric oxide synthase expression induced by smoking.	Simvastatin	0-11	nitric oxide synthase 3	Homo sapiens	84-117
16226933-6	2005	Nicotinamide adenine dinucleotide phosphate oxidase and the uncoupled endothelial nitric oxide synthase may be O2- -producing enzymes.	Superoxides	111-113	nitric oxide synthase 3	Homo sapiens	70-103
16002570-8	2005	In human lung microvascular endothelial cells, simvastatin increased expression of endothelial nitric oxide synthase mRNA.	Simvastatin	47-58	nitric oxide synthase 3	Homo sapiens	83-116
16244776-8	2005	Apart from the disease, eNOS T-786C and G894T polymorphisms independently affected the deformability index (OR, -786CC+TC = 2.81, p = 0.01 and OR, 894TT+GT = 2.5, p = 0.02, respectively), in particular in subjects in whom the contemporary presence of the two rare alleles was observed (OR, -786CC+TC and 894TT+GT combined genotype = 6.9, p&lt;0.0001).	Technetium	119-121	nitric oxide synthase 3	Homo sapiens	24-28
16009356-2	2005	Enzymatic systems such as the mitochondrial respiratory chain, vascular NAD(P)H oxidases, xanthine oxidase, and uncoupled endothelial nitric oxide synthase (eNOS) produce superoxide anion (O2*-) in vascular cells.	Superoxides	171-187	nitric oxide synthase 3	Homo sapiens	122-155
16009356-2	2005	Enzymatic systems such as the mitochondrial respiratory chain, vascular NAD(P)H oxidases, xanthine oxidase, and uncoupled endothelial nitric oxide synthase (eNOS) produce superoxide anion (O2*-) in vascular cells.	Superoxides	189-191	nitric oxide synthase 3	Homo sapiens	122-155
16244776-8	2005	Apart from the disease, eNOS T-786C and G894T polymorphisms independently affected the deformability index (OR, -786CC+TC = 2.81, p = 0.01 and OR, 894TT+GT = 2.5, p = 0.02, respectively), in particular in subjects in whom the contemporary presence of the two rare alleles was observed (OR, -786CC+TC and 894TT+GT combined genotype = 6.9, p&lt;0.0001).	Technetium	297-299	nitric oxide synthase 3	Homo sapiens	24-28
16270749-0	2005	Phospho-eNOS Ser-114 in human mesenchymal stem cells: constitutive phosphorylation, nuclear localization and upregulation during mitosis.	Serine	13-16	nitric oxide synthase 3	Homo sapiens	8-12
16270749-1	2005	Activity of endothelial nitric oxide synthase (eNOS) is modulated by protein-protein interaction and phosphorylation at specific serine or threonine residues.	Serine	129-135	nitric oxide synthase 3	Homo sapiens	12-45
16270749-3	2005	Examination of phosphorylated eNOS subspecies revealed that eNOS phosphorylated at Ser-114 is heavily enriched in the nucleus, whereas eNOS phosphorylated at Ser-1177 is localized at filamentous structures in the cytosol that are abundant in the perinuclear region.	Serine	83-86	nitric oxide synthase 3	Homo sapiens	30-34
16270749-1	2005	Activity of endothelial nitric oxide synthase (eNOS) is modulated by protein-protein interaction and phosphorylation at specific serine or threonine residues.	Serine	129-135	nitric oxide synthase 3	Homo sapiens	47-51
16270749-3	2005	Examination of phosphorylated eNOS subspecies revealed that eNOS phosphorylated at Ser-114 is heavily enriched in the nucleus, whereas eNOS phosphorylated at Ser-1177 is localized at filamentous structures in the cytosol that are abundant in the perinuclear region.	Serine	83-86	nitric oxide synthase 3	Homo sapiens	60-64
16270749-1	2005	Activity of endothelial nitric oxide synthase (eNOS) is modulated by protein-protein interaction and phosphorylation at specific serine or threonine residues.	Threonine	139-148	nitric oxide synthase 3	Homo sapiens	12-45
16270749-3	2005	Examination of phosphorylated eNOS subspecies revealed that eNOS phosphorylated at Ser-114 is heavily enriched in the nucleus, whereas eNOS phosphorylated at Ser-1177 is localized at filamentous structures in the cytosol that are abundant in the perinuclear region.	Serine	83-86	nitric oxide synthase 3	Homo sapiens	60-64
16270749-4	2005	Phosphorylation of eNOS at Ser-114 but not at Ser-1177 was strongly increased in cells shortly before mitosis and decreased to normal level after completed cell division.	Serine	27-30	nitric oxide synthase 3	Homo sapiens	19-23
16270749-5	2005	Double immunofluorescence analysis revealed that subcellular localization of 8-hydroxyguanosine immunoreactivity was overlapping with eNOS phosphorylated at Ser-114 in human MSCs providing evidence that phosphorylation at this residue is linked to the generation of superoxide anions.	8-hydroxyguanosine	77-95	nitric oxide synthase 3	Homo sapiens	134-138
16270749-5	2005	Double immunofluorescence analysis revealed that subcellular localization of 8-hydroxyguanosine immunoreactivity was overlapping with eNOS phosphorylated at Ser-114 in human MSCs providing evidence that phosphorylation at this residue is linked to the generation of superoxide anions.	Serine	157-160	nitric oxide synthase 3	Homo sapiens	134-138
16270749-6	2005	As expected there was only a weak colocalization between eNOS phosphorylated at Ser-1177 and caveolin-1.	Serine	80-83	nitric oxide synthase 3	Homo sapiens	57-61
16107535-0	2005	Dietary soy isoflavone induced increases in antioxidant and eNOS gene expression lead to improved endothelial function and reduced blood pressure in vivo.	Isoflavones	12-22	nitric oxide synthase 3	Homo sapiens	60-64
16107535-4	2005	Improved vascular reactivity in animals fed an SP diet was paralleled by increased mitochondrial glutathione and mRNA levels for endothelial nitric oxide synthase (eNOS) and the antioxidant enzymes manganese superoxide dismutase and cytochrome c oxidase.	sp	47-49	nitric oxide synthase 3	Homo sapiens	129-162
16107535-4	2005	Improved vascular reactivity in animals fed an SP diet was paralleled by increased mitochondrial glutathione and mRNA levels for endothelial nitric oxide synthase (eNOS) and the antioxidant enzymes manganese superoxide dismutase and cytochrome c oxidase.	sp	47-49	nitric oxide synthase 3	Homo sapiens	164-168
16107535-5	2005	Reduced eNOS and antioxidant gene expression, impaired endothelial function, and elevated blood pressure in animals fed a soy-deficient diet was reversed after refeeding them an SP diet for 6 months.	sp	178-180	nitric oxide synthase 3	Homo sapiens	8-12
16107535-6	2005	Our findings suggest that an SP diet increases eNOS and antioxidant gene expression in the vasculature and other tissues, resulting in reduced oxidative stress and increased NO bioavailability.	sp	29-31	nitric oxide synthase 3	Homo sapiens	47-51
16270749-1	2005	Activity of endothelial nitric oxide synthase (eNOS) is modulated by protein-protein interaction and phosphorylation at specific serine or threonine residues.	Threonine	139-148	nitric oxide synthase 3	Homo sapiens	47-51
16093452-1	2005	Endothelial function is dependent on the generation of nitric oxide (NO) by the enzyme endothelial NO synthase (eNOS).	Nitric Oxide	55-67	nitric oxide synthase 3	Homo sapiens	112-116
16210014-6	2005	RESULT(S): Estradiol 17-beta (E2) induced a dose- and time-dependent increase in the expression of eNOS mRNA and protein and iNOS protein in HES cells which could be blocked by the estrogen receptor antagonist ICI 182,780.	Estradiol	11-28	nitric oxide synthase 3	Homo sapiens	99-103
16210014-7	2005	Estradiol increased the expression of eNOS mRNA and protein in primary endometrial cells.	Estradiol	0-9	nitric oxide synthase 3	Homo sapiens	38-42
16210014-9	2005	Progesterone in physiologic concentrations augmented the effect of estrogen on the expression of both eNOS and peNOS but not of iNOS.	Progesterone	0-12	nitric oxide synthase 3	Homo sapiens	102-106
16148605-6	2005	However, eNOS genotype showed a significant association with cardiovascular mortality in statistical models, including traditional risk factors and factors peculiar to ESRD, and became even stronger when plasma ADMA was forced into the Cox model (P=0.006).	N,N-dimethylarginine	211-215	nitric oxide synthase 3	Homo sapiens	9-13
16154428-0	2005	Possible interactions of the endothelial constitutive nitric oxide synthase genotype with alcohol drinking and walking time for high serum uric acid levels among Japanese.	Alcohols	90-97	nitric oxide synthase 3	Homo sapiens	29-75
16154428-0	2005	Possible interactions of the endothelial constitutive nitric oxide synthase genotype with alcohol drinking and walking time for high serum uric acid levels among Japanese.	Uric Acid	139-148	nitric oxide synthase 3	Homo sapiens	29-75
16154428-1	2005	A variable number of tandem repeat polymorphism located in intron 4 of the gene for endothelial constitutive nitric oxide synthase (ecNOS) is reported to be significantly associated with the nitric oxide level, which influences serum uric acid (SUA).	Nitric Oxide	109-121	nitric oxide synthase 3	Homo sapiens	132-137
16154428-1	2005	A variable number of tandem repeat polymorphism located in intron 4 of the gene for endothelial constitutive nitric oxide synthase (ecNOS) is reported to be significantly associated with the nitric oxide level, which influences serum uric acid (SUA).	Uric Acid	234-243	nitric oxide synthase 3	Homo sapiens	84-130
16154428-1	2005	A variable number of tandem repeat polymorphism located in intron 4 of the gene for endothelial constitutive nitric oxide synthase (ecNOS) is reported to be significantly associated with the nitric oxide level, which influences serum uric acid (SUA).	Uric Acid	234-243	nitric oxide synthase 3	Homo sapiens	132-137
16154428-1	2005	A variable number of tandem repeat polymorphism located in intron 4 of the gene for endothelial constitutive nitric oxide synthase (ecNOS) is reported to be significantly associated with the nitric oxide level, which influences serum uric acid (SUA).	sua	245-248	nitric oxide synthase 3	Homo sapiens	84-130
16154428-1	2005	A variable number of tandem repeat polymorphism located in intron 4 of the gene for endothelial constitutive nitric oxide synthase (ecNOS) is reported to be significantly associated with the nitric oxide level, which influences serum uric acid (SUA).	sua	245-248	nitric oxide synthase 3	Homo sapiens	132-137
16154428-9	2005	This study indicated that the ecNOS variable number of tandem repeat polymorphism influences the SUA level in men.	sua	97-100	nitric oxide synthase 3	Homo sapiens	30-35
16154438-1	2005	It has been demonstrated that the enzyme endothelial nitric oxide synthase (eNOS) is present in adipose tissue, resulting in nitric oxide production and subsequent inhibition of lipolysis.	Nitric Oxide	53-65	nitric oxide synthase 3	Homo sapiens	76-80
16157773-7	2005	A nitric oxide (NO) scavenger and an inhibitor of NO synthase 3 (NOS3) reversed the effects of testosterone on APD, which suggests that NO released from NOS3 is responsible for the electrophysiological effects of testosterone.	Nitric Oxide	2-14	nitric oxide synthase 3	Homo sapiens	153-157
16266057-1	2005	OBJECT: Increased cerebrospinal fluid (CSF) levels of asymmetric dimethyl L-arginine (ADMA), an endogenous inhibitor of endothelial nitric oxide synthase (eNOS), are associated with delayed vasospasm after subarachnoid hemorrhage (SAH); however, the source, cellular mechanisms, and pharmacological inhibition of ADMA production following SAH are unknown.	N,N-dimethylarginine	65-84	nitric oxide synthase 3	Homo sapiens	120-153
16266057-1	2005	OBJECT: Increased cerebrospinal fluid (CSF) levels of asymmetric dimethyl L-arginine (ADMA), an endogenous inhibitor of endothelial nitric oxide synthase (eNOS), are associated with delayed vasospasm after subarachnoid hemorrhage (SAH); however, the source, cellular mechanisms, and pharmacological inhibition of ADMA production following SAH are unknown.	N,N-dimethylarginine	86-90	nitric oxide synthase 3	Homo sapiens	120-153
16266057-1	2005	OBJECT: Increased cerebrospinal fluid (CSF) levels of asymmetric dimethyl L-arginine (ADMA), an endogenous inhibitor of endothelial nitric oxide synthase (eNOS), are associated with delayed vasospasm after subarachnoid hemorrhage (SAH); however, the source, cellular mechanisms, and pharmacological inhibition of ADMA production following SAH are unknown.	N,N-dimethylarginine	313-317	nitric oxide synthase 3	Homo sapiens	120-153
16195486-4	2005	This is caused by increased vascular superoxide production and a supersensitivity to vasoconstrictors secondary to a tonic activation of protein kinase C. NADPH oxidase(s) and uncoupled endothelial nitric oxide synthase have been proposed as superoxide sources.	Superoxides	37-47	nitric oxide synthase 3	Homo sapiens	186-219
16195486-4	2005	This is caused by increased vascular superoxide production and a supersensitivity to vasoconstrictors secondary to a tonic activation of protein kinase C. NADPH oxidase(s) and uncoupled endothelial nitric oxide synthase have been proposed as superoxide sources.	Superoxides	242-252	nitric oxide synthase 3	Homo sapiens	186-219
16157773-7	2005	A nitric oxide (NO) scavenger and an inhibitor of NO synthase 3 (NOS3) reversed the effects of testosterone on APD, which suggests that NO released from NOS3 is responsible for the electrophysiological effects of testosterone.	Testosterone	95-107	nitric oxide synthase 3	Homo sapiens	50-63
16157773-7	2005	A nitric oxide (NO) scavenger and an inhibitor of NO synthase 3 (NOS3) reversed the effects of testosterone on APD, which suggests that NO released from NOS3 is responsible for the electrophysiological effects of testosterone.	Testosterone	95-107	nitric oxide synthase 3	Homo sapiens	65-69
16157773-7	2005	A nitric oxide (NO) scavenger and an inhibitor of NO synthase 3 (NOS3) reversed the effects of testosterone on APD, which suggests that NO released from NOS3 is responsible for the electrophysiological effects of testosterone.	Testosterone	95-107	nitric oxide synthase 3	Homo sapiens	153-157
16157773-7	2005	A nitric oxide (NO) scavenger and an inhibitor of NO synthase 3 (NOS3) reversed the effects of testosterone on APD, which suggests that NO released from NOS3 is responsible for the electrophysiological effects of testosterone.	Testosterone	213-225	nitric oxide synthase 3	Homo sapiens	50-63
16157773-7	2005	A nitric oxide (NO) scavenger and an inhibitor of NO synthase 3 (NOS3) reversed the effects of testosterone on APD, which suggests that NO released from NOS3 is responsible for the electrophysiological effects of testosterone.	Testosterone	213-225	nitric oxide synthase 3	Homo sapiens	65-69
16157773-7	2005	A nitric oxide (NO) scavenger and an inhibitor of NO synthase 3 (NOS3) reversed the effects of testosterone on APD, which suggests that NO released from NOS3 is responsible for the electrophysiological effects of testosterone.	Testosterone	213-225	nitric oxide synthase 3	Homo sapiens	153-157
16157773-9	2005	Immunoblot analysis revealed that testosterone induced phosphorylation of Akt and NOS3.	Testosterone	34-46	nitric oxide synthase 3	Homo sapiens	82-86
16164743-2	2005	In humans, a common polymorphism exists in the eNOS gene that results in the conversion of glutamate to aspartate for codon 298.	Glutamic Acid	91-100	nitric oxide synthase 3	Homo sapiens	47-51
16118242-6	2005	While the shear-stress-induced tyrosine phosphorylation of PECAM-1 as well as the serine phosphorylation of Akt and eNOS were abolished by the pre-treatment of cells with the tyrosine kinase inhibitor PP1 the phosphorylation of AMPK was unaffected.	Tyrosine	31-39	nitric oxide synthase 3	Homo sapiens	116-120
16118242-6	2005	While the shear-stress-induced tyrosine phosphorylation of PECAM-1 as well as the serine phosphorylation of Akt and eNOS were abolished by the pre-treatment of cells with the tyrosine kinase inhibitor PP1 the phosphorylation of AMPK was unaffected.	Serine	82-88	nitric oxide synthase 3	Homo sapiens	116-120
16118242-9	2005	These data indicate that the shear-stress-induced activation of Akt and eNOS in endothelial cells is modulated by the tyrosine phosphorylation of PECAM-1 whereas the shear-stress-induced phosphorylation of AMPK is controlled by an alternative signaling pathway.	Tyrosine	118-126	nitric oxide synthase 3	Homo sapiens	72-76
16164743-2	2005	In humans, a common polymorphism exists in the eNOS gene that results in the conversion of glutamate to aspartate for codon 298.	Aspartic Acid	104-113	nitric oxide synthase 3	Homo sapiens	47-51
16102116-8	2005	This effect was significantly reduced by the addition of the K+ channel blocker iberiotoxin (100 nmol L(-1)), eNOS inhibitor L-NMMA (300 micromol L(-1)), or the MEK inhibitor PD 98059 (20 micromol L(-1)).	omega-N-Methylarginine	125-131	nitric oxide synthase 3	Homo sapiens	110-114
15894566-2	2005	The aim of the present study was to evaluate the possible role of the NO system in the development of cold-induced hypertension (CIH) by testing the hypothesis that adenoviral delivery of human eNOS gene increases NO production and attenuates CIH in rats.	cih	129-132	nitric oxide synthase 3	Homo sapiens	194-198
15894566-2	2005	The aim of the present study was to evaluate the possible role of the NO system in the development of cold-induced hypertension (CIH) by testing the hypothesis that adenoviral delivery of human eNOS gene increases NO production and attenuates CIH in rats.	cih	243-246	nitric oxide synthase 3	Homo sapiens	194-198
16410222-7	2005	Atorvastatin stimulated the expression of angiopoietin (Ang)-2 and moderately enhanced the expression of endothelial nitric oxide synthase (eNOS), whereas heme oxygenase-1 (HO-1) was not significantly affected.	Atorvastatin	0-12	nitric oxide synthase 3	Homo sapiens	105-138
16020752-1	2005	OBJECTIVE: We recently reported that the peroxisome proliferator-activated receptor gamma (PPARgamma) ligands 15-deoxy-Delta(12,14)-prostaglandin J2 (15d-PGJ2) and ciglitazone increased cultured endothelial cell nitric oxide (NO) release without increasing the expression of endothelial nitric oxide synthase (eNOS).	15-deoxy-delta	110-124	nitric oxide synthase 3	Homo sapiens	275-308
16020752-1	2005	OBJECTIVE: We recently reported that the peroxisome proliferator-activated receptor gamma (PPARgamma) ligands 15-deoxy-Delta(12,14)-prostaglandin J2 (15d-PGJ2) and ciglitazone increased cultured endothelial cell nitric oxide (NO) release without increasing the expression of endothelial nitric oxide synthase (eNOS).	9-deoxy-delta-9-prostaglandin D2	132-148	nitric oxide synthase 3	Homo sapiens	275-308
16020752-1	2005	OBJECTIVE: We recently reported that the peroxisome proliferator-activated receptor gamma (PPARgamma) ligands 15-deoxy-Delta(12,14)-prostaglandin J2 (15d-PGJ2) and ciglitazone increased cultured endothelial cell nitric oxide (NO) release without increasing the expression of endothelial nitric oxide synthase (eNOS).	9-deoxy-delta-9-prostaglandin D2	154-158	nitric oxide synthase 3	Homo sapiens	275-308
16123371-0	2005	Variation in the eNOS gene modifies the association between total energy expenditure and glucose intolerance.	Glucose	89-96	nitric oxide synthase 3	Homo sapiens	17-21
16123371-2	2005	Energy expenditure induces the endothelial NO synthase (eNOS) gene, providing a mechanism for insulin-independent glucose disposal.	Glucose	114-121	nitric oxide synthase 3	Homo sapiens	31-54
16123371-2	2005	Energy expenditure induces the endothelial NO synthase (eNOS) gene, providing a mechanism for insulin-independent glucose disposal.	Glucose	114-121	nitric oxide synthase 3	Homo sapiens	56-60
16123371-9	2005	Genetic variation at the eNOS locus is associated with diabetes, which may be attributable to an enhanced effect of total energy expenditure on glucose disposal in individuals with specific eNOS haplotypes.	Glucose	144-151	nitric oxide synthase 3	Homo sapiens	25-29
16123371-9	2005	Genetic variation at the eNOS locus is associated with diabetes, which may be attributable to an enhanced effect of total energy expenditure on glucose disposal in individuals with specific eNOS haplotypes.	Glucose	144-151	nitric oxide synthase 3	Homo sapiens	190-194
16076760-6	2005	These results suggested that the NADPH oxidase, MnSOD, and e-NOS polymorphisms, but not catalase, might play a role in the development of arsenic-related hypertension, especially in subjects with high triglyceride levels.	Arsenic	138-145	nitric oxide synthase 3	Homo sapiens	59-64
16102116-11	2005	An increase of +101% MAPK phosphorylation was induced by HGF, which was blocked, if the cells were treated with L-NMMA (n = 20; P &lt; 0.05), whereas HGF-induced phosphorylation of the eNOS was not affected by MEK inhibition.	omega-N-Methylarginine	112-118	nitric oxide synthase 3	Homo sapiens	185-189
16102116-12	2005	CONCLUSIONS: Hepatocyte growth factor modulates endothelial K+ channels causing an activation of the eNOS; the increase of nitric oxide is necessary for the phosphorylation of the MAPK inducing the proliferation of HUCVEC.	Nitric Oxide	123-135	nitric oxide synthase 3	Homo sapiens	101-105
16100023-1	2005	BACKGROUND AND PURPOSE: Endothelial nitric oxide exerts a variety of protective effects on endothelial cells and blood vessels, and therefore the nitric oxide synthase 3 gene (NOS3) is a logical candidate gene for stroke susceptibility.	Nitric Oxide	36-48	nitric oxide synthase 3	Homo sapiens	146-169
16329468-6	2005	Sesamol induced NO release from endothelial cells in a dose-dependent manner (from 1 to 10 microM), as measured 24 h after treatment; the expression of the eNOS gene at both transcription and translation levels; and NOS activity in endothelial cells.	sesamol	0-7	nitric oxide synthase 3	Homo sapiens	156-160
16329468-8	2005	The transcription of eNOS induced by sesamol was confirmed through the activation of PI-3 kinase-Akt (protein kinase B) signaling.	sesamol	37-44	nitric oxide synthase 3	Homo sapiens	21-25
16100023-1	2005	BACKGROUND AND PURPOSE: Endothelial nitric oxide exerts a variety of protective effects on endothelial cells and blood vessels, and therefore the nitric oxide synthase 3 gene (NOS3) is a logical candidate gene for stroke susceptibility.	Nitric Oxide	36-48	nitric oxide synthase 3	Homo sapiens	176-180
15551057-6	2005	E2 alone enhanced prostaglandin E(2) (PGE(2)) and nitric oxide (NO) production by 2.8-fold and 2.0-fold, respectively, and stimulated endothelial nitric oxide synthase protein expression by 2.5-fold.	Estradiol	0-2	nitric oxide synthase 3	Homo sapiens	134-167
15933248-8	2005	Because BH4 is an essential cofactor for production of NO by both iNOS and endothelial nitric oxide synthase (eNOS), these results suggest that iNOS may reduce production of NO by eNOS by limiting availability of BH4.	sapropterin	8-11	nitric oxide synthase 3	Homo sapiens	75-108
15933248-8	2005	Because BH4 is an essential cofactor for production of NO by both iNOS and endothelial nitric oxide synthase (eNOS), these results suggest that iNOS may reduce production of NO by eNOS by limiting availability of BH4.	sapropterin	213-216	nitric oxide synthase 3	Homo sapiens	75-108
16136006-3	2005	METHODS: Three-step immunoperoxidase reaction on acetone-fixed cryostat sections was performed using both polyclonal and monoclonal antibodies against eNOS and iNOS.	Acetone	49-56	nitric oxide synthase 3	Homo sapiens	151-155
15819614-4	2005	The loss of immunoprecipitable eNOS from Cav-1-enriched fractions was accompanied by a decrease both in phosphorylation of eNOS and in enzymatic activity (conversion of arginine into citrulline).	Arginine	169-177	nitric oxide synthase 3	Homo sapiens	31-35
15819614-4	2005	The loss of immunoprecipitable eNOS from Cav-1-enriched fractions was accompanied by a decrease both in phosphorylation of eNOS and in enzymatic activity (conversion of arginine into citrulline).	Citrulline	183-193	nitric oxide synthase 3	Homo sapiens	31-35
15772123-7	2005	Furthermore, leptin induces NOS III phosphorylation at Ser(1179) and Thr(497), but not when adipocytes are pretreated with H-89 or U0126.	Serine	55-58	nitric oxide synthase 3	Homo sapiens	28-35
15879305-3	2005	Superoxide produced by the NADPH oxidase may react with NO released by endothelial nitric oxide synthase (eNOS), thereby generating peroxynitrite.	Superoxides	0-10	nitric oxide synthase 3	Homo sapiens	71-104
15879305-3	2005	Superoxide produced by the NADPH oxidase may react with NO released by endothelial nitric oxide synthase (eNOS), thereby generating peroxynitrite.	Peroxynitrous Acid	132-145	nitric oxide synthase 3	Homo sapiens	71-104
15778808-3	2005	The purpose of this study was to examine the Glu298Asp variant of the endothelial nitric oxide synthase (eNOS) gene to determine whether this polymorphism was associated with susceptibility to CSA in patients with HCM.	Cyclosporine	193-196	nitric oxide synthase 3	Homo sapiens	70-103
15778808-3	2005	The purpose of this study was to examine the Glu298Asp variant of the endothelial nitric oxide synthase (eNOS) gene to determine whether this polymorphism was associated with susceptibility to CSA in patients with HCM.	Cyclosporine	193-196	nitric oxide synthase 3	Homo sapiens	105-109
15778808-11	2005	In conclusion, the Asp298 variant of the eNOS gene may be associated with CSA in HCM patients.	Cyclosporine	74-77	nitric oxide synthase 3	Homo sapiens	41-45
16136006-5	2005	RESULTS: The immunoreactivity to eNOS antibody was observed in the endothelial lining of vessels in PGA, PGH and in the rim of normal parathyroid gland adjacent to PGA sample.	GH2 protein, human	105-108	nitric oxide synthase 3	Homo sapiens	33-37
16136006-9	2005	MAIN RESULT: Our findings confirm that eNOS is regularly expressed in the vasculature of PGA and PGH.	GH2 protein, human	97-100	nitric oxide synthase 3	Homo sapiens	39-43
15933265-6	2005	Hypoxia reduced endothelial NOS (eNOS) activity and eNOS phosphorylation at Ser(1177), but increased eNOS protein level.	Serine	76-79	nitric oxide synthase 3	Homo sapiens	52-56
16007000-1	2005	OBJECTIVES: Controversy exists regarding the effects of polymorphisms in the endothelial nitric oxide synthase (eNOS) gene on nitrites/nitrates (NOx) plasma concentrations.	Nitrites	126-134	nitric oxide synthase 3	Homo sapiens	77-110
16007000-1	2005	OBJECTIVES: Controversy exists regarding the effects of polymorphisms in the endothelial nitric oxide synthase (eNOS) gene on nitrites/nitrates (NOx) plasma concentrations.	Nitrites	126-134	nitric oxide synthase 3	Homo sapiens	112-116
16007000-1	2005	OBJECTIVES: Controversy exists regarding the effects of polymorphisms in the endothelial nitric oxide synthase (eNOS) gene on nitrites/nitrates (NOx) plasma concentrations.	Nitrates	135-143	nitric oxide synthase 3	Homo sapiens	77-110
16007000-1	2005	OBJECTIVES: Controversy exists regarding the effects of polymorphisms in the endothelial nitric oxide synthase (eNOS) gene on nitrites/nitrates (NOx) plasma concentrations.	Nitrates	135-143	nitric oxide synthase 3	Homo sapiens	112-116
16007000-1	2005	OBJECTIVES: Controversy exists regarding the effects of polymorphisms in the endothelial nitric oxide synthase (eNOS) gene on nitrites/nitrates (NOx) plasma concentrations.	nicotine 1-N-oxide	145-148	nitric oxide synthase 3	Homo sapiens	77-110
16007000-1	2005	OBJECTIVES: Controversy exists regarding the effects of polymorphisms in the endothelial nitric oxide synthase (eNOS) gene on nitrites/nitrates (NOx) plasma concentrations.	nicotine 1-N-oxide	145-148	nitric oxide synthase 3	Homo sapiens	112-116
16007000-2	2005	In this study we compared the distribution of haplotypes involving three relevant eNOS polymorphisms (T-786C in the promoter region; b/a in intron 4, and Glu298Asp in exon 7) in healthy subjects with low and high circulating NOx levels.	nicotine 1-N-oxide	225-228	nitric oxide synthase 3	Homo sapiens	82-86
16007000-10	2005	The frequencies of the remaining haplotypes were not different among group L and H. CONCLUSIONS: While eNOS genotypes are not significantly associated with changes in the circulating NOx concentrations, the specific eNOS haplotype that includes the "C", "4b", and "Glu" alleles is associated with lower circulating NOx concentrations.	nicotine 1-N-oxide	315-318	nitric oxide synthase 3	Homo sapiens	216-220
15933265-6	2005	Hypoxia reduced endothelial NOS (eNOS) activity and eNOS phosphorylation at Ser(1177), but increased eNOS protein level.	Serine	76-79	nitric oxide synthase 3	Homo sapiens	52-56
15852033-5	2005	A possible reason for the lack of effect of prednisolone may due to an inhibition of eNOS expression.	Prednisolone	44-56	nitric oxide synthase 3	Homo sapiens	85-89
15852033-18	2005	Finally, eNOS protein expression was significantly reduced by prednisolone.	Prednisolone	62-74	nitric oxide synthase 3	Homo sapiens	9-13
15817516-5	2005	Here we show that E2-mediated activation of endothelial nitric oxide synthase (eNOS) increases the production of nitric oxide (NO), which, under Abeta(E22Q)-induced oxidative damage, results in the formation of peroxynitrite and increased nitration of tyrosine residues.	Estradiol	18-20	nitric oxide synthase 3	Homo sapiens	44-77
15852033-20	2005	Prednisolone increases O(2)(*-) in porcine PAECs through a downregulation of endogenous eNOS expression.	Prednisolone	0-12	nitric oxide synthase 3	Homo sapiens	88-92
15817516-5	2005	Here we show that E2-mediated activation of endothelial nitric oxide synthase (eNOS) increases the production of nitric oxide (NO), which, under Abeta(E22Q)-induced oxidative damage, results in the formation of peroxynitrite and increased nitration of tyrosine residues.	Estradiol	18-20	nitric oxide synthase 3	Homo sapiens	79-83
15905312-0	2005	Endothelial nitric oxide synthase -786T&gt;C, but not 894G&gt;T and 4a4b, polymorphism influences plasma homocysteine concentrations in persons with normal vitamin status.	Homocysteine	105-117	nitric oxide synthase 3	Homo sapiens	0-33
15817516-5	2005	Here we show that E2-mediated activation of endothelial nitric oxide synthase (eNOS) increases the production of nitric oxide (NO), which, under Abeta(E22Q)-induced oxidative damage, results in the formation of peroxynitrite and increased nitration of tyrosine residues.	Nitric Oxide	56-68	nitric oxide synthase 3	Homo sapiens	79-83
15817516-5	2005	Here we show that E2-mediated activation of endothelial nitric oxide synthase (eNOS) increases the production of nitric oxide (NO), which, under Abeta(E22Q)-induced oxidative damage, results in the formation of peroxynitrite and increased nitration of tyrosine residues.	Peroxynitrous Acid	211-224	nitric oxide synthase 3	Homo sapiens	44-77
15817516-5	2005	Here we show that E2-mediated activation of endothelial nitric oxide synthase (eNOS) increases the production of nitric oxide (NO), which, under Abeta(E22Q)-induced oxidative damage, results in the formation of peroxynitrite and increased nitration of tyrosine residues.	Peroxynitrous Acid	211-224	nitric oxide synthase 3	Homo sapiens	79-83
15817516-5	2005	Here we show that E2-mediated activation of endothelial nitric oxide synthase (eNOS) increases the production of nitric oxide (NO), which, under Abeta(E22Q)-induced oxidative damage, results in the formation of peroxynitrite and increased nitration of tyrosine residues.	Tyrosine	252-260	nitric oxide synthase 3	Homo sapiens	44-77
15817516-5	2005	Here we show that E2-mediated activation of endothelial nitric oxide synthase (eNOS) increases the production of nitric oxide (NO), which, under Abeta(E22Q)-induced oxidative damage, results in the formation of peroxynitrite and increased nitration of tyrosine residues.	Tyrosine	252-260	nitric oxide synthase 3	Homo sapiens	79-83
15817516-6	2005	Inhibition of eNOS prevents nitrotyrosination and permits E2-mediated protection against Abeta(E22Q) on endothelial cells.	Estradiol	58-60	nitric oxide synthase 3	Homo sapiens	14-18
15870070-9	2005	Importantly, methylthioadenosine also prevented the trichostatin A-mediated increase in eNOS mRNA transcript levels in nonendothelial cells.	5'-methylthioadenosine	13-32	nitric oxide synthase 3	Homo sapiens	88-92
15956830-5	2005	An infusion of recombinant high-density lipoprotein cholesterol can immediately release nitric oxide, a potent vasodilator and responder to changes in rheology, into the arteries by activation of endothelial nitric oxide synthase.	Nitric Oxide	88-100	nitric oxide synthase 3	Homo sapiens	196-229
15870070-3	2005	Within endothelial cells, but not a variety of nonendothelial cells, the nucleosomes that encompassed the eNOS core promoter and proximal downstream coding regions were highly enriched in acetylated histones H3 and H4 and methylated lysine 4 of histone H3.	Lysine	233-239	nitric oxide synthase 3	Homo sapiens	106-110
15870070-9	2005	Importantly, methylthioadenosine also prevented the trichostatin A-mediated increase in eNOS mRNA transcript levels in nonendothelial cells.	trichostatin A	52-66	nitric oxide synthase 3	Homo sapiens	88-92
15870070-7	2005	Inhibition of histone deacetylase activity by trichostatin A increased acetylation of histones H3 and H4 at the eNOS proximal promoter in nonexpressing cell types and led to increased steady-state eNOS mRNA transcript levels.	trichostatin A	46-60	nitric oxide synthase 3	Homo sapiens	112-116
15937123-3	2005	In this work, we show by a variety of methods (ozone chemiluminescence, biotin switch, and mass spectrometry) that the molecular chaperone Hsp90 is a target of S-nitrosylation and identify a susceptible cysteine residue in the region of the C-terminal domain that interacts with endothelial nitric oxide synthase (eNOS).	Cysteine	203-211	nitric oxide synthase 3	Homo sapiens	279-312
15870070-7	2005	Inhibition of histone deacetylase activity by trichostatin A increased acetylation of histones H3 and H4 at the eNOS proximal promoter in nonexpressing cell types and led to increased steady-state eNOS mRNA transcript levels.	trichostatin A	46-60	nitric oxide synthase 3	Homo sapiens	197-201
15870070-8	2005	H3 lysine 4 methylation was also essential for eNOS expression, since treatment of endothelial cells with methylthioadenosine, a known lysine 4 methylation inhibitor, decreased eNOS RNA levels, H3 lysine 4 methylation, and RNA polymerase II loading at the eNOS proximal promoter.	Lysine	3-9	nitric oxide synthase 3	Homo sapiens	47-51
15870070-8	2005	H3 lysine 4 methylation was also essential for eNOS expression, since treatment of endothelial cells with methylthioadenosine, a known lysine 4 methylation inhibitor, decreased eNOS RNA levels, H3 lysine 4 methylation, and RNA polymerase II loading at the eNOS proximal promoter.	5'-methylthioadenosine	106-125	nitric oxide synthase 3	Homo sapiens	47-51
15870070-8	2005	H3 lysine 4 methylation was also essential for eNOS expression, since treatment of endothelial cells with methylthioadenosine, a known lysine 4 methylation inhibitor, decreased eNOS RNA levels, H3 lysine 4 methylation, and RNA polymerase II loading at the eNOS proximal promoter.	5'-methylthioadenosine	106-125	nitric oxide synthase 3	Homo sapiens	177-181
15870070-8	2005	H3 lysine 4 methylation was also essential for eNOS expression, since treatment of endothelial cells with methylthioadenosine, a known lysine 4 methylation inhibitor, decreased eNOS RNA levels, H3 lysine 4 methylation, and RNA polymerase II loading at the eNOS proximal promoter.	5'-methylthioadenosine	106-125	nitric oxide synthase 3	Homo sapiens	177-181
15870070-8	2005	H3 lysine 4 methylation was also essential for eNOS expression, since treatment of endothelial cells with methylthioadenosine, a known lysine 4 methylation inhibitor, decreased eNOS RNA levels, H3 lysine 4 methylation, and RNA polymerase II loading at the eNOS proximal promoter.	Lysine	135-141	nitric oxide synthase 3	Homo sapiens	47-51
15941833-1	2005	Recent studies demonstrate that oxidative inactivation of tetrahydrobiopterin (H4B) may cause uncoupling of endothelial nitric oxide synthase (eNOS) to produce superoxide (O2*-).	sapropterin	58-77	nitric oxide synthase 3	Homo sapiens	108-141
15941833-1	2005	Recent studies demonstrate that oxidative inactivation of tetrahydrobiopterin (H4B) may cause uncoupling of endothelial nitric oxide synthase (eNOS) to produce superoxide (O2*-).	Superoxides	160-170	nitric oxide synthase 3	Homo sapiens	108-141
15941833-1	2005	Recent studies demonstrate that oxidative inactivation of tetrahydrobiopterin (H4B) may cause uncoupling of endothelial nitric oxide synthase (eNOS) to produce superoxide (O2*-).	Superoxides	172-174	nitric oxide synthase 3	Homo sapiens	108-141
15919417-6	2005	The eNOS protein level was studied by immunohistochemistry with avidin-biotin complex immunoperoxidase procedure.	avidin-biotin	64-77	nitric oxide synthase 3	Homo sapiens	4-8
15905462-7	2005	ENOS transcripts with longer poly(A) tails had prolonged half-lives (6 hours in static cells versus 18 hours in sheared cells).	Poly A	29-36	nitric oxide synthase 3	Homo sapiens	0-4
15905462-10	2005	Furthermore, hydrogen peroxide and HMG Co-A reductase inhibitors, other stimuli known to modulate eNOS expression posttranscriptionally, also induced eNOS 3" poly(A) tail lengthening.	Hydrogen Peroxide	13-30	nitric oxide synthase 3	Homo sapiens	98-102
15905462-10	2005	Furthermore, hydrogen peroxide and HMG Co-A reductase inhibitors, other stimuli known to modulate eNOS expression posttranscriptionally, also induced eNOS 3" poly(A) tail lengthening.	Hydrogen Peroxide	13-30	nitric oxide synthase 3	Homo sapiens	150-154
15925745-4	2005	When uncoupled from essential cofactors, NO synthase III (NOS III) can also produce O(2)(*-).	Superoxides	84-88	nitric oxide synthase 3	Homo sapiens	41-56
15925745-4	2005	When uncoupled from essential cofactors, NO synthase III (NOS III) can also produce O(2)(*-).	Superoxides	84-88	nitric oxide synthase 3	Homo sapiens	58-65
15925745-10	2005	A reduction in O(2)(*-) production in response to L-NAME occurred in the remaining patients and indicates O(2)(*-) production by the uncoupled NOS III enzyme.	Superoxides	15-19	nitric oxide synthase 3	Homo sapiens	143-150
15925745-10	2005	A reduction in O(2)(*-) production in response to L-NAME occurred in the remaining patients and indicates O(2)(*-) production by the uncoupled NOS III enzyme.	NG-Nitroarginine Methyl Ester	50-56	nitric oxide synthase 3	Homo sapiens	143-150
15925745-10	2005	A reduction in O(2)(*-) production in response to L-NAME occurred in the remaining patients and indicates O(2)(*-) production by the uncoupled NOS III enzyme.	Superoxides	15-23	nitric oxide synthase 3	Homo sapiens	143-150
15925745-11	2005	CONCLUSIONS: This study provides first published evidence that NOS III can reside in the uncoupled state in patients with hypertension and, to a greater extent, in patients with coexisting hypertension and diabetes, and that it contributes significantly to increased superoxide production in these disease states.	Superoxides	267-277	nitric oxide synthase 3	Homo sapiens	63-70
15845030-2	2005	The recent therapeutic application of nitric oxide (NO) in HA disorders, for the improvement of oxygenation and vasodilation, ushered us to investigate the endothelial nitric oxide synthase gene (NOS3) with respect to HA adaptation.	Nitric Oxide	38-50	nitric oxide synthase 3	Homo sapiens	156-189
15737995-11	2005	Moreover, overexpression of PDK1, but not Akt, reversed Hsp90 inhibition-induced loss of eNOS serine 1179 phosphorylation and salvaged enzymatic activity.	Serine	94-100	nitric oxide synthase 3	Homo sapiens	89-93
15737995-13	2005	Inhibition of Hsp90 function resulted in PDK1 depletion and thus triggered a cascade of Akt deactivation, loss of eNOS serine 1179 phosphorylation, and decrease of enzyme function.	Serine	119-125	nitric oxide synthase 3	Homo sapiens	114-118
15905730-9	2005	The eNOS mRNA showed a 54% and 65% reduction for 15- and 30-microM ritonavir-treated rings, respectively (P &lt; 0.05).	Ritonavir	67-76	nitric oxide synthase 3	Homo sapiens	4-8
15905730-12	2005	HCAECs treated with ritonavir showed significant reductions in mRNA and protein levels of eNOS (P &lt; 0.05).	Ritonavir	20-29	nitric oxide synthase 3	Homo sapiens	90-94
15905730-13	2005	Thus, ritonavir significantly impairs vasomotor function and reduces eNOS expression in porcine coronary artery endothelial cells as well as HCAECs.	Ritonavir	6-15	nitric oxide synthase 3	Homo sapiens	69-73
15718036-0	2005	Influence of the Glu298Asp polymorphism of NOS3 on age at onset and homocysteine levels in AD patients.	Homocysteine	68-80	nitric oxide synthase 3	Homo sapiens	43-47
15737995-2	2005	Besides acting as an allosteric enhancer, Hsp90 was shown to serve as a module recruiting Akt to phosphorylate the serine 1179/1177 (bovine/human) residue of eNOS.	Serine	115-121	nitric oxide synthase 3	Homo sapiens	158-162
15737995-6	2005	Both geldanamycin and radicicol, two structurally different Hsp90 inhibitors, selectively reduced serine 1179-phosphorylated eNOS, leading to decreased enzyme activity.	geldanamycin	5-17	nitric oxide synthase 3	Homo sapiens	125-129
15737995-6	2005	Both geldanamycin and radicicol, two structurally different Hsp90 inhibitors, selectively reduced serine 1179-phosphorylated eNOS, leading to decreased enzyme activity.	monorden	22-31	nitric oxide synthase 3	Homo sapiens	125-129
15737995-6	2005	Both geldanamycin and radicicol, two structurally different Hsp90 inhibitors, selectively reduced serine 1179-phosphorylated eNOS, leading to decreased enzyme activity.	Serine	98-104	nitric oxide synthase 3	Homo sapiens	125-129
15737995-10	2005	Silencing the PDK1 gene by small interfering RNA was sufficient to induce reduction of phospho-Akt and consequent loss of serine 1179-phosphorylated eNOS.	Serine	122-128	nitric oxide synthase 3	Homo sapiens	149-153
15845030-2	2005	The recent therapeutic application of nitric oxide (NO) in HA disorders, for the improvement of oxygenation and vasodilation, ushered us to investigate the endothelial nitric oxide synthase gene (NOS3) with respect to HA adaptation.	Nitric Oxide	38-50	nitric oxide synthase 3	Homo sapiens	196-200
15808421-9	2005	Similarly, DEM and CDNB inhibited TNF-alpha-induced Akt and eNOS phosphorylation, suggesting that thiol modification is involved in eNOS inductive pathways.	diethyl maleate	11-14	nitric oxide synthase 3	Homo sapiens	60-64
15821416-3	2005	Studies in animal models and in patients with congestive heart failure or hypertension indicate that aldosterone induces oxidative stress and impairs endothelial nitric oxide synthase through a mineralocorticoid receptor-dependent mechanism.	Aldosterone	101-112	nitric oxide synthase 3	Homo sapiens	150-183
15808421-9	2005	Similarly, DEM and CDNB inhibited TNF-alpha-induced Akt and eNOS phosphorylation, suggesting that thiol modification is involved in eNOS inductive pathways.	diethyl maleate	11-14	nitric oxide synthase 3	Homo sapiens	132-136
15808421-2	2005	Recent reports show that H(2)O(2) induces phosphorylation and activation of endothelial nitric oxide synthase (eNOS) through an Akt-phosphorylation-dependent pathway.	Hydrogen Peroxide	25-33	nitric oxide synthase 3	Homo sapiens	76-109
15808421-2	2005	Recent reports show that H(2)O(2) induces phosphorylation and activation of endothelial nitric oxide synthase (eNOS) through an Akt-phosphorylation-dependent pathway.	Hydrogen Peroxide	25-33	nitric oxide synthase 3	Homo sapiens	111-115
15808421-9	2005	Similarly, DEM and CDNB inhibited TNF-alpha-induced Akt and eNOS phosphorylation, suggesting that thiol modification is involved in eNOS inductive pathways.	Dinitrochlorobenzene	19-23	nitric oxide synthase 3	Homo sapiens	60-64
15808421-4	2005	Whereas moderate levels of H(2)O(2) (100 microM) activated the Akt/eNOS pathway, higher levels (500 microM) did not, suggesting differential effects by differing levels of oxidative stress.	Hydrogen Peroxide	27-35	nitric oxide synthase 3	Homo sapiens	67-71
15808421-9	2005	Similarly, DEM and CDNB inhibited TNF-alpha-induced Akt and eNOS phosphorylation, suggesting that thiol modification is involved in eNOS inductive pathways.	Dinitrochlorobenzene	19-23	nitric oxide synthase 3	Homo sapiens	132-136
15808421-7	2005	However, down-regulation of cell membrane surface and intracellular free thiols was associated with the inhibition of phosphorylation, suggesting that oxidation of non-GSH thiols inhibits the H(2)O(2)-induced phosphorylation of eNOS and Akt.	Hydrogen Peroxide	192-200	nitric oxide synthase 3	Homo sapiens	228-232
15808421-9	2005	Similarly, DEM and CDNB inhibited TNF-alpha-induced Akt and eNOS phosphorylation, suggesting that thiol modification is involved in eNOS inductive pathways.	Sulfhydryl Compounds	98-103	nitric oxide synthase 3	Homo sapiens	60-64
15808421-9	2005	Similarly, DEM and CDNB inhibited TNF-alpha-induced Akt and eNOS phosphorylation, suggesting that thiol modification is involved in eNOS inductive pathways.	Sulfhydryl Compounds	98-103	nitric oxide synthase 3	Homo sapiens	132-136
15808421-10	2005	Our findings suggest that eNOS activation is exquisitely sensitive to regulation by redox and that cell surface thiols, other than glutathione, regulate signal transduction leading to phosphorylation of Akt and eNOS.	Sulfhydryl Compounds	112-118	nitric oxide synthase 3	Homo sapiens	211-215
15864134-0	2005	Increase in the transcriptional activity of the endothelial nitric oxide synthase gene with fluvastatin: a relation with the -786T&gt;C polymorphism.	Fluvastatin	92-103	nitric oxide synthase 3	Homo sapiens	48-81
15864129-5	2005	RESULTS: Two polymorphisms in the sodium channel gamma-subunit promotor gene, and a polymorphism in the endothelial nitric oxide synthase gene, were significantly associated with blood pressure response to hydrochlorothiazide.	Hydrochlorothiazide	206-225	nitric oxide synthase 3	Homo sapiens	104-137
15864129-9	2005	CONCLUSIONS: Two polymorphisms in the sodium channel gamma-subunit promotor gene, and a polymorphism in the endothelial nitric oxide synthase gene, were associated with significant differences in odds of DBP response to hydrochlorothiazide.	Hydrochlorothiazide	220-239	nitric oxide synthase 3	Homo sapiens	108-141
15864134-2	2005	We examined endothelial nitric oxide synthase (eNOS) mRNA levels, mRNA stability and the transcriptional activities of the eNOS gene in human umbilical vein endothelial cells treated with fluvastatin and simvastatin.	Fluvastatin	188-199	nitric oxide synthase 3	Homo sapiens	12-45
15864134-2	2005	We examined endothelial nitric oxide synthase (eNOS) mRNA levels, mRNA stability and the transcriptional activities of the eNOS gene in human umbilical vein endothelial cells treated with fluvastatin and simvastatin.	Fluvastatin	188-199	nitric oxide synthase 3	Homo sapiens	123-127
15860762-5	2005	Recent studies have shown that H2O2 stimulates reactive oxygen species production via enhanced intracellular iron uptake, mitochondrial damage, and sources of vascular NAD(P)H oxidases, xanthine oxidase, and uncoupled endothelial nitric oxide synthase (eNOS).	Hydrogen Peroxide	31-35	nitric oxide synthase 3	Homo sapiens	218-251
15864134-2	2005	We examined endothelial nitric oxide synthase (eNOS) mRNA levels, mRNA stability and the transcriptional activities of the eNOS gene in human umbilical vein endothelial cells treated with fluvastatin and simvastatin.	Simvastatin	204-215	nitric oxide synthase 3	Homo sapiens	123-127
15864134-4	2005	Utilizing the real-time reverse transcription-polymerase chain reaction, fluvastatin significantly increased eNOS mRNA levels and mRNA stability, and decreased RPA1 mRNA levels.	Fluvastatin	73-84	nitric oxide synthase 3	Homo sapiens	109-113
15864134-5	2005	Luciferase reporter gene assays revealed that fluvastatin significantly increased the transcriptional activity of the eNOS gene.	Fluvastatin	46-57	nitric oxide synthase 3	Homo sapiens	118-122
15864134-7	2005	Simvastatin increased eNOS mRNA levels and mRNA stability, but did not affect the transcriptional activity of the eNOS gene.	Simvastatin	0-11	nitric oxide synthase 3	Homo sapiens	22-26
15864134-8	2005	Fluvastatin increased eNOS mRNA levels by enhancing both the transcriptional activity and mRNA stability.	Fluvastatin	0-11	nitric oxide synthase 3	Homo sapiens	22-26
15864134-10	2005	Simvastatin increased eNOS mRNA levels only by enhancing mRNA stability.	Simvastatin	0-11	nitric oxide synthase 3	Homo sapiens	22-26
15806288-7	2005	Functional analysis demonstrated that the YCPRYVRRKLENELLVL peptide shared by two clones inhibited the expression of ICAM-1, increased nitric oxide concentration in the culture media, and upregulated the expression of caveolin-1 and eNOS.	Nitric Oxide	135-147	nitric oxide synthase 3	Homo sapiens	233-237
15722551-4	2005	Induction of eNOS expression by histone deacetylase (HDAC) inhibitors trichostatin A (TSA) and sodium butyrate was observed in all four different types of non-endothelial cells examined.	trichostatin A	70-84	nitric oxide synthase 3	Homo sapiens	13-17
15722551-4	2005	Induction of eNOS expression by histone deacetylase (HDAC) inhibitors trichostatin A (TSA) and sodium butyrate was observed in all four different types of non-endothelial cells examined.	trichostatin A	86-89	nitric oxide synthase 3	Homo sapiens	13-17
15722551-4	2005	Induction of eNOS expression by histone deacetylase (HDAC) inhibitors trichostatin A (TSA) and sodium butyrate was observed in all four different types of non-endothelial cells examined.	Butyric Acid	95-110	nitric oxide synthase 3	Homo sapiens	13-17
15722551-6	2005	Moreover, DNA methylation-mediated repression of eNOS promoter activity was partially reversed by TSA treatment, and combined treatment of TSA and 5-aza-2"-deoxycytidine (AzadC) synergistically induced eNOS expression in non-endothelial cells.	trichostatin A	98-101	nitric oxide synthase 3	Homo sapiens	49-53
15722551-6	2005	Moreover, DNA methylation-mediated repression of eNOS promoter activity was partially reversed by TSA treatment, and combined treatment of TSA and 5-aza-2"-deoxycytidine (AzadC) synergistically induced eNOS expression in non-endothelial cells.	trichostatin A	98-101	nitric oxide synthase 3	Homo sapiens	202-206
15722551-6	2005	Moreover, DNA methylation-mediated repression of eNOS promoter activity was partially reversed by TSA treatment, and combined treatment of TSA and 5-aza-2"-deoxycytidine (AzadC) synergistically induced eNOS expression in non-endothelial cells.	trichostatin A	139-142	nitric oxide synthase 3	Homo sapiens	49-53
15722551-6	2005	Moreover, DNA methylation-mediated repression of eNOS promoter activity was partially reversed by TSA treatment, and combined treatment of TSA and 5-aza-2"-deoxycytidine (AzadC) synergistically induced eNOS expression in non-endothelial cells.	trichostatin A	139-142	nitric oxide synthase 3	Homo sapiens	202-206
15722551-6	2005	Moreover, DNA methylation-mediated repression of eNOS promoter activity was partially reversed by TSA treatment, and combined treatment of TSA and 5-aza-2"-deoxycytidine (AzadC) synergistically induced eNOS expression in non-endothelial cells.	Decitabine	147-169	nitric oxide synthase 3	Homo sapiens	202-206
15722551-6	2005	Moreover, DNA methylation-mediated repression of eNOS promoter activity was partially reversed by TSA treatment, and combined treatment of TSA and 5-aza-2"-deoxycytidine (AzadC) synergistically induced eNOS expression in non-endothelial cells.	Decitabine	171-176	nitric oxide synthase 3	Homo sapiens	49-53
15722551-6	2005	Moreover, DNA methylation-mediated repression of eNOS promoter activity was partially reversed by TSA treatment, and combined treatment of TSA and 5-aza-2"-deoxycytidine (AzadC) synergistically induced eNOS expression in non-endothelial cells.	Decitabine	171-176	nitric oxide synthase 3	Homo sapiens	202-206
15722551-10	2005	Combined TSA and AzadC treatment increased Sp1 binding to the endogenous eNOS promoter but decreased the association between HDAC1 and Sp1 in HeLa cells.	trichostatin A	9-12	nitric oxide synthase 3	Homo sapiens	73-77
15722551-10	2005	Combined TSA and AzadC treatment increased Sp1 binding to the endogenous eNOS promoter but decreased the association between HDAC1 and Sp1 in HeLa cells.	Decitabine	17-22	nitric oxide synthase 3	Homo sapiens	73-77
15740722-3	2005	Superoxide dismutase (SOD), tempol (membrane permeable SOD mimetic) and the NADPH oxidase inhibitors, 4-(2-aminoethyl)-benzenesulfonyl fluoride and apocynin, but not allopurinol, inhibited HUVEC proliferation and migration, as well as activity of endothelial NOS (eNOS).	4-(2-aminoethyl)benzenesulfonylfluoride	102-143	nitric oxide synthase 3	Homo sapiens	247-262
15590897-1	2005	Recently, we demonstrated that the peroxisome proliferator-activated receptor-gamma (PPAR-gamma) ligands, either 15-deoxy-Delta12,14-prostaglandin J2 (15d-PGJ2) or ciglitazone, increased endothelial nitric oxide (.NO) release without altering endothelial nitric oxide synthase (eNOS) expression (4).	14-prostaglandin j2	130-149	nitric oxide synthase 3	Homo sapiens	243-276
15705930-1	2005	UNLABELLED: Background- We have recently identified that endothelium-derived hydrogen peroxide (H2O2) is an endothelium-derived hyperpolarizing factor (EDHF) in animals and humans, for which endothelial nitric oxide synthase (eNOS) is an important source.	Hydrogen Peroxide	77-94	nitric oxide synthase 3	Homo sapiens	191-224
15705930-1	2005	UNLABELLED: Background- We have recently identified that endothelium-derived hydrogen peroxide (H2O2) is an endothelium-derived hyperpolarizing factor (EDHF) in animals and humans, for which endothelial nitric oxide synthase (eNOS) is an important source.	Hydrogen Peroxide	96-100	nitric oxide synthase 3	Homo sapiens	191-224
15705930-1	2005	UNLABELLED: Background- We have recently identified that endothelium-derived hydrogen peroxide (H2O2) is an endothelium-derived hyperpolarizing factor (EDHF) in animals and humans, for which endothelial nitric oxide synthase (eNOS) is an important source.	endothelium-derived hyperpolarizing factor	108-150	nitric oxide synthase 3	Homo sapiens	191-224
15705930-1	2005	UNLABELLED: Background- We have recently identified that endothelium-derived hydrogen peroxide (H2O2) is an endothelium-derived hyperpolarizing factor (EDHF) in animals and humans, for which endothelial nitric oxide synthase (eNOS) is an important source.	edhf	152-156	nitric oxide synthase 3	Homo sapiens	191-224
15665327-0	2005	Flow shear stress stimulates Gab1 tyrosine phosphorylation to mediate protein kinase B and endothelial nitric-oxide synthase activation in endothelial cells.	Tyrosine	34-42	nitric oxide synthase 3	Homo sapiens	91-124
15665327-5	2005	Gab1 phosphorylation as well as activation of Akt and eNOS by flow was inhibited by the Src kinase inhibitor PP2 (4-amino-5-(4-chlorophenyl)-7-(t-butyl)pyrazolo[3,4-d]pyrimidine) and VEGFR2 kinase inhibitors SU1498 and VTI, suggesting that flow-mediated Gab1 phosphorylation is Src kinase-dependent and VEGFR2-dependent.	pp2	109-112	nitric oxide synthase 3	Homo sapiens	54-58
15665327-5	2005	Gab1 phosphorylation as well as activation of Akt and eNOS by flow was inhibited by the Src kinase inhibitor PP2 (4-amino-5-(4-chlorophenyl)-7-(t-butyl)pyrazolo[3,4-d]pyrimidine) and VEGFR2 kinase inhibitors SU1498 and VTI, suggesting that flow-mediated Gab1 phosphorylation is Src kinase-dependent and VEGFR2-dependent.	4-amino-5-(4-chlorophenyl	114-139	nitric oxide synthase 3	Homo sapiens	54-58
15665327-5	2005	Gab1 phosphorylation as well as activation of Akt and eNOS by flow was inhibited by the Src kinase inhibitor PP2 (4-amino-5-(4-chlorophenyl)-7-(t-butyl)pyrazolo[3,4-d]pyrimidine) and VEGFR2 kinase inhibitors SU1498 and VTI, suggesting that flow-mediated Gab1 phosphorylation is Src kinase-dependent and VEGFR2-dependent.	-7-(t-butyl)pyrazolo[3,4-d]pyrimidine	140-177	nitric oxide synthase 3	Homo sapiens	54-58
15640399-0	2005	Bradykinin down-regulates, whereas arginine analogs up-regulates, endothelial nitric-oxide synthase expression in coronary endothelial cells.	Arginine	35-43	nitric oxide synthase 3	Homo sapiens	66-99
15615701-5	2005	Importantly, resveratrol activated MAPK and endothelial nitric-oxide synthase (eNOS) at nm concentrations (i.e. an order of magnitude less than that required for ER genomic activity) and concentrations possibly achieved transiently in serum following oral red wine consumption.	Resveratrol	13-24	nitric oxide synthase 3	Homo sapiens	44-77
15665327-5	2005	Gab1 phosphorylation as well as activation of Akt and eNOS by flow was inhibited by the Src kinase inhibitor PP2 (4-amino-5-(4-chlorophenyl)-7-(t-butyl)pyrazolo[3,4-d]pyrimidine) and VEGFR2 kinase inhibitors SU1498 and VTI, suggesting that flow-mediated Gab1 phosphorylation is Src kinase-dependent and VEGFR2-dependent.	SU 1498	208-214	nitric oxide synthase 3	Homo sapiens	54-58
15665327-5	2005	Gab1 phosphorylation as well as activation of Akt and eNOS by flow was inhibited by the Src kinase inhibitor PP2 (4-amino-5-(4-chlorophenyl)-7-(t-butyl)pyrazolo[3,4-d]pyrimidine) and VEGFR2 kinase inhibitors SU1498 and VTI, suggesting that flow-mediated Gab1 phosphorylation is Src kinase-dependent and VEGFR2-dependent.	N-{n-[4-(Acetylamino)-3,5-Dichlorobenzyl]carbamimidoyl}-2-(1h-Indol-1-Yl)acetamide	219-222	nitric oxide synthase 3	Homo sapiens	54-58
15784500-7	2005	A23187-stimulated activation of eNOS was, however, also accompanied by phosphorylation of eNOS S1179 and dephosphorylation of T497, demonstrating that an increase in [Ca(2+)](i) may not be the sole mechanism of activation.	Calcimycin	0-6	nitric oxide synthase 3	Homo sapiens	32-36
15784500-7	2005	A23187-stimulated activation of eNOS was, however, also accompanied by phosphorylation of eNOS S1179 and dephosphorylation of T497, demonstrating that an increase in [Ca(2+)](i) may not be the sole mechanism of activation.	Calcimycin	0-6	nitric oxide synthase 3	Homo sapiens	90-94
15784500-8	2005	The physiologic relevance of this was further underscored by the finding that ATP dose-dependently increased peak [Ca(2+)](i) and eNOS activity in COS-7/oeNOS, but also increased eNOS p-S1179 and decreased p-T497.	Adenosine Triphosphate	78-81	nitric oxide synthase 3	Homo sapiens	130-134
15784500-8	2005	The physiologic relevance of this was further underscored by the finding that ATP dose-dependently increased peak [Ca(2+)](i) and eNOS activity in COS-7/oeNOS, but also increased eNOS p-S1179 and decreased p-T497.	Adenosine Triphosphate	78-81	nitric oxide synthase 3	Homo sapiens	154-158
15784500-8	2005	The physiologic relevance of this was further underscored by the finding that ATP dose-dependently increased peak [Ca(2+)](i) and eNOS activity in COS-7/oeNOS, but also increased eNOS p-S1179 and decreased p-T497.	cos-7	147-152	nitric oxide synthase 3	Homo sapiens	130-134
15784500-9	2005	This finding was similar to those in ovine P-UAEC treated with the Ca(2+)-mobilizing agonist ATP, wherein activation of eNOS was again concomitant with a rise p-S1179 as well as a slight decrease in p-T497.	Adenosine Triphosphate	93-96	nitric oxide synthase 3	Homo sapiens	120-124
15784500-10	2005	In conclusion, we describe the full-length ovine eNOS cDNA sequence and show that both physiologic and nonphysiologic calcium-mobilizing agents, which activate ovine eNOS in COS-7 and P-UAEC, do so in association with changes in eNOS phosphorylation.	Calcium	118-125	nitric oxide synthase 3	Homo sapiens	49-53
15784500-10	2005	In conclusion, we describe the full-length ovine eNOS cDNA sequence and show that both physiologic and nonphysiologic calcium-mobilizing agents, which activate ovine eNOS in COS-7 and P-UAEC, do so in association with changes in eNOS phosphorylation.	Calcium	118-125	nitric oxide synthase 3	Homo sapiens	166-170
15784500-10	2005	In conclusion, we describe the full-length ovine eNOS cDNA sequence and show that both physiologic and nonphysiologic calcium-mobilizing agents, which activate ovine eNOS in COS-7 and P-UAEC, do so in association with changes in eNOS phosphorylation.	Calcium	118-125	nitric oxide synthase 3	Homo sapiens	166-170
15733940-0	2005	Pitavastatin at low dose activates endothelial nitric oxide synthase through PI3K-AKT pathway in endothelial cells.	pitavastatin	0-12	nitric oxide synthase 3	Homo sapiens	35-68
15733940-2	2005	Previously, we have reported that pitavastatin induces the activation of endothelial nitric oxide synthase (eNOS) and increases nitric oxide (NO) production in vascular endothelial cells (EC).	pitavastatin	34-46	nitric oxide synthase 3	Homo sapiens	73-106
15733940-2	2005	Previously, we have reported that pitavastatin induces the activation of endothelial nitric oxide synthase (eNOS) and increases nitric oxide (NO) production in vascular endothelial cells (EC).	pitavastatin	34-46	nitric oxide synthase 3	Homo sapiens	108-112
15733940-2	2005	Previously, we have reported that pitavastatin induces the activation of endothelial nitric oxide synthase (eNOS) and increases nitric oxide (NO) production in vascular endothelial cells (EC).	Nitric Oxide	85-97	nitric oxide synthase 3	Homo sapiens	108-112
15733940-3	2005	However, the mechanism of eNOS activation by pitavastatin remains unknown.	pitavastatin	45-57	nitric oxide synthase 3	Homo sapiens	26-30
15733940-4	2005	Here, we examined the implications of pitavastatin-induced signaling in eNOS phosphorylation in EC.	pitavastatin	38-50	nitric oxide synthase 3	Homo sapiens	72-76
15733940-5	2005	We found that treatment of EC with a low dose of pitavastatin induced eNOS phosphorylation at Ser-1177, activated Akt phosphorylation at Ser-473 in a time-and dose-dependent manner, and increased NO production.	pitavastatin	49-61	nitric oxide synthase 3	Homo sapiens	70-74
15733940-5	2005	We found that treatment of EC with a low dose of pitavastatin induced eNOS phosphorylation at Ser-1177, activated Akt phosphorylation at Ser-473 in a time-and dose-dependent manner, and increased NO production.	Serine	94-97	nitric oxide synthase 3	Homo sapiens	70-74
15733940-8	2005	These results suggest that the activation of eNOS with a low dose of pitavastatin (0.1 microM) involves phosphoinositide 3-kinase and the Akt pathway and produces NO in EC, which is dependent on post-transcriptional regulation.	pitavastatin	69-81	nitric oxide synthase 3	Homo sapiens	45-49
15531748-0	2005	Endothelin-1 decreases endothelial NOS expression and activity through ETA receptor-mediated generation of hydrogen peroxide.	Hydrogen Peroxide	107-124	nitric oxide synthase 3	Homo sapiens	23-38
15531748-10	2005	In FPAEC in monoculture treated with 0-100 microM H2O2, 12 microM had no effect on eNOS promoter activity, but it increased eNOS protein levels by 50%.	Hydrogen Peroxide	50-54	nitric oxide synthase 3	Homo sapiens	124-128
15531748-11	2005	However, at 100 microM, H2O2 decreased eNOS promoter activity and protein levels in FPAEC by 79 and 40%, respectively.	Hydrogen Peroxide	24-28	nitric oxide synthase 3	Homo sapiens	39-43
15531748-12	2005	These data suggest a role for smooth muscle cell-derived H2O2 in ET-1-mediated downregulation of eNOS expression in children born with PPHN.	Hydrogen Peroxide	57-61	nitric oxide synthase 3	Homo sapiens	97-101
15721870-1	2005	OBJECTIVE: Oxidized low-density lipoprotein (ox-LDL) increases superoxide anion (O(2)(-)) production by the endothelial nitric oxide (NO) synthase (eNOS).	Superoxides	63-79	nitric oxide synthase 3	Homo sapiens	148-152
15721870-9	2005	In COS-7 cells, a T495A eNOS mutant generated significantly more O(2)(-) than a T495D mutant did, indicating that the dephosphorylation of Thr(495) alone can increase O(2)(-) production by eNOS.	Threonine	139-142	nitric oxide synthase 3	Homo sapiens	189-193
15721870-1	2005	OBJECTIVE: Oxidized low-density lipoprotein (ox-LDL) increases superoxide anion (O(2)(-)) production by the endothelial nitric oxide (NO) synthase (eNOS).	Superoxides	81-84	nitric oxide synthase 3	Homo sapiens	148-152
15721870-9	2005	In COS-7 cells, a T495A eNOS mutant generated significantly more O(2)(-) than a T495D mutant did, indicating that the dephosphorylation of Thr(495) alone can increase O(2)(-) production by eNOS.	Superoxides	167-171	nitric oxide synthase 3	Homo sapiens	24-28
15721870-10	2005	However, although the dephosphorylation of Thr(495) in histamine-stimulated endothelial cells enhanced the binding of calmodulin to eNOS, calmodulin no longer bound to eNOS from ox-LDL-treated endothelial cells.	Threonine	43-46	nitric oxide synthase 3	Homo sapiens	132-136
15721870-10	2005	However, although the dephosphorylation of Thr(495) in histamine-stimulated endothelial cells enhanced the binding of calmodulin to eNOS, calmodulin no longer bound to eNOS from ox-LDL-treated endothelial cells.	Histamine	55-64	nitric oxide synthase 3	Homo sapiens	132-136
15810551-4	2005	Here the production of NA, a nitroso-arginine, which was shown to be synthesised by brain NO-synthase (bNOS), was studied in eNOS preparations.	nitroso-arginine	29-45	nitric oxide synthase 3	Homo sapiens	125-129
15810551-6	2005	Using microelectrodes, NA and nitrite were simultaneously measured in pure recombinant eNOS giving similar enzyme activity.	Nitrites	30-37	nitric oxide synthase 3	Homo sapiens	87-91
15721870-3	2005	METHODS AND RESULTS: In unstimulated human endothelial cells, eNOS Thr(495) was constitutively phosphorylated.	Threonine	67-70	nitric oxide synthase 3	Homo sapiens	62-66
15721870-5	2005	ox-LDL, but not native LDL, induced a time- and concentration-dependent decrease in the phosphorylation of eNOS on Thr(495).	Threonine	115-118	nitric oxide synthase 3	Homo sapiens	107-111
15721870-9	2005	In COS-7 cells, a T495A eNOS mutant generated significantly more O(2)(-) than a T495D mutant did, indicating that the dephosphorylation of Thr(495) alone can increase O(2)(-) production by eNOS.	carbonyl sulfide	3-6	nitric oxide synthase 3	Homo sapiens	24-28
15721870-9	2005	In COS-7 cells, a T495A eNOS mutant generated significantly more O(2)(-) than a T495D mutant did, indicating that the dephosphorylation of Thr(495) alone can increase O(2)(-) production by eNOS.	Superoxides	65-69	nitric oxide synthase 3	Homo sapiens	24-28
15721870-9	2005	In COS-7 cells, a T495A eNOS mutant generated significantly more O(2)(-) than a T495D mutant did, indicating that the dephosphorylation of Thr(495) alone can increase O(2)(-) production by eNOS.	Threonine	139-142	nitric oxide synthase 3	Homo sapiens	24-28
15698605-1	2005	BACKGROUND: Nitric oxide (NO) produced by endothelial NO synthase (eNOS) mediates endothelium-dependent vasodilation and antithrombotic action.	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	67-71
15740982-4	2005	In these cells, eNOS activity is modulated by tyrosine- and serine-phosphorylation.	Tyrosine	46-54	nitric oxide synthase 3	Homo sapiens	16-20
15565175-1	2005	Mutations in the endothelial nitric oxide synthase (eNOS) gene may be associated with abnormal nitric oxide (NO) production and cardiovascular diseases.	Nitric Oxide	29-41	nitric oxide synthase 3	Homo sapiens	52-56
15740982-4	2005	In these cells, eNOS activity is modulated by tyrosine- and serine-phosphorylation.	Serine	60-66	nitric oxide synthase 3	Homo sapiens	16-20
15740983-9	2005	The anthocyanins cyanidin, the hydroxycinnamic acids p-coumaric acid and caffeic acid, and the phenolic acids benzoic acid and vanillic acid also enhanced eNOS expression moderately (with no effect on eNOS promoter activity).	phenolic acid	95-109	nitric oxide synthase 3	Homo sapiens	155-159
15740982-7	2005	Therefore, the present results indicate that the molecular mechanism of clinically observed anti-inflammatory action of ESW should include tyrosine-dephosphorylation of eNOS, a successive increase in NO production and suppression of NF-kappaB activation.	Tyrosine	139-147	nitric oxide synthase 3	Homo sapiens	169-173
15740983-9	2005	The anthocyanins cyanidin, the hydroxycinnamic acids p-coumaric acid and caffeic acid, and the phenolic acids benzoic acid and vanillic acid also enhanced eNOS expression moderately (with no effect on eNOS promoter activity).	phenolic acid	95-109	nitric oxide synthase 3	Homo sapiens	201-205
15740983-2	2005	Especially red wine is a rich source of polyphenols, and we have previously shown that French red wine upregulates eNOS, a protective enzyme in the cardiovascular system.	Polyphenols	40-51	nitric oxide synthase 3	Homo sapiens	115-119
15740983-9	2005	The anthocyanins cyanidin, the hydroxycinnamic acids p-coumaric acid and caffeic acid, and the phenolic acids benzoic acid and vanillic acid also enhanced eNOS expression moderately (with no effect on eNOS promoter activity).	Benzoic Acid	110-122	nitric oxide synthase 3	Homo sapiens	155-159
15740983-4	2005	Of the compounds tested, we found 3,4",5-trihydroxy-trans-stilbene (trans-resveratrol) to be the most efficacious stimulator of eNOS expression (and eNOS transcription), but this compound alone could not explain the total stimulatory effect of red wine.	Resveratrol	34-66	nitric oxide synthase 3	Homo sapiens	128-132
15740983-4	2005	Of the compounds tested, we found 3,4",5-trihydroxy-trans-stilbene (trans-resveratrol) to be the most efficacious stimulator of eNOS expression (and eNOS transcription), but this compound alone could not explain the total stimulatory effect of red wine.	Resveratrol	34-66	nitric oxide synthase 3	Homo sapiens	149-153
15740983-9	2005	The anthocyanins cyanidin, the hydroxycinnamic acids p-coumaric acid and caffeic acid, and the phenolic acids benzoic acid and vanillic acid also enhanced eNOS expression moderately (with no effect on eNOS promoter activity).	Vanillic Acid	127-140	nitric oxide synthase 3	Homo sapiens	155-159
15740983-4	2005	Of the compounds tested, we found 3,4",5-trihydroxy-trans-stilbene (trans-resveratrol) to be the most efficacious stimulator of eNOS expression (and eNOS transcription), but this compound alone could not explain the total stimulatory effect of red wine.	Resveratrol	68-85	nitric oxide synthase 3	Homo sapiens	128-132
15740983-9	2005	The anthocyanins cyanidin, the hydroxycinnamic acids p-coumaric acid and caffeic acid, and the phenolic acids benzoic acid and vanillic acid also enhanced eNOS expression moderately (with no effect on eNOS promoter activity).	Vanillic Acid	127-140	nitric oxide synthase 3	Homo sapiens	201-205
15740983-4	2005	Of the compounds tested, we found 3,4",5-trihydroxy-trans-stilbene (trans-resveratrol) to be the most efficacious stimulator of eNOS expression (and eNOS transcription), but this compound alone could not explain the total stimulatory effect of red wine.	Resveratrol	68-85	nitric oxide synthase 3	Homo sapiens	149-153
15740983-10	2005	Thus, the increase in eNOS in response to red wine involves several polyphenolic compounds with a major contribution from trans-resveratrol and lesser contributions from cinnamic and hydroxycinnamic acids, cyanidin, and some phenolic acids.	Ellagic Acid	68-80	nitric oxide synthase 3	Homo sapiens	22-26
15740983-6	2005	The flavonol quercetin inhibited eNOS expression (with no effect on eNOS promoter activity).	3-hydroxyflavone	4-12	nitric oxide synthase 3	Homo sapiens	33-37
15740983-10	2005	Thus, the increase in eNOS in response to red wine involves several polyphenolic compounds with a major contribution from trans-resveratrol and lesser contributions from cinnamic and hydroxycinnamic acids, cyanidin, and some phenolic acids.	Resveratrol	122-139	nitric oxide synthase 3	Homo sapiens	22-26
15740983-10	2005	Thus, the increase in eNOS in response to red wine involves several polyphenolic compounds with a major contribution from trans-resveratrol and lesser contributions from cinnamic and hydroxycinnamic acids, cyanidin, and some phenolic acids.	Coumaric Acids	183-204	nitric oxide synthase 3	Homo sapiens	22-26
15740983-10	2005	Thus, the increase in eNOS in response to red wine involves several polyphenolic compounds with a major contribution from trans-resveratrol and lesser contributions from cinnamic and hydroxycinnamic acids, cyanidin, and some phenolic acids.	cyanidin	206-214	nitric oxide synthase 3	Homo sapiens	22-26
15740983-6	2005	The flavonol quercetin inhibited eNOS expression (with no effect on eNOS promoter activity).	Quercetin	13-22	nitric oxide synthase 3	Homo sapiens	33-37
15740983-10	2005	Thus, the increase in eNOS in response to red wine involves several polyphenolic compounds with a major contribution from trans-resveratrol and lesser contributions from cinnamic and hydroxycinnamic acids, cyanidin, and some phenolic acids.	phenolic acid	225-239	nitric oxide synthase 3	Homo sapiens	22-26
15740983-7	2005	Cinnamic acid was a rather potent enhancer of eNOS expression, however with an efficacy of only 170%.	cinnamic acid	0-13	nitric oxide synthase 3	Homo sapiens	46-50
15740983-9	2005	The anthocyanins cyanidin, the hydroxycinnamic acids p-coumaric acid and caffeic acid, and the phenolic acids benzoic acid and vanillic acid also enhanced eNOS expression moderately (with no effect on eNOS promoter activity).	anthocyanins cyanidin	4-25	nitric oxide synthase 3	Homo sapiens	155-159
15740983-9	2005	The anthocyanins cyanidin, the hydroxycinnamic acids p-coumaric acid and caffeic acid, and the phenolic acids benzoic acid and vanillic acid also enhanced eNOS expression moderately (with no effect on eNOS promoter activity).	hydroxycinnamic acids p-coumaric acid	31-68	nitric oxide synthase 3	Homo sapiens	155-159
15642349-2	2005	N-SMase induced translocation of endothelial NOS (eNOS) from plasma membrane caveolae to intracellular region, eNOS phosphorylation on serine 1179, and an increase of ceramide level in endothelial cells.	Serine	135-141	nitric oxide synthase 3	Homo sapiens	111-115
15846275-5	2005	METHODS: Patients who have congestive heart failure were tested for the presence of an eNOS promoter polymorphism (thymidine to cytosine transition [T(-786)C]).	Thymidine	115-124	nitric oxide synthase 3	Homo sapiens	87-91
15846275-5	2005	METHODS: Patients who have congestive heart failure were tested for the presence of an eNOS promoter polymorphism (thymidine to cytosine transition [T(-786)C]).	Cytosine	128-136	nitric oxide synthase 3	Homo sapiens	87-91
15720205-3	2005	Homocysteine seems to promote the formation of reactive oxygen species primarily by a biochemical mechanism involving endothelial nitric oxide synthase, as increased endothelial lipid peroxidation and oxidation of the redox-sensitve dye 2",7"-dichlorofluoresceine could only be observed after incubation of endothelial cells with L-, but not with D-homocysteine, and could be prevented by inhibition of endothelial nitric oxide synthase.	Homocysteine	0-12	nitric oxide synthase 3	Homo sapiens	118-151
15720205-3	2005	Homocysteine seems to promote the formation of reactive oxygen species primarily by a biochemical mechanism involving endothelial nitric oxide synthase, as increased endothelial lipid peroxidation and oxidation of the redox-sensitve dye 2",7"-dichlorofluoresceine could only be observed after incubation of endothelial cells with L-, but not with D-homocysteine, and could be prevented by inhibition of endothelial nitric oxide synthase.	Homocysteine	0-12	nitric oxide synthase 3	Homo sapiens	403-436
15720205-3	2005	Homocysteine seems to promote the formation of reactive oxygen species primarily by a biochemical mechanism involving endothelial nitric oxide synthase, as increased endothelial lipid peroxidation and oxidation of the redox-sensitve dye 2",7"-dichlorofluoresceine could only be observed after incubation of endothelial cells with L-, but not with D-homocysteine, and could be prevented by inhibition of endothelial nitric oxide synthase.	Reactive Oxygen Species	47-70	nitric oxide synthase 3	Homo sapiens	118-151
15720205-3	2005	Homocysteine seems to promote the formation of reactive oxygen species primarily by a biochemical mechanism involving endothelial nitric oxide synthase, as increased endothelial lipid peroxidation and oxidation of the redox-sensitve dye 2",7"-dichlorofluoresceine could only be observed after incubation of endothelial cells with L-, but not with D-homocysteine, and could be prevented by inhibition of endothelial nitric oxide synthase.	Reactive Oxygen Species	47-70	nitric oxide synthase 3	Homo sapiens	403-436
15583003-9	2005	Blockade of endothelial NOS (eNOS) activation using geldanamycin and radicicol, inhibitors of heat shock protein 90, in endothelium-intact arteries suppressed both LPS-induced relaxation and LPS-induced iNOS expression (9.0 +/- 8.0% and 2.0 +/- 6.2%, respectively).	geldanamycin	52-64	nitric oxide synthase 3	Homo sapiens	12-27
15583003-9	2005	Blockade of endothelial NOS (eNOS) activation using geldanamycin and radicicol, inhibitors of heat shock protein 90, in endothelium-intact arteries suppressed both LPS-induced relaxation and LPS-induced iNOS expression (9.0 +/- 8.0% and 2.0 +/- 6.2%, respectively).	monorden	69-78	nitric oxide synthase 3	Homo sapiens	12-27
15655515-4	2005	We hypothesized that isoflavones may affect the expression of endothelial-type nitric oxide synthase (eNOS) and thereby NO formation in vitro.	Isoflavones	21-32	nitric oxide synthase 3	Homo sapiens	62-100
15655515-4	2005	We hypothesized that isoflavones may affect the expression of endothelial-type nitric oxide synthase (eNOS) and thereby NO formation in vitro.	Isoflavones	21-32	nitric oxide synthase 3	Homo sapiens	102-106
15655515-7	2005	Active eNOS was detected by quantifying conversion of L-arginine to L-citrulline and by measuring NO released from endothelial cells using the fluorescent probe DAF-2 (20-96 h).eNOS promoter activity increased in response to isoflavone treatment (20 h).	Arginine	54-64	nitric oxide synthase 3	Homo sapiens	7-11
15655515-7	2005	Active eNOS was detected by quantifying conversion of L-arginine to L-citrulline and by measuring NO released from endothelial cells using the fluorescent probe DAF-2 (20-96 h).eNOS promoter activity increased in response to isoflavone treatment (20 h).	Arginine	54-64	nitric oxide synthase 3	Homo sapiens	177-181
15655515-7	2005	Active eNOS was detected by quantifying conversion of L-arginine to L-citrulline and by measuring NO released from endothelial cells using the fluorescent probe DAF-2 (20-96 h).eNOS promoter activity increased in response to isoflavone treatment (20 h).	Citrulline	68-80	nitric oxide synthase 3	Homo sapiens	7-11
15655515-7	2005	Active eNOS was detected by quantifying conversion of L-arginine to L-citrulline and by measuring NO released from endothelial cells using the fluorescent probe DAF-2 (20-96 h).eNOS promoter activity increased in response to isoflavone treatment (20 h).	Citrulline	68-80	nitric oxide synthase 3	Homo sapiens	177-181
15655515-7	2005	Active eNOS was detected by quantifying conversion of L-arginine to L-citrulline and by measuring NO released from endothelial cells using the fluorescent probe DAF-2 (20-96 h).eNOS promoter activity increased in response to isoflavone treatment (20 h).	Isoflavones	225-235	nitric oxide synthase 3	Homo sapiens	7-11
15655515-7	2005	Active eNOS was detected by quantifying conversion of L-arginine to L-citrulline and by measuring NO released from endothelial cells using the fluorescent probe DAF-2 (20-96 h).eNOS promoter activity increased in response to isoflavone treatment (20 h).	Isoflavones	225-235	nitric oxide synthase 3	Homo sapiens	177-181
15655515-8	2005	NO and L-citrulline production by EA.hy926 cells rose up to 1.7-fold of control levels after stimulation with genistein for 48-96 h. From these results, we conclude that the suggested positive effects of soy isoflavones on vascular reactivity may be indeed mediated via a long-term effect on the eNOS system.	Genistein	110-119	nitric oxide synthase 3	Homo sapiens	296-300
15722114-1	2005	Nitric oxide (NO) is a gaseous lipophilic free radical cellular messenger generated by three distinct isoforms of nitric oxide synthases (NOS), neuronal (nNOS), inducible (iNOS) and endothelial NOS (eNOS).	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	182-197
15642349-4	2005	We propose the involvement of N-SMase and ceramide in Ca(2+)-independent eNOS activation and NO production in endothelial cells in situ, linking to endothelium-dependent vasorelaxation.	Ceramides	42-50	nitric oxide synthase 3	Homo sapiens	73-77
16301818-12	2005	In addition, the beta3 adrenoceptor-dependent increase in cGMP and activation of NOS were blocked by the inhibition of phospholipase C (PLC), calcium/calmodulin (CaM), endothelial NOS activity and cGMP accumulation.	Cyclic GMP	58-62	nitric oxide synthase 3	Homo sapiens	168-183
15353403-0	2005	A high-salt diet stimulates thick ascending limb eNOS expression by raising medullary osmolality and increasing release of endothelin-1.	Salts	7-11	nitric oxide synthase 3	Homo sapiens	49-53
15353403-1	2005	A high-salt diet increases renal endothelin (ET) production and thick ascending limb (THAL) endothelial nitric oxide synthase (eNOS) expression.	Salts	7-11	nitric oxide synthase 3	Homo sapiens	92-125
15353403-1	2005	A high-salt diet increases renal endothelin (ET) production and thick ascending limb (THAL) endothelial nitric oxide synthase (eNOS) expression.	Salts	7-11	nitric oxide synthase 3	Homo sapiens	127-131
15353403-4	2005	We hypothesized that a high-salt diet raises medullary osmolality, increases ET release by the THAL, and thus enhances eNOS expression.	Salts	28-32	nitric oxide synthase 3	Homo sapiens	119-123
15353403-5	2005	Seven days of high salt (1% NaCl in drinking water) increased eNOS expression in THALs by 125 +/- 31%.	Salts	19-23	nitric oxide synthase 3	Homo sapiens	62-66
15353403-5	2005	Seven days of high salt (1% NaCl in drinking water) increased eNOS expression in THALs by 125 +/- 31%.	Sodium Chloride	28-32	nitric oxide synthase 3	Homo sapiens	62-66
15353403-5	2005	Seven days of high salt (1% NaCl in drinking water) increased eNOS expression in THALs by 125 +/- 31%.	Water	45-50	nitric oxide synthase 3	Homo sapiens	62-66
15353403-9	2005	In primary cultures of medullary THALs, raising osmolality from 300 to 350 and 400 mosmol/kg H(2)O using NaCl increased eNOS expression by 39 +/- 11% (P &lt; 0.05) and 71 +/- 16%, respectively (P &lt; 0.05).	Sodium Chloride	105-109	nitric oxide synthase 3	Homo sapiens	120-124
15353403-11	2005	BQ-788, an ET(B) receptor antagonist (1 muM), blocked the stimulatory effect of 400 mosmol/kg H(2)O on eNOS expression (70 +/- 13% vs. -5 +/- 10%; paired difference, 74 +/- 15%; P &lt; 0.05).	BQ 788	0-6	nitric oxide synthase 3	Homo sapiens	103-107
15353403-13	2005	We concluded that high salt stimulates THAL eNOS expression by increasing outer medullary osmolality, ET-1 release by the THAL and ET(B) receptor activation.	Salts	23-27	nitric oxide synthase 3	Homo sapiens	44-48
15569838-1	2004	BACKGROUND: Arginase competes with endothelial nitric oxide synthase (eNOS) for the substrate l-arginine and decreases NO production.	Arginine	94-104	nitric oxide synthase 3	Homo sapiens	35-68
16036314-12	2005	Phosphorylation of eNOS Ser1177 under shear stress was elevated by 20 min, a response that was blocked by PI-3K (phosphatidylinositol 3-kinase) inhibitors wortmannin and LY294002, but not the MEK (MAPK kinase) inhibitor UO126.	Wortmannin	155-165	nitric oxide synthase 3	Homo sapiens	19-23
16036314-12	2005	Phosphorylation of eNOS Ser1177 under shear stress was elevated by 20 min, a response that was blocked by PI-3K (phosphatidylinositol 3-kinase) inhibitors wortmannin and LY294002, but not the MEK (MAPK kinase) inhibitor UO126.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	170-178	nitric oxide synthase 3	Homo sapiens	19-23
16036314-12	2005	Phosphorylation of eNOS Ser1177 under shear stress was elevated by 20 min, a response that was blocked by PI-3K (phosphatidylinositol 3-kinase) inhibitors wortmannin and LY294002, but not the MEK (MAPK kinase) inhibitor UO126.	U 0126	220-225	nitric oxide synthase 3	Homo sapiens	19-23
15526284-0	2005	Up-regulation of the association between heat shock protein 90 and endothelial nitric oxide synthase prevents high glucose-induced apoptosis in human endothelial cells.	Glucose	115-122	nitric oxide synthase 3	Homo sapiens	67-100
15526284-3	2005	High glucose can trigger endothelial cell apoptosis by de-activation of endothelial nitric oxide synthase (eNOS).	Glucose	5-12	nitric oxide synthase 3	Homo sapiens	72-105
15526284-3	2005	High glucose can trigger endothelial cell apoptosis by de-activation of endothelial nitric oxide synthase (eNOS).	Glucose	5-12	nitric oxide synthase 3	Homo sapiens	107-111
15526284-5	2005	Yet, little is known about the molecular mechanisms that regulate eNOS activity during high glucose exposure.	Glucose	92-99	nitric oxide synthase 3	Homo sapiens	66-70
15526284-6	2005	The present study was designed to determine the involvement of protein interactions between eNOS and HSP90 in high glucose-induced endothelial cell apoptosis.	Glucose	115-122	nitric oxide synthase 3	Homo sapiens	92-96
15526284-8	2005	The results showed that the protein interactions between eNOS and HSP90 and between eNOS and Akt and the phosphorylation of eNOS were up-regulated by high glucose exposure for 2-4 h. With longer exposures, these effects decreased gradually.	Glucose	155-162	nitric oxide synthase 3	Homo sapiens	57-61
15526284-8	2005	The results showed that the protein interactions between eNOS and HSP90 and between eNOS and Akt and the phosphorylation of eNOS were up-regulated by high glucose exposure for 2-4 h. With longer exposures, these effects decreased gradually.	Glucose	155-162	nitric oxide synthase 3	Homo sapiens	84-88
15526284-8	2005	The results showed that the protein interactions between eNOS and HSP90 and between eNOS and Akt and the phosphorylation of eNOS were up-regulated by high glucose exposure for 2-4 h. With longer exposures, these effects decreased gradually.	Glucose	155-162	nitric oxide synthase 3	Homo sapiens	84-88
15526284-9	2005	During early hours of exposure, the protein interactions of eNOS/HSP90 and eNOS/Akt and the phosphorylation of eNOS were all inhibited by geldanamycin, an HSP90 inhibitor.	geldanamycin	138-150	nitric oxide synthase 3	Homo sapiens	60-64
15526284-9	2005	During early hours of exposure, the protein interactions of eNOS/HSP90 and eNOS/Akt and the phosphorylation of eNOS were all inhibited by geldanamycin, an HSP90 inhibitor.	geldanamycin	138-150	nitric oxide synthase 3	Homo sapiens	75-79
15526284-9	2005	During early hours of exposure, the protein interactions of eNOS/HSP90 and eNOS/Akt and the phosphorylation of eNOS were all inhibited by geldanamycin, an HSP90 inhibitor.	geldanamycin	138-150	nitric oxide synthase 3	Homo sapiens	75-79
15526284-11	2005	LY294002, a phosphatidylinositol 3 (PI3) kinase inhibitor, inhibited the association of eNOS/Akt and the phosphorylation of eNOS but had no effect on the interaction between eNOS and HSP90 during early hours of exposure.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	0-8	nitric oxide synthase 3	Homo sapiens	88-92
15526284-11	2005	LY294002, a phosphatidylinositol 3 (PI3) kinase inhibitor, inhibited the association of eNOS/Akt and the phosphorylation of eNOS but had no effect on the interaction between eNOS and HSP90 during early hours of exposure.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	0-8	nitric oxide synthase 3	Homo sapiens	124-128
15526284-11	2005	LY294002, a phosphatidylinositol 3 (PI3) kinase inhibitor, inhibited the association of eNOS/Akt and the phosphorylation of eNOS but had no effect on the interaction between eNOS and HSP90 during early hours of exposure.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	0-8	nitric oxide synthase 3	Homo sapiens	124-128
15526284-12	2005	From our results we propose that, in HUVECs, during early phase of high glucose exposure, apoptosis can be prevented by enhancement of eNOS activity through augmentation of the protein interaction between eNOS and HSP90 and recruitment of the activated Akt.	Glucose	72-79	nitric oxide synthase 3	Homo sapiens	135-139
15526284-12	2005	From our results we propose that, in HUVECs, during early phase of high glucose exposure, apoptosis can be prevented by enhancement of eNOS activity through augmentation of the protein interaction between eNOS and HSP90 and recruitment of the activated Akt.	Glucose	72-79	nitric oxide synthase 3	Homo sapiens	205-209
15526284-14	2005	The present study provides a molecular basis for the effects of eNOS in the prevention of endothelial cells apoptosis during early phase of high glucose exposure.	Glucose	145-152	nitric oxide synthase 3	Homo sapiens	64-68
15719745-12	2005	CONCLUSION: CSI could partially prevent the occurrence of tolerance to nitrate ester, with the effect better than vitamin C, the mechanism might be related with its regulation on eNOS, ET-1 mRNA expression and protection on vascular endothelial function.	nitrate ester	71-84	nitric oxide synthase 3	Homo sapiens	179-183
15769392-6	2005	These effects of simvastatin and lovastatin on eNOS mRNA expression correlated with changes in nitric oxide production.	Simvastatin	17-28	nitric oxide synthase 3	Homo sapiens	47-51
15769392-6	2005	These effects of simvastatin and lovastatin on eNOS mRNA expression correlated with changes in nitric oxide production.	Lovastatin	33-43	nitric oxide synthase 3	Homo sapiens	47-51
15769392-6	2005	These effects of simvastatin and lovastatin on eNOS mRNA expression correlated with changes in nitric oxide production.	Nitric Oxide	95-107	nitric oxide synthase 3	Homo sapiens	47-51
15943229-5	2005	Measuring of eNOS activity in platelets using diaminofluorescein diacetate (DAF-2A) showed that in carriers of 786C/C promoter genotype NO-producing activity is 2.1 times lower than in normal homozygotes (P=0.03) and 2.9 times lower comparing to heterozygotes (P&gt;0.05).	diaminofluorescein diacetate	46-74	nitric oxide synthase 3	Homo sapiens	13-17
15912652-1	2005	The increase of vascular nitrotyrosine and cytochines accumulation is accompanied by an increase of endothelial nitric oxide synthase (eNOS) expression].	3-nitrotyrosine	25-38	nitric oxide synthase 3	Homo sapiens	100-133
15912652-14	2005	A significant positive correlation was found between nitrotyrosin and eNOS expression and systolic arterial pressure.	nitrotyrosin	53-65	nitric oxide synthase 3	Homo sapiens	70-74
17315398-2	2005	HDL promote endothelium proliferation and diminish endothelial apoptosis; they play a key role in vasorelaxation by increasing the release of nitric oxide and prostacyclin through the induction of the expression and the activity of endothelial nitric oxide synthase and the coupling of cyclooxygenase 2 and prostacyclin synthase.	Nitric Oxide	142-154	nitric oxide synthase 3	Homo sapiens	232-265
17315398-2	2005	HDL promote endothelium proliferation and diminish endothelial apoptosis; they play a key role in vasorelaxation by increasing the release of nitric oxide and prostacyclin through the induction of the expression and the activity of endothelial nitric oxide synthase and the coupling of cyclooxygenase 2 and prostacyclin synthase.	Epoprostenol	159-171	nitric oxide synthase 3	Homo sapiens	232-265
15636445-1	2004	Endothelial nitric oxide synthase (eNOS) catalyzes the formation of nitric oxide (NO) which has vasodilatory, antithrombotic, antiinflammatory and antiproliferative actions through which NO regulates blood pressure and modulates the process of atherosclerosis.	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	35-39
15622377-11	2004	In addition, eNOS immunoreactivity was reduced in the homocysteine group, but the combined homocysteine and curcumin group showed eNOS levels comparable to those in the control group.	Homocysteine	91-103	nitric oxide synthase 3	Homo sapiens	130-134
15607645-8	2004	DHCA also increased nitric oxide synthase activity in a dose-dependent manner in cultured cells, which was associated with a comparable increase in endothelial nitric oxide synthase protein.	3,4-dihydroxyphenylpropionic acid	0-4	nitric oxide synthase 3	Homo sapiens	148-181
15739773-5	2004	We determined, within our case study, the level of NAA to e-NOS in blood and tears of patients with diabetic retinopathy and in donors.	1-naphthaleneacetic acid	51-54	nitric oxide synthase 3	Homo sapiens	58-63
15739773-6	2004	The level of NAA to e-NOS was found to be twice higher in tears versus blood in all groups of patients.	1-naphthaleneacetic acid	13-16	nitric oxide synthase 3	Homo sapiens	20-25
15514213-3	2004	METHODS AND RESULTS: Here we show that HDL, modified with physiologically relevant HOCl concentrations, attenuates the expression and activity of vasculoprotective endothelial nitric oxide synthase.	Hypochlorous Acid	83-87	nitric oxide synthase 3	Homo sapiens	164-197
15514213-4	2004	HOCl-HDL promotes dislocalization of endothelial nitric oxide synthase from the plasma membrane and perinuclear location of human umbilical venous endothelial cells.	Hypochlorous Acid	0-4	nitric oxide synthase 3	Homo sapiens	37-70
15704255-3	2004	We showed that the 894 G&gt;T single-nucleotide polymorphism in the human endothelial nitric oxide synthase gene (eNOS) increased the risk of recurrent venous thrombosis in individuals with elevated homocysteine levels, indicating that the pathophysiological mechanism in HHcy involves impaired NO-mediated vasodilatation.	Homocysteine	199-211	nitric oxide synthase 3	Homo sapiens	74-107
15622377-11	2004	In addition, eNOS immunoreactivity was reduced in the homocysteine group, but the combined homocysteine and curcumin group showed eNOS levels comparable to those in the control group.	Homocysteine	54-66	nitric oxide synthase 3	Homo sapiens	13-17
15622377-11	2004	In addition, eNOS immunoreactivity was reduced in the homocysteine group, but the combined homocysteine and curcumin group showed eNOS levels comparable to those in the control group.	Curcumin	108-116	nitric oxide synthase 3	Homo sapiens	130-134
15622377-14	2004	In addition, curcumin significantly blocked homocysteine-induced superoxide anion production and eNOS down-regulation.	Curcumin	13-21	nitric oxide synthase 3	Homo sapiens	97-101
15465001-1	2004	We report the novel observation that medroxyprogesterone acetate (MPA) attenuates the induction by 17beta estradiol (E2) of both nitric oxide (NO) production and endothelial nitric oxide synthase (eNOS) activity in human umbilical vein endothelial cells.	Medroxyprogesterone Acetate	37-64	nitric oxide synthase 3	Homo sapiens	162-195
15634400-4	2004	It is 0.28 and 0.22 by MTT test, 4691 and 3995 by (3)H-TdR permeate separately at the time of 120 h. CONCLUSIONS: eNOS-overexpressing endothelial cells inhibited significantly smooth muscle cells proliferation and platelet aggregation in vitro; which shows powerful effect 48 hours post transfection and lasts up to 120 hours at the least; and were held back by L-NAME.	monooxyethylene trimethylolpropane tristearate	23-26	nitric oxide synthase 3	Homo sapiens	114-118
15634400-4	2004	It is 0.28 and 0.22 by MTT test, 4691 and 3995 by (3)H-TdR permeate separately at the time of 120 h. CONCLUSIONS: eNOS-overexpressing endothelial cells inhibited significantly smooth muscle cells proliferation and platelet aggregation in vitro; which shows powerful effect 48 hours post transfection and lasts up to 120 hours at the least; and were held back by L-NAME.	NG-Nitroarginine Methyl Ester	362-368	nitric oxide synthase 3	Homo sapiens	114-118
15319431-7	2004	In particular, AbetaP enhances eNOS phosphorylation on threonine 495 and serine 116 and reduces acetylcholine-induced phosphorylation on serine 1177.	Threonine	55-64	nitric oxide synthase 3	Homo sapiens	31-35
15319431-9	2004	In fact, selective inhibition of the calcium-dependent group of PKC is able to rescue beta-amyloid-induced alteration of eNOS phosphorylation, NO production, and endothelial vasorelaxation.	Calcium	37-44	nitric oxide synthase 3	Homo sapiens	121-125
15319431-11	2004	Our data demonstrate that globular AbetaP-induced endothelial NO dysfunction can be attributed to an alteration of intracellular Ca(2+) homeostasis, which could lead to the activation of calcium-dependent group of PKC with a consequent change of the eNOS phosphorylation pattern.	Calcium	187-194	nitric oxide synthase 3	Homo sapiens	250-254
15465001-1	2004	We report the novel observation that medroxyprogesterone acetate (MPA) attenuates the induction by 17beta estradiol (E2) of both nitric oxide (NO) production and endothelial nitric oxide synthase (eNOS) activity in human umbilical vein endothelial cells.	Medroxyprogesterone Acetate	66-69	nitric oxide synthase 3	Homo sapiens	162-195
15465001-1	2004	We report the novel observation that medroxyprogesterone acetate (MPA) attenuates the induction by 17beta estradiol (E2) of both nitric oxide (NO) production and endothelial nitric oxide synthase (eNOS) activity in human umbilical vein endothelial cells.	Estradiol	99-115	nitric oxide synthase 3	Homo sapiens	162-195
15523316-3	2004	Endothelial NO is synthesized from the amino acid l-arginine by the endothelial isoform of NO synthase (eNOS).	amino acid l-arginine	39-60	nitric oxide synthase 3	Homo sapiens	104-108
15517628-1	2004	OBJECTIVE: In systemic lupus erythematosus (SLE), endothelial nitric oxide synthase (eNOS) gene locus has been found to be suggestive of linkage with disease, nitric oxide (NO) is produced in significant amounts, and endothelial cell dysfunction is observed.	Nitric Oxide	62-74	nitric oxide synthase 3	Homo sapiens	85-89
15479220-2	2004	The aim of this study was to investigate whether vitamin(s) C and/or E modulate hyperglycaemia-induced oxidative stress by regulating enzymatic activities of prooxidant, i.e. NAD(P)H oxidase and/or antioxidant enzymes, namely endothelial nitric oxide synthase (eNOS), superoxide dismutase, catalase and glutathione peroxidase, using coronary microvascular endothelial cells (CMEC).	vitamin(s) c	49-61	nitric oxide synthase 3	Homo sapiens	226-259
15459608-1	2004	BACKGROUND: We evaluated the effect of the point mutation of guanine to thymine at nucleotide position 894 (G894T) of the endothelial nitric oxide synthase (eNOS) gene on inflammatory and oxidative stress markers.	Guanine	61-68	nitric oxide synthase 3	Homo sapiens	122-155
15483745-1	2004	Nitric oxide is synthesized from L-arginine by endothelial nitric oxide synthase encoded by eNOS gene.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	47-80
15483745-1	2004	Nitric oxide is synthesized from L-arginine by endothelial nitric oxide synthase encoded by eNOS gene.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	92-96
15483745-1	2004	Nitric oxide is synthesized from L-arginine by endothelial nitric oxide synthase encoded by eNOS gene.	Arginine	33-43	nitric oxide synthase 3	Homo sapiens	47-80
15483745-1	2004	Nitric oxide is synthesized from L-arginine by endothelial nitric oxide synthase encoded by eNOS gene.	Arginine	33-43	nitric oxide synthase 3	Homo sapiens	92-96
15483745-2	2004	This study was performed to investigate the relationship between the serum nitric oxide level and eNOS gene polymorphism in the Turkish population with angiographically diagnosed coronary artery disease (63.47 +/- 9.10 years old, n=250) and control subjects without any history and/or risk factors of coronary artery disease (60.71 +/- 9.14 years old, n=150).	Nitric Oxide	75-87	nitric oxide synthase 3	Homo sapiens	98-102
15483745-4	2004	It was found that Glu/Glu, Glu/Asp and Asp/Asp genotype frequencies of the eNOS were 49.3%, 41.3% and 9.3% respectively in the control group, and 45.6%, 41.2% and 13.2% in the patient group.	Glutamic Acid	18-21	nitric oxide synthase 3	Homo sapiens	75-79
15483745-4	2004	It was found that Glu/Glu, Glu/Asp and Asp/Asp genotype frequencies of the eNOS were 49.3%, 41.3% and 9.3% respectively in the control group, and 45.6%, 41.2% and 13.2% in the patient group.	Glutamic Acid	22-25	nitric oxide synthase 3	Homo sapiens	75-79
15483745-4	2004	It was found that Glu/Glu, Glu/Asp and Asp/Asp genotype frequencies of the eNOS were 49.3%, 41.3% and 9.3% respectively in the control group, and 45.6%, 41.2% and 13.2% in the patient group.	Glutamic Acid	22-25	nitric oxide synthase 3	Homo sapiens	75-79
15483745-4	2004	It was found that Glu/Glu, Glu/Asp and Asp/Asp genotype frequencies of the eNOS were 49.3%, 41.3% and 9.3% respectively in the control group, and 45.6%, 41.2% and 13.2% in the patient group.	Aspartic Acid	31-34	nitric oxide synthase 3	Homo sapiens	75-79
15483745-4	2004	It was found that Glu/Glu, Glu/Asp and Asp/Asp genotype frequencies of the eNOS were 49.3%, 41.3% and 9.3% respectively in the control group, and 45.6%, 41.2% and 13.2% in the patient group.	Aspartic Acid	39-42	nitric oxide synthase 3	Homo sapiens	75-79
15483745-4	2004	It was found that Glu/Glu, Glu/Asp and Asp/Asp genotype frequencies of the eNOS were 49.3%, 41.3% and 9.3% respectively in the control group, and 45.6%, 41.2% and 13.2% in the patient group.	Aspartic Acid	39-42	nitric oxide synthase 3	Homo sapiens	75-79
15375006-7	2004	Pretreatment of these cells with a decoy oligonucleotide comprising position -800 to -779 of the C-type nos-3 promoter reconstituted shear stress-induced NOS-3 expression.	decoy oligonucleotide	35-56	nitric oxide synthase 3	Homo sapiens	104-109
15375006-7	2004	Pretreatment of these cells with a decoy oligonucleotide comprising position -800 to -779 of the C-type nos-3 promoter reconstituted shear stress-induced NOS-3 expression.	decoy oligonucleotide	35-56	nitric oxide synthase 3	Homo sapiens	154-159
15459608-1	2004	BACKGROUND: We evaluated the effect of the point mutation of guanine to thymine at nucleotide position 894 (G894T) of the endothelial nitric oxide synthase (eNOS) gene on inflammatory and oxidative stress markers.	Guanine	61-68	nitric oxide synthase 3	Homo sapiens	157-161
15459608-1	2004	BACKGROUND: We evaluated the effect of the point mutation of guanine to thymine at nucleotide position 894 (G894T) of the endothelial nitric oxide synthase (eNOS) gene on inflammatory and oxidative stress markers.	Thymine	72-79	nitric oxide synthase 3	Homo sapiens	122-155
15459608-1	2004	BACKGROUND: We evaluated the effect of the point mutation of guanine to thymine at nucleotide position 894 (G894T) of the endothelial nitric oxide synthase (eNOS) gene on inflammatory and oxidative stress markers.	Thymine	72-79	nitric oxide synthase 3	Homo sapiens	157-161
15494775-5	2004	RESULTS: Subjects with the eNOS Asp298 allele (n=15) showed significantly reduced FMD:GTN compared with those without this allele (n=38) (0.23+/-0.13 [mean +/- SD] versus 0.35+/-0.14, P=0.0072), whereas there was no significant difference in GTN between these two groups.	Nitroglycerin	242-245	nitric oxide synthase 3	Homo sapiens	27-31
15494775-1	2004	BACKGROUND: The guanine to thymine polymorphism at position 894 of the eNOS gene (resulting in a change from glutamate to aspartate [Asp] at codon 298 [Asp298]) and the methylenetetrahydrofolate reductase (MTHFR) gene polymorphism (C677T) have been reported to be associated with atherosclerosis and cardiovascular disease.	Guanine	16-23	nitric oxide synthase 3	Homo sapiens	71-75
15284089-7	2004	When HUVECs were subjected to a 0.5s impulse of 12 dynes/cm2, a transient disruption of the eNOS/PECAM-1 complex was observed, accompanied by an increase in eNOS activity (cGMP production).	Cyclic GMP	172-176	nitric oxide synthase 3	Homo sapiens	92-96
15284089-7	2004	When HUVECs were subjected to a 0.5s impulse of 12 dynes/cm2, a transient disruption of the eNOS/PECAM-1 complex was observed, accompanied by an increase in eNOS activity (cGMP production).	Cyclic GMP	172-176	nitric oxide synthase 3	Homo sapiens	157-161
15494775-6	2004	Although subjects with the MTHFR T677 allele did not show significantly reduced levels of FMD:GTN, subjects with the eNOS Asp298 allele and who were carriers of the MTHFR T677 allele demonstrated markedly reduced levels of FMD:GTN compared with noncarriers (0.14+/-0.05 versus 0.28+/-0.13, P=0.04).	Nitroglycerin	227-230	nitric oxide synthase 3	Homo sapiens	117-121
15494775-1	2004	BACKGROUND: The guanine to thymine polymorphism at position 894 of the eNOS gene (resulting in a change from glutamate to aspartate [Asp] at codon 298 [Asp298]) and the methylenetetrahydrofolate reductase (MTHFR) gene polymorphism (C677T) have been reported to be associated with atherosclerosis and cardiovascular disease.	Thymine	27-34	nitric oxide synthase 3	Homo sapiens	71-75
15560113-0	2004	15-deoxy-delta12,14-prostaglandin-J2 inhibits expression of eNOS in human endothelial cells.	15-deoxy-delta12	0-16	nitric oxide synthase 3	Homo sapiens	60-64
15494775-1	2004	BACKGROUND: The guanine to thymine polymorphism at position 894 of the eNOS gene (resulting in a change from glutamate to aspartate [Asp] at codon 298 [Asp298]) and the methylenetetrahydrofolate reductase (MTHFR) gene polymorphism (C677T) have been reported to be associated with atherosclerosis and cardiovascular disease.	Glutamic Acid	109-118	nitric oxide synthase 3	Homo sapiens	71-75
15494775-1	2004	BACKGROUND: The guanine to thymine polymorphism at position 894 of the eNOS gene (resulting in a change from glutamate to aspartate [Asp] at codon 298 [Asp298]) and the methylenetetrahydrofolate reductase (MTHFR) gene polymorphism (C677T) have been reported to be associated with atherosclerosis and cardiovascular disease.	Aspartic Acid	122-131	nitric oxide synthase 3	Homo sapiens	71-75
15494775-1	2004	BACKGROUND: The guanine to thymine polymorphism at position 894 of the eNOS gene (resulting in a change from glutamate to aspartate [Asp] at codon 298 [Asp298]) and the methylenetetrahydrofolate reductase (MTHFR) gene polymorphism (C677T) have been reported to be associated with atherosclerosis and cardiovascular disease.	Aspartic Acid	133-136	nitric oxide synthase 3	Homo sapiens	71-75
15494775-5	2004	RESULTS: Subjects with the eNOS Asp298 allele (n=15) showed significantly reduced FMD:GTN compared with those without this allele (n=38) (0.23+/-0.13 [mean +/- SD] versus 0.35+/-0.14, P=0.0072), whereas there was no significant difference in GTN between these two groups.	Nitroglycerin	86-89	nitric oxide synthase 3	Homo sapiens	27-31
15490108-9	2004	In contrast, chronic exposure to elevated glucose (25 mmol/l for 7 days) reduced total nitrite levels (46% reduction), levels of eNOS mRNA (46% reduction) and eNOS protein (65% reduction).	Glucose	42-49	nitric oxide synthase 3	Homo sapiens	159-163
15490108-14	2004	CONCLUSIONS/INTERPRETATION: In diabetes, the expression and activity of eNOS is regulated through glucose-mediated mitochondrial production of reactive oxygen species and activation of the oxidative stress transcription factor AP-1.	Glucose	98-105	nitric oxide synthase 3	Homo sapiens	72-76
15490108-14	2004	CONCLUSIONS/INTERPRETATION: In diabetes, the expression and activity of eNOS is regulated through glucose-mediated mitochondrial production of reactive oxygen species and activation of the oxidative stress transcription factor AP-1.	Reactive Oxygen Species	143-166	nitric oxide synthase 3	Homo sapiens	72-76
15272035-8	2004	Gestational diabetes and NBMPR effects involved eNOS, PKC and p42/44(mapk) activation, and were blocked by the A(2a) purinoceptor antagonist ZM-241385.	4-nitrobenzylthioinosine	25-30	nitric oxide synthase 3	Homo sapiens	48-52
15272035-8	2004	Gestational diabetes and NBMPR effects involved eNOS, PKC and p42/44(mapk) activation, and were blocked by the A(2a) purinoceptor antagonist ZM-241385.	ZM 241385	141-150	nitric oxide synthase 3	Homo sapiens	48-52
15485778-0	2004	[Effect of total Panax notoginseng saponins on the activity of human endothelial nitric oxide synthase gene promoter].	Saponins	35-43	nitric oxide synthase 3	Homo sapiens	69-102
15485778-1	2004	OBJECTIVE: To study the mechanism of total Panax notoginseng saponin (tPNS) in regulating the transcription activity of human endothelial nitric oxide synthase (heNOS) gene promoter.	Saponins	61-68	nitric oxide synthase 3	Homo sapiens	126-159
15490108-0	2004	Hyperglycaemia-induced superoxide production decreases eNOS expression via AP-1 activation in aortic endothelial cells.	Superoxides	23-33	nitric oxide synthase 3	Homo sapiens	55-59
15490108-3	2004	The aim of this study was to investigate the regulation of endothelial nitric oxide synthase (eNOS) activity by acute and chronic elevated glucose.	Glucose	139-146	nitric oxide synthase 3	Homo sapiens	59-92
15490108-3	2004	The aim of this study was to investigate the regulation of endothelial nitric oxide synthase (eNOS) activity by acute and chronic elevated glucose.	Glucose	139-146	nitric oxide synthase 3	Homo sapiens	94-98
15490108-6	2004	The expression and activity of eNOS were measured using quantitative PCR and nitrite measurements respectively.	Nitrites	77-84	nitric oxide synthase 3	Homo sapiens	31-35
15490108-8	2004	RESULTS: Acute exposure (4 h) of human aortic endothelial cells to 25 mmol/l glucose moderately increased eNOS activity and eNOS mRNA and protein expression.	Glucose	77-84	nitric oxide synthase 3	Homo sapiens	106-110
15490108-8	2004	RESULTS: Acute exposure (4 h) of human aortic endothelial cells to 25 mmol/l glucose moderately increased eNOS activity and eNOS mRNA and protein expression.	Glucose	77-84	nitric oxide synthase 3	Homo sapiens	124-128
15490108-9	2004	In contrast, chronic exposure to elevated glucose (25 mmol/l for 7 days) reduced total nitrite levels (46% reduction), levels of eNOS mRNA (46% reduction) and eNOS protein (65% reduction).	Glucose	42-49	nitric oxide synthase 3	Homo sapiens	129-133
15465788-1	2004	L-arginine, the principal substrate for endothelial nitric oxide synthase, is oxidized to L-citrulline and nitric oxide.	Arginine	0-10	nitric oxide synthase 3	Homo sapiens	40-73
15465788-1	2004	L-arginine, the principal substrate for endothelial nitric oxide synthase, is oxidized to L-citrulline and nitric oxide.	Citrulline	90-102	nitric oxide synthase 3	Homo sapiens	40-73
15375496-5	2004	There was a close relationship between the expression of nitrotyrosine and all three NOS isoforms (for all p&lt;0.0005), catalase (p&lt;0.0005) and MnSOD (p=0.043), in addition enlarged tumor size was in association with high nitrotyrosine (p=0.046), eNOS (p=0.005) and VEGF (p=0.046) levels.	3-nitrotyrosine	57-70	nitric oxide synthase 3	Homo sapiens	251-255
15375508-5	2004	Both estradiol and LiCl enhanced the expression of eNOS mRNA with the phosphorylation of GSK-3beta, but not Akt.	Estradiol	5-14	nitric oxide synthase 3	Homo sapiens	51-55
15375508-5	2004	Both estradiol and LiCl enhanced the expression of eNOS mRNA with the phosphorylation of GSK-3beta, but not Akt.	Lithium Chloride	19-23	nitric oxide synthase 3	Homo sapiens	51-55
15375508-7	2004	We conclude that the estradiol-induced eNOS expression is modulated by PI3-kinase-dependent GSK-3beta pathway.	Estradiol	21-30	nitric oxide synthase 3	Homo sapiens	39-43
15560113-0	2004	15-deoxy-delta12,14-prostaglandin-J2 inhibits expression of eNOS in human endothelial cells.	14-prostaglandin-j2	17-36	nitric oxide synthase 3	Homo sapiens	60-64
15560113-3	2004	Our aim was to investigated the effect of 15d-PGJ2 on eNOS in human umbilical vein endothelial cells (HUVEC).	15-deoxy-delta(12,14)-prostaglandin J2	42-50	nitric oxide synthase 3	Homo sapiens	54-58
15560113-8	2004	Since none of the observed effects could be mimicked by troglitazone, a more potent PPARgamma ligand, we suppose that 15d-PGJ2 diminishes expression of eNOS via PPARgamma-independent mechanisms.	15-deoxy-delta(12,14)-prostaglandin J2	118-126	nitric oxide synthase 3	Homo sapiens	152-156
15289285-8	2004	Additionally, endothelial NO synthase (eNOS) activity was measured in EA.hy 926 cell homogenates by an l-[(3)H]citrulline/l-[(3)H]arginine conversion assay.	-[(3)h]citrulline	104-121	nitric oxide synthase 3	Homo sapiens	39-43
15140758-9	2004	We concluded that eNOS in the renal glomerular capillary endothelial cells is suppressed by activity of PKC at high-glucose concentrations comparable to those in diabetic animals and humans.	Glucose	116-123	nitric oxide synthase 3	Homo sapiens	18-22
15234981-10	2004	Finally, the histone deacetylase inhibitor trichostatin A is known to regulate the expression of eNOS via a post-transcriptional mechanism.	trichostatin A	43-57	nitric oxide synthase 3	Homo sapiens	97-101
15234981-11	2004	We found that trichostatin A treatment of vascular endothelial cells increased expression of sONE mRNA levels prior to the observed decrease in eNOS mRNA expression.	trichostatin A	14-28	nitric oxide synthase 3	Homo sapiens	144-148
15288814-7	2004	Nitric oxide predictably inhibited both endothelial nitric oxide synthase and glyceraldehyde 3-phosphate dehydrogenase, and ascorbate partially prevented inhibition of the latter enzyme.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	40-73
15289285-8	2004	Additionally, endothelial NO synthase (eNOS) activity was measured in EA.hy 926 cell homogenates by an l-[(3)H]citrulline/l-[(3)H]arginine conversion assay.	Arginine	130-138	nitric oxide synthase 3	Homo sapiens	39-43
15289285-13	2004	Incubation of soluble eNOS for 15 min with 100 microm aspirin or acetylating aspirin analogues increased the l-[(3)H]citrulline yield by 40-80%, while salicylic acid had no effect.	Aspirin	54-61	nitric oxide synthase 3	Homo sapiens	22-26
15289285-13	2004	Incubation of soluble eNOS for 15 min with 100 microm aspirin or acetylating aspirin analogues increased the l-[(3)H]citrulline yield by 40-80%, while salicylic acid had no effect.	Aspirin	77-84	nitric oxide synthase 3	Homo sapiens	22-26
15289285-13	2004	Incubation of soluble eNOS for 15 min with 100 microm aspirin or acetylating aspirin analogues increased the l-[(3)H]citrulline yield by 40-80%, while salicylic acid had no effect.	l-[(3)h]citrulline	109-127	nitric oxide synthase 3	Homo sapiens	22-26
15289285-13	2004	Incubation of soluble eNOS for 15 min with 100 microm aspirin or acetylating aspirin analogues increased the l-[(3)H]citrulline yield by 40-80%, while salicylic acid had no effect.	Salicylic Acid	151-165	nitric oxide synthase 3	Homo sapiens	22-26
15333482-1	2004	OBJECTIVE: We examined the endothelial nitric oxide (eNOS) gene polymorphisms to assess its possible association with diabetic retinopathy and macular edema.	Nitric Oxide	39-51	nitric oxide synthase 3	Homo sapiens	53-57
15288120-0	2004	Alpha-tocopherol amplifies phosphorylation of endothelial nitric oxide synthase at serine 1177 and its short-chain derivative trolox stabilizes tetrahydrobiopterin.	alpha-Tocopherol	0-16	nitric oxide synthase 3	Homo sapiens	46-79
15288120-0	2004	Alpha-tocopherol amplifies phosphorylation of endothelial nitric oxide synthase at serine 1177 and its short-chain derivative trolox stabilizes tetrahydrobiopterin.	Serine	83-89	nitric oxide synthase 3	Homo sapiens	46-79
15288120-0	2004	Alpha-tocopherol amplifies phosphorylation of endothelial nitric oxide synthase at serine 1177 and its short-chain derivative trolox stabilizes tetrahydrobiopterin.	sapropterin	144-163	nitric oxide synthase 3	Homo sapiens	46-79
15288120-4	2004	Ionomycin induced citrulline and cGMP formation partially through phosphorylation of endothelial NO synthase (eNOS) at its serine residue 1177, which was mediated mainly by calmodulin-dependent kinase II.	Ionomycin	0-9	nitric oxide synthase 3	Homo sapiens	110-114
15288120-4	2004	Ionomycin induced citrulline and cGMP formation partially through phosphorylation of endothelial NO synthase (eNOS) at its serine residue 1177, which was mediated mainly by calmodulin-dependent kinase II.	Citrulline	18-28	nitric oxide synthase 3	Homo sapiens	110-114
15288120-4	2004	Ionomycin induced citrulline and cGMP formation partially through phosphorylation of endothelial NO synthase (eNOS) at its serine residue 1177, which was mediated mainly by calmodulin-dependent kinase II.	Cyclic GMP	33-37	nitric oxide synthase 3	Homo sapiens	110-114
15288120-4	2004	Ionomycin induced citrulline and cGMP formation partially through phosphorylation of endothelial NO synthase (eNOS) at its serine residue 1177, which was mediated mainly by calmodulin-dependent kinase II.	Serine	123-129	nitric oxide synthase 3	Homo sapiens	110-114
15288120-5	2004	Preincubation of cells with alpha-tocopherol or trolox increased eNOS activity in a concentration-dependent manner without changing eNOS expression.	alpha-Tocopherol	28-44	nitric oxide synthase 3	Homo sapiens	65-69
15288120-5	2004	Preincubation of cells with alpha-tocopherol or trolox increased eNOS activity in a concentration-dependent manner without changing eNOS expression.	6-hydroxy-2,5,7,8-tetramethylchroman-2-carboxylic acid	48-54	nitric oxide synthase 3	Homo sapiens	65-69
15288120-6	2004	The effect of the water-soluble trolox was due to chemical stabilization of the eNOS cofactor tetrahydrobiopterin.	Water	18-23	nitric oxide synthase 3	Homo sapiens	80-84
15288120-6	2004	The effect of the water-soluble trolox was due to chemical stabilization of the eNOS cofactor tetrahydrobiopterin.	6-hydroxy-2,5,7,8-tetramethylchroman-2-carboxylic acid	32-38	nitric oxide synthase 3	Homo sapiens	80-84
15288120-6	2004	The effect of the water-soluble trolox was due to chemical stabilization of the eNOS cofactor tetrahydrobiopterin.	sapropterin	94-113	nitric oxide synthase 3	Homo sapiens	80-84
15288120-7	2004	On the contrary, alpha-tocopherol, located mainly in cellular membranes, did not affect tetrahydrobiopterin but increased ionomycin-induced eNOS phosphorylation at serine 1177.	alpha-Tocopherol	17-33	nitric oxide synthase 3	Homo sapiens	140-144
15288120-7	2004	On the contrary, alpha-tocopherol, located mainly in cellular membranes, did not affect tetrahydrobiopterin but increased ionomycin-induced eNOS phosphorylation at serine 1177.	Ionomycin	122-131	nitric oxide synthase 3	Homo sapiens	140-144
15288120-7	2004	On the contrary, alpha-tocopherol, located mainly in cellular membranes, did not affect tetrahydrobiopterin but increased ionomycin-induced eNOS phosphorylation at serine 1177.	Serine	164-170	nitric oxide synthase 3	Homo sapiens	140-144
15288120-8	2004	The effects of alpha-tocopherol on citrulline and cGMP formation and eNOS phosphorylation were amplified by co-incubation with ascorbate, which is suggested to regenerate oxidized alpha-tocopherol and to act synergistically with alpha-tocopherol.	Ascorbic Acid	127-136	nitric oxide synthase 3	Homo sapiens	69-73
15288120-8	2004	The effects of alpha-tocopherol on citrulline and cGMP formation and eNOS phosphorylation were amplified by co-incubation with ascorbate, which is suggested to regenerate oxidized alpha-tocopherol and to act synergistically with alpha-tocopherol.	alpha-Tocopherol	180-196	nitric oxide synthase 3	Homo sapiens	69-73
15283697-1	2004	In this issue of Clinical Science, Agema and co-workers report the results of a genetic association study of eNOS (endothelial nitric oxide synthase) gene polymorphisms (-786T --&gt; C, intron 4b --&gt; a and Glu298 --&gt; Asp) in patients with angiographic CAD (coronary artery disease), and/or prior MI (myocardial infarction) and a group of healthy population-based controls.	Aspartic Acid	223-226	nitric oxide synthase 3	Homo sapiens	115-148
15288120-8	2004	The effects of alpha-tocopherol on citrulline and cGMP formation and eNOS phosphorylation were amplified by co-incubation with ascorbate, which is suggested to regenerate oxidized alpha-tocopherol and to act synergistically with alpha-tocopherol.	alpha-Tocopherol	180-196	nitric oxide synthase 3	Homo sapiens	69-73
15136572-0	2004	Targeting of endothelial nitric-oxide synthase to the cytoplasmic face of the Golgi complex or plasma membrane regulates Akt- versus calcium-dependent mechanisms for nitric oxide release.	Calcium	133-140	nitric oxide synthase 3	Homo sapiens	13-46
15299097-1	2004	BACKGROUND: Nitric oxide (NO) synthesized by endothelial cell NO synthase (ecNOS) is a potent regulator of intrarenal haemodynamics.	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	75-80
15351621-10	2004	RESULTS: The least expression of endothelial NOS (eNOS) and inducible NOS (iNOS) in HCSMCs was observed in cells exposed to 27 mM glucose alone.	Glucose	130-137	nitric oxide synthase 3	Homo sapiens	33-48
15351621-10	2004	RESULTS: The least expression of endothelial NOS (eNOS) and inducible NOS (iNOS) in HCSMCs was observed in cells exposed to 27 mM glucose alone.	Glucose	130-137	nitric oxide synthase 3	Homo sapiens	50-54
15256611-2	2004	In the arterial wall, redox imbalance and oxidation of tetrahydrobiopterin (BH4) uncouples endothelial nitric oxide synthase (eNOS).	sapropterin	55-74	nitric oxide synthase 3	Homo sapiens	91-124
15256611-2	2004	In the arterial wall, redox imbalance and oxidation of tetrahydrobiopterin (BH4) uncouples endothelial nitric oxide synthase (eNOS).	sapropterin	76-79	nitric oxide synthase 3	Homo sapiens	91-124
15356084-5	2004	In vitro, DHEA increased EC expression of endothelial nitric oxide synthase and activity of extracellular signal-regulated kinase 1/2.	Dehydroepiandrosterone	10-14	nitric oxide synthase 3	Homo sapiens	42-75
15123766-1	2004	Nitric oxide (NO) produced by endothelial nitric-oxide synthase (eNOS) represents an antithrombotic and anti-atherosclerotic principle in the vasculature.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	30-63
15123766-1	2004	Nitric oxide (NO) produced by endothelial nitric-oxide synthase (eNOS) represents an antithrombotic and anti-atherosclerotic principle in the vasculature.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	65-69
15123766-9	2004	Interestingly, the flavonoids luteolin and cynaroside increased eNOS promoter activity and eNOS mRNA expression, whereas the caffeoylquinic acids cynarin and chlorogenic acid were without effect.	Flavonoids	19-29	nitric oxide synthase 3	Homo sapiens	64-68
15123766-9	2004	Interestingly, the flavonoids luteolin and cynaroside increased eNOS promoter activity and eNOS mRNA expression, whereas the caffeoylquinic acids cynarin and chlorogenic acid were without effect.	Flavonoids	19-29	nitric oxide synthase 3	Homo sapiens	91-95
15123766-9	2004	Interestingly, the flavonoids luteolin and cynaroside increased eNOS promoter activity and eNOS mRNA expression, whereas the caffeoylquinic acids cynarin and chlorogenic acid were without effect.	Luteolin	30-38	nitric oxide synthase 3	Homo sapiens	64-68
15123766-9	2004	Interestingly, the flavonoids luteolin and cynaroside increased eNOS promoter activity and eNOS mRNA expression, whereas the caffeoylquinic acids cynarin and chlorogenic acid were without effect.	Luteolin	30-38	nitric oxide synthase 3	Homo sapiens	91-95
15123766-9	2004	Interestingly, the flavonoids luteolin and cynaroside increased eNOS promoter activity and eNOS mRNA expression, whereas the caffeoylquinic acids cynarin and chlorogenic acid were without effect.	luteolin-7-glucoside	43-53	nitric oxide synthase 3	Homo sapiens	64-68
15123766-9	2004	Interestingly, the flavonoids luteolin and cynaroside increased eNOS promoter activity and eNOS mRNA expression, whereas the caffeoylquinic acids cynarin and chlorogenic acid were without effect.	luteolin-7-glucoside	43-53	nitric oxide synthase 3	Homo sapiens	91-95
15123766-11	2004	Artichoke flavonoids are likely to represent the active ingredients mediating eNOS up-regulation.	Flavonoids	10-20	nitric oxide synthase 3	Homo sapiens	78-82
15082754-3	2004	Activated Akt phosphorylates human eNOS at serine 1177 and subsequently increases NOS activity.	Serine	43-49	nitric oxide synthase 3	Homo sapiens	35-39
15276426-3	2004	Nitric oxide (NO), formed by endothelial NO synthase (eNOS), plays a crucial role in the vascular system.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	54-58
15276426-4	2004	Decreased availability of biologically active NO in the endothelium is implicated in the pathophysiology of several vascular diseases and inhibition of eNOS by arsenic is one of the proposed mechanism s for arsenic-induced vascular diseases.	Arsenic	160-167	nitric oxide synthase 3	Homo sapiens	152-156
15276426-4	2004	Decreased availability of biologically active NO in the endothelium is implicated in the pathophysiology of several vascular diseases and inhibition of eNOS by arsenic is one of the proposed mechanism s for arsenic-induced vascular diseases.	Arsenic	207-214	nitric oxide synthase 3	Homo sapiens	152-156
15166218-0	2004	Three different oxygen-induced radical species in endothelial nitric-oxide synthase oxygenase domain under regulation by L-arginine and tetrahydrobiopterin.	Oxygen	16-22	nitric oxide synthase 3	Homo sapiens	50-83
15166218-0	2004	Three different oxygen-induced radical species in endothelial nitric-oxide synthase oxygenase domain under regulation by L-arginine and tetrahydrobiopterin.	Arginine	121-131	nitric oxide synthase 3	Homo sapiens	50-83
15166218-0	2004	Three different oxygen-induced radical species in endothelial nitric-oxide synthase oxygenase domain under regulation by L-arginine and tetrahydrobiopterin.	sapropterin	136-155	nitric oxide synthase 3	Homo sapiens	50-83
15231445-6	2004	Platelet endothelial NO synthase (eNOS) activity was examined through the conversion of l-[(14)C]arginine to l-[(14)C]citrulline.	l-[(14)c]arginine	88-105	nitric oxide synthase 3	Homo sapiens	34-38
15136572-0	2004	Targeting of endothelial nitric-oxide synthase to the cytoplasmic face of the Golgi complex or plasma membrane regulates Akt- versus calcium-dependent mechanisms for nitric oxide release.	Nitric Oxide	166-178	nitric oxide synthase 3	Homo sapiens	13-46
15231445-6	2004	Platelet endothelial NO synthase (eNOS) activity was examined through the conversion of l-[(14)C]arginine to l-[(14)C]citrulline.	l-[(14)c]citrulline	109-128	nitric oxide synthase 3	Homo sapiens	34-38
15183461-3	2004	In addition to the rapid effect, we have also found that the eNOS mRNA and protein expression were augmented in HUVECs treated with PAHs at concentration as low as 0.1 microM for 24 h. These effects were abolished when the HUVECs were pretreated with the BAPTA, NiCl(2) and SKF96365, as well as SKF525A.	Polycyclic Aromatic Hydrocarbons	132-136	nitric oxide synthase 3	Homo sapiens	61-65
15183461-3	2004	In addition to the rapid effect, we have also found that the eNOS mRNA and protein expression were augmented in HUVECs treated with PAHs at concentration as low as 0.1 microM for 24 h. These effects were abolished when the HUVECs were pretreated with the BAPTA, NiCl(2) and SKF96365, as well as SKF525A.	1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid	255-260	nitric oxide synthase 3	Homo sapiens	61-65
15183461-3	2004	In addition to the rapid effect, we have also found that the eNOS mRNA and protein expression were augmented in HUVECs treated with PAHs at concentration as low as 0.1 microM for 24 h. These effects were abolished when the HUVECs were pretreated with the BAPTA, NiCl(2) and SKF96365, as well as SKF525A.	nicl	262-266	nitric oxide synthase 3	Homo sapiens	61-65
15183461-3	2004	In addition to the rapid effect, we have also found that the eNOS mRNA and protein expression were augmented in HUVECs treated with PAHs at concentration as low as 0.1 microM for 24 h. These effects were abolished when the HUVECs were pretreated with the BAPTA, NiCl(2) and SKF96365, as well as SKF525A.	1-(2-(3-(4-methoxyphenyl)propoxy)-4-methoxyphenylethyl)-1H-imidazole	274-282	nitric oxide synthase 3	Homo sapiens	61-65
15183461-3	2004	In addition to the rapid effect, we have also found that the eNOS mRNA and protein expression were augmented in HUVECs treated with PAHs at concentration as low as 0.1 microM for 24 h. These effects were abolished when the HUVECs were pretreated with the BAPTA, NiCl(2) and SKF96365, as well as SKF525A.	Proadifen	295-302	nitric oxide synthase 3	Homo sapiens	61-65
15183461-4	2004	Our results revealed that, for the first time, PAHs induce the activation of eNOS and enhance eNOS protein expression in HUVECs both in a Ca(2+)-dependent manner.	Polycyclic Aromatic Hydrocarbons	47-51	nitric oxide synthase 3	Homo sapiens	77-81
15183461-4	2004	Our results revealed that, for the first time, PAHs induce the activation of eNOS and enhance eNOS protein expression in HUVECs both in a Ca(2+)-dependent manner.	Polycyclic Aromatic Hydrocarbons	47-51	nitric oxide synthase 3	Homo sapiens	94-98
15295390-4	2004	The eNOS activity was determined in the samples by the conversion of (14)C-L-arginine to (14)C-L-citrulline, and the eNOS concentration was determined by a human eNOS immunoassay.	(14)c-l-arginine	69-85	nitric oxide synthase 3	Homo sapiens	4-8
15211444-1	2004	BACKGROUND: Synthesis of nitric oxide by endothelial nitric oxide synthase (ENOS) plays a key role in the atherosclerotic process.	Nitric Oxide	25-37	nitric oxide synthase 3	Homo sapiens	41-74
15211444-1	2004	BACKGROUND: Synthesis of nitric oxide by endothelial nitric oxide synthase (ENOS) plays a key role in the atherosclerotic process.	Nitric Oxide	25-37	nitric oxide synthase 3	Homo sapiens	76-80
15295390-4	2004	The eNOS activity was determined in the samples by the conversion of (14)C-L-arginine to (14)C-L-citrulline, and the eNOS concentration was determined by a human eNOS immunoassay.	(14)c-l-citrulline	89-107	nitric oxide synthase 3	Homo sapiens	4-8
15224139-5	2004	Therefore, the present study was performed on cultured primary porcine pulmonary artery endothelial cells (PAECs) to investigate the effects of histamine on eNOS gene expression, and to explore the role of CaMK II in eNOS gene expression.	Histamine	144-153	nitric oxide synthase 3	Homo sapiens	157-161
15240653-3	2004	Recently, we found that human endothelial cells obtained from carriers of the Arg(972) IRS-1 polymorphism exhibited reduced eNOS expression in response to chronic exposure to insulin.	Arginine	78-81	nitric oxide synthase 3	Homo sapiens	124-128
15219988-0	2004	CO exchange of the oxyferrous complexes of endothelial nitric-oxide synthase oxygenase domain in the presence of 4-amino-tetrahydrobiopterin.	4-amino-tetrahydrobiopterin	113-140	nitric oxide synthase 3	Homo sapiens	43-76
15335153-11	2004	HPMC expressed eNOS (NOSIII) when grown in L-arginine-supplemented medium, shown by immunocytochemistry and by reverse transcriptase-polymer chain reaction.	Arginine	43-53	nitric oxide synthase 3	Homo sapiens	21-27
15224139-7	2004	The results showed that histamine upregulated eNOS mRNA and protein levels in a concentration- and time-dependent manner.	Histamine	24-33	nitric oxide synthase 3	Homo sapiens	46-50
15224139-8	2004	Incubation with 10 micromol/L histamine for 24 h could increase eNOS mRNA and protein level to 160.8+/-12.2% (P&lt;0.05) and 136.2+/-11.2% (P&lt;0.05), respectively, of the control values.	Histamine	30-39	nitric oxide synthase 3	Homo sapiens	64-68
15224139-11	2004	The results suggested that eNOS gene promoter activity was enhanced to 148.2+/-33.7% (P&lt;0.05) of the control after PAECs were incubated with 10 micromol/L histamine for 24 h. The nitrite and nitrate content in culture media measured by colorimetric method after incubation with 10 micromol/L histamine for 24 h indicated that the NO production in PAECs was increased.	Histamine	158-167	nitric oxide synthase 3	Homo sapiens	27-31
15224139-11	2004	The results suggested that eNOS gene promoter activity was enhanced to 148.2+/-33.7% (P&lt;0.05) of the control after PAECs were incubated with 10 micromol/L histamine for 24 h. The nitrite and nitrate content in culture media measured by colorimetric method after incubation with 10 micromol/L histamine for 24 h indicated that the NO production in PAECs was increased.	Nitrites	182-189	nitric oxide synthase 3	Homo sapiens	27-31
15224139-11	2004	The results suggested that eNOS gene promoter activity was enhanced to 148.2+/-33.7% (P&lt;0.05) of the control after PAECs were incubated with 10 micromol/L histamine for 24 h. The nitrite and nitrate content in culture media measured by colorimetric method after incubation with 10 micromol/L histamine for 24 h indicated that the NO production in PAECs was increased.	Nitrates	194-201	nitric oxide synthase 3	Homo sapiens	27-31
15224139-11	2004	The results suggested that eNOS gene promoter activity was enhanced to 148.2+/-33.7% (P&lt;0.05) of the control after PAECs were incubated with 10 micromol/L histamine for 24 h. The nitrite and nitrate content in culture media measured by colorimetric method after incubation with 10 micromol/L histamine for 24 h indicated that the NO production in PAECs was increased.	Histamine	295-304	nitric oxide synthase 3	Homo sapiens	27-31
15224139-12	2004	These results suggest that histamine up-regulates eNOS gene transcription and enhances NO production in PAECs by a signaling pathway involving CaMK II, which might be one of the mechanisms of histamine modulating pulmonary vascular tone.	Histamine	27-36	nitric oxide synthase 3	Homo sapiens	50-54
15224139-12	2004	These results suggest that histamine up-regulates eNOS gene transcription and enhances NO production in PAECs by a signaling pathway involving CaMK II, which might be one of the mechanisms of histamine modulating pulmonary vascular tone.	Histamine	192-201	nitric oxide synthase 3	Homo sapiens	50-54
15136061-8	2004	We propose that hyperhomocysteinemia in MTHFR 677TT homozygote smokers is the consequence of mild intracellular folate deficiency caused by a smoking-related reduction of NOS3 activity that is exacerbated when serum folate is low.	Folic Acid	112-118	nitric oxide synthase 3	Homo sapiens	171-175
15168725-1	2004	In endothelial cells nitric oxide (NO) is synthesized by endothelial-nitric oxide synthase (e-NOS), constitutively expressed and encoded by a 26-exon gene, located on chromosome 7q35-36.	Nitric Oxide	21-33	nitric oxide synthase 3	Homo sapiens	57-90
14992685-4	2004	In the present study, we investigated the ability of 7-oxocholesterol and LPC to regulate the activation of eNOS (endothelial nitric oxide synthase) and cPLA2 (cytosolic phospholipase A2) that synthesize two essential factors for vascular wall integrity, NO (nitric oxide) and arachidonic acid.	7-ketocholesterol	53-69	nitric oxide synthase 3	Homo sapiens	114-147
14992685-4	2004	In the present study, we investigated the ability of 7-oxocholesterol and LPC to regulate the activation of eNOS (endothelial nitric oxide synthase) and cPLA2 (cytosolic phospholipase A2) that synthesize two essential factors for vascular wall integrity, NO (nitric oxide) and arachidonic acid.	Lysophosphatidylcholines	74-77	nitric oxide synthase 3	Homo sapiens	114-147
14992685-4	2004	In the present study, we investigated the ability of 7-oxocholesterol and LPC to regulate the activation of eNOS (endothelial nitric oxide synthase) and cPLA2 (cytosolic phospholipase A2) that synthesize two essential factors for vascular wall integrity, NO (nitric oxide) and arachidonic acid.	Arachidonic Acid	277-293	nitric oxide synthase 3	Homo sapiens	114-147
15073390-9	2004	CONCLUSIONS: The eNOS Glu298--&gt;Asp polymorphism may be related to early atherogenesis.	Aspartic Acid	34-37	nitric oxide synthase 3	Homo sapiens	17-21
15158908-5	2004	In addition, we demonstrate that high concentrations of magnesium did not modulate the levels of plasminogen activator inhibitor-1, but enhanced the synthesis of nitric oxide, in part through the up-regulation of endothelial nitric oxide synthase.	Magnesium	56-65	nitric oxide synthase 3	Homo sapiens	213-246
15158908-5	2004	In addition, we demonstrate that high concentrations of magnesium did not modulate the levels of plasminogen activator inhibitor-1, but enhanced the synthesis of nitric oxide, in part through the up-regulation of endothelial nitric oxide synthase.	Nitric Oxide	162-174	nitric oxide synthase 3	Homo sapiens	213-246
15134582-8	2004	This folate shuttle facilitates the important recoupling of the uncoupled endothelial nitric oxide synthase enzyme reaction and may restore the synthesis of the omnipotent endothelial nitric oxide to the vasculature.	Folic Acid	5-11	nitric oxide synthase 3	Homo sapiens	74-107
15228081-1	2004	The endothelial type (NOS-3) of three isoforms of nitric oxide (NO) synthase occurs in porcine oocytes and granulosa cells, but the regulation of NO synthesis in oocytes remains unknown.	Nitric Oxide	50-62	nitric oxide synthase 3	Homo sapiens	22-27
15069547-0	2004	Tyrosine phosphorylation of NOS3 in a breast cancer cell line and Src-transformed cells.	Tyrosine	0-8	nitric oxide synthase 3	Homo sapiens	28-32
15069547-1	2004	We investigated the tyrosine phosphorylation of NOS3 by active Src.	Tyrosine	20-28	nitric oxide synthase 3	Homo sapiens	48-52
15069547-2	2004	In a cell line derived from human breast cancer, BT474, we found activation of c-Src and tyrosine phosphorylation of NOS3.	bt474	49-54	nitric oxide synthase 3	Homo sapiens	117-121
15069547-2	2004	In a cell line derived from human breast cancer, BT474, we found activation of c-Src and tyrosine phosphorylation of NOS3.	Tyrosine	89-97	nitric oxide synthase 3	Homo sapiens	117-121
15069547-3	2004	Phosphorylation of NOS3 was suppressed by treatment of BT474 with PP1, an Src kinase inhibitor, in a dose-dependent manner, suggesting that phosphorylation of NOS3 is catalyzed by active c-Src.	bt474	55-60	nitric oxide synthase 3	Homo sapiens	19-23
15069547-3	2004	Phosphorylation of NOS3 was suppressed by treatment of BT474 with PP1, an Src kinase inhibitor, in a dose-dependent manner, suggesting that phosphorylation of NOS3 is catalyzed by active c-Src.	bt474	55-60	nitric oxide synthase 3	Homo sapiens	159-163
14985356-6	2004	Closer examination of ICAM-1-deficient cells revealed decreased Akt Thr(308) and endothelial nitric-oxide synthase Ser(1177) phosphorylation and NO bioavailability, increased actin stress fiber formation, and a lack of distinct cell polarity compared with wild-type endothelium.	Serine	115-118	nitric oxide synthase 3	Homo sapiens	81-114
15063353-2	2004	Evidence supports the importance of nitric oxide derived from endothelial nitric oxide synthase as a vasoprotective substance, and of vascular NAD(P)H oxidase-derived reactive oxygen species as important signaling molecules in vascular cells.	Nitric Oxide	36-48	nitric oxide synthase 3	Homo sapiens	62-95
15063353-3	2004	Recent studies show that dysfunction of endothelial nitric oxide synthase in atherosclerosis generates O(2)(-) rather than nitric oxide, and that upregulation of vascular NAD(P)H oxidase is closely associated with atherosclerotic progression and plaque instability.	o(2)(-)	103-110	nitric oxide synthase 3	Homo sapiens	40-73
15305696-1	2004	Constitutive nitric oxide (NO) is generated by constitutively expressed types of NO-synthase enzymes (NOS-I and -III), being involved in physiological processes such as nervous transmission and vasodilatation.	Nitric Oxide	13-25	nitric oxide synthase 3	Homo sapiens	102-116
15004019-0	2004	Evidence of two distinct oxygen complexes of reduced endothelial nitric oxide synthase.	Oxygen	25-31	nitric oxide synthase 3	Homo sapiens	53-86
15004019-1	2004	Oxygen binding to the oxygenase domain of reduced endothelial nitric oxide synthase (eNOS) results in two distinct species differing in their Soret and visible absorbance maxima and in their capacity to exchange oxygen by CO.	Oxygen	0-6	nitric oxide synthase 3	Homo sapiens	50-83
15004019-1	2004	Oxygen binding to the oxygenase domain of reduced endothelial nitric oxide synthase (eNOS) results in two distinct species differing in their Soret and visible absorbance maxima and in their capacity to exchange oxygen by CO.	Oxygen	22-28	nitric oxide synthase 3	Homo sapiens	50-83
15004019-1	2004	Oxygen binding to the oxygenase domain of reduced endothelial nitric oxide synthase (eNOS) results in two distinct species differing in their Soret and visible absorbance maxima and in their capacity to exchange oxygen by CO.	Carbon Monoxide	222-224	nitric oxide synthase 3	Homo sapiens	50-83
15212666-6	2004	METHOD: The aim of our study was to investigate, whether two polymorphisms in the AT1R and NOS3 genes shown to result in maternal vasoconstriction are associated with an increased risk for RSA.	rabbit sperm membrane autoantigen	189-192	nitric oxide synthase 3	Homo sapiens	91-95
15099281-8	2004	CONCLUSION: The results of the present study demonstrate that the eNOS 894 G &gt; T variation interacts with elevated tHcy levels, leading to an increased risk of recurrent thrombotic events.	thcy	118-122	nitric oxide synthase 3	Homo sapiens	66-70
14751809-5	2004	Our data show that treatment with fenofibrate for 48 hours resulted in an increase in eNOS activity.	Fenofibrate	34-45	nitric oxide synthase 3	Homo sapiens	86-90
14751809-7	2004	Fenofibrate also increased eNOS protein as well as its mRNA levels.	Fenofibrate	0-11	nitric oxide synthase 3	Homo sapiens	27-31
14751809-8	2004	RU486, which has been shown to antagonize PPARalpha action, inhibited the fenofibrate-induced upregulation of eNOS protein expression.	Mifepristone	0-5	nitric oxide synthase 3	Homo sapiens	110-114
14751809-8	2004	RU486, which has been shown to antagonize PPARalpha action, inhibited the fenofibrate-induced upregulation of eNOS protein expression.	Fenofibrate	74-85	nitric oxide synthase 3	Homo sapiens	110-114
14751809-9	2004	WY14643 and bezafibrate also increased eNOS protein levels, whereas rosiglitazone did not.	pirinixic acid	0-7	nitric oxide synthase 3	Homo sapiens	39-43
14751809-9	2004	WY14643 and bezafibrate also increased eNOS protein levels, whereas rosiglitazone did not.	Bezafibrate	12-23	nitric oxide synthase 3	Homo sapiens	39-43
14751809-11	2004	Actinomycin D studies demonstrated that the half-life of eNOS mRNA increased with fenofibrate treatment.	Dactinomycin	0-13	nitric oxide synthase 3	Homo sapiens	57-61
14751809-11	2004	Actinomycin D studies demonstrated that the half-life of eNOS mRNA increased with fenofibrate treatment.	Fenofibrate	82-93	nitric oxide synthase 3	Homo sapiens	57-61
15168725-1	2004	In endothelial cells nitric oxide (NO) is synthesized by endothelial-nitric oxide synthase (e-NOS), constitutively expressed and encoded by a 26-exon gene, located on chromosome 7q35-36.	Nitric Oxide	21-33	nitric oxide synthase 3	Homo sapiens	92-97
15168725-2	2004	The prevalence of the T rare variant of the G894T polymorphism in exon 7 of the e-NOS gene (Glu--&gt;Asp amino acid substitution) has been reported to be significantly higher in patients with coronary spasm and coronary artery disease.	asp amino acid	101-115	nitric oxide synthase 3	Homo sapiens	80-85
15039923-3	2004	A common variant of the gene for endothelial nitric oxide synthase (NOS3 G894T) was recently added to this group of NTD candidate genes, based on a report demonstrating that homozygosity for the T allele of this variant is associated with increased homocysteine levels in normal adult populations.	Homocysteine	249-261	nitric oxide synthase 3	Homo sapiens	33-66
15095278-5	2004	In accordance with these temporal effects, reduced bone mineral density, bone microhardness, and osteocalcin expression could be restored to normal, wild-type values after 21 days in vivo administration of the nitric oxide donor glyceryl trinitrate to 4-week-old endothelial nitric oxide synthase knockout mice, but there was no significant effect in older animals.	Nitric Oxide	210-222	nitric oxide synthase 3	Homo sapiens	263-296
15095278-5	2004	In accordance with these temporal effects, reduced bone mineral density, bone microhardness, and osteocalcin expression could be restored to normal, wild-type values after 21 days in vivo administration of the nitric oxide donor glyceryl trinitrate to 4-week-old endothelial nitric oxide synthase knockout mice, but there was no significant effect in older animals.	Nitroglycerin	229-248	nitric oxide synthase 3	Homo sapiens	263-296
15016421-0	2004	Poorer cognitive performance in humans with mild cognitive impairment carrying the T variant of the Glu/Asp NOS3 polymorphism.	Glutamic Acid	100-103	nitric oxide synthase 3	Homo sapiens	108-112
15016421-0	2004	Poorer cognitive performance in humans with mild cognitive impairment carrying the T variant of the Glu/Asp NOS3 polymorphism.	Aspartic Acid	104-107	nitric oxide synthase 3	Homo sapiens	108-112
15016421-2	2004	The endothelial nitric oxide synthase (NOS3) gene encodes endothelial NOS, an enzyme that regulates the production of the vasodilatory nitric oxide associated with the cerebral small vessel pathology observed in early AD.	Nitric Oxide	16-28	nitric oxide synthase 3	Homo sapiens	39-43
15016421-2	2004	The endothelial nitric oxide synthase (NOS3) gene encodes endothelial NOS, an enzyme that regulates the production of the vasodilatory nitric oxide associated with the cerebral small vessel pathology observed in early AD.	Nitric Oxide	16-28	nitric oxide synthase 3	Homo sapiens	58-73
15016421-3	2004	We studied the distribution of genotype and allele frequencies of the NOS3 Glu/Asp polymorphism in a sample of 62 MCI subjects and 136 controls.	Glutamic Acid	75-78	nitric oxide synthase 3	Homo sapiens	70-74
15016421-3	2004	We studied the distribution of genotype and allele frequencies of the NOS3 Glu/Asp polymorphism in a sample of 62 MCI subjects and 136 controls.	Aspartic Acid	79-82	nitric oxide synthase 3	Homo sapiens	70-74
14656731-1	2004	Nitric oxide (NO), produced by endothelial nitric oxide synthase (eNOS), is a key signaling molecule in vascular homeostasis.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	31-64
14656742-6	2004	For instance, eNOS transcription rates increase in response to lysophosphatidylcholine, shear stress, and TGF-beta, among others.	Lysophosphatidylcholines	63-86	nitric oxide synthase 3	Homo sapiens	14-18
15115168-1	2004	OBJECTIVES: Polymorphisms of the angiotensin converting enzyme (ACE) and endothelial nitric oxide (eNOS) genes have been implicated in asthma pathogenesis.	Nitric Oxide	85-97	nitric oxide synthase 3	Homo sapiens	99-103
14656731-0	2004	Regulation of endothelial nitric oxide synthase by tetrahydrobiopterin in vascular disease.	sapropterin	51-70	nitric oxide synthase 3	Homo sapiens	14-47
15370068-4	2004	The authors recently discovered that physiologically relevant concentrations of ONOO- oxidize the zinc thiolate center in endothelial nitric oxide synthase (eNOS).	onoo	80-84	nitric oxide synthase 3	Homo sapiens	122-155
15370068-4	2004	The authors recently discovered that physiologically relevant concentrations of ONOO- oxidize the zinc thiolate center in endothelial nitric oxide synthase (eNOS).	zinc thiolate	98-111	nitric oxide synthase 3	Homo sapiens	122-155
15039923-3	2004	A common variant of the gene for endothelial nitric oxide synthase (NOS3 G894T) was recently added to this group of NTD candidate genes, based on a report demonstrating that homozygosity for the T allele of this variant is associated with increased homocysteine levels in normal adult populations.	Homocysteine	249-261	nitric oxide synthase 3	Homo sapiens	68-72
14744923-9	2004	In normal placenta, adequate concentration of l-arginine orients ecNOS toward NO.	Arginine	46-56	nitric oxide synthase 3	Homo sapiens	65-70
14988829-2	2004	We hypothesized that simvastatin, which enhances Akt-dependent endothelial nitric oxide synthase phosphorylation, may increase hepatic nitric oxide release and decrease hepatic resistance in patients with cirrhosis and portal hypertension.	Simvastatin	21-32	nitric oxide synthase 3	Homo sapiens	63-96
14966047-8	2004	CONCLUSIONS: The non-BB genotype of the ecNOS 4a/4b gene polymorphism is a protective factor against the development of ACS.	boeravinone B	21-23	nitric oxide synthase 3	Homo sapiens	40-45
14966047-9	2004	The GG genotype of the ecNOS Glu298Asp polymorphism exerts a benefit in addition to the non-BB genotype in the Korean population.	boeravinone B	92-94	nitric oxide synthase 3	Homo sapiens	23-28
14980706-0	2004	L-Homocysteine and L-homocystine stereospecifically induce endothelial nitric oxide synthase-dependent lipid peroxidation in endothelial cells.	Homocysteine	0-14	nitric oxide synthase 3	Homo sapiens	59-92
14980706-0	2004	L-Homocysteine and L-homocystine stereospecifically induce endothelial nitric oxide synthase-dependent lipid peroxidation in endothelial cells.	Homocystine	19-32	nitric oxide synthase 3	Homo sapiens	59-92
14980706-7	2004	Mechanistically, the pro-oxidant effect of homocysteine appears to involve endothelial nitric oxide synthase (eNOS), as it is blocked by the eNOS inhibitor L-N(G)-nitroarginine methyl ester.	Homocysteine	43-55	nitric oxide synthase 3	Homo sapiens	75-108
14980706-7	2004	Mechanistically, the pro-oxidant effect of homocysteine appears to involve endothelial nitric oxide synthase (eNOS), as it is blocked by the eNOS inhibitor L-N(G)-nitroarginine methyl ester.	Homocysteine	43-55	nitric oxide synthase 3	Homo sapiens	110-114
14980706-7	2004	Mechanistically, the pro-oxidant effect of homocysteine appears to involve endothelial nitric oxide synthase (eNOS), as it is blocked by the eNOS inhibitor L-N(G)-nitroarginine methyl ester.	Homocysteine	43-55	nitric oxide synthase 3	Homo sapiens	141-145
14980706-7	2004	Mechanistically, the pro-oxidant effect of homocysteine appears to involve endothelial nitric oxide synthase (eNOS), as it is blocked by the eNOS inhibitor L-N(G)-nitroarginine methyl ester.	l-n(g)-nitroarginine methyl ester	156-189	nitric oxide synthase 3	Homo sapiens	75-108
14980706-7	2004	Mechanistically, the pro-oxidant effect of homocysteine appears to involve endothelial nitric oxide synthase (eNOS), as it is blocked by the eNOS inhibitor L-N(G)-nitroarginine methyl ester.	l-n(g)-nitroarginine methyl ester	156-189	nitric oxide synthase 3	Homo sapiens	110-114
14980706-7	2004	Mechanistically, the pro-oxidant effect of homocysteine appears to involve endothelial nitric oxide synthase (eNOS), as it is blocked by the eNOS inhibitor L-N(G)-nitroarginine methyl ester.	l-n(g)-nitroarginine methyl ester	156-189	nitric oxide synthase 3	Homo sapiens	141-145
14744923-10	2004	In preeclampsia, a lower than normal l-arginine concentration caused by arginase II overexpression redirects ecNOS toward peroxynitrite.	Arginine	37-47	nitric oxide synthase 3	Homo sapiens	109-114
14744923-10	2004	In preeclampsia, a lower than normal l-arginine concentration caused by arginase II overexpression redirects ecNOS toward peroxynitrite.	Peroxynitrous Acid	122-135	nitric oxide synthase 3	Homo sapiens	109-114
15091107-6	2004	of wortmannin, an inhibitor of phosphatidylinositol 3-kinase (PI-3K), significantly inhibited the increases in both eNOS mRNA and its protein with concomitant inhibition of Akt activation.	Wortmannin	3-13	nitric oxide synthase 3	Homo sapiens	116-120
15091107-8	2004	Both eNOS up-regulation and acquisition of ischemic tolerance observed at 3 days after preconditioning ischemia were significantly inhibited by pretreatment with wortmannin.	Wortmannin	162-172	nitric oxide synthase 3	Homo sapiens	5-9
14963277-2	2004	Nitric oxide (NO) synthesized by endothelial nitric oxide synthase (eNOS) is a key mediator of endothelial function.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	33-66
15068229-1	2004	BACKGROUND: Insulin increases endothelial nitric oxide (NO) production by activating endothelial nitric oxide synthase (eNOS) through protein kinase B (Akt)-mediated phosphorylation of serine residue 1179 (p-eNOS serine 1179).	Nitric Oxide	42-54	nitric oxide synthase 3	Homo sapiens	85-118
15068229-1	2004	BACKGROUND: Insulin increases endothelial nitric oxide (NO) production by activating endothelial nitric oxide synthase (eNOS) through protein kinase B (Akt)-mediated phosphorylation of serine residue 1179 (p-eNOS serine 1179).	Serine	185-191	nitric oxide synthase 3	Homo sapiens	85-118
15076784-10	2004	CONCLUSION: Exercise training enhances endothelium-dependent vasorelaxation after 5-FU-induced vasoconstriction, and this may be due, at least in part, to an increase in aortic eNOS protein content and activity.	Fluorouracil	82-86	nitric oxide synthase 3	Homo sapiens	177-181
15068229-1	2004	BACKGROUND: Insulin increases endothelial nitric oxide (NO) production by activating endothelial nitric oxide synthase (eNOS) through protein kinase B (Akt)-mediated phosphorylation of serine residue 1179 (p-eNOS serine 1179).	Serine	213-219	nitric oxide synthase 3	Homo sapiens	85-118
14661033-2	2004	Exposure to hypoxia (pO(2)=10 mmHg) for periods up to 3 h resulted in a time-dependent increase in eNOS protein expression and an early (15 min) and sustained increase in eNOS phosphorylation at Ser-1177.	Serine	195-198	nitric oxide synthase 3	Homo sapiens	171-175
14764132-0	2004	Endothelial nitric oxide synthase expression in neurogenic urinary bladders treated with intravesical resiniferatoxin.	resiniferatoxin	102-117	nitric oxide synthase 3	Homo sapiens	0-33
14764132-1	2004	OBJECTIVE: To investigate endothelial nitric oxide synthase (eNOS) immunoreactivity in bladder biopsies from patients with neurogenic detrusor overactivity (NDO) before and after treatment with intravesical resiniferatoxin, and compare this with control material; the distribution of two other vascular markers, von Willebrand Factor (vWF) and the vascular endothelial growth factor (VEGF), was also studied.	resiniferatoxin	207-222	nitric oxide synthase 3	Homo sapiens	26-59
15005272-1	2004	Shear stress caused by blood flow is a potent physiological stimulus for the generation of nitric oxide (NO) in endothelial cells, which is believed to derive from the up-regulation and post-transcriptional activation of endothelial constitutive NO synthase (ecNOS).	Nitric Oxide	91-103	nitric oxide synthase 3	Homo sapiens	259-264
15049129-7	2004	In addition, the expression of endothelial nitric oxide synthase was strongly induced by Pitavastatin, and was suppressed by mevalonic acid and geranylgeranyl pyrophosphate by Western blot analysis.	pitavastatin	89-101	nitric oxide synthase 3	Homo sapiens	31-64
15049129-7	2004	In addition, the expression of endothelial nitric oxide synthase was strongly induced by Pitavastatin, and was suppressed by mevalonic acid and geranylgeranyl pyrophosphate by Western blot analysis.	Mevalonic Acid	125-139	nitric oxide synthase 3	Homo sapiens	31-64
15049129-7	2004	In addition, the expression of endothelial nitric oxide synthase was strongly induced by Pitavastatin, and was suppressed by mevalonic acid and geranylgeranyl pyrophosphate by Western blot analysis.	geranylgeranyl pyrophosphate	144-172	nitric oxide synthase 3	Homo sapiens	31-64
14983058-6	2004	Exposure of purified human eNOS protein to NO donors or calcium-mediated activation of the enzyme resulted in a shift in eNOS from a predominantly dimeric to a predominantly monomeric enzyme.	Calcium	56-63	nitric oxide synthase 3	Homo sapiens	27-31
14983058-6	2004	Exposure of purified human eNOS protein to NO donors or calcium-mediated activation of the enzyme resulted in a shift in eNOS from a predominantly dimeric to a predominantly monomeric enzyme.	Calcium	56-63	nitric oxide synthase 3	Homo sapiens	121-125
14764132-7	2004	There was a trend to higher eNOS values before treatment in those responding than in those not responding to resiniferatoxin (P = 0.059), and a significant reduction in eNOS immunoreactivity after successful treatment (P = 0.016).	resiniferatoxin	109-124	nitric oxide synthase 3	Homo sapiens	28-32
14764132-10	2004	CONCLUSIONS: The trend for higher eNOS expression in patients with NDO who responded to resiniferatoxin suggests that increased vasculature or vasodilatation in the suburothelium may be necessary for successful intravesical treatment.	resiniferatoxin	88-103	nitric oxide synthase 3	Homo sapiens	34-38
14661033-3	2004	Exposure to hypoxia for 30 min led to a doubling in eNOS activity (control=6.2+/-4.4 vs hypoxia=14.1+/-5.0 fmol cGMP/microg protein, P&lt;0.05) and NO release (control=5.9+/-0.8 vs hypoxia=11.8+/-1.2 nM/microg protein, P&lt;0.05).	Cyclic GMP	112-116	nitric oxide synthase 3	Homo sapiens	52-56
14661033-5	2004	Pretreatment of cells with either 1 microg/ml geldanamycin (a specific inhibitor of Hsp90) or 500 nM wortmannin (a specific PI3 kinase inhibitor) suppressed hypoxia-stimulated Akt and eNOS phosphorylation and significantly attenuated hypoxia-stimulated Hsp90 binding to eNOS.	geldanamycin	46-58	nitric oxide synthase 3	Homo sapiens	184-188
14661033-5	2004	Pretreatment of cells with either 1 microg/ml geldanamycin (a specific inhibitor of Hsp90) or 500 nM wortmannin (a specific PI3 kinase inhibitor) suppressed hypoxia-stimulated Akt and eNOS phosphorylation and significantly attenuated hypoxia-stimulated Hsp90 binding to eNOS.	geldanamycin	46-58	nitric oxide synthase 3	Homo sapiens	270-274
14661033-5	2004	Pretreatment of cells with either 1 microg/ml geldanamycin (a specific inhibitor of Hsp90) or 500 nM wortmannin (a specific PI3 kinase inhibitor) suppressed hypoxia-stimulated Akt and eNOS phosphorylation and significantly attenuated hypoxia-stimulated Hsp90 binding to eNOS.	Wortmannin	101-111	nitric oxide synthase 3	Homo sapiens	184-188
14661033-5	2004	Pretreatment of cells with either 1 microg/ml geldanamycin (a specific inhibitor of Hsp90) or 500 nM wortmannin (a specific PI3 kinase inhibitor) suppressed hypoxia-stimulated Akt and eNOS phosphorylation and significantly attenuated hypoxia-stimulated Hsp90 binding to eNOS.	Wortmannin	101-111	nitric oxide synthase 3	Homo sapiens	270-274
14661033-6	2004	Both eNOS activity and NO production were inhibited by geldanamycin and wortmannin.	geldanamycin	55-67	nitric oxide synthase 3	Homo sapiens	5-9
14661033-6	2004	Both eNOS activity and NO production were inhibited by geldanamycin and wortmannin.	Wortmannin	72-82	nitric oxide synthase 3	Homo sapiens	5-9
14742696-5	2004	Therefore, we used either ERalpha or ERbeta expression vector to investigate the effect of 17beta-estradiol treatment on eNOS promoter activity using eNOS promoter/luciferase vector in cultured human myometrial cells.	Estradiol	91-107	nitric oxide synthase 3	Homo sapiens	121-125
14570928-8	2004	While NFkappaB activation is generally viewed as a proinflammatory stimulus, the current data indicate that its transient activation by shear may increase expression of eNOS, which via production of nitric oxide could convey anti-inflammatory and anti-atherosclerotic properties.	Nitric Oxide	199-211	nitric oxide synthase 3	Homo sapiens	169-173
14742696-6	2004	17beta-estradiol treatment significantly augmented eNOS promoter activity in cells co-transfected with either ERalpha or ERbeta, and this augmentation was dose-dependently suppressed by ICI 182780, an estrogen antagonist.	Estradiol	0-16	nitric oxide synthase 3	Homo sapiens	51-55
15050533-2	2004	We have shown previously that dexamethasone downregulates the expression of the endothelial NO synthase (eNOS) gene in human endothelial cells and in the rat and that this may contribute to the blood pressure-raising effect of the steroid [Proc.	Dexamethasone	30-43	nitric oxide synthase 3	Homo sapiens	105-109
15050533-2	2004	We have shown previously that dexamethasone downregulates the expression of the endothelial NO synthase (eNOS) gene in human endothelial cells and in the rat and that this may contribute to the blood pressure-raising effect of the steroid [Proc.	Steroids	231-238	nitric oxide synthase 3	Homo sapiens	105-109
15106837-0	2004	17 Beta-estradiol regulates nNOS and eNOS activity in the hippocampus.	Estradiol	0-17	nitric oxide synthase 3	Homo sapiens	37-41
15134564-2	2004	NO derives from a) the actions of enzymes, the NO Synthases (NOS), which are constitutives (endothelial NOS (eNOS) and nervous NOS (nNOS)) and generate small amounts of NO and have homeostatic functions: and b) from the actions of inducible NOS (iNOS), which generate large amounts of NO and exert protective actions against noxious agents but also toxic effects (e.g. inhibition of enzymes) through the production of peroxynitrite (ONOO-).	Peroxynitrous Acid	418-431	nitric oxide synthase 3	Homo sapiens	92-107
15218542-5	2004	Among many enzymatic systems that are capable of producing O(2)(*-), NAD(P)H oxidase and uncoupled endothelial NO synthase (eNOS) apparently are the main sources of O(2)(*-) in the endothelial cells.	Superoxides	59-63	nitric oxide synthase 3	Homo sapiens	124-128
15218542-5	2004	Among many enzymatic systems that are capable of producing O(2)(*-), NAD(P)H oxidase and uncoupled endothelial NO synthase (eNOS) apparently are the main sources of O(2)(*-) in the endothelial cells.	Superoxides	165-169	nitric oxide synthase 3	Homo sapiens	124-128
15218542-6	2004	It seems that O(2)(*-) generated by NAD(P)H oxidase may trigger eNOS uncoupling and contribute to the endothelial balance between NO and O(2)(*-).	Superoxides	14-18	nitric oxide synthase 3	Homo sapiens	64-68
15218542-6	2004	It seems that O(2)(*-) generated by NAD(P)H oxidase may trigger eNOS uncoupling and contribute to the endothelial balance between NO and O(2)(*-).	Superoxides	137-141	nitric oxide synthase 3	Homo sapiens	64-68
15777017-2	2004	Superoxide-producing enzymes involved in increased oxidative stress within vascular tissue include NAD(P)H-oxidase, xanthine oxidase and endothelial nitric oxide synthase in an uncoupled state.	Superoxides	0-10	nitric oxide synthase 3	Homo sapiens	137-170
15134564-2	2004	NO derives from a) the actions of enzymes, the NO Synthases (NOS), which are constitutives (endothelial NOS (eNOS) and nervous NOS (nNOS)) and generate small amounts of NO and have homeostatic functions: and b) from the actions of inducible NOS (iNOS), which generate large amounts of NO and exert protective actions against noxious agents but also toxic effects (e.g. inhibition of enzymes) through the production of peroxynitrite (ONOO-).	oxido nitrite	433-438	nitric oxide synthase 3	Homo sapiens	92-107
14597568-9	2004	Activity of eNOS in HPMEC, measured over 48 h, either as the basal production of nitric oxide (NO) or as the accumulation of intracellular cGMP was not detectable.	Nitric Oxide	81-93	nitric oxide synthase 3	Homo sapiens	12-16
15612667-2	2004	The present study was designed to generate a recombinant adenovirus containing the tetracycline (Tet)-regulated endothelial nitric oxide synthase (eNOS) gene and to detect the controllable expression of the gene in esophageal smooth muscle cells (ESMC).	Tetracycline	83-95	nitric oxide synthase 3	Homo sapiens	112-145
15612667-2	2004	The present study was designed to generate a recombinant adenovirus containing the tetracycline (Tet)-regulated endothelial nitric oxide synthase (eNOS) gene and to detect the controllable expression of the gene in esophageal smooth muscle cells (ESMC).	Tetracycline	83-95	nitric oxide synthase 3	Homo sapiens	147-151
15612667-2	2004	The present study was designed to generate a recombinant adenovirus containing the tetracycline (Tet)-regulated endothelial nitric oxide synthase (eNOS) gene and to detect the controllable expression of the gene in esophageal smooth muscle cells (ESMC).	Tetracycline	97-100	nitric oxide synthase 3	Homo sapiens	112-145
15612667-2	2004	The present study was designed to generate a recombinant adenovirus containing the tetracycline (Tet)-regulated endothelial nitric oxide synthase (eNOS) gene and to detect the controllable expression of the gene in esophageal smooth muscle cells (ESMC).	Tetracycline	97-100	nitric oxide synthase 3	Homo sapiens	147-151
15612667-4	2004	Cultured ESMC were coinfected by Adeno-X-TRE-eNOS and regulation virus (Adeno-X Tet-off virus), and the Dox-regulated eNOS expression was detected by RT-PCR and western blot.	Doxycycline	104-107	nitric oxide synthase 3	Homo sapiens	118-122
15612667-8	2004	CONCLUSIONS: A Tet- (or Dox-) regulated recombinant adenovirus carrying eNOS was successfully generated and controllable expression of eNOS in ESMC was achieved, which provides some material for conducting further gene therapy studies with eNOS.	Tetracycline	15-18	nitric oxide synthase 3	Homo sapiens	72-76
15612667-8	2004	CONCLUSIONS: A Tet- (or Dox-) regulated recombinant adenovirus carrying eNOS was successfully generated and controllable expression of eNOS in ESMC was achieved, which provides some material for conducting further gene therapy studies with eNOS.	Tetracycline	15-18	nitric oxide synthase 3	Homo sapiens	135-139
15612667-8	2004	CONCLUSIONS: A Tet- (or Dox-) regulated recombinant adenovirus carrying eNOS was successfully generated and controllable expression of eNOS in ESMC was achieved, which provides some material for conducting further gene therapy studies with eNOS.	Tetracycline	15-18	nitric oxide synthase 3	Homo sapiens	135-139
15612667-8	2004	CONCLUSIONS: A Tet- (or Dox-) regulated recombinant adenovirus carrying eNOS was successfully generated and controllable expression of eNOS in ESMC was achieved, which provides some material for conducting further gene therapy studies with eNOS.	Doxycycline	24-27	nitric oxide synthase 3	Homo sapiens	72-76
15612667-8	2004	CONCLUSIONS: A Tet- (or Dox-) regulated recombinant adenovirus carrying eNOS was successfully generated and controllable expression of eNOS in ESMC was achieved, which provides some material for conducting further gene therapy studies with eNOS.	Doxycycline	24-27	nitric oxide synthase 3	Homo sapiens	135-139
15612667-8	2004	CONCLUSIONS: A Tet- (or Dox-) regulated recombinant adenovirus carrying eNOS was successfully generated and controllable expression of eNOS in ESMC was achieved, which provides some material for conducting further gene therapy studies with eNOS.	Doxycycline	24-27	nitric oxide synthase 3	Homo sapiens	135-139
15612667-8	2004	CONCLUSIONS: A Tet- (or Dox-) regulated recombinant adenovirus carrying eNOS was successfully generated and controllable expression of eNOS in ESMC was achieved, which provides some material for conducting further gene therapy studies with eNOS.	esmc	143-147	nitric oxide synthase 3	Homo sapiens	72-76
15612667-8	2004	CONCLUSIONS: A Tet- (or Dox-) regulated recombinant adenovirus carrying eNOS was successfully generated and controllable expression of eNOS in ESMC was achieved, which provides some material for conducting further gene therapy studies with eNOS.	esmc	143-147	nitric oxide synthase 3	Homo sapiens	135-139
15612667-8	2004	CONCLUSIONS: A Tet- (or Dox-) regulated recombinant adenovirus carrying eNOS was successfully generated and controllable expression of eNOS in ESMC was achieved, which provides some material for conducting further gene therapy studies with eNOS.	esmc	143-147	nitric oxide synthase 3	Homo sapiens	135-139
14597568-9	2004	Activity of eNOS in HPMEC, measured over 48 h, either as the basal production of nitric oxide (NO) or as the accumulation of intracellular cGMP was not detectable.	Cyclic GMP	139-143	nitric oxide synthase 3	Homo sapiens	12-16
15061658-0	2004	Three repeats of CCCCTCC on the pyrimidine-rich sequence in the proximal 5" flanking region are required for efficient transcriptional activity of the human endothelial nitric oxide synthase gene.	pyrimidine	32-42	nitric oxide synthase 3	Homo sapiens	157-190
15061658-5	2004	Dinucleotide-substitution mutants at the repeat sequences reduced their transcriptional activities of the eNOS gene in transient transfection assays as diminishing their abilities to form the complex.	Dinucleoside Phosphates	0-12	nitric oxide synthase 3	Homo sapiens	106-110
14718923-1	2004	Three nitric oxide synthase (NOS) isoforms, eNOS, nNOS and iNOS, generate nitric oxide (NO) crucial to the cardiovascular, nervous and host defense systems, respectively.	Nitric Oxide	6-18	nitric oxide synthase 3	Homo sapiens	44-48
14718923-3	2004	Crystal structures of nNOS-selective dipeptide inhibitors in complex with both nNOS and eNOS were solved and the inhibitors were found to adopt a curled conformation in nNOS but an extended conformation in eNOS.	Dipeptides	37-46	nitric oxide synthase 3	Homo sapiens	88-92
14718923-3	2004	Crystal structures of nNOS-selective dipeptide inhibitors in complex with both nNOS and eNOS were solved and the inhibitors were found to adopt a curled conformation in nNOS but an extended conformation in eNOS.	Dipeptides	37-46	nitric oxide synthase 3	Homo sapiens	206-210
14718923-6	2004	Therefore, a single-residue difference is responsible for more than two orders of magnitude selectivity in inhibition of nNOS over eNOS by L-N(omega)-nitroarginine-containing dipeptide inhibitors.	l-n(omega)-nitroarginine	139-163	nitric oxide synthase 3	Homo sapiens	131-135
14718923-6	2004	Therefore, a single-residue difference is responsible for more than two orders of magnitude selectivity in inhibition of nNOS over eNOS by L-N(omega)-nitroarginine-containing dipeptide inhibitors.	Dipeptides	175-184	nitric oxide synthase 3	Homo sapiens	131-135
15740692-7	2004	Thus, the present study describes for the first time the modulation and spatial distribution of eNOS and iNOS expression during the oestrous cycle and early pregnancy, suggesting that ovarian steroids are differently involved in the regulation of each NOS.	Steroids	192-200	nitric oxide synthase 3	Homo sapiens	96-100
15193362-1	2004	Increased shear stress to the endothelium increases activity of endothelial nitric oxide synthase (eNOS) with subsequent release of small quantities (nMol) of nitric oxide (NO) into the circulation.	Nitric Oxide	76-88	nitric oxide synthase 3	Homo sapiens	99-103
15532370-1	2004	AIM: To study association of the complex of polymorphic markers of ACE genes (ACE complex), aldosteron synthetase gene (CYP11B2) and endothelial synthetase of nitric oxide (NOS3) with onset, course and progression of chronic glomerulonephritis (CGN).	Nitric Oxide	159-171	nitric oxide synthase 3	Homo sapiens	173-177
14664902-5	2003	Interestingly, the endothelial nitric oxide synthase may become uncoupled in the presence of high ADMA levels further contributing to the vascular oxidative stress burden.	N,N-dimethylarginine	98-102	nitric oxide synthase 3	Homo sapiens	19-52
15381390-2	2004	Human platelets synthesize nitric oxide (NO) through an endothelial-type NO synthase (ecNOS) activated also by substances enhancing 3",5"-cyclic adenosine monophosphate (cAMP) concentrations, such as catecholamines, beta-adrenoceptor agonists and adenosine.	Nitric Oxide	27-39	nitric oxide synthase 3	Homo sapiens	86-91
15381390-2	2004	Human platelets synthesize nitric oxide (NO) through an endothelial-type NO synthase (ecNOS) activated also by substances enhancing 3",5"-cyclic adenosine monophosphate (cAMP) concentrations, such as catecholamines, beta-adrenoceptor agonists and adenosine.	3",5"-cyclic adenosine monophosphate	132-168	nitric oxide synthase 3	Homo sapiens	86-91
15381390-2	2004	Human platelets synthesize nitric oxide (NO) through an endothelial-type NO synthase (ecNOS) activated also by substances enhancing 3",5"-cyclic adenosine monophosphate (cAMP) concentrations, such as catecholamines, beta-adrenoceptor agonists and adenosine.	Cyclic AMP	170-174	nitric oxide synthase 3	Homo sapiens	86-91
15381390-2	2004	Human platelets synthesize nitric oxide (NO) through an endothelial-type NO synthase (ecNOS) activated also by substances enhancing 3",5"-cyclic adenosine monophosphate (cAMP) concentrations, such as catecholamines, beta-adrenoceptor agonists and adenosine.	Catecholamines	200-214	nitric oxide synthase 3	Homo sapiens	86-91
15381390-2	2004	Human platelets synthesize nitric oxide (NO) through an endothelial-type NO synthase (ecNOS) activated also by substances enhancing 3",5"-cyclic adenosine monophosphate (cAMP) concentrations, such as catecholamines, beta-adrenoceptor agonists and adenosine.	Adenosine	145-154	nitric oxide synthase 3	Homo sapiens	86-91
15381390-3	2004	To verify whether cAMP directly activates ecNOS through the cAMP-dependent protein kinase A (PKA), we evaluated (i) the influence of 8-Br-cAMP, adenosine and forskolin on ecNOS activity and phosphorylation at Ser(1177) and (ii) the effect of PKA inhibition on ecNOS activity.	Cyclic AMP	18-22	nitric oxide synthase 3	Homo sapiens	42-47
15381390-3	2004	To verify whether cAMP directly activates ecNOS through the cAMP-dependent protein kinase A (PKA), we evaluated (i) the influence of 8-Br-cAMP, adenosine and forskolin on ecNOS activity and phosphorylation at Ser(1177) and (ii) the effect of PKA inhibition on ecNOS activity.	Colforsin	158-167	nitric oxide synthase 3	Homo sapiens	171-176
15381390-3	2004	To verify whether cAMP directly activates ecNOS through the cAMP-dependent protein kinase A (PKA), we evaluated (i) the influence of 8-Br-cAMP, adenosine and forskolin on ecNOS activity and phosphorylation at Ser(1177) and (ii) the effect of PKA inhibition on ecNOS activity.	Colforsin	158-167	nitric oxide synthase 3	Homo sapiens	171-176
15381390-8	2004	Platelet exposure to 8-Br-cAMP and forskolin, beside the phosphorylation of the specific PKA substrate VASP, markedly increased the expression of ecNOS protein phosphorylated at Ser(1177).	8-Bromo Cyclic Adenosine Monophosphate	21-30	nitric oxide synthase 3	Homo sapiens	146-151
15381390-8	2004	Platelet exposure to 8-Br-cAMP and forskolin, beside the phosphorylation of the specific PKA substrate VASP, markedly increased the expression of ecNOS protein phosphorylated at Ser(1177).	Colforsin	35-44	nitric oxide synthase 3	Homo sapiens	146-151
15381390-8	2004	Platelet exposure to 8-Br-cAMP and forskolin, beside the phosphorylation of the specific PKA substrate VASP, markedly increased the expression of ecNOS protein phosphorylated at Ser(1177).	Serine	178-181	nitric oxide synthase 3	Homo sapiens	146-151
14675775-2	2003	Surprisingly, its role in endothelial nitric oxide (NO) synthetase (eNOS) regulation and NO release is basically unknown.	Nitric Oxide	38-50	nitric oxide synthase 3	Homo sapiens	68-72
14667883-0	2003	Effects of mifepristone on expression of endothelial nitric oxide synthase in human endometrium during the implantation phase.	Mifepristone	11-23	nitric oxide synthase 3	Homo sapiens	41-74
14667883-1	2003	OBJECTIVE: To investigate the effects of the antiprogestin mifepristone on expression of endothelial (eNOS) nitric oxide synthase in human endometrium during the implantation phase.	Mifepristone	59-71	nitric oxide synthase 3	Homo sapiens	102-106
14667883-10	2003	Treatment with mifepristone significantly decreased eNOS expression in the endometrial glandular epithelium but did not affect endothelial eNOS.	Mifepristone	15-27	nitric oxide synthase 3	Homo sapiens	52-56
14667883-11	2003	CONCLUSION(S): Mifepristone has differential effects on eNOS expression in the epithelium and endothelium in the human endometrium at the time of implantation.	Mifepristone	15-27	nitric oxide synthase 3	Homo sapiens	56-60
14667898-0	2003	The Glu298--&gt;Asp polymorphism of the endothelial nitric oxide synthase gene is associated with endometriosis.	Aspartic Acid	16-19	nitric oxide synthase 3	Homo sapiens	40-73
14581231-1	2003	The kinetics of formation and transformation of oxygen complexes of two heme-thiolate proteins (the F393H mutant of cytochrome P450 BM3 and the oxygenase domain of endothelial nitric oxide synthase, eNOS) were studied under high pressure.	Oxygen	48-54	nitric oxide synthase 3	Homo sapiens	164-197
14639046-1	2003	An association study was performed between apolipoprotein E (apoE) polymorphism and the common structural polymorphism Glu/Asp at codon 298 of the nitric oxide synthase (NOS3) gene in late-onset sporadic Alzheimer"s dementia probands (LOAD), diffuse Lewy body dementia cases (DLBD) and controls in a Hungarian sample.	Glutamic Acid	119-122	nitric oxide synthase 3	Homo sapiens	170-174
12952971-0	2003	Phosphorylation of threonine 497 in endothelial nitric-oxide synthase coordinates the coupling of L-arginine metabolism to efficient nitric oxide production.	Threonine	19-28	nitric oxide synthase 3	Homo sapiens	36-69
12952971-0	2003	Phosphorylation of threonine 497 in endothelial nitric-oxide synthase coordinates the coupling of L-arginine metabolism to efficient nitric oxide production.	Arginine	98-108	nitric oxide synthase 3	Homo sapiens	36-69
12952971-0	2003	Phosphorylation of threonine 497 in endothelial nitric-oxide synthase coordinates the coupling of L-arginine metabolism to efficient nitric oxide production.	Nitric Oxide	133-145	nitric oxide synthase 3	Homo sapiens	36-69
14613648-9	2003	(3) In 42 paraffin-embedded GCT specimens, the positive expression rates of NOS1, NOS2, and NOS3 protein were 85.7%, 59.5%, and 31.0% in MGC, 54.8%, 28.6%, and 14.3% in MC, respectively.	Paraffin	10-18	nitric oxide synthase 3	Homo sapiens	92-96
14613648-9	2003	(3) In 42 paraffin-embedded GCT specimens, the positive expression rates of NOS1, NOS2, and NOS3 protein were 85.7%, 59.5%, and 31.0% in MGC, 54.8%, 28.6%, and 14.3% in MC, respectively.	Methylcholanthrene	169-171	nitric oxide synthase 3	Homo sapiens	92-96
14613286-8	2003	CONCLUSION: Our findings show that the Glu/Asp(298) polymorphism of the eNOS gene is associated with GCA susceptibility.	Glutamic Acid	39-42	nitric oxide synthase 3	Homo sapiens	72-76
14613286-8	2003	CONCLUSION: Our findings show that the Glu/Asp(298) polymorphism of the eNOS gene is associated with GCA susceptibility.	Aspartic Acid	43-46	nitric oxide synthase 3	Homo sapiens	72-76
14979680-12	2003	However, according to recent studies on endothelial nitric oxide synthase (eNOS) gene polymorphisms, it is likely that only certain patients could benefit from n-3 fatty acid supplementation.	Fatty Acids, Omega-3	160-174	nitric oxide synthase 3	Homo sapiens	40-73
14979680-12	2003	However, according to recent studies on endothelial nitric oxide synthase (eNOS) gene polymorphisms, it is likely that only certain patients could benefit from n-3 fatty acid supplementation.	Fatty Acids, Omega-3	160-174	nitric oxide synthase 3	Homo sapiens	75-79
14682408-6	2003	On comparing pulmonary artery pressures in different eNOS genotypes, the mean pulmonary artery pressure (Ppa) in patients with the BB genotype was significantly higher than in patients with the nonBB genotypes (41.3 +/- 17.7 mmHg vs. 27.3 +/- 11.2 mmHg, P = 0.02).	boeravinone B	131-133	nitric oxide synthase 3	Homo sapiens	53-57
14599552-5	2003	However, if sufficient citrulline is present in the medium, A23187-activated NO production by eNOS does not rely on extracellular arginine.	Citrulline	23-33	nitric oxide synthase 3	Homo sapiens	94-98
14599552-5	2003	However, if sufficient citrulline is present in the medium, A23187-activated NO production by eNOS does not rely on extracellular arginine.	Calcimycin	60-66	nitric oxide synthase 3	Homo sapiens	94-98
14556284-2	2003	Recent studies on the leech central nervous system (CNS), in which synapse regeneration is successful, have shown that nitric oxide (NO) generated immediately after injury by endothelial nitric oxide synthase (eNOS) stops migrating microglia at the lesion.	Nitric Oxide	119-131	nitric oxide synthase 3	Homo sapiens	175-208
14551376-1	2003	BACKGROUND: Asymmetric dimethylarginine (ADMA), an endogenous inhibitor of endothelial nitric oxide synthase and a proposed cardiovascular risk factor, is elevated in chronic kidney disease (CKD).	dimethylarginine	23-39	nitric oxide synthase 3	Homo sapiens	75-108
14624405-3	2003	This study was designed to investigate whether SUA could be influenced by a 27-bp repeat polymorphism in intron 4 of ecNOS gene.	sua	47-50	nitric oxide synthase 3	Homo sapiens	117-122
14551376-1	2003	BACKGROUND: Asymmetric dimethylarginine (ADMA), an endogenous inhibitor of endothelial nitric oxide synthase and a proposed cardiovascular risk factor, is elevated in chronic kidney disease (CKD).	N,N-dimethylarginine	41-45	nitric oxide synthase 3	Homo sapiens	75-108
14512444-2	2003	For a better understanding of the underlying pathophysiological mechanisms, we aimed to characterize the intracellular arginine sources of eNOS.	Arginine	119-127	nitric oxide synthase 3	Homo sapiens	139-143
14624405-6	2003	The mean SUA level of patients having type 2 diabetes was significantly lower than that of control subjects (6.1 +/- 1.8 mg/dL v 6.6 +/- 1.8 mg/dL, P&lt;.001); and the mean SUA level of diabetic patients with ecNOS ab/aa genotypes was lower than that of patients with bb genotype (5.7 +/- 1.6 mg/dL v 6.2 +/- 1.8 mg/dL, P=.008).	sua	9-12	nitric oxide synthase 3	Homo sapiens	209-214
14624405-8	2003	Using Pearson"s correlation analysis and multiple linear regression analysis, ecNOS genotype was noticed to be an independent factor in contributing to SUA variability in female diabetic patients.	sua	152-155	nitric oxide synthase 3	Homo sapiens	78-83
14512444-3	2003	Our previous studies in human endothelial EA.hy926 cells suggested the existence of two arginine pools: pool I can be depleted by extracellular lysine, whereas pool II is not freely exchangeable with the extracellular space, but accessible to eNOS.	Arginine	88-96	nitric oxide synthase 3	Homo sapiens	243-247
14510774-0	2003	NOS 3 subcellular localization in the regulation of nitric oxide production.	Nitric Oxide	52-64	nitric oxide synthase 3	Homo sapiens	0-5
14510774-5	2003	Our laboratory has previously published that in salt-dependent hypertension there is an altered localization of NOS 3, with an increase in cytosolic expression.	Salts	48-52	nitric oxide synthase 3	Homo sapiens	112-117
14553962-0	2003	Effects of endothelial nitric oxide synthase, alpha-adducin, and other candidate gene polymorphisms on blood pressure response to hydrochlorothiazide.	Hydrochlorothiazide	130-149	nitric oxide synthase 3	Homo sapiens	11-44
14553962-6	2003	After adjustment for covariates, the endothelial nitric oxide synthase Glu298--&gt;Asp polymorphism made an additional statistically significant contribution to predicting diastolic BP response to hydrochlorothiazide, accounting for another 1% of interindividual variation in response (P =.034).	Aspartic Acid	83-86	nitric oxide synthase 3	Homo sapiens	37-70
14553962-6	2003	After adjustment for covariates, the endothelial nitric oxide synthase Glu298--&gt;Asp polymorphism made an additional statistically significant contribution to predicting diastolic BP response to hydrochlorothiazide, accounting for another 1% of interindividual variation in response (P =.034).	Hydrochlorothiazide	197-216	nitric oxide synthase 3	Homo sapiens	37-70
14520629-3	2003	Recently, a gene polymorphism of the endothelial NO synthase (ENOS) gene was identified that is associated with circulating nitrate levels.	Nitrates	124-131	nitric oxide synthase 3	Homo sapiens	62-66
14583343-1	2003	Changes in plasma nitrite concentration in the human forearm circulation have recently been shown to reflect acute changes in endothelial nitric oxide synthase (eNOS)-activity.	Nitrites	18-25	nitric oxide synthase 3	Homo sapiens	126-159
12969157-9	2003	Patients with ADPKD have defective nitric oxide generation from diminished cNOS activity.	Nitric Oxide	35-47	nitric oxide synthase 3	Homo sapiens	75-79
12919953-0	2003	Transcriptional stimulation of the eNOS gene by the stable prostacyclin analogue beraprost is mediated through cAMP-responsive element in vascular endothelial cells: close link between PGI2 signal and NO pathways.	Epoprostenol	59-71	nitric oxide synthase 3	Homo sapiens	35-39
12919953-0	2003	Transcriptional stimulation of the eNOS gene by the stable prostacyclin analogue beraprost is mediated through cAMP-responsive element in vascular endothelial cells: close link between PGI2 signal and NO pathways.	Cyclic AMP	111-115	nitric oxide synthase 3	Homo sapiens	35-39
12919953-0	2003	Transcriptional stimulation of the eNOS gene by the stable prostacyclin analogue beraprost is mediated through cAMP-responsive element in vascular endothelial cells: close link between PGI2 signal and NO pathways.	Epoprostenol	185-189	nitric oxide synthase 3	Homo sapiens	35-39
12919953-4	2003	Treatment of these cells with BPS increased the eNOS expression as assessed by Northern blots, Western blots, and NO production by NO-specific fluorescence (DAF2-DA) and by the Griess method.	beraprost	30-33	nitric oxide synthase 3	Homo sapiens	48-52
12919953-6	2003	In addition, BPS increased the promoter activity of the human eNOS gene, as determined by luciferase assays of the eNOS promoter gene.	beraprost	13-16	nitric oxide synthase 3	Homo sapiens	62-66
12919953-6	2003	In addition, BPS increased the promoter activity of the human eNOS gene, as determined by luciferase assays of the eNOS promoter gene.	beraprost	13-16	nitric oxide synthase 3	Homo sapiens	115-119
12876216-0	2003	Inhibition of GTP-dependent vesicle trafficking impairs internalization of plasmalemmal eNOS and cellular nitric oxide production.	Guanosine Triphosphate	14-17	nitric oxide synthase 3	Homo sapiens	88-92
12927592-5	2003	Surprisingly, agonist-induced increases in eNOS activity were reduced to 42 and 50% in the presence of the proteasome inhibiting drugs MG132 and clasto-lactacystin-beta-lactone, respectively (P &lt; 0.01).	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	135-140	nitric oxide synthase 3	Homo sapiens	43-47
12824189-2	2003	Nitric oxide (NO), generated from endothelial nitric-oxide synthase (eNOS), prevents resorption, whereas receptor activator of nuclear kappa B ligand (RANKL) promotes resorption through regulating osteoclast activity.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	34-67
12824189-2	2003	Nitric oxide (NO), generated from endothelial nitric-oxide synthase (eNOS), prevents resorption, whereas receptor activator of nuclear kappa B ligand (RANKL) promotes resorption through regulating osteoclast activity.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	69-73
12876216-1	2003	The Ca2+ mobilizing peptide, bradykinin (BK), stimulates endothelial nitric oxide synthase (eNOS)-derived cellular nitric oxide (NO) production in association with altering the subcellular distribution of the enzyme.	Nitric Oxide	69-81	nitric oxide synthase 3	Homo sapiens	92-96
12876216-4	2003	This was associated with the mobilization of eNOS-GFP protein into Triton X-100-insoluble fractions of cell lysates, and an internalization of plasmalemmal eNOS-GFP in live and fixed ECV 304 cells.	Octoxynol	67-79	nitric oxide synthase 3	Homo sapiens	45-49
12876216-5	2003	Incubation of digitonin-permeabilized ECV304 cells with the non-hydrolyzed GTP analog, GTP-gamma-S, abrogated the BK-mediated internalization of eNOS-GFP as assessed by confocal microscopy.	Digitonin	14-23	nitric oxide synthase 3	Homo sapiens	145-149
12876216-5	2003	Incubation of digitonin-permeabilized ECV304 cells with the non-hydrolyzed GTP analog, GTP-gamma-S, abrogated the BK-mediated internalization of eNOS-GFP as assessed by confocal microscopy.	Guanosine Triphosphate	75-78	nitric oxide synthase 3	Homo sapiens	145-149
12876216-5	2003	Incubation of digitonin-permeabilized ECV304 cells with the non-hydrolyzed GTP analog, GTP-gamma-S, abrogated the BK-mediated internalization of eNOS-GFP as assessed by confocal microscopy.	Guanosine 5'-O-(3-Thiotriphosphate)	87-98	nitric oxide synthase 3	Homo sapiens	145-149
12876216-9	2003	These studies demonstrate that disruption of dynamin- and GTP-dependent, but clathrin-independent, vesicle trafficking pathways impairs BK-dependent cellular NO production, via inhibition of the internalization of eNOS-containing plasmalemmal vesicles.	Guanosine Triphosphate	58-61	nitric oxide synthase 3	Homo sapiens	214-218
12923396-9	2003	Those subjects with normal plasma homocysteine values had an increased hypertensive risk with an odds ratio of 2.6 for the PP genotype of the PPARgamma2 gene and an odds ratio of 1.8 for the a allele of the eNOS gene.	Homocysteine	34-46	nitric oxide synthase 3	Homo sapiens	207-211
14623174-2	2003	7-Methoxyindazole (7-MI) was the most active compound of this series and displayed selectivity toward the constitutive neuronal (NOS I) and endothelial (NOS III) NOS isoforms, the inducible NOS II being almost insensitive to this inhibitor.	7-methoxyindazole	0-17	nitric oxide synthase 3	Homo sapiens	153-160
12967769-3	2003	Although several mechanisms are proposed to explain the reduction of cNOS activity, reduced substrate availability, caused by a combination of increased arginase activity and decreased cellular uptake of L-arginine, appears to play a key role.	Arginine	204-214	nitric oxide synthase 3	Homo sapiens	69-73
14583660-8	2003	Indomethacin increased both NO(x), eNOS and L-citrulline levels.	Indomethacin	0-12	nitric oxide synthase 3	Homo sapiens	35-39
12893742-2	2003	Nitric oxide (NO) produced by endothelial NO synthase (eNOS) plays an essential role in regulation of vascular function and structure by blood flow, but the molecular mechanisms that transduce mechanical force to eNOS activation are not well understood.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	55-59
12893742-2	2003	Nitric oxide (NO) produced by endothelial NO synthase (eNOS) plays an essential role in regulation of vascular function and structure by blood flow, but the molecular mechanisms that transduce mechanical force to eNOS activation are not well understood.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	213-217
12893742-6	2003	Decreasing VEGFR2 expression with antisense VEGFR2 oligonucleotides significantly attenuates activation of Akt and eNOS.	Oligonucleotides	51-67	nitric oxide synthase 3	Homo sapiens	115-119
12730050-2	2003	During oxidative stress, endothelial nitric oxide (NO) synthase (eNOS) becomes uncoupled because of decreased bioavailability of tetrahydrobiopterin (BH4), an essential cofactor of eNOS.	sapropterin	150-153	nitric oxide synthase 3	Homo sapiens	65-69
12791703-2	2003	AMP-activated protein kinase (AMPK) has previously been demonstrated to phosphorylate and activate eNOS at Ser-1177 in vitro, yet the function of AMPK in endothelium is poorly characterized.	Serine	107-110	nitric oxide synthase 3	Homo sapiens	99-103
12791703-4	2003	AICAR caused the time- and dose-dependent stimulation of AMPK activity, with a concomitant increase in eNOS Ser-1177 phosphorylation and NO production.	Serine	108-111	nitric oxide synthase 3	Homo sapiens	103-107
12791703-8	2003	Expression of dominant negative AMPK attenuated AICAR-stimulated AMPK activity, eNOS Ser-1177 phosphorylation and NO production and was without effect on AICAR-stimulated protein kinase B Ser-473 phosphorylation or NO production stimulated by insulin or A23187.	Serine	85-88	nitric oxide synthase 3	Homo sapiens	80-84
12791703-9	2003	These data suggest that AICAR-stimulated NO production is mediated by AMPK as a consequence of increased Ser-1177 phosphorylation of eNOS.	Serine	105-108	nitric oxide synthase 3	Homo sapiens	133-137
12730050-2	2003	During oxidative stress, endothelial nitric oxide (NO) synthase (eNOS) becomes uncoupled because of decreased bioavailability of tetrahydrobiopterin (BH4), an essential cofactor of eNOS.	nitric	37-43	nitric oxide synthase 3	Homo sapiens	65-69
12730050-2	2003	During oxidative stress, endothelial nitric oxide (NO) synthase (eNOS) becomes uncoupled because of decreased bioavailability of tetrahydrobiopterin (BH4), an essential cofactor of eNOS.	sapropterin	129-148	nitric oxide synthase 3	Homo sapiens	65-69
12730050-2	2003	During oxidative stress, endothelial nitric oxide (NO) synthase (eNOS) becomes uncoupled because of decreased bioavailability of tetrahydrobiopterin (BH4), an essential cofactor of eNOS.	sapropterin	150-153	nitric oxide synthase 3	Homo sapiens	181-185
12730050-2	2003	During oxidative stress, endothelial nitric oxide (NO) synthase (eNOS) becomes uncoupled because of decreased bioavailability of tetrahydrobiopterin (BH4), an essential cofactor of eNOS.	sapropterin	129-148	nitric oxide synthase 3	Homo sapiens	181-185
12918531-0	2003	Red wine polyphenols enhance endothelial nitric oxide synthase expression and subsequent nitric oxide release from endothelial cells.	Polyphenols	9-20	nitric oxide synthase 3	Homo sapiens	29-62
12864782-10	2003	In contrast, cNOS activity remained unchanged upon homocysteine treatment.	Homocysteine	51-63	nitric oxide synthase 3	Homo sapiens	13-17
12738794-6	2003	Dopamine and SKF R-38393 induced overexpression of the nitric-oxide synthase (NOS) isoforms neuronal NOS, inducible NOS (iNOS), and endothelial NOS in a protein kinase A-dependent manner.	Dopamine	0-8	nitric oxide synthase 3	Homo sapiens	132-147
12865324-4	2003	We show that DHEA administration to human endothelial cells triggers nitric oxide synthesis, due to enhanced expression and stabilization of endothelial nitric oxide synthase (eNOS).	Dehydroepiandrosterone	13-17	nitric oxide synthase 3	Homo sapiens	141-174
12874836-7	2003	Heating also increased cNOs phosphorylation at tyrosine residues.	Tyrosine	47-55	nitric oxide synthase 3	Homo sapiens	23-27
12852865-2	2003	A major structural component is the membrane protein caveolin-1 which associates with numerous signalling molecules, including endothelial nitric oxide (eNOS).	Nitric Oxide	139-151	nitric oxide synthase 3	Homo sapiens	153-157
12738794-6	2003	Dopamine and SKF R-38393 induced overexpression of the nitric-oxide synthase (NOS) isoforms neuronal NOS, inducible NOS (iNOS), and endothelial NOS in a protein kinase A-dependent manner.	skf r-38393	13-24	nitric oxide synthase 3	Homo sapiens	132-147
12974195-8	2003	The intensities of i-NOS and c-NOS of MG were significantly higher in group I than in group II (p &lt; 0.05) with no significant differences in other areas (p &gt; 0.05, respectively).	Magnesium	38-40	nitric oxide synthase 3	Homo sapiens	29-34
12738608-0	2003	Association of a missense mutation in the NOS3 gene with exhaled nitric oxide levels.	Nitric Oxide	65-77	nitric oxide synthase 3	Homo sapiens	42-46
12738608-2	2003	We identified a strong association between a known functional NOS3 missense sequence variant in the endothelial nitric oxide gene (G894T) and FENO level in a cohort of subjects with asthma.	Nitric Oxide	112-124	nitric oxide synthase 3	Homo sapiens	62-66
12738608-2	2003	We identified a strong association between a known functional NOS3 missense sequence variant in the endothelial nitric oxide gene (G894T) and FENO level in a cohort of subjects with asthma.	flubendiamide	142-146	nitric oxide synthase 3	Homo sapiens	62-66
12824263-0	2003	High glucose-induced tyrosine nitration in endothelial cells: role of eNOS uncoupling and aldose reductase activation.	Glucose	5-12	nitric oxide synthase 3	Homo sapiens	70-74
12860247-7	2003	Human aortic endothelial cells incubated with simvastatin exhibited up to threefold higher intracellular oxidation of DHR-123 along with a twofold increase in total e-NOS protein.	Simvastatin	46-57	nitric oxide synthase 3	Homo sapiens	165-170
12746044-2	2003	Nitric oxide (NO) can be generated by constitutive and inducible nitric oxide synthases (cNOS and iNOS) in pulmonary endothelial and epithelial cells.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	89-93
12746044-4	2003	Infusion of L-N(G)-nitroarginine methyl ester (L-NAME) (100 micro M), an inhibitor of cNOS and iNOS, via pulmonary circulation for 90 minutes resulted in a decrease of lung surfactant secretion (1.55%+/-0.15% in control versus 0.79%+/-0.16% in L-NAME-treated lungs, P &lt;.05).	l-n(g)-nitroarginine methyl ester	12-45	nitric oxide synthase 3	Homo sapiens	86-90
12746044-4	2003	Infusion of L-N(G)-nitroarginine methyl ester (L-NAME) (100 micro M), an inhibitor of cNOS and iNOS, via pulmonary circulation for 90 minutes resulted in a decrease of lung surfactant secretion (1.55%+/-0.15% in control versus 0.79%+/-0.16% in L-NAME-treated lungs, P &lt;.05).	NG-Nitroarginine Methyl Ester	47-53	nitric oxide synthase 3	Homo sapiens	86-90
12824263-9	2003	CONCLUSIONS: Increases in glucose levels and osmotic stress similar to those in diabetic patients increase the formation of nitrotyrosine in retinal endothelial cells because of their actions increasing NOS activity and causing superoxide formation due to eNOS uncoupling and AR activation.	Glucose	26-33	nitric oxide synthase 3	Homo sapiens	256-260
12824263-9	2003	CONCLUSIONS: Increases in glucose levels and osmotic stress similar to those in diabetic patients increase the formation of nitrotyrosine in retinal endothelial cells because of their actions increasing NOS activity and causing superoxide formation due to eNOS uncoupling and AR activation.	3-nitrotyrosine	124-137	nitric oxide synthase 3	Homo sapiens	256-260
12824263-7	2003	RESULTS: Increased concentrations of glucose or 3-methyL-o-glucose stimulated formation of nitric oxide (NO) and superoxide induced protein nitration on tyrosine and increased expression and activity of endothelial nitric oxide synthase (eNOS).	Glucose	37-44	nitric oxide synthase 3	Homo sapiens	203-236
12824263-7	2003	RESULTS: Increased concentrations of glucose or 3-methyL-o-glucose stimulated formation of nitric oxide (NO) and superoxide induced protein nitration on tyrosine and increased expression and activity of endothelial nitric oxide synthase (eNOS).	Glucose	37-44	nitric oxide synthase 3	Homo sapiens	238-242
12824263-7	2003	RESULTS: Increased concentrations of glucose or 3-methyL-o-glucose stimulated formation of nitric oxide (NO) and superoxide induced protein nitration on tyrosine and increased expression and activity of endothelial nitric oxide synthase (eNOS).	3-methyl-o-glucose	48-66	nitric oxide synthase 3	Homo sapiens	203-236
12824263-7	2003	RESULTS: Increased concentrations of glucose or 3-methyL-o-glucose stimulated formation of nitric oxide (NO) and superoxide induced protein nitration on tyrosine and increased expression and activity of endothelial nitric oxide synthase (eNOS).	3-methyl-o-glucose	48-66	nitric oxide synthase 3	Homo sapiens	238-242
12824263-7	2003	RESULTS: Increased concentrations of glucose or 3-methyL-o-glucose stimulated formation of nitric oxide (NO) and superoxide induced protein nitration on tyrosine and increased expression and activity of endothelial nitric oxide synthase (eNOS).	Superoxides	113-123	nitric oxide synthase 3	Homo sapiens	203-236
12824263-7	2003	RESULTS: Increased concentrations of glucose or 3-methyL-o-glucose stimulated formation of nitric oxide (NO) and superoxide induced protein nitration on tyrosine and increased expression and activity of endothelial nitric oxide synthase (eNOS).	Superoxides	113-123	nitric oxide synthase 3	Homo sapiens	238-242
12692136-0	2003	Interactions of peroxynitrite, tetrahydrobiopterin, ascorbic acid, and thiols: implications for uncoupling endothelial nitric-oxide synthase.	Peroxynitrous Acid	16-29	nitric oxide synthase 3	Homo sapiens	107-140
12787407-4	2003	The aim of the present study was to characterize and localize in situ the nitric oxide synthase (NOS) isoforms (NOS1, NOS2, and NOS3) expressed in human normal kidney, and soluble guanylyl cyclase, the well-known target for nitric oxide.	Nitric Oxide	74-86	nitric oxide synthase 3	Homo sapiens	128-132
12692136-0	2003	Interactions of peroxynitrite, tetrahydrobiopterin, ascorbic acid, and thiols: implications for uncoupling endothelial nitric-oxide synthase.	sapropterin	31-50	nitric oxide synthase 3	Homo sapiens	107-140
12692136-0	2003	Interactions of peroxynitrite, tetrahydrobiopterin, ascorbic acid, and thiols: implications for uncoupling endothelial nitric-oxide synthase.	Ascorbic Acid	52-65	nitric oxide synthase 3	Homo sapiens	107-140
12692136-0	2003	Interactions of peroxynitrite, tetrahydrobiopterin, ascorbic acid, and thiols: implications for uncoupling endothelial nitric-oxide synthase.	Sulfhydryl Compounds	71-77	nitric oxide synthase 3	Homo sapiens	107-140
12692136-1	2003	Tetrahydrobiopterin (BH4) serves as a critical co-factor for the endothelial nitric-oxide synthase (eNOS).	sapropterin	0-19	nitric oxide synthase 3	Homo sapiens	65-98
12692136-1	2003	Tetrahydrobiopterin (BH4) serves as a critical co-factor for the endothelial nitric-oxide synthase (eNOS).	sapropterin	21-24	nitric oxide synthase 3	Homo sapiens	65-98
12689917-0	2003	Genetic evidence that nitric oxide modulates homocysteine: the NOS3 894TT genotype is a risk factor for hyperhomocystenemia.	Nitric Oxide	22-34	nitric oxide synthase 3	Homo sapiens	63-67
14592555-7	2003	RESULTS: Incubation of HUVECs and PC-12 with 10(-5) mol/l of aspirin increased cNOS expression by 70 +/- 7% and 50 +/- 5, respectively.	PC 12 ester	34-39	nitric oxide synthase 3	Homo sapiens	79-83
14592555-7	2003	RESULTS: Incubation of HUVECs and PC-12 with 10(-5) mol/l of aspirin increased cNOS expression by 70 +/- 7% and 50 +/- 5, respectively.	Aspirin	61-68	nitric oxide synthase 3	Homo sapiens	79-83
12734108-4	2003	Confocal microscopy of PAEC, in which eNOS was labeled with fluorescein, F-actin was labeled with Texas red-phalloidin, and G-actin was labeled with deoxyribonuclease I conjugated with Texas red, also demonstrated an association between eNOS and F-actin or G-actin.	Fluorescein	60-71	nitric oxide synthase 3	Homo sapiens	38-42
12734108-7	2003	Incubation of PAEC with swinholide A, an actin filament disruptor, resulted in an increase in eNOS activity, eNOS protein content, and association of eNOS with G-actin and in a decrease in the association of eNOS with F-actin.	paec	14-18	nitric oxide synthase 3	Homo sapiens	94-98
12734108-7	2003	Incubation of PAEC with swinholide A, an actin filament disruptor, resulted in an increase in eNOS activity, eNOS protein content, and association of eNOS with G-actin and in a decrease in the association of eNOS with F-actin.	paec	14-18	nitric oxide synthase 3	Homo sapiens	109-113
12734108-7	2003	Incubation of PAEC with swinholide A, an actin filament disruptor, resulted in an increase in eNOS activity, eNOS protein content, and association of eNOS with G-actin and in a decrease in the association of eNOS with F-actin.	paec	14-18	nitric oxide synthase 3	Homo sapiens	109-113
12734108-7	2003	Incubation of PAEC with swinholide A, an actin filament disruptor, resulted in an increase in eNOS activity, eNOS protein content, and association of eNOS with G-actin and in a decrease in the association of eNOS with F-actin.	paec	14-18	nitric oxide synthase 3	Homo sapiens	109-113
12689917-9	2003	CONCLUSIONS: These data indicate that the NOS3 894TT genotype is a risk factor for elevated tHcy in healthy nonsmoking adults with low serum folate and supports the hypothesis that nitric oxide modulates homocysteine through an effect on folate catabolism.	thcy	92-96	nitric oxide synthase 3	Homo sapiens	42-46
12689917-9	2003	CONCLUSIONS: These data indicate that the NOS3 894TT genotype is a risk factor for elevated tHcy in healthy nonsmoking adults with low serum folate and supports the hypothesis that nitric oxide modulates homocysteine through an effect on folate catabolism.	Folic Acid	141-147	nitric oxide synthase 3	Homo sapiens	42-46
12689917-9	2003	CONCLUSIONS: These data indicate that the NOS3 894TT genotype is a risk factor for elevated tHcy in healthy nonsmoking adults with low serum folate and supports the hypothesis that nitric oxide modulates homocysteine through an effect on folate catabolism.	Nitric Oxide	181-193	nitric oxide synthase 3	Homo sapiens	42-46
12689917-9	2003	CONCLUSIONS: These data indicate that the NOS3 894TT genotype is a risk factor for elevated tHcy in healthy nonsmoking adults with low serum folate and supports the hypothesis that nitric oxide modulates homocysteine through an effect on folate catabolism.	Homocysteine	204-216	nitric oxide synthase 3	Homo sapiens	42-46
12689917-9	2003	CONCLUSIONS: These data indicate that the NOS3 894TT genotype is a risk factor for elevated tHcy in healthy nonsmoking adults with low serum folate and supports the hypothesis that nitric oxide modulates homocysteine through an effect on folate catabolism.	Folic Acid	238-244	nitric oxide synthase 3	Homo sapiens	42-46
12689917-0	2003	Genetic evidence that nitric oxide modulates homocysteine: the NOS3 894TT genotype is a risk factor for hyperhomocystenemia.	Homocysteine	45-57	nitric oxide synthase 3	Homo sapiens	63-67
12689917-4	2003	METHODS AND RESULTS: The hypothesis that the endothelial nitric oxide synthase (NOS3) G894T polymorphism is a genetic determinant of tHcy concentrations was tested in 2 independent healthy adult populations.	thcy	133-137	nitric oxide synthase 3	Homo sapiens	45-78
12689917-4	2003	METHODS AND RESULTS: The hypothesis that the endothelial nitric oxide synthase (NOS3) G894T polymorphism is a genetic determinant of tHcy concentrations was tested in 2 independent healthy adult populations.	thcy	133-137	nitric oxide synthase 3	Homo sapiens	80-84
12689917-5	2003	In both populations, NOS3 genotype was significantly associated with tHcy concentrations in nonsmokers with low folate (P=0.03 for each).	thcy	69-73	nitric oxide synthase 3	Homo sapiens	21-25
12689917-5	2003	In both populations, NOS3 genotype was significantly associated with tHcy concentrations in nonsmokers with low folate (P=0.03 for each).	Folic Acid	112-118	nitric oxide synthase 3	Homo sapiens	21-25
12689917-7	2003	NOS3 genotype remained a significant determinant of tHcy concentrations after adjustment.	thcy	52-56	nitric oxide synthase 3	Homo sapiens	0-4
12766119-2	2003	Endothelium-dependent vasodilation of the renal vasculature cannot be easily assessed, but infusion of L-arginine, the substrate of endothelial nitric oxide synthase, leads to an increase in renal plasma flow (RPF) in humans.	Arginine	103-113	nitric oxide synthase 3	Homo sapiens	132-165
12974139-1	2003	Endothelial nitric oxide synthase (eNOS or NOS3) is the main responsible for nitric oxide (NO) production in vascular system and different polymorphisms have been identified in epidemiological studies.	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	35-39
12974139-1	2003	Endothelial nitric oxide synthase (eNOS or NOS3) is the main responsible for nitric oxide (NO) production in vascular system and different polymorphisms have been identified in epidemiological studies.	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	43-47
12757846-4	2003	In the present study, we show that superoxide generated in several enzymatic or chemical systems (e.g., xanthine/xanthine oxidase, endothelial nitric oxide synthase, or potassium superoxide) oxidizes HE to a fluorescent product (excitation, 480 nm; emission, 567 nm) that is totally different from E+.	Superoxides	35-45	nitric oxide synthase 3	Homo sapiens	131-164
12757846-4	2003	In the present study, we show that superoxide generated in several enzymatic or chemical systems (e.g., xanthine/xanthine oxidase, endothelial nitric oxide synthase, or potassium superoxide) oxidizes HE to a fluorescent product (excitation, 480 nm; emission, 567 nm) that is totally different from E+.	hydroethidine	200-202	nitric oxide synthase 3	Homo sapiens	131-164
12869534-0	2003	Regulation of endothelial nitric oxide synthase by protein kinase C. Endothelial nitric oxide synthase (eNOS) is a key enzyme in nitric oxide-mediated signal transduction in mammalian cells.	Nitric Oxide	26-38	nitric oxide synthase 3	Homo sapiens	69-102
12756290-1	2003	The enzyme endothelial nitric oxide synthase (eNOS) catalyzes the conversion of arginine, oxygen and NADPH to NO and citrulline.	Arginine	80-88	nitric oxide synthase 3	Homo sapiens	11-44
12869534-0	2003	Regulation of endothelial nitric oxide synthase by protein kinase C. Endothelial nitric oxide synthase (eNOS) is a key enzyme in nitric oxide-mediated signal transduction in mammalian cells.	Nitric Oxide	26-38	nitric oxide synthase 3	Homo sapiens	104-108
12756290-1	2003	The enzyme endothelial nitric oxide synthase (eNOS) catalyzes the conversion of arginine, oxygen and NADPH to NO and citrulline.	Arginine	80-88	nitric oxide synthase 3	Homo sapiens	46-50
12756290-1	2003	The enzyme endothelial nitric oxide synthase (eNOS) catalyzes the conversion of arginine, oxygen and NADPH to NO and citrulline.	Oxygen	90-96	nitric oxide synthase 3	Homo sapiens	46-50
12756290-1	2003	The enzyme endothelial nitric oxide synthase (eNOS) catalyzes the conversion of arginine, oxygen and NADPH to NO and citrulline.	Oxygen	90-96	nitric oxide synthase 3	Homo sapiens	11-44
12756290-1	2003	The enzyme endothelial nitric oxide synthase (eNOS) catalyzes the conversion of arginine, oxygen and NADPH to NO and citrulline.	NADP	101-106	nitric oxide synthase 3	Homo sapiens	11-44
12756290-1	2003	The enzyme endothelial nitric oxide synthase (eNOS) catalyzes the conversion of arginine, oxygen and NADPH to NO and citrulline.	NADP	101-106	nitric oxide synthase 3	Homo sapiens	46-50
12756290-1	2003	The enzyme endothelial nitric oxide synthase (eNOS) catalyzes the conversion of arginine, oxygen and NADPH to NO and citrulline.	Citrulline	117-127	nitric oxide synthase 3	Homo sapiens	11-44
12756290-1	2003	The enzyme endothelial nitric oxide synthase (eNOS) catalyzes the conversion of arginine, oxygen and NADPH to NO and citrulline.	Citrulline	117-127	nitric oxide synthase 3	Homo sapiens	46-50
12785010-7	2003	CS and/or TC reduced apoptosis induced by hypoxia in a dose-dependent manner, and significantly increased BK and ecNOS expression.	Cesium	0-2	nitric oxide synthase 3	Homo sapiens	113-118
12785010-7	2003	CS and/or TC reduced apoptosis induced by hypoxia in a dose-dependent manner, and significantly increased BK and ecNOS expression.	Technetium	10-12	nitric oxide synthase 3	Homo sapiens	113-118
12785010-10	2003	Both CS and TC can ameliorate hypoxia-induced apoptosis in HAEC through inhibiting caspase-3 activation by enhancing ecNOS activity, via the accumulation of BK.	Cesium	5-7	nitric oxide synthase 3	Homo sapiens	117-122
12785010-10	2003	Both CS and TC can ameliorate hypoxia-induced apoptosis in HAEC through inhibiting caspase-3 activation by enhancing ecNOS activity, via the accumulation of BK.	Technetium	12-14	nitric oxide synthase 3	Homo sapiens	117-122
12707234-0	2003	Histamine upregulates gene expression of endothelial nitric oxide synthase in human vascular endothelial cells.	Histamine	0-9	nitric oxide synthase 3	Homo sapiens	41-74
12819869-3	2003	This study tested the hypothesis that polymorphisms in eNOS are associated with susceptibility to CAF after cadaveric renal transplantation.	cafestol palmitate	98-101	nitric oxide synthase 3	Homo sapiens	55-59
12707234-1	2003	BACKGROUND: Histamine has a short-term, transient, stimulating effect on endothelial nitric oxide synthase (eNOS) activity; however, long-term effects on eNOS have not been described yet.	Histamine	12-21	nitric oxide synthase 3	Homo sapiens	73-106
12707234-7	2003	The histamine-induced eNOS expression was completely prevented by KN-93, an inhibitor of CaMK II.	Histamine	4-13	nitric oxide synthase 3	Homo sapiens	22-26
12707234-1	2003	BACKGROUND: Histamine has a short-term, transient, stimulating effect on endothelial nitric oxide synthase (eNOS) activity; however, long-term effects on eNOS have not been described yet.	Histamine	12-21	nitric oxide synthase 3	Homo sapiens	108-112
12707234-7	2003	The histamine-induced eNOS expression was completely prevented by KN-93, an inhibitor of CaMK II.	KN 93	66-71	nitric oxide synthase 3	Homo sapiens	22-26
12707234-1	2003	BACKGROUND: Histamine has a short-term, transient, stimulating effect on endothelial nitric oxide synthase (eNOS) activity; however, long-term effects on eNOS have not been described yet.	Histamine	12-21	nitric oxide synthase 3	Homo sapiens	154-158
12707234-8	2003	Histamine increased the activity of a 1.6-kb human eNOS promoter fragment (luciferase reporter gene assay), an effect that was also blocked by mepyramine.	Histamine	0-9	nitric oxide synthase 3	Homo sapiens	51-55
12707234-2	2003	In addition, the vascular effect of histamine seems to depend critically on eNOS functionality.	Histamine	36-45	nitric oxide synthase 3	Homo sapiens	76-80
12707234-8	2003	Histamine increased the activity of a 1.6-kb human eNOS promoter fragment (luciferase reporter gene assay), an effect that was also blocked by mepyramine.	Pyrilamine	143-153	nitric oxide synthase 3	Homo sapiens	51-55
12707234-3	2003	Therefore, we studied the effects of histamine on eNOS gene expression and function.	Histamine	37-46	nitric oxide synthase 3	Homo sapiens	50-54
12707234-10	2003	Under conditions of oxidative stress, however, the eNOS upregulated by histamine produced reactive oxygen species (CM-H2DCFDA oxidation-based fluorescence assay).	Histamine	71-80	nitric oxide synthase 3	Homo sapiens	51-55
12707234-4	2003	METHODS AND RESULTS: In human umbilical vein endothelial cells (HUVECs) and HUVEC-derived EA.hy 926 cells, histamine upregulated eNOS mRNA (RNase protection assay) and protein (electron microscopic immunocytochemistry) expression.	Histamine	107-116	nitric oxide synthase 3	Homo sapiens	129-133
12707234-10	2003	Under conditions of oxidative stress, however, the eNOS upregulated by histamine produced reactive oxygen species (CM-H2DCFDA oxidation-based fluorescence assay).	Reactive Oxygen Species	90-113	nitric oxide synthase 3	Homo sapiens	51-55
12707234-5	2003	The upregulation of eNOS could be prevented by mepyramine, a selective antagonist at the H1 receptor, but not by H2 and H3 receptor antagonists.	Pyrilamine	47-57	nitric oxide synthase 3	Homo sapiens	20-24
12875691-7	2003	Both H(2)O(2) and LPS significantly increased the eNOS transcript levels and the increases were significantly attenuated after pretreatment with propofol.	Hydrogen Peroxide	5-13	nitric oxide synthase 3	Homo sapiens	50-54
12707234-10	2003	Under conditions of oxidative stress, however, the eNOS upregulated by histamine produced reactive oxygen species (CM-H2DCFDA oxidation-based fluorescence assay).	Curium	115-117	nitric oxide synthase 3	Homo sapiens	51-55
12707234-10	2003	Under conditions of oxidative stress, however, the eNOS upregulated by histamine produced reactive oxygen species (CM-H2DCFDA oxidation-based fluorescence assay).	2',7'-dichlorodihydrofluorescein diacetate	118-125	nitric oxide synthase 3	Homo sapiens	51-55
12707234-12	2003	This eNOS upregulation may be protective under normal conditions, but it may become harmful under conditions of oxidative stress when eNOS produces reactive oxygen species at the expense of nitric oxide.	Reactive Oxygen Species	148-171	nitric oxide synthase 3	Homo sapiens	5-9
12707234-12	2003	This eNOS upregulation may be protective under normal conditions, but it may become harmful under conditions of oxidative stress when eNOS produces reactive oxygen species at the expense of nitric oxide.	Reactive Oxygen Species	148-171	nitric oxide synthase 3	Homo sapiens	134-138
12707234-12	2003	This eNOS upregulation may be protective under normal conditions, but it may become harmful under conditions of oxidative stress when eNOS produces reactive oxygen species at the expense of nitric oxide.	Nitric Oxide	190-202	nitric oxide synthase 3	Homo sapiens	5-9
12707234-12	2003	This eNOS upregulation may be protective under normal conditions, but it may become harmful under conditions of oxidative stress when eNOS produces reactive oxygen species at the expense of nitric oxide.	Nitric Oxide	190-202	nitric oxide synthase 3	Homo sapiens	134-138
12707237-0	2003	Reactive oxygen species are involved in smoking-induced dysfunction of nitric oxide biosynthesis and upregulation of endothelial nitric oxide synthase: an in vitro demonstration in human coronary artery endothelial cells.	Reactive Oxygen Species	0-23	nitric oxide synthase 3	Homo sapiens	117-150
12707237-1	2003	BACKGROUND: Our group has previously shown that human umbilical vein endothelial cells exposed to smokers" serum decreased nitric oxide (NO) production and endothelial nitric oxide synthase (eNOS) activity in the presence of increased eNOS expression.	Nitric Oxide	123-135	nitric oxide synthase 3	Homo sapiens	235-239
12707237-7	2003	In smokers, addition of PEG-SOD, PEG-SOD+PEG-catalase, or tetrahydrobiopterin significantly (P&lt;0.05) improved NO levels and eNOS activity.	sapropterin	58-77	nitric oxide synthase 3	Homo sapiens	127-131
12707237-10	2003	Furthermore, these data support other studies suggesting a role for hydrogen peroxide in the upregulation of eNOS.	Hydrogen Peroxide	68-85	nitric oxide synthase 3	Homo sapiens	109-113
12875691-8	2003	Both H(2)O(2) and LPS significantly increased the eNOS protein expression and the increase was attenuated after pretreatment with propofol.	Hydrogen Peroxide	5-13	nitric oxide synthase 3	Homo sapiens	50-54
12875691-8	2003	Both H(2)O(2) and LPS significantly increased the eNOS protein expression and the increase was attenuated after pretreatment with propofol.	Propofol	130-138	nitric oxide synthase 3	Homo sapiens	50-54
12875691-9	2003	CONCLUSION: Propofol could protect endothelial cells against oxidative stress by inhibiting eNOS transcription and protein expression, but could not antagonise endotoxin induced cell injuries.	Propofol	12-20	nitric oxide synthase 3	Homo sapiens	92-96
12875691-7	2003	Both H(2)O(2) and LPS significantly increased the eNOS transcript levels and the increases were significantly attenuated after pretreatment with propofol.	Propofol	145-153	nitric oxide synthase 3	Homo sapiens	50-54
12657742-0	2003	Trichloroethylene decreases heat shock protein 90 interactions with endothelial nitric oxide synthase: implications for endothelial cell proliferation.	Trichloroethylene	0-17	nitric oxide synthase 3	Homo sapiens	68-101
12727149-1	2003	AIMS: Endothelial nitric oxide synthase (eNOS) catalyzes the formation of nitric oxide which has vasodilatory, antithrombotic, antiinflammatory and antiproliferative properties.	Nitric Oxide	18-30	nitric oxide synthase 3	Homo sapiens	41-45
12826063-0	2003	Competition and binding of arginine, imidazole, and aminoguanidine to endothelial nitric oxide synthase: aminoguanidine is a poor model for substrate, intermediate, and arginine analog inhibitor binding.	Arginine	27-35	nitric oxide synthase 3	Homo sapiens	70-103
12826063-0	2003	Competition and binding of arginine, imidazole, and aminoguanidine to endothelial nitric oxide synthase: aminoguanidine is a poor model for substrate, intermediate, and arginine analog inhibitor binding.	imidazole	37-46	nitric oxide synthase 3	Homo sapiens	70-103
12826063-0	2003	Competition and binding of arginine, imidazole, and aminoguanidine to endothelial nitric oxide synthase: aminoguanidine is a poor model for substrate, intermediate, and arginine analog inhibitor binding.	pimagedine	52-66	nitric oxide synthase 3	Homo sapiens	70-103
12826063-0	2003	Competition and binding of arginine, imidazole, and aminoguanidine to endothelial nitric oxide synthase: aminoguanidine is a poor model for substrate, intermediate, and arginine analog inhibitor binding.	pimagedine	105-119	nitric oxide synthase 3	Homo sapiens	70-103
12657742-2	2003	Endothelial nitric oxide synthase (eNOS) generation of nitric oxide (NO) plays an important role in endothelial cell proliferation, which is considered essential for normal blood vessel growth and development.	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	35-39
12657742-11	2003	These data show that TRI alters hsp90 interactions with eNOS and induces eNOS to shift from NO to O2- generation.	Superoxides	98-100	nitric oxide synthase 3	Homo sapiens	73-77
12591925-0	2003	Compensatory phosphorylation and protein-protein interactions revealed by loss of function and gain of function mutants of multiple serine phosphorylation sites in endothelial nitric-oxide synthase.	Serine	132-138	nitric oxide synthase 3	Homo sapiens	164-197
12591925-1	2003	We examined the influence of individual serine phosphorylation sites in endothelial nitric-oxide synthase (eNOS) on basal and stimulated NO release, cooperative phosphorylation, and co-association with hsp90 and Akt.	Serine	40-46	nitric oxide synthase 3	Homo sapiens	72-105
12569550-0	2003	Reactive oxygen species-mediated regulation of eNOS and iNOS expression in multicellular prostate tumor spheroids.	Reactive Oxygen Species	0-23	nitric oxide synthase 3	Homo sapiens	47-51
12569550-1	2003	Nitric oxide (NO) generated by either endothelial nitric oxide synthase (eNOS) or inducible nitric oxide synthase (iNOS) may be involved in prostate tumorigenesis through the inhibition of reactive oxygen species (ROS)-induced apoptosis.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	38-71
12569550-1	2003	Nitric oxide (NO) generated by either endothelial nitric oxide synthase (eNOS) or inducible nitric oxide synthase (iNOS) may be involved in prostate tumorigenesis through the inhibition of reactive oxygen species (ROS)-induced apoptosis.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	73-77
12569550-1	2003	Nitric oxide (NO) generated by either endothelial nitric oxide synthase (eNOS) or inducible nitric oxide synthase (iNOS) may be involved in prostate tumorigenesis through the inhibition of reactive oxygen species (ROS)-induced apoptosis.	Reactive Oxygen Species	189-212	nitric oxide synthase 3	Homo sapiens	38-71
12569550-1	2003	Nitric oxide (NO) generated by either endothelial nitric oxide synthase (eNOS) or inducible nitric oxide synthase (iNOS) may be involved in prostate tumorigenesis through the inhibition of reactive oxygen species (ROS)-induced apoptosis.	Reactive Oxygen Species	189-212	nitric oxide synthase 3	Homo sapiens	73-77
12569550-1	2003	Nitric oxide (NO) generated by either endothelial nitric oxide synthase (eNOS) or inducible nitric oxide synthase (iNOS) may be involved in prostate tumorigenesis through the inhibition of reactive oxygen species (ROS)-induced apoptosis.	Reactive Oxygen Species	214-217	nitric oxide synthase 3	Homo sapiens	38-71
12569550-5	2003	Elevation of ROS by treatment of tumor spheroids with either buthionine sulfoximine (BSO) or hydrogen peroxide resulted in upregulation of eNOS, whereas iNOS was downregulated.	Reactive Oxygen Species	13-16	nitric oxide synthase 3	Homo sapiens	139-143
12569550-5	2003	Elevation of ROS by treatment of tumor spheroids with either buthionine sulfoximine (BSO) or hydrogen peroxide resulted in upregulation of eNOS, whereas iNOS was downregulated.	Buthionine Sulfoximine	61-83	nitric oxide synthase 3	Homo sapiens	139-143
12569550-5	2003	Elevation of ROS by treatment of tumor spheroids with either buthionine sulfoximine (BSO) or hydrogen peroxide resulted in upregulation of eNOS, whereas iNOS was downregulated.	Buthionine Sulfoximine	85-88	nitric oxide synthase 3	Homo sapiens	139-143
12569550-5	2003	Elevation of ROS by treatment of tumor spheroids with either buthionine sulfoximine (BSO) or hydrogen peroxide resulted in upregulation of eNOS, whereas iNOS was downregulated.	Hydrogen Peroxide	93-110	nitric oxide synthase 3	Homo sapiens	139-143
12569550-7	2003	Upregulation of eNOS after treatment with hydrogen peroxide was apparently transduced through receptor tyrosine kinase signaling pathways since it was abolished by the protein kinase C (PKC) inhibitor bisindolylmaleimide-1 (BIM-1), the p21(ras) inhibitor S-trans-trans-farnesylthiosalicylic acid (FTS), the c-Raf inhibitor ZM 336372 and PD98059, which inhibits ERK1/2 activation.	Hydrogen Peroxide	42-59	nitric oxide synthase 3	Homo sapiens	16-20
12569550-7	2003	Upregulation of eNOS after treatment with hydrogen peroxide was apparently transduced through receptor tyrosine kinase signaling pathways since it was abolished by the protein kinase C (PKC) inhibitor bisindolylmaleimide-1 (BIM-1), the p21(ras) inhibitor S-trans-trans-farnesylthiosalicylic acid (FTS), the c-Raf inhibitor ZM 336372 and PD98059, which inhibits ERK1/2 activation.	bisindolylmaleimide-1	201-222	nitric oxide synthase 3	Homo sapiens	16-20
12569550-7	2003	Upregulation of eNOS after treatment with hydrogen peroxide was apparently transduced through receptor tyrosine kinase signaling pathways since it was abolished by the protein kinase C (PKC) inhibitor bisindolylmaleimide-1 (BIM-1), the p21(ras) inhibitor S-trans-trans-farnesylthiosalicylic acid (FTS), the c-Raf inhibitor ZM 336372 and PD98059, which inhibits ERK1/2 activation.	bisindolylmaleimide I	224-229	nitric oxide synthase 3	Homo sapiens	16-20
12569550-7	2003	Upregulation of eNOS after treatment with hydrogen peroxide was apparently transduced through receptor tyrosine kinase signaling pathways since it was abolished by the protein kinase C (PKC) inhibitor bisindolylmaleimide-1 (BIM-1), the p21(ras) inhibitor S-trans-trans-farnesylthiosalicylic acid (FTS), the c-Raf inhibitor ZM 336372 and PD98059, which inhibits ERK1/2 activation.	farnesylthiosalicylic acid	255-295	nitric oxide synthase 3	Homo sapiens	16-20
12569550-7	2003	Upregulation of eNOS after treatment with hydrogen peroxide was apparently transduced through receptor tyrosine kinase signaling pathways since it was abolished by the protein kinase C (PKC) inhibitor bisindolylmaleimide-1 (BIM-1), the p21(ras) inhibitor S-trans-trans-farnesylthiosalicylic acid (FTS), the c-Raf inhibitor ZM 336372 and PD98059, which inhibits ERK1/2 activation.	farnesylthiosalicylic acid	297-300	nitric oxide synthase 3	Homo sapiens	16-20
12569550-7	2003	Upregulation of eNOS after treatment with hydrogen peroxide was apparently transduced through receptor tyrosine kinase signaling pathways since it was abolished by the protein kinase C (PKC) inhibitor bisindolylmaleimide-1 (BIM-1), the p21(ras) inhibitor S-trans-trans-farnesylthiosalicylic acid (FTS), the c-Raf inhibitor ZM 336372 and PD98059, which inhibits ERK1/2 activation.	N-(5-(3-dimethylaminobenzamido)-2-methylphenyl)-4-hydroxybenzamide	323-332	nitric oxide synthase 3	Homo sapiens	16-20
12569550-7	2003	Upregulation of eNOS after treatment with hydrogen peroxide was apparently transduced through receptor tyrosine kinase signaling pathways since it was abolished by the protein kinase C (PKC) inhibitor bisindolylmaleimide-1 (BIM-1), the p21(ras) inhibitor S-trans-trans-farnesylthiosalicylic acid (FTS), the c-Raf inhibitor ZM 336372 and PD98059, which inhibits ERK1/2 activation.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	337-344	nitric oxide synthase 3	Homo sapiens	16-20
12547825-7	2003	We further show that, 1) 17-epiestriol induces the expression of endothelial nitric-oxide synthase mRNA and protein, 2) 17-epiestriol prevents TNFalpha-induced migration of NFkappaB into the nucleus, 3) N(G)-nitro-l-arginine methyl ester, an inhibitor of NO synthesis, abolishes 17-epiestriol-mediated inhibition of TNFalpha-induced VCAM-1 expression and migration of NFkappaB from the cytoplasm to the nucleus.	17-Epiestriol	25-38	nitric oxide synthase 3	Homo sapiens	65-98
12682286-2	2003	We previously demonstrated that estrogen rapidly induces nitric oxide release via a phosphatidylinositol 3-kinase/Akt/endothelial nitric-oxide synthase (eNOS) pathway in EA.hy926 cells (immortalized human endothelial cells), which express a 46-kDa ER.	Nitric Oxide	57-69	nitric oxide synthase 3	Homo sapiens	118-151
12692005-0	2003	Nebivolol prevents vascular NOS III uncoupling in experimental hyperlipidemia and inhibits NADPH oxidase activity in inflammatory cells.	Nebivolol	0-9	nitric oxide synthase 3	Homo sapiens	28-35
12665482-2	2003	When uncoupled from essential cofactors, endothelial nitric oxide synthase (eNOS) produces O2*-.	Superoxides	91-95	nitric oxide synthase 3	Homo sapiens	41-74
12665482-2	2003	When uncoupled from essential cofactors, endothelial nitric oxide synthase (eNOS) produces O2*-.	Superoxides	91-95	nitric oxide synthase 3	Homo sapiens	76-80
12665482-5	2003	When eNOS is functioning normally, incorporation of Nomega-Nitro-L-Arginine methyl ester (L-NAME, 1 mmol/L), results in increased O2*- detection, as inhibition of NO production prevents NO scavenging of O2*-.	NG-Nitroarginine Methyl Ester	52-88	nitric oxide synthase 3	Homo sapiens	5-9
12665482-5	2003	When eNOS is functioning normally, incorporation of Nomega-Nitro-L-Arginine methyl ester (L-NAME, 1 mmol/L), results in increased O2*- detection, as inhibition of NO production prevents NO scavenging of O2*-.	NG-Nitroarginine Methyl Ester	90-96	nitric oxide synthase 3	Homo sapiens	5-9
12665482-5	2003	When eNOS is functioning normally, incorporation of Nomega-Nitro-L-Arginine methyl ester (L-NAME, 1 mmol/L), results in increased O2*- detection, as inhibition of NO production prevents NO scavenging of O2*-.	Superoxides	130-132	nitric oxide synthase 3	Homo sapiens	5-9
12665482-7	2003	In the remaining 9 CCF patients, incorporation of L-NAME reduced O2*- production by 39%, indicating O2*- production by eNOS uncoupling.	Superoxides	100-104	nitric oxide synthase 3	Homo sapiens	119-123
12665482-9	2003	Endothelium-dependent and -independent vasodilator responses to acetylcholine and sodium nitroprusside recorded using venous occlusion plethysmography were significantly impaired in patients exhibiting eNOS uncoupling.	Acetylcholine	64-77	nitric oxide synthase 3	Homo sapiens	202-206
12665482-9	2003	Endothelium-dependent and -independent vasodilator responses to acetylcholine and sodium nitroprusside recorded using venous occlusion plethysmography were significantly impaired in patients exhibiting eNOS uncoupling.	Nitroprusside	82-102	nitric oxide synthase 3	Homo sapiens	202-206
12668492-5	2003	The polymorphism in exon 7 of NOS3, a G-T transition at position 894 that results in a Glu to Asp amino acid substitution for codon 298, was genotyped and subjects were followed prospectively to the end point of death or heart transplantation.	Glutamic Acid	87-90	nitric oxide synthase 3	Homo sapiens	30-34
12668492-5	2003	The polymorphism in exon 7 of NOS3, a G-T transition at position 894 that results in a Glu to Asp amino acid substitution for codon 298, was genotyped and subjects were followed prospectively to the end point of death or heart transplantation.	asp amino acid	94-108	nitric oxide synthase 3	Homo sapiens	30-34
14967938-7	2003	A significant synthesis of NO by oocytes was observed in the presence of ionomycin, but not in the absence of ionomycin, indicating that oocyte NOS-3 functions in response to transient elevations in the intracellular calcium level.	Ionomycin	73-82	nitric oxide synthase 3	Homo sapiens	144-149
12676608-5	2003	In cultured human aortic endothelial cells, treatment with arsenite resulted in a concentration-dependent inhibition of endothelial nitric oxide synthase (eNOS).	arsenite	59-67	nitric oxide synthase 3	Homo sapiens	120-153
12701065-7	2003	In addition, the expression of endothelial nitric oxide synthase (eNOS) was altered, with linoleic acid increasing eNOS activity.	Linoleic Acid	90-103	nitric oxide synthase 3	Homo sapiens	31-64
12709683-3	2003	Furthermore, this signaling system is coupled to constitutive nitric oxide synthase (cNOS)-derived nitric oxide (NO) release in both vertebrates and invertebrates, thereby regulating neural, immune, and vascular-like functions in these divergent organisms.	Nitric Oxide	62-74	nitric oxide synthase 3	Homo sapiens	85-89
14967938-7	2003	A significant synthesis of NO by oocytes was observed in the presence of ionomycin, but not in the absence of ionomycin, indicating that oocyte NOS-3 functions in response to transient elevations in the intracellular calcium level.	Calcium	217-224	nitric oxide synthase 3	Homo sapiens	144-149
12628472-1	2003	Nitric oxide (NO) is synthesized from L-arginine by neuronal, endothelial and inducible isoforms of NO synthase (nNOS, eNOS and iNOS, respectively) and is involved in the regulation of a variety of physiological functions, including immune activity.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	119-123
12709683-4	2003	In human endothelial cells from various blood vessels, CB1 immunoreactive components are present as is its coupling to anandamide-stimulated cNOS-derived NO production, which exerts an autoregulatory role on cNOS release.	anandamide	119-129	nitric oxide synthase 3	Homo sapiens	141-145
12709683-4	2003	In human endothelial cells from various blood vessels, CB1 immunoreactive components are present as is its coupling to anandamide-stimulated cNOS-derived NO production, which exerts an autoregulatory role on cNOS release.	anandamide	119-129	nitric oxide synthase 3	Homo sapiens	208-212
12670736-2	2003	Many recent mechanistic studies have focused on the ability of estradiol to stimulate endothelial nitric oxide synthase (eNOS) and the subsequent generation of nitric oxide (NO).	Estradiol	63-72	nitric oxide synthase 3	Homo sapiens	86-119
12670736-2	2003	Many recent mechanistic studies have focused on the ability of estradiol to stimulate endothelial nitric oxide synthase (eNOS) and the subsequent generation of nitric oxide (NO).	Estradiol	63-72	nitric oxide synthase 3	Homo sapiens	121-125
12670736-2	2003	Many recent mechanistic studies have focused on the ability of estradiol to stimulate endothelial nitric oxide synthase (eNOS) and the subsequent generation of nitric oxide (NO).	Nitric Oxide	98-110	nitric oxide synthase 3	Homo sapiens	121-125
12651037-1	2003	OBJECTIVES: We sought to investigate whether two polymorphisms located in the promoter (T(-786)C) and exon 7 (Glu298Asp) of the endothelial nitric oxide (NO) synthase (eNOS) gene affected agonists-mediated NO release.	Nitric Oxide	140-152	nitric oxide synthase 3	Homo sapiens	168-172
12519764-1	2003	Endothelial nitric oxide synthase (eNOS), which generates the endogenous vasodilator, nitric oxide (NO), is highly regulated by post-translational modifications and protein interactions.	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	35-39
12519764-7	2003	HSP90 also significantly increased the rate of NADPH-dependent cytochrome c reduction by eNOS at both low and high Ca(2+) concentrations.	NADP	47-52	nitric oxide synthase 3	Homo sapiens	89-93
12519764-9	2003	At 100 nm Ca(2+), HSP90 promoted dose-dependent CaM binding to eNOS that was fully inhibitable by GA. At high calcium, HSP90 did not affect CaM binding to eNOS, but GA inhibited HSP90 binding to eNOS.	geldanamycin	98-100	nitric oxide synthase 3	Homo sapiens	63-67
12519764-10	2003	At high Ca(2+), HSP90 caused the V(max) of eNOS for l-arginine to increase by 2-fold, but the K(m) of eNOS was unchanged.	Arginine	52-62	nitric oxide synthase 3	Homo sapiens	43-47
12600864-10	2003	Mixed tocopherols were more potent than alpha-tocopherol alone in modulating NO release and ecNOS activation but not SOD protein content or PKC activation.	alpha-Tocopherol	40-56	nitric oxide synthase 3	Homo sapiens	92-97
12600864-12	2003	Effects of mixed tocopherols were associated with increased NO release, ecNOS activation, and SOD protein content in platelets, which may contribute to the effect on platelet aggregation.	Tocopherols	17-28	nitric oxide synthase 3	Homo sapiens	72-77
12600864-6	2003	ADP and phorbol 12-myristate 13-acetate-induced platelet aggregation, nitric oxide (NO) release, activation of endothelial constitutive nitric-oxide synthase (ecNOS; EC 1.14.13.39) and of protein kinase C (PKC), and ecNOS, superoxide dismutase (SOD; EC 1.15.1.1), and PKC protein content in platelets were measured before and after 8 wk of administration of tocopherols.	Tetradecanoylphorbol Acetate	8-39	nitric oxide synthase 3	Homo sapiens	111-157
12600864-6	2003	ADP and phorbol 12-myristate 13-acetate-induced platelet aggregation, nitric oxide (NO) release, activation of endothelial constitutive nitric-oxide synthase (ecNOS; EC 1.14.13.39) and of protein kinase C (PKC), and ecNOS, superoxide dismutase (SOD; EC 1.15.1.1), and PKC protein content in platelets were measured before and after 8 wk of administration of tocopherols.	Tetradecanoylphorbol Acetate	8-39	nitric oxide synthase 3	Homo sapiens	159-164
12600864-6	2003	ADP and phorbol 12-myristate 13-acetate-induced platelet aggregation, nitric oxide (NO) release, activation of endothelial constitutive nitric-oxide synthase (ecNOS; EC 1.14.13.39) and of protein kinase C (PKC), and ecNOS, superoxide dismutase (SOD; EC 1.15.1.1), and PKC protein content in platelets were measured before and after 8 wk of administration of tocopherols.	Tetradecanoylphorbol Acetate	8-39	nitric oxide synthase 3	Homo sapiens	216-221
12600864-8	2003	NO release, ecNOS activation, and SOD protein content in platelets increased in the tocopherol-treated groups.	Tocopherols	84-94	nitric oxide synthase 3	Homo sapiens	12-17
12600864-10	2003	Mixed tocopherols were more potent than alpha-tocopherol alone in modulating NO release and ecNOS activation but not SOD protein content or PKC activation.	Tocopherols	6-17	nitric oxide synthase 3	Homo sapiens	92-97
12590932-5	2003	Menadione increased L-arginine uptake by the cells, but inhibited endothelial nitric oxide synthase, an effect that was prevented by acute loading with ascorbate.	Vitamin K 3	0-9	nitric oxide synthase 3	Homo sapiens	66-99
12590926-0	2003	Differential effects of mutations in human endothelial nitric oxide synthase at residues Tyr-357 and Arg-365 on L-arginine hydroxylation and GN-hydroxy-L-arginine oxidation.	Tyrosine	89-92	nitric oxide synthase 3	Homo sapiens	43-76
12590932-5	2003	Menadione increased L-arginine uptake by the cells, but inhibited endothelial nitric oxide synthase, an effect that was prevented by acute loading with ascorbate.	Ascorbic Acid	152-161	nitric oxide synthase 3	Homo sapiens	66-99
12590926-0	2003	Differential effects of mutations in human endothelial nitric oxide synthase at residues Tyr-357 and Arg-365 on L-arginine hydroxylation and GN-hydroxy-L-arginine oxidation.	Arginine	112-122	nitric oxide synthase 3	Homo sapiens	43-76
12607129-1	2003	OBJECTIVE: Although it has been shown recently that acetylcholine (ACh)-induced vasodilation of forearm resistance vessels is predominantly mediated by nitric oxide, direct biochemical evidence for eNOS stimulation by bradykinin (BK) in the human arterial circulation is still lacking.	Acetylcholine	67-70	nitric oxide synthase 3	Homo sapiens	198-202
12600950-2	2003	This study investigated the relationship of the eNOS Glu(298)--&gt;Asp and T(786)--&gt;C polymorphisms with the presence and severity of CAD in the Italian population.	Glutamic Acid	53-56	nitric oxide synthase 3	Homo sapiens	48-52
12600950-10	2003	CONCLUSIONS: The present study provides evidence that the Glu(298)--&gt;Asp and T(786)--&gt;C polymorphisms of the eNOS gene are associated with the presence and severity of angiographically defined CAD in the Italian population and that those individuals carrying both eNOS variants simultaneously might have a higher risk of developing CAD.	Glutamic Acid	58-61	nitric oxide synthase 3	Homo sapiens	115-119
12600950-10	2003	CONCLUSIONS: The present study provides evidence that the Glu(298)--&gt;Asp and T(786)--&gt;C polymorphisms of the eNOS gene are associated with the presence and severity of angiographically defined CAD in the Italian population and that those individuals carrying both eNOS variants simultaneously might have a higher risk of developing CAD.	Glutamic Acid	58-61	nitric oxide synthase 3	Homo sapiens	270-274
12641536-1	2003	OBJECTIVE: Conflicting data exists about the possible contribution of the homozygous Asp/Asp genotype of the Glu298Asp polymorphism of endothelial nitric oxide synthase to human atherosclerotic vascular disease.	Aspartic Acid	85-88	nitric oxide synthase 3	Homo sapiens	135-168
12641536-1	2003	OBJECTIVE: Conflicting data exists about the possible contribution of the homozygous Asp/Asp genotype of the Glu298Asp polymorphism of endothelial nitric oxide synthase to human atherosclerotic vascular disease.	Aspartic Acid	89-92	nitric oxide synthase 3	Homo sapiens	135-168
12631094-10	2003	A positive linear relationship was found between cNOS activity in cortex and creatinine clearance.	Creatinine	77-87	nitric oxide synthase 3	Homo sapiens	49-53
12640355-2	2003	Unlike classical steroid transcription mediated pathways, estrogen"s acute vasodilatory effect is mediated by calcium dependent cell surface estrogen receptors that stimulate constitutive endothelial nitric oxide synthase (eNOS) activity.	Calcium	110-117	nitric oxide synthase 3	Homo sapiens	188-221
12640355-2	2003	Unlike classical steroid transcription mediated pathways, estrogen"s acute vasodilatory effect is mediated by calcium dependent cell surface estrogen receptors that stimulate constitutive endothelial nitric oxide synthase (eNOS) activity.	Calcium	110-117	nitric oxide synthase 3	Homo sapiens	223-227
12640355-3	2003	The transient release of eNOS derived nitric oxide exerts profound physiological effects on the vasculature exerting a state of cellular inhibition (i.e. vasodilation).	Nitric Oxide	38-50	nitric oxide synthase 3	Homo sapiens	25-29
12488320-0	2003	The proline-rich domain of dynamin-2 is responsible for dynamin-dependent in vitro potentiation of endothelial nitric-oxide synthase activity via selective effects on reductase domain function.	Proline	4-11	nitric oxide synthase 3	Homo sapiens	99-132
12488320-1	2003	The GTPase dynamin-2 (dyn-2) binds and positively regulates the nitric oxide-generating enzyme, endothelial nitric-oxide synthase (eNOS) (Cao, S., Yao, Y., McCabe, T., Yao, Q., Katusic, Z., Sessa, W., and Shah, V. (2001) J. Biol.	Nitric Oxide	64-76	nitric oxide synthase 3	Homo sapiens	96-129
12615295-6	2003	Studies in experimental models of ischemic stroke show that statin therapy reduces brain infarct size and improves neurologic outcome by directly upregulating brain endothelial nitric oxide synthase.	statin	60-66	nitric oxide synthase 3	Homo sapiens	165-198
12588285-0	2003	The effect of lipoproteins on endothelial nitric oxide synthase is modulated by lipoperoxides.	Lipid Peroxides	80-93	nitric oxide synthase 3	Homo sapiens	30-63
12480940-3	2003	UV-visible and electron paramagnetic resonance (EPR) spectral characterization for the resting eNOS(ox) and its complexes with various ligands indicated a standard NOS heme structure as a thiolate hemeprotein.	Heme	168-172	nitric oxide synthase 3	Homo sapiens	95-99
12480940-4	2003	Two low spin imidazole heme complexes but not the isolated eNOS(ox) were resolved by EPR indicating slight difference in heme geometry of the dimeric eNOS(ox) domain.	imidazole heme	13-27	nitric oxide synthase 3	Homo sapiens	150-154
12480940-4	2003	Two low spin imidazole heme complexes but not the isolated eNOS(ox) were resolved by EPR indicating slight difference in heme geometry of the dimeric eNOS(ox) domain.	Heme	23-27	nitric oxide synthase 3	Homo sapiens	150-154
12480940-5	2003	Stoichiometric titration of eNOS(ox) demonstrated that the heme has a capacity for a reducing equivalent of 1-1.5.	Heme	59-63	nitric oxide synthase 3	Homo sapiens	28-32
12480940-8	2003	Ferrous eNOS(ox), in the presence of l-arginine, is fully functional in forming the tetrahydrobiopterin radical upon mixing with oxygen as demonstrated by rapid-freeze EPR measurements.	Arginine	37-47	nitric oxide synthase 3	Homo sapiens	8-12
12480940-8	2003	Ferrous eNOS(ox), in the presence of l-arginine, is fully functional in forming the tetrahydrobiopterin radical upon mixing with oxygen as demonstrated by rapid-freeze EPR measurements.	tetrahydrobiopterin radical	84-111	nitric oxide synthase 3	Homo sapiens	8-12
12480940-8	2003	Ferrous eNOS(ox), in the presence of l-arginine, is fully functional in forming the tetrahydrobiopterin radical upon mixing with oxygen as demonstrated by rapid-freeze EPR measurements.	Oxygen	129-135	nitric oxide synthase 3	Homo sapiens	8-12
12480940-12	2003	This first redox characterization on both eNOS domains by stoichiometric titration and the generation of a high quality EPR spectrum for the BH(4) radical intermediate illustrated the usefulness of these tools in future detailed investigations into the reaction mechanism of eNOS.	bh(4) radical	141-154	nitric oxide synthase 3	Homo sapiens	275-279
12588285-10	2003	In HMEC-1 and in HUVEC, mildly oxidized LDLs stimulated both e-NOS and NO2/NO3 accumulation; the effect on e-NOS was potentiated by vitamin C in HMEC-1.	Ascorbic Acid	132-141	nitric oxide synthase 3	Homo sapiens	107-112
12574107-1	2003	Endothelium-dependent vasorelaxation plays an important role in reduction of blood pressure and is mediated through release of nitric oxide (NO), which is generated by constitutively expressed endothelial nitric oxide synthase (NOS3).	Nitric Oxide	127-139	nitric oxide synthase 3	Homo sapiens	193-226
12552477-10	2003	The blunted blood pressure increase of smokers compared to controls following CPT, may represent altered nitric oxide production in the macro and microcirculation through differential upregulation of endothelial nitric oxide synthase (eNOS) and inducible NOS respectively.	Nitric Oxide	105-117	nitric oxide synthase 3	Homo sapiens	200-233
12574107-1	2003	Endothelium-dependent vasorelaxation plays an important role in reduction of blood pressure and is mediated through release of nitric oxide (NO), which is generated by constitutively expressed endothelial nitric oxide synthase (NOS3).	Nitric Oxide	127-139	nitric oxide synthase 3	Homo sapiens	228-232
12594242-5	2003	In addition, NOS3 overexpression impaired neuronal Mt function as demonstrated by the reduced levels of 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide and nicotinamide adenine dinucleotide (reduced form)-tetrazolium reductase activities and MitoTracker Red fluorescence.	thiazolyl blue	104-164	nitric oxide synthase 3	Homo sapiens	13-17
12594242-5	2003	In addition, NOS3 overexpression impaired neuronal Mt function as demonstrated by the reduced levels of 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide and nicotinamide adenine dinucleotide (reduced form)-tetrazolium reductase activities and MitoTracker Red fluorescence.	NAD	169-202	nitric oxide synthase 3	Homo sapiens	13-17
12594242-5	2003	In addition, NOS3 overexpression impaired neuronal Mt function as demonstrated by the reduced levels of 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide and nicotinamide adenine dinucleotide (reduced form)-tetrazolium reductase activities and MitoTracker Red fluorescence.	Tetrazolium Salts	145-156	nitric oxide synthase 3	Homo sapiens	13-17
12594242-6	2003	These adverse effects of NOS3 were associated with increased cellular levels of reactive oxygen species and impaired membrane integrity and were not produced in cells that were transfected with a cDNA encoding catalytically inactive NOS3.	reactive	80-88	nitric oxide synthase 3	Homo sapiens	25-29
12594242-6	2003	These adverse effects of NOS3 were associated with increased cellular levels of reactive oxygen species and impaired membrane integrity and were not produced in cells that were transfected with a cDNA encoding catalytically inactive NOS3.	oxygen species	89-103	nitric oxide synthase 3	Homo sapiens	25-29
12594242-7	2003	Importantly, modest elevations in NOS3 expression, achieved by infection with low multiplicities of adenovirus-NOS3 infection, did not cause apoptosis but rendered the cells more sensitive to oxidative injury by H(2)O(2) or diethyldithiocarbamate.	h(2)o	212-217	nitric oxide synthase 3	Homo sapiens	34-38
12594242-7	2003	Importantly, modest elevations in NOS3 expression, achieved by infection with low multiplicities of adenovirus-NOS3 infection, did not cause apoptosis but rendered the cells more sensitive to oxidative injury by H(2)O(2) or diethyldithiocarbamate.	Ditiocarb	224-246	nitric oxide synthase 3	Homo sapiens	34-38
12559774-3	2003	Normally, endothelial nitric oxide synthase (eNOS) produces a tonic amount of nitric oxide (NO), which is responsible for the homeostasis between the endothelium and surrounding tissues.	Nitric Oxide	22-34	nitric oxide synthase 3	Homo sapiens	45-49
12586536-5	2003	The mutant was activated by BH4 with an EC(50) of 0.24+/-0.04 microM, a value comparable to that obtained with WT eNOS (0.22+/-0.02 microM).	sapropterin	28-31	nitric oxide synthase 3	Homo sapiens	114-118
12503100-1	2003	Through the nitric oxide (NO) production in the vascular system, the endothelial nitric oxide synthase (eNOS or NOS3) is a key enzyme in blood pressure regulation and atherosclerosis control.	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	69-102
12503100-1	2003	Through the nitric oxide (NO) production in the vascular system, the endothelial nitric oxide synthase (eNOS or NOS3) is a key enzyme in blood pressure regulation and atherosclerosis control.	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	104-108
12503100-1	2003	Through the nitric oxide (NO) production in the vascular system, the endothelial nitric oxide synthase (eNOS or NOS3) is a key enzyme in blood pressure regulation and atherosclerosis control.	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	112-116
12431978-1	2003	17beta-Estradiol activates endothelial nitric oxide synthase (eNOS), enhancing nitric oxide (NO) release from endothelial cells via the phosphatidylinositol 3-kinase (PI3-kinase)/Akt pathway.	Estradiol	0-16	nitric oxide synthase 3	Homo sapiens	27-60
12490885-1	2003	Dinucleotide CA repeats of variable length in an intron of the human endothelial nitric oxide synthase gene act as regulatory signals for splicing of the gene"s pre-mRNA.	Dinucleoside Phosphates	0-12	nitric oxide synthase 3	Homo sapiens	69-102
12521608-2	2003	Increased expression of endothelial nitric oxide synthase (eNOS) has been shown to play an important role in maintaining high levels of (*)NO generation to offset the increase in O(2)(*-) that occurs during proliferation.	Superoxides	179-183	nitric oxide synthase 3	Homo sapiens	24-57
15000126-7	2003	Cultured bone cells also rapidly produce nitric oxide (NO) in response to fluid flow as a result of activation of endothelial nitric oxide synthase (ecNOS), which enzyme also mediates the adaptive response of bone tissue to mechanical loading.	Nitric Oxide	41-53	nitric oxide synthase 3	Homo sapiens	114-147
15000126-7	2003	Cultured bone cells also rapidly produce nitric oxide (NO) in response to fluid flow as a result of activation of endothelial nitric oxide synthase (ecNOS), which enzyme also mediates the adaptive response of bone tissue to mechanical loading.	Nitric Oxide	41-53	nitric oxide synthase 3	Homo sapiens	149-154
12482742-1	2003	The endothelial nitric oxide synthase (eNOS), the expression of which is regulated by a range of transcriptional and posttranscriptional mechanisms, generates nitric oxide (NO) in response to a number of stimuli.	Nitric Oxide	16-28	nitric oxide synthase 3	Homo sapiens	39-43
12482742-4	2003	Two amino acids seem to be particularly important in regulating eNOS activity and these are a serine residue in the reductase domain (Ser(1177)) and a threonine residue (Thr(495)) located within the CaM-binding domain.	Serine	94-100	nitric oxide synthase 3	Homo sapiens	64-68
12482742-4	2003	Two amino acids seem to be particularly important in regulating eNOS activity and these are a serine residue in the reductase domain (Ser(1177)) and a threonine residue (Thr(495)) located within the CaM-binding domain.	Serine	134-137	nitric oxide synthase 3	Homo sapiens	64-68
12482742-4	2003	Two amino acids seem to be particularly important in regulating eNOS activity and these are a serine residue in the reductase domain (Ser(1177)) and a threonine residue (Thr(495)) located within the CaM-binding domain.	Threonine	151-160	nitric oxide synthase 3	Homo sapiens	64-68
12482742-4	2003	Two amino acids seem to be particularly important in regulating eNOS activity and these are a serine residue in the reductase domain (Ser(1177)) and a threonine residue (Thr(495)) located within the CaM-binding domain.	Threonine	170-173	nitric oxide synthase 3	Homo sapiens	64-68
12482742-5	2003	Simultaneous alterations in the phosphorylation of Ser(1177) and Thr(495) in response to a variety of stimuli are regulated by a number of kinases and phosphatases that continuously associate with and dissociate from the eNOS signaling complex.	Serine	51-54	nitric oxide synthase 3	Homo sapiens	221-225
12482742-5	2003	Simultaneous alterations in the phosphorylation of Ser(1177) and Thr(495) in response to a variety of stimuli are regulated by a number of kinases and phosphatases that continuously associate with and dissociate from the eNOS signaling complex.	Threonine	65-68	nitric oxide synthase 3	Homo sapiens	221-225
12524222-7	2003	Our data indicate that AII increased the expression of endothelial NOS, inducible NOS, and NAD(P)H oxidase in a dose-dependent manner, which was attenuated by incubation with either E2, superoxide dismutase, or the AII type 1 receptor (AT1R) inhibitor candesartan.	candesartan	252-263	nitric oxide synthase 3	Homo sapiens	55-70
12474221-2	2003	Nitric oxide is produced by the nitric oxide synthases, endothelial NOS (eNOS), neural NOS (nNOS), and inducible NOS (iNOS).	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	56-71
12474221-2	2003	Nitric oxide is produced by the nitric oxide synthases, endothelial NOS (eNOS), neural NOS (nNOS), and inducible NOS (iNOS).	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	73-77
12524661-6	2003	Treatment of HAECs with gly-ox-HDL attenuated the expression of endothelial nitric oxide synthase (eNOS), but not inducible nitric oxide synthase (iNOS), and this was followed by decreased production of nitric oxide (NO) by the cells.	Glycine	24-27	nitric oxide synthase 3	Homo sapiens	64-97
14580231-1	2003	INTRODUCTION: Endothelial nitric oxide synthase (ecNOS) is a key regulator of vascular nitric oxide production.	Nitric Oxide	26-38	nitric oxide synthase 3	Homo sapiens	49-54
14610325-5	2003	In addition, we evaluated the effect of glucose on the expression of endothelial nitric oxide synthase (eNOS) in HGECs by Western blotting.	Glucose	40-47	nitric oxide synthase 3	Homo sapiens	69-102
14610325-5	2003	In addition, we evaluated the effect of glucose on the expression of endothelial nitric oxide synthase (eNOS) in HGECs by Western blotting.	Glucose	40-47	nitric oxide synthase 3	Homo sapiens	104-108
14989558-0	2003	Interactive effects of the ACE DD polymorphism with the NOS III homozygous G849T (Glu298--&gt;Asp) variant in determining endothelial function in coronary artery disease.	Aspartic Acid	94-97	nitric oxide synthase 3	Homo sapiens	56-63
14610325-7	2003	However, Western blot analysis revealed that eNOS protein expression was significantly upregulated at 12 h after exposure to high glucose concentrations (30 mM), reaching a peak at 48 h (twofold increase over baseline levels).	Glucose	130-137	nitric oxide synthase 3	Homo sapiens	45-49
14610325-10	2003	CONCLUSIONS: The present study demonstrated that high glucose increased eNOS protein expression, but decreased NO release finally.	Glucose	54-61	nitric oxide synthase 3	Homo sapiens	72-76
15981946-4	2003	PKC-mediated superoxide production may inactivate nitric oxide (NO) derived from endothelial NOS III, but also may inhibit the activity and/or expression of the NO downstream target, the soluble guanylyl cyclase.	Superoxides	13-23	nitric oxide synthase 3	Homo sapiens	93-100
15981946-4	2003	PKC-mediated superoxide production may inactivate nitric oxide (NO) derived from endothelial NOS III, but also may inhibit the activity and/or expression of the NO downstream target, the soluble guanylyl cyclase.	Nitric Oxide	50-62	nitric oxide synthase 3	Homo sapiens	93-100
12534448-0	2002	Prior aspirin use in unstable angina patients with modified plasma inflammatory markers and endothelial nitric oxide synthase in neutrophils.	Aspirin	6-13	nitric oxide synthase 3	Homo sapiens	92-125
12388304-9	2002	In vitro tube formation was inhibited by N(G)-nitro-l-arginine methyl ester in wild-type mice and restored by a NO donor, diethylenetriamine-NO, in eNOS(-/-) mice (P &lt; 0.05).	diethylenetriamine-no	122-143	nitric oxide synthase 3	Homo sapiens	148-152
14597854-2	2003	Changes in iron availability can affect an important regulator of vascular tone, the endothelial nitric oxide synthase (eNOS), activated by a heme-dependent dimerization.	Iron	11-15	nitric oxide synthase 3	Homo sapiens	85-118
14597854-2	2003	Changes in iron availability can affect an important regulator of vascular tone, the endothelial nitric oxide synthase (eNOS), activated by a heme-dependent dimerization.	Iron	11-15	nitric oxide synthase 3	Homo sapiens	120-124
14597854-2	2003	Changes in iron availability can affect an important regulator of vascular tone, the endothelial nitric oxide synthase (eNOS), activated by a heme-dependent dimerization.	Heme	142-146	nitric oxide synthase 3	Homo sapiens	85-118
14597854-2	2003	Changes in iron availability can affect an important regulator of vascular tone, the endothelial nitric oxide synthase (eNOS), activated by a heme-dependent dimerization.	Heme	142-146	nitric oxide synthase 3	Homo sapiens	120-124
14597854-3	2003	OBJECTIVE: To study the regulation of the anti-hypertensive eNOS in human endothelial cells, in correlation with iron metabolism alterations and stimuli triggering them in vivo, such as inflammation or infection.	Iron	113-117	nitric oxide synthase 3	Homo sapiens	60-64
14597854-7	2003	METHODS: eNOS protein expression was evaluated by separating the monomeric from the active dimeric form by low-temperature sodium dodecyl sulphate poly-acrylamide gel electrophoresis (SDS-PAGE), and mRNA was analyzed by semi-quantitative reverse transcriptase (RT)-polymerase chain reaction (PCR).	Sodium Dodecyl Sulfate	123-146	nitric oxide synthase 3	Homo sapiens	9-13
14597854-7	2003	METHODS: eNOS protein expression was evaluated by separating the monomeric from the active dimeric form by low-temperature sodium dodecyl sulphate poly-acrylamide gel electrophoresis (SDS-PAGE), and mRNA was analyzed by semi-quantitative reverse transcriptase (RT)-polymerase chain reaction (PCR).	Acrylamide	152-162	nitric oxide synthase 3	Homo sapiens	9-13
14597854-7	2003	METHODS: eNOS protein expression was evaluated by separating the monomeric from the active dimeric form by low-temperature sodium dodecyl sulphate poly-acrylamide gel electrophoresis (SDS-PAGE), and mRNA was analyzed by semi-quantitative reverse transcriptase (RT)-polymerase chain reaction (PCR).	Sodium Dodecyl Sulfate	184-187	nitric oxide synthase 3	Homo sapiens	9-13
14597854-10	2003	CONCLUSIONS: The results of this study suggest a down-regulating effect of infectious and inflammatory stimuli on eNOS expression, both at the mRNA level and protein expression or stability and dimerization, enhanced by heme and iron shortage, and indicate eNOS as a possible link between infection and hypertension.	Heme	220-224	nitric oxide synthase 3	Homo sapiens	114-118
14597854-10	2003	CONCLUSIONS: The results of this study suggest a down-regulating effect of infectious and inflammatory stimuli on eNOS expression, both at the mRNA level and protein expression or stability and dimerization, enhanced by heme and iron shortage, and indicate eNOS as a possible link between infection and hypertension.	Iron	229-233	nitric oxide synthase 3	Homo sapiens	114-118
12534448-2	2002	The aim of this study was to explore if prior aspirin therapy in unstable angina (UA) patients could modify systemic inflammatory markers such as interleukin-6 (IL-6), tumour necrosis factor-alpha (TNF-alpha) and intercellular adhesion molecule-1 (ICAM-1) and the expression of endothelial nitric oxide synthase (eNOS) in neutrophils.	Aspirin	46-53	nitric oxide synthase 3	Homo sapiens	278-311
12534448-2	2002	The aim of this study was to explore if prior aspirin therapy in unstable angina (UA) patients could modify systemic inflammatory markers such as interleukin-6 (IL-6), tumour necrosis factor-alpha (TNF-alpha) and intercellular adhesion molecule-1 (ICAM-1) and the expression of endothelial nitric oxide synthase (eNOS) in neutrophils.	Aspirin	46-53	nitric oxide synthase 3	Homo sapiens	313-317
12534448-9	2002	The eNOS protein expression was also higher in neutrophils from the UA patients taking aspirin than in those not taking aspirin.	Aspirin	87-94	nitric oxide synthase 3	Homo sapiens	4-8
12534448-9	2002	The eNOS protein expression was also higher in neutrophils from the UA patients taking aspirin than in those not taking aspirin.	Aspirin	120-127	nitric oxide synthase 3	Homo sapiens	4-8
12534448-10	2002	CONCLUSION: Patients taking aspirin before UA showed a lower systemic inflammatory response and higher eNOS protein expression in their neutrophils	Aspirin	28-35	nitric oxide synthase 3	Homo sapiens	103-107
12489993-1	2002	Previously, we have demonstrated that increased superoxide generation plays a role in the nitric oxide (NO)-mediated inhibition of endothelial NO synthase (NOS III) in endothelial cells (ECs).	Superoxides	48-58	nitric oxide synthase 3	Homo sapiens	156-163
12512694-0	2002	Cerivastatin potentiates nitric oxide release and enos expression through inhibition of isoprenoids synthesis.	cerivastatin	0-12	nitric oxide synthase 3	Homo sapiens	50-54
12512694-3	2002	The long-term effect of cerivastatin on NO release from endothelial cells was determined by using highly sensitive electrochemical microsensors and was correlated with endothelial NO synthase (eNOS) levels.	cerivastatin	24-36	nitric oxide synthase 3	Homo sapiens	193-197
12512694-5	2002	Cerivastatin increased spontaneous (by 53% +/- 6) and an eNOS-stimulated NO release (by 41 +/- 6% for calcium ionophore and by 47 +/- 5% acetylcholine) as well as eNOS expression (by 118 +/- 6%) in the same concentration-range.	cerivastatin	0-12	nitric oxide synthase 3	Homo sapiens	57-61
12512694-5	2002	Cerivastatin increased spontaneous (by 53% +/- 6) and an eNOS-stimulated NO release (by 41 +/- 6% for calcium ionophore and by 47 +/- 5% acetylcholine) as well as eNOS expression (by 118 +/- 6%) in the same concentration-range.	Calcium	102-109	nitric oxide synthase 3	Homo sapiens	57-61
12512694-6	2002	Cerivastatin-dependent increase in both NO release and eNOS expression was revealed after approximately 4 h of exposure reaching the maximum after approximately 10 h. Co-treatment with MVA or GGPP, but not FPP or LDL, reversed the effects of cerivastatin.	cerivastatin	0-12	nitric oxide synthase 3	Homo sapiens	55-59
12512694-6	2002	Cerivastatin-dependent increase in both NO release and eNOS expression was revealed after approximately 4 h of exposure reaching the maximum after approximately 10 h. Co-treatment with MVA or GGPP, but not FPP or LDL, reversed the effects of cerivastatin.	geranylgeranyl pyrophosphate	192-196	nitric oxide synthase 3	Homo sapiens	55-59
12512694-6	2002	Cerivastatin-dependent increase in both NO release and eNOS expression was revealed after approximately 4 h of exposure reaching the maximum after approximately 10 h. Co-treatment with MVA or GGPP, but not FPP or LDL, reversed the effects of cerivastatin.	cerivastatin	242-254	nitric oxide synthase 3	Homo sapiens	55-59
12512694-7	2002	These findings indicate that the long-term effect of cerivastatin resulting in enhanced NO bioavailabilty in endothelial cell is, at least in part, due to up-regulation of eNOS by blocking isoprenoids synthesis.	cerivastatin	53-65	nitric oxide synthase 3	Homo sapiens	172-176
12512694-7	2002	These findings indicate that the long-term effect of cerivastatin resulting in enhanced NO bioavailabilty in endothelial cell is, at least in part, due to up-regulation of eNOS by blocking isoprenoids synthesis.	Terpenes	189-200	nitric oxide synthase 3	Homo sapiens	172-176
12429631-4	2002	EXPERIMENTAL DESIGN: In this study, we characterized the Glu-Asp298 ecNOS polymorphism in a series of 161 prostate cancer cases.	Glutamic Acid	57-60	nitric oxide synthase 3	Homo sapiens	68-73
12444902-1	2002	AIMS: We have evaluated, in cultured human cavernosal smooth muscle cells, the expression and activity of calcium-dependent constitutive nitric oxide synthase (cNOS) and the ability of insulin to induce nitric oxide (NO) production and to increase intracellular cyclic nucleotides guanosine 3",5"-cyclic monophosphate (cGMP) and adenosine 3",5"-cyclic monophosphate (cAMP).	Calcium	106-113	nitric oxide synthase 3	Homo sapiens	160-164
12444902-1	2002	AIMS: We have evaluated, in cultured human cavernosal smooth muscle cells, the expression and activity of calcium-dependent constitutive nitric oxide synthase (cNOS) and the ability of insulin to induce nitric oxide (NO) production and to increase intracellular cyclic nucleotides guanosine 3",5"-cyclic monophosphate (cGMP) and adenosine 3",5"-cyclic monophosphate (cAMP).	Nitric Oxide	137-149	nitric oxide synthase 3	Homo sapiens	160-164
12444902-7	2002	CONCLUSION: Human cavernosal smooth muscle cells, by expressing cNOS activity, are a source of NO and not only its target; in these cells, insulin rapidly activates cNOS through a PI 3-kinase pathway, with a consequent increase of both cyclic nucleotides, thus directly influencing the mechanisms involved in penile vascular tone and interplaying with classical haemodynamic mediators.	Nucleotides, Cyclic	236-254	nitric oxide synthase 3	Homo sapiens	165-169
12483466-0	2002	Endothelial nitric oxide synthase genotype modulates the improvement of coronary blood flow by pravastatin: a placebo-controlled PET study.	Pravastatin	95-106	nitric oxide synthase 3	Homo sapiens	0-33
12483466-1	2002	The objective was to study whether coronary blood flow or its response to pravastatin are affected by genetic variation in the endothelial nitric oxide synthase (eNOS) gene.	Pravastatin	74-85	nitric oxide synthase 3	Homo sapiens	127-160
12483466-1	2002	The objective was to study whether coronary blood flow or its response to pravastatin are affected by genetic variation in the endothelial nitric oxide synthase (eNOS) gene.	Pravastatin	74-85	nitric oxide synthase 3	Homo sapiens	162-166
12483466-12	2002	More specifically, after pravastatin treatment the adenosine-stimulated flow increased by 54.5% in men with the eNOS ba genotype, whereas in the men with the bb genotype no significant change in flow was observed ( P=0.002 for ba versus bb).	Pravastatin	25-36	nitric oxide synthase 3	Homo sapiens	112-116
12483466-12	2002	More specifically, after pravastatin treatment the adenosine-stimulated flow increased by 54.5% in men with the eNOS ba genotype, whereas in the men with the bb genotype no significant change in flow was observed ( P=0.002 for ba versus bb).	Adenosine	51-60	nitric oxide synthase 3	Homo sapiens	112-116
12483466-12	2002	More specifically, after pravastatin treatment the adenosine-stimulated flow increased by 54.5% in men with the eNOS ba genotype, whereas in the men with the bb genotype no significant change in flow was observed ( P=0.002 for ba versus bb).	Barium	117-119	nitric oxide synthase 3	Homo sapiens	112-116
12483466-15	2002	Our results suggest that adenosine-stimulated myocardial perfusion improves after treatment with pravastatin in subjects with the eNOS ba genotype but not in those with the bb genotype.	Adenosine	25-34	nitric oxide synthase 3	Homo sapiens	130-134
12483466-15	2002	Our results suggest that adenosine-stimulated myocardial perfusion improves after treatment with pravastatin in subjects with the eNOS ba genotype but not in those with the bb genotype.	Pravastatin	97-108	nitric oxide synthase 3	Homo sapiens	130-134
12446767-1	2002	Endothelial nitric oxide synthase (eNOS) is an important regulator of cardiovascular homeostasis by production of nitric oxide (NO) from vascular endothelial cells.	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	35-39
12446767-4	2002	Using adenovirus-mediated gene transfer in human umbilical vein endothelial cells (HUVECs), we show here that both active RhoA and ROCK not only downregulate eNOS gene expression as reported previously but also inhibit eNOS phosphorylation at Ser-1177 and cellular NO production with concomitant suppression of PKB activation.	Serine	243-246	nitric oxide synthase 3	Homo sapiens	158-162
12480752-5	2002	In addition, a theoretical capsule summary is presented detailing how AD may develop from chronic cerebral hypoperfusion and the role of critically attained threshold of cerebral hypoperfusion (CATCH) and of vascular nitric oxide derived from endothelial nitric oxide synthase in triggering the cataclysmic cerebromicrovascular pathology.	Nitric Oxide	217-229	nitric oxide synthase 3	Homo sapiens	243-276
12411399-4	2002	The HDAC inhibitors TSA, butyric acid (BuA), and MS-275 time- and concentration-dependently suppressed eNOS protein levels to 41+/-2%, 46+/-12%, and 40+/-12% of control, respectively.	trichostatin A	20-23	nitric oxide synthase 3	Homo sapiens	103-107
12411399-4	2002	The HDAC inhibitors TSA, butyric acid (BuA), and MS-275 time- and concentration-dependently suppressed eNOS protein levels to 41+/-2%, 46+/-12%, and 40+/-12% of control, respectively.	Butyric Acid	25-37	nitric oxide synthase 3	Homo sapiens	103-107
12411399-4	2002	The HDAC inhibitors TSA, butyric acid (BuA), and MS-275 time- and concentration-dependently suppressed eNOS protein levels to 41+/-2%, 46+/-12%, and 40+/-12% of control, respectively.	Butyric Acid	39-42	nitric oxide synthase 3	Homo sapiens	103-107
12411399-9	2002	Although TSA decreased both eNOS protein and mRNA levels, TSA paradoxically enhanced the activity of the eNOS promoter, and did not alter the eNOS transcription rate in nuclear run-on experiments, suggesting that TSA posttranscriptionally targets eNOS mRNA.	trichostatin A	9-12	nitric oxide synthase 3	Homo sapiens	28-32
12411399-9	2002	Although TSA decreased both eNOS protein and mRNA levels, TSA paradoxically enhanced the activity of the eNOS promoter, and did not alter the eNOS transcription rate in nuclear run-on experiments, suggesting that TSA posttranscriptionally targets eNOS mRNA.	trichostatin A	58-61	nitric oxide synthase 3	Homo sapiens	105-109
12411399-9	2002	Although TSA decreased both eNOS protein and mRNA levels, TSA paradoxically enhanced the activity of the eNOS promoter, and did not alter the eNOS transcription rate in nuclear run-on experiments, suggesting that TSA posttranscriptionally targets eNOS mRNA.	trichostatin A	58-61	nitric oxide synthase 3	Homo sapiens	105-109
12411399-9	2002	Although TSA decreased both eNOS protein and mRNA levels, TSA paradoxically enhanced the activity of the eNOS promoter, and did not alter the eNOS transcription rate in nuclear run-on experiments, suggesting that TSA posttranscriptionally targets eNOS mRNA.	trichostatin A	58-61	nitric oxide synthase 3	Homo sapiens	105-109
12489993-1	2002	Previously, we have demonstrated that increased superoxide generation plays a role in the nitric oxide (NO)-mediated inhibition of endothelial NO synthase (NOS III) in endothelial cells (ECs).	Nitric Oxide	90-102	nitric oxide synthase 3	Homo sapiens	156-163
12489993-2	2002	In this study we demonstrate that the source of the superoxide is likely due to both NADPH oxidase and NOS III itself.	Superoxides	52-62	nitric oxide synthase 3	Homo sapiens	103-110
12489993-8	2002	In conclusion, our results indicate that superoxide and peroxynitrite are involved in the inhibition of NOS III by NO, and that the scavenging of superoxide may be necessary to prevent NOS III inhibition during treatments that involve inhaled NO or NO donors.	Superoxides	41-51	nitric oxide synthase 3	Homo sapiens	104-111
12489993-8	2002	In conclusion, our results indicate that superoxide and peroxynitrite are involved in the inhibition of NOS III by NO, and that the scavenging of superoxide may be necessary to prevent NOS III inhibition during treatments that involve inhaled NO or NO donors.	Peroxynitrous Acid	56-69	nitric oxide synthase 3	Homo sapiens	104-111
12363386-0	2002	Decreased calcium-dependent constitutive nitric oxide synthase (cNOS) activity in prefrontal cortex in schizophrenia and depression.	Calcium	10-17	nitric oxide synthase 3	Homo sapiens	64-68
12381413-9	2002	Stills others such as the immunosuppressants cyclosporine A and FK506/tacrolimus or erythropoietin have inconsistent effects on eNOS.	Cyclosporine	45-59	nitric oxide synthase 3	Homo sapiens	128-132
12381413-9	2002	Stills others such as the immunosuppressants cyclosporine A and FK506/tacrolimus or erythropoietin have inconsistent effects on eNOS.	Tacrolimus	64-69	nitric oxide synthase 3	Homo sapiens	128-132
12381413-9	2002	Stills others such as the immunosuppressants cyclosporine A and FK506/tacrolimus or erythropoietin have inconsistent effects on eNOS.	Tacrolimus	70-80	nitric oxide synthase 3	Homo sapiens	128-132
12390956-6	2002	C6-ceramide stimulated eNOS transcription by a signaling mechanism involving protein phosphatase PP2A but did not modify the stability of the eNOS mRNA.	N-caproylsphingosine	0-11	nitric oxide synthase 3	Homo sapiens	23-27
12392844-9	2002	Nuclear run-on experiments showed that high doses of glyc-oxLDL can reduce the transcription rate of nascent NOSIII mRNA (densitometric analysis revealed a reduction of 25% [p &lt; 0.05 vs. untreated cells, nLDL, and glycLDL] after treatment of cells with 300 microg/ml glyc-oxLDL).	glyc-oxldl	53-63	nitric oxide synthase 3	Homo sapiens	109-115
12392844-9	2002	Nuclear run-on experiments showed that high doses of glyc-oxLDL can reduce the transcription rate of nascent NOSIII mRNA (densitometric analysis revealed a reduction of 25% [p &lt; 0.05 vs. untreated cells, nLDL, and glycLDL] after treatment of cells with 300 microg/ml glyc-oxLDL).	glyc-oxldl	270-280	nitric oxide synthase 3	Homo sapiens	109-115
12392844-11	2002	CONCLUSIONS: These results indicate that glyc-oxLDL, per se, may influence signal transduction pathways involving NO-mediated regulatory signals and NOSIII activity in human endothelial cells.	glyc-oxldl	41-51	nitric oxide synthase 3	Homo sapiens	149-155
12370098-11	2002	MLB inhibited H/R-induced increases in [Ca2+]i and eNOS mRNA expression, stimulated NO release and iNOS mRNA expression (P &lt;0.05).	r	16-17	nitric oxide synthase 3	Homo sapiens	51-55
12364359-11	2002	The functional difference in NO generation depending on eNOS with either glutamate or aspartate at position 298 was also confirmed in vitro.	Glutamic Acid	73-82	nitric oxide synthase 3	Homo sapiens	56-60
12364359-11	2002	The functional difference in NO generation depending on eNOS with either glutamate or aspartate at position 298 was also confirmed in vitro.	Aspartic Acid	86-95	nitric oxide synthase 3	Homo sapiens	56-60
12270851-0	2002	Red wine polyphenols enhance endothelial nitric oxide synthase expression and subsequent nitric oxide release from endothelial cells.	Polyphenols	9-20	nitric oxide synthase 3	Homo sapiens	29-62
12270851-3	2002	This study examines the influence of red wine polyphenols on the regulation of endothelial nitric oxide synthase (eNOS) expression and subsequent NO synthesis, focusing on the putative long-lasting antiatherosclerotic effects of red wine.	Polyphenols	46-57	nitric oxide synthase 3	Homo sapiens	79-112
12270851-3	2002	This study examines the influence of red wine polyphenols on the regulation of endothelial nitric oxide synthase (eNOS) expression and subsequent NO synthesis, focusing on the putative long-lasting antiatherosclerotic effects of red wine.	Polyphenols	46-57	nitric oxide synthase 3	Homo sapiens	114-118
12270851-7	2002	Furthermore, we found an increased human eNOS promotor activity (up to 2-fold) in response to red wine polyphenols (18 hours, 100 to 600 microg/mL), as demonstrated by a luciferase reporter gene assay.	Polyphenols	103-114	nitric oxide synthase 3	Homo sapiens	41-45
12270851-9	2002	Increased active eNOS levels may antagonize the development of endothelial dysfunction and atherosclerosis, a hypothesis that supports the view that red wine indeed may have long-term protective cardiovascular properties mediated by its polyphenols.	Polyphenols	237-248	nitric oxide synthase 3	Homo sapiens	17-21
12270858-0	2002	Resveratrol, a polyphenolic phytoalexin present in red wine, enhances expression and activity of endothelial nitric oxide synthase.	Resveratrol	0-11	nitric oxide synthase 3	Homo sapiens	97-130
12270858-0	2002	Resveratrol, a polyphenolic phytoalexin present in red wine, enhances expression and activity of endothelial nitric oxide synthase.	polyphenolic phytoalexin	15-39	nitric oxide synthase 3	Homo sapiens	97-130
12270858-4	2002	METHODS AND RESULTS: Incubation of human umbilical vein endothelial cells (HUVEC) and HUVEC-derived EA.hy 926 cells with resveratrol for 24 to 72 hours upregulated eNOS mRNA expression in a time- and concentration-dependent manner (up to 2.8-fold).	Resveratrol	121-132	nitric oxide synthase 3	Homo sapiens	164-168
12270858-5	2002	eNOS protein expression and eNOS-derived NO production were also increased after long-term incubation with resveratrol.	Resveratrol	107-118	nitric oxide synthase 3	Homo sapiens	0-4
12270858-5	2002	eNOS protein expression and eNOS-derived NO production were also increased after long-term incubation with resveratrol.	Resveratrol	107-118	nitric oxide synthase 3	Homo sapiens	28-32
12270858-6	2002	Resveratrol increased the activity of the eNOS promoter (3.5-kb fragment) in a concentration-dependent fashion, with the essential trans-stimulated sequence being located in the proximal 263 bp of the promoter sequence.	Resveratrol	0-11	nitric oxide synthase 3	Homo sapiens	42-46
12270858-7	2002	In addition, eNOS mRNA was stabilized by resveratrol.	Resveratrol	41-52	nitric oxide synthase 3	Homo sapiens	13-17
12270858-8	2002	The effect of resveratrol on eNOS expression was not modified by the estrogen receptor antagonists ICI 182780 and RU 58668.	Resveratrol	14-25	nitric oxide synthase 3	Homo sapiens	29-33
12270858-10	2002	In addition to its long-term effects on eNOS expression, resveratrol also enhanced the production of bioactive NO in the short-term (after a 2-minute incubation).	Resveratrol	57-68	nitric oxide synthase 3	Homo sapiens	40-44
12270858-11	2002	CONCLUSIONS: In concert with other effects, the stimulation of eNOS expression and activity may contribute to the cardiovascular protective effects attributed to resveratrol.	Resveratrol	162-173	nitric oxide synthase 3	Homo sapiens	63-67
12182860-2	2002	Selectivity versus e-NOS was increased to approximately 100-fold through appropriate substitution at the benzene ring.	Benzene	105-112	nitric oxide synthase 3	Homo sapiens	19-24
12201830-5	2002	During TERT, platelet cNOS activity rose in A and B (0.6 +/- 0.1 vs. 1.8 +/- 0.1 fmol/min/109 plts, P &lt; 0.05 and 0.7 +/- 0.1 vs. 2.4 +/- 0.2, P &lt; 0.001, A1 vs. A2 and B1 vs. B2, respectively).	tert	7-11	nitric oxide synthase 3	Homo sapiens	22-26
12186793-7	2002	Actinomycin D studies suggested that eNOS downregulation was related to decreased mRNA stability.	Dactinomycin	0-13	nitric oxide synthase 3	Homo sapiens	37-41
12269787-4	2002	Retinoic acid had an inhibitory effect on the level of oocyte eNOS mRNA in a dose-dependent manner if COCs were exposed to retinoic acid before FSH stimulation.	Tretinoin	0-13	nitric oxide synthase 3	Homo sapiens	62-66
12269787-4	2002	Retinoic acid had an inhibitory effect on the level of oocyte eNOS mRNA in a dose-dependent manner if COCs were exposed to retinoic acid before FSH stimulation.	Tretinoin	123-136	nitric oxide synthase 3	Homo sapiens	62-66
12269787-6	2002	eNOS protein also decreased to approximately 50% of the control after exposure to 10 microM retinoic acid.	Tretinoin	92-105	nitric oxide synthase 3	Homo sapiens	0-4
12269787-8	2002	These results suggest that retinoic acid has a strong inhibitory action on eNOS mRNA level and NO synthesis in the porcine oocyte.	Tretinoin	27-40	nitric oxide synthase 3	Homo sapiens	75-79
12553744-1	2002	L-arginine is the substrate for endothelial nitric oxide synthase (eNOS), and the precursor for the synthesis of nitric oxide (NO).	Arginine	0-10	nitric oxide synthase 3	Homo sapiens	32-65
12135947-4	2002	Both in vivo and in vitro phosphorylation of endothelial nitric oxide synthase (eNOS) by Akt were reduced by hyperglycemia and hexosamine activation.	Hexosamines	127-137	nitric oxide synthase 3	Homo sapiens	45-78
12089165-1	2002	BACKGROUND: NO synthesized from L-arginine by the constitutive endothelial NO synthase (eNOS) plays a key role in the atherosclerotic process.	Arginine	32-42	nitric oxide synthase 3	Homo sapiens	88-92
11934890-2	2002	Based on previous data from our laboratory, we hypothesized that DHEA binds to specific cell-surface receptors to activate intracellular G-proteins and endothelial nitric-oxide synthase (eNOS).	Dehydroepiandrosterone	65-69	nitric oxide synthase 3	Homo sapiens	152-185
12323127-5	2002	The constitutive forms of nitric oxide synthase (cNOS) in neurons and endothelial cells are calcium-dependent.	Calcium	92-99	nitric oxide synthase 3	Homo sapiens	49-53
11980473-0	2002	Resonance Raman detection of the Fe-S bond in endothelial nitric oxide synthase.	Iron	33-37	nitric oxide synthase 3	Homo sapiens	46-79
11980473-1	2002	We report the first low-frequency resonance Raman spectra of ferric endothelial nitric oxide synthase (eNOS) holoenzyme, including the frequency of the Fe-S vibration in the presence of the substrate L-arginine.	Arginine	200-210	nitric oxide synthase 3	Homo sapiens	68-101
12384247-8	2002	In addition, double immunolabeling studies revealed that in these glial cells iNOS and eNOS are co-localized with nitrotyrosine.	3-nitrotyrosine	114-127	nitric oxide synthase 3	Homo sapiens	87-91
12390956-10	2002	The partial reversal of this reduction by BH(4) and the diminution of ROS generation by L-NAME suggest that ceramide promotes NADPH oxidase activity of eNOS, leading to ROS formation at the expense of NO synthesis.	Reactive Oxygen Species	70-73	nitric oxide synthase 3	Homo sapiens	152-156
12390956-10	2002	The partial reversal of this reduction by BH(4) and the diminution of ROS generation by L-NAME suggest that ceramide promotes NADPH oxidase activity of eNOS, leading to ROS formation at the expense of NO synthesis.	NG-Nitroarginine Methyl Ester	88-94	nitric oxide synthase 3	Homo sapiens	152-156
12390956-10	2002	The partial reversal of this reduction by BH(4) and the diminution of ROS generation by L-NAME suggest that ceramide promotes NADPH oxidase activity of eNOS, leading to ROS formation at the expense of NO synthesis.	Ceramides	108-116	nitric oxide synthase 3	Homo sapiens	152-156
12390956-10	2002	The partial reversal of this reduction by BH(4) and the diminution of ROS generation by L-NAME suggest that ceramide promotes NADPH oxidase activity of eNOS, leading to ROS formation at the expense of NO synthesis.	Reactive Oxygen Species	169-172	nitric oxide synthase 3	Homo sapiens	152-156
12390956-11	2002	The ceramide-induced upregulation of eNOS gene transcription can be considered an ineffective compensatory mechanism.	Ceramides	4-12	nitric oxide synthase 3	Homo sapiens	37-41
12372469-6	2002	MAIN OUTCOME MEASURE(S): Expression of eNOS and alpha(v)beta(3) integrin protein in the endometrium and peritoneal fluid levels of nitric oxide.	Nitric Oxide	131-143	nitric oxide synthase 3	Homo sapiens	39-43
12352326-9	2002	Endothelial NOS mRNA was increased in cyclosporine-and tacrolimus-treated patients in comparison with controls (0.92 +/- 0.09, 0.96 +/- 0.04, and 0.37 +/- 0.05 respectively; p &lt; 0.001), whereas no difference was found between patients and controls in HO-1 mRNA.	Cyclosporine	38-50	nitric oxide synthase 3	Homo sapiens	0-15
12352326-9	2002	Endothelial NOS mRNA was increased in cyclosporine-and tacrolimus-treated patients in comparison with controls (0.92 +/- 0.09, 0.96 +/- 0.04, and 0.37 +/- 0.05 respectively; p &lt; 0.001), whereas no difference was found between patients and controls in HO-1 mRNA.	Tacrolimus	55-65	nitric oxide synthase 3	Homo sapiens	0-15
12352326-11	2002	Ramipril also reduced p22 (to 0.83 +/- 0.05 in cyclosporine, p &lt; 0.03 and to 0.81 +/- 0.08 in tacrolimus; p &lt; 0.01) and TGF-beta mRNA (to 0.72 +/- 01 in cyclosporine, p &lt; 0.02, and to 0.73 +/- 0.05 in tacrolimus; p &lt; 0.01) with no difference between groups, but it did not change HO-1 and ecNOS mRNA.	Ramipril	0-8	nitric oxide synthase 3	Homo sapiens	301-306
12359981-0	2002	The Glu298Asp polymorphism of the NOS 3 gene as a determinant of the baseline production of nitric oxide.	Nitric Oxide	92-104	nitric oxide synthase 3	Homo sapiens	34-39
12359981-2	2002	OBJECTIVE: To investigate functional differences between the various genotypes with respect to basal nitric oxide (NO) production, we estimated the response to endothelial NO synthase (ecNOS) inhibition by infusion of increasing doses of N(G)-monomethyl-L-arginine (L-NMMA) into the brachial artery during venous occlusion plethysmography.	omega-N-Methylarginine	238-264	nitric oxide synthase 3	Homo sapiens	185-190
12471479-18	2002	In the L-NAME group, cNOS activity was lower than in the untreated NEC group.	NG-Nitroarginine Methyl Ester	7-13	nitric oxide synthase 3	Homo sapiens	21-25
12471479-20	2002	However, in L-arg control loops, cNOS activity was greater than in the L-NAME group.	Arginine	12-17	nitric oxide synthase 3	Homo sapiens	33-37
12471479-23	2002	L-NAME significantly decreases cNOS activity and correlates with our previously published histopathologic findings confirming the protective role of cNOS-derived NO in NEC-injured gut mucosa.	NG-Nitroarginine Methyl Ester	0-6	nitric oxide synthase 3	Homo sapiens	31-35
12471479-23	2002	L-NAME significantly decreases cNOS activity and correlates with our previously published histopathologic findings confirming the protective role of cNOS-derived NO in NEC-injured gut mucosa.	NG-Nitroarginine Methyl Ester	0-6	nitric oxide synthase 3	Homo sapiens	149-153
12181148-11	2002	These results strongly support the hypothesis that 17beta-estradiol increases coronary blood flow in the unanesthetized nonpregnant ewe via an ER-dependent mechanism that results in an increase in both eNOS and iNOS expression.	Estradiol	51-67	nitric oxide synthase 3	Homo sapiens	202-206
12176133-1	2002	OBJECTIVES: Tetrahydrobiopterin (BH4) is an essential cofactor for endothelial nitric oxide synthase (eNOS) activity.	sapropterin	12-31	nitric oxide synthase 3	Homo sapiens	67-100
12176133-1	2002	OBJECTIVES: Tetrahydrobiopterin (BH4) is an essential cofactor for endothelial nitric oxide synthase (eNOS) activity.	sapropterin	12-31	nitric oxide synthase 3	Homo sapiens	102-106
12176133-1	2002	OBJECTIVES: Tetrahydrobiopterin (BH4) is an essential cofactor for endothelial nitric oxide synthase (eNOS) activity.	sapropterin	33-36	nitric oxide synthase 3	Homo sapiens	67-100
12176133-1	2002	OBJECTIVES: Tetrahydrobiopterin (BH4) is an essential cofactor for endothelial nitric oxide synthase (eNOS) activity.	sapropterin	33-36	nitric oxide synthase 3	Homo sapiens	102-106
12176133-3	2002	BH4 activates and promotes homodimerisation of purified eNOS protein, but the intracellular mechanisms underlying BH4-mediated eNOS regulation in endothelial cells remain less clear.	sapropterin	0-3	nitric oxide synthase 3	Homo sapiens	56-60
12176133-3	2002	BH4 activates and promotes homodimerisation of purified eNOS protein, but the intracellular mechanisms underlying BH4-mediated eNOS regulation in endothelial cells remain less clear.	sapropterin	114-117	nitric oxide synthase 3	Homo sapiens	127-131
12176133-4	2002	We aimed to investigate the role of BH4 levels in intracellular eNOS regulation, by targeting the BH4 synthetic pathway as a novel strategy to modulate intracellular BH4 levels.	sapropterin	36-39	nitric oxide synthase 3	Homo sapiens	64-68
12176133-4	2002	We aimed to investigate the role of BH4 levels in intracellular eNOS regulation, by targeting the BH4 synthetic pathway as a novel strategy to modulate intracellular BH4 levels.	sapropterin	98-101	nitric oxide synthase 3	Homo sapiens	64-68
12176133-4	2002	We aimed to investigate the role of BH4 levels in intracellular eNOS regulation, by targeting the BH4 synthetic pathway as a novel strategy to modulate intracellular BH4 levels.	sapropterin	98-101	nitric oxide synthase 3	Homo sapiens	64-68
12176133-10	2002	CONCLUSIONS: These findings suggest that GTPCH gene transfer is a valid approach to increase BH4 levels in human endothelial cells, and provide new evidence for the relative importance of different mechanisms underlying BH4-mediated eNOS regulation in intact human endothelial cells.	sapropterin	220-223	nitric oxide synthase 3	Homo sapiens	233-237
12226742-1	2002	Nitric oxide (NO), formed by endothelial constitutive nitric oxide synthase (eNOS) maintains endothelium-dependent vasodilatation and also mediates antithrombotic actions.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	29-75
12226742-1	2002	Nitric oxide (NO), formed by endothelial constitutive nitric oxide synthase (eNOS) maintains endothelium-dependent vasodilatation and also mediates antithrombotic actions.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	77-81
12269787-0	2002	Retinoic acid suppression of endothelial nitric oxide synthase in porcine oocyte.	Tretinoin	0-13	nitric oxide synthase 3	Homo sapiens	29-62
12269787-2	2002	The present study was designed to determine the effect of retinoic acid on eNOS regulation in porcine oocytes during follicle-stimulating hormone (FSH) stimulation.	Tretinoin	58-71	nitric oxide synthase 3	Homo sapiens	75-79
12214669-10	2002	N-butyl N"-hydroxyguanidine is also a good substrate for NOS I and NOS III.	N-butyl-N'-hydroxyguanidine	0-27	nitric oxide synthase 3	Homo sapiens	67-74
12175813-2	2002	All of these cell types are capable of producing nitric oxide (NO), either constitutively or in response to inflammatory cytokines, through the activity of nitric oxide synthases (NOSs): eNOS (NOS3; endothelial NOS) and iNOS (NOS2; inducible NOS), respectively.	Nitric Oxide	49-61	nitric oxide synthase 3	Homo sapiens	187-191
12175813-2	2002	All of these cell types are capable of producing nitric oxide (NO), either constitutively or in response to inflammatory cytokines, through the activity of nitric oxide synthases (NOSs): eNOS (NOS3; endothelial NOS) and iNOS (NOS2; inducible NOS), respectively.	Nitric Oxide	49-61	nitric oxide synthase 3	Homo sapiens	193-197
11983711-2	2002	The ansamycin antibiotic geldanamycin has frequently been used as an inhibitor of heat shock protein 90 (Hsp90), and this agent has been widely employed as a probe to examine the interactions of Hsp90 with endothelial nitric-oxide synthase.	Rifabutin	4-13	nitric oxide synthase 3	Homo sapiens	206-239
11983711-2	2002	The ansamycin antibiotic geldanamycin has frequently been used as an inhibitor of heat shock protein 90 (Hsp90), and this agent has been widely employed as a probe to examine the interactions of Hsp90 with endothelial nitric-oxide synthase.	geldanamycin	25-37	nitric oxide synthase 3	Homo sapiens	206-239
11983711-5	2002	The treatment of endothelial cells with geldanamycin resulted in a dramatic increase in O(2)(*)(-) generation, which was independent of endothelial nitric-oxide synthase, because it was not inhibited by N-nitro-l-arginine methyl ester and also occurred in vascular smooth muscle cells.	geldanamycin	40-52	nitric oxide synthase 3	Homo sapiens	136-169
12093770-6	2002	All of these effects of hypoxia on eNOS were reversed by cotreatment with hydroxyfasudil.	hydroxyfasudil	74-88	nitric oxide synthase 3	Homo sapiens	35-39
12093770-8	2002	Indeed, disruption of the actin cytoskeleton, the downstream target of Rho-kinase, by cytochalasin D also upregulated eNOS expression.	Cytochalasin D	86-100	nitric oxide synthase 3	Homo sapiens	118-122
12093770-9	2002	Hypoxia reduced eNOS mRNA half-life from 22+/-2 to 13+/-2 hours, which was reversed by cotreatment with hydroxyfasudil.	hydroxyfasudil	104-118	nitric oxide synthase 3	Homo sapiens	16-20
12055099-7	2002	The data strongly suggest, but do not definitely prove, that glucose indeed has the ability to stimulate both cNOS and iNOS in the islets and that NO might serve as a negative feedback inhibitor of glucose-stimulated insulin release.	Glucose	61-68	nitric oxide synthase 3	Homo sapiens	110-114
12060567-3	2002	The addition of 3",4"-dichlorobenzamil hydrochloride, an inhibitor of the Na+/Ca2+ exchanger (NCX), prevented the increase of eNOS activity with alkalosis.	3",4"-dichlorobenzamil hydrochloride	16-52	nitric oxide synthase 3	Homo sapiens	126-130
12086682-2	2002	One hypothesis is n-LDL increases caveolin-1 (Cav-1), which decreases nitric oxide (*NO) production by binding endothelial nitric oxide synthase (eNOS) in an inactive state.	Nitric Oxide	70-82	nitric oxide synthase 3	Homo sapiens	111-144
12086682-2	2002	One hypothesis is n-LDL increases caveolin-1 (Cav-1), which decreases nitric oxide (*NO) production by binding endothelial nitric oxide synthase (eNOS) in an inactive state.	Nitric Oxide	70-82	nitric oxide synthase 3	Homo sapiens	146-150
12086682-10	2002	These data support the hypothesis that n-LDL increases O(2)(*-), which scavenges *NO, and suggest that n-LDL uncouples eNOS activity by decreasing the association of hsp90 as an initial step in signaling eNOS to generate O(2)(*-).	Nitrogen	46-47	nitric oxide synthase 3	Homo sapiens	119-123
12086682-10	2002	These data support the hypothesis that n-LDL increases O(2)(*-), which scavenges *NO, and suggest that n-LDL uncouples eNOS activity by decreasing the association of hsp90 as an initial step in signaling eNOS to generate O(2)(*-).	Nitrogen	46-47	nitric oxide synthase 3	Homo sapiens	204-208
12049652-3	2002	To investigate the molecular mechanisms underlying the rapid deactivation of eNOS after stimulation with receptor agonists, we measured the time courses of eNOS activation and intracellular free Ca2+ concentration ([Ca2+]i) in response to bradykinin (BK) and ATP.	Adenosine Triphosphate	259-262	nitric oxide synthase 3	Homo sapiens	77-81
12049652-9	2002	However, when ATP was added to BK-pretreated cells or, conversely, BK to ATP-pretreated cells, activation of eNOS was comparable with that of untreated cells, suggesting that BK and ATP affect different pools of eNOS.	Adenosine Triphosphate	14-17	nitric oxide synthase 3	Homo sapiens	109-113
12049652-9	2002	However, when ATP was added to BK-pretreated cells or, conversely, BK to ATP-pretreated cells, activation of eNOS was comparable with that of untreated cells, suggesting that BK and ATP affect different pools of eNOS.	Adenosine Triphosphate	14-17	nitric oxide synthase 3	Homo sapiens	212-216
12049652-9	2002	However, when ATP was added to BK-pretreated cells or, conversely, BK to ATP-pretreated cells, activation of eNOS was comparable with that of untreated cells, suggesting that BK and ATP affect different pools of eNOS.	Adenosine Triphosphate	73-76	nitric oxide synthase 3	Homo sapiens	109-113
12049652-9	2002	However, when ATP was added to BK-pretreated cells or, conversely, BK to ATP-pretreated cells, activation of eNOS was comparable with that of untreated cells, suggesting that BK and ATP affect different pools of eNOS.	Adenosine Triphosphate	73-76	nitric oxide synthase 3	Homo sapiens	212-216
12049652-9	2002	However, when ATP was added to BK-pretreated cells or, conversely, BK to ATP-pretreated cells, activation of eNOS was comparable with that of untreated cells, suggesting that BK and ATP affect different pools of eNOS.	Adenosine Triphosphate	73-76	nitric oxide synthase 3	Homo sapiens	109-113
12049652-9	2002	However, when ATP was added to BK-pretreated cells or, conversely, BK to ATP-pretreated cells, activation of eNOS was comparable with that of untreated cells, suggesting that BK and ATP affect different pools of eNOS.	Adenosine Triphosphate	73-76	nitric oxide synthase 3	Homo sapiens	212-216
12049652-10	2002	The desensitization of eNOS was reversible, since removal of ATP or BK from the incubation buffer restored the response to the respective agonist within 20 min.	Adenosine Triphosphate	61-64	nitric oxide synthase 3	Homo sapiens	23-27
12003772-3	2002	Incubation of PAEC with taxol (15 microM) for 2-4 h resulted in an increase in NO production, eNOS activity, and the amount of HSP90 binding to eNOS.	paec	14-18	nitric oxide synthase 3	Homo sapiens	94-98
12003772-3	2002	Incubation of PAEC with taxol (15 microM) for 2-4 h resulted in an increase in NO production, eNOS activity, and the amount of HSP90 binding to eNOS.	paec	14-18	nitric oxide synthase 3	Homo sapiens	144-148
12003772-3	2002	Incubation of PAEC with taxol (15 microM) for 2-4 h resulted in an increase in NO production, eNOS activity, and the amount of HSP90 binding to eNOS.	Paclitaxel	24-29	nitric oxide synthase 3	Homo sapiens	94-98
12003772-3	2002	Incubation of PAEC with taxol (15 microM) for 2-4 h resulted in an increase in NO production, eNOS activity, and the amount of HSP90 binding to eNOS.	Paclitaxel	24-29	nitric oxide synthase 3	Homo sapiens	144-148
12003772-4	2002	Incubation of PAEC with nocodazole (50 microM) for 2-4 h induced a decrease in NO production, eNOS activity, and the amount of HSP90 binding to eNOS.	paec	14-18	nitric oxide synthase 3	Homo sapiens	94-98
12003772-4	2002	Incubation of PAEC with nocodazole (50 microM) for 2-4 h induced a decrease in NO production, eNOS activity, and the amount of HSP90 binding to eNOS.	paec	14-18	nitric oxide synthase 3	Homo sapiens	144-148
12003772-4	2002	Incubation of PAEC with nocodazole (50 microM) for 2-4 h induced a decrease in NO production, eNOS activity, and the amount of HSP90 binding to eNOS.	Nocodazole	24-34	nitric oxide synthase 3	Homo sapiens	94-98
12003772-4	2002	Incubation of PAEC with nocodazole (50 microM) for 2-4 h induced a decrease in NO production, eNOS activity, and the amount of HSP90 binding to eNOS.	Nocodazole	24-34	nitric oxide synthase 3	Homo sapiens	144-148
12003772-5	2002	The presence of taxol in the culture medium prevented the effects of nocodazole on NO production and eNOS activity in PAEC.	Paclitaxel	16-21	nitric oxide synthase 3	Homo sapiens	101-105
12003772-6	2002	Geldanamycin, a HSP90 inhibitor, prevented the taxol-induced increase in eNOS activity.	geldanamycin	0-12	nitric oxide synthase 3	Homo sapiens	73-77
12003772-6	2002	Geldanamycin, a HSP90 inhibitor, prevented the taxol-induced increase in eNOS activity.	Paclitaxel	47-52	nitric oxide synthase 3	Homo sapiens	73-77
12052455-3	2002	Nitric oxide (NO) inhibits osteoclastic bone destruction, and in normal bone cells its generation by endothelial nitric oxide synthase (eNOS, the predominant bone isoform) is enhanced by mechanical stimuli and estrogen, which both protect against fracture.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	101-134
12052455-3	2002	Nitric oxide (NO) inhibits osteoclastic bone destruction, and in normal bone cells its generation by endothelial nitric oxide synthase (eNOS, the predominant bone isoform) is enhanced by mechanical stimuli and estrogen, which both protect against fracture.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	136-140
12121349-1	2002	The gene encoding endothelial nitric oxide synthase (eNOS) is involved in abnormalities in nitric oxide (NO) synthesis that mediates functional damage of vascular cells, especially of endothelial cells (ECs), a common characteristic in cardiovascular diseases.	Nitric Oxide	30-42	nitric oxide synthase 3	Homo sapiens	53-57
12010932-2	2002	OBJECTIVE: To assess whether Glu298--&gt;Asp polymorphism of the eNOS gene is associated with the occurrence and severity of angiographically defined coronary artery disease in the Italian population.	Aspartic Acid	41-44	nitric oxide synthase 3	Homo sapiens	65-69
12010932-3	2002	METHODS: Polymerase chain reaction/restriction fragment length polymorphism analysis was done to detect the Glu298--&gt;Asp variant of the eNOS gene in 201 patients with coronary artery disease and 114 controls.	Aspartic Acid	120-123	nitric oxide synthase 3	Homo sapiens	139-143
12010932-5	2002	RESULTS: The frequencies of the eNOS Glu/Glu, Glu/Asp, and Asp/Asp genotypes in the coronary artery disease group were significantly different from those of controls (45.3%, 38.8%, and 15.9% v 42.1%, 51.8%, and 6.1%, respectively; chi2 = 8.589, p = 0.0136).	Glutamic Acid	37-40	nitric oxide synthase 3	Homo sapiens	32-36
12010932-6	2002	In comparison with subjects who had a Glu298 allele in the eNOS gene, the risk of coronary artery disease was increased among Asp/Asp carriers (odds ratio 2.9, 95% confidence interval 1.2 to 6.8, p = 0.01) and was independent of the other common risk factors (p = 0.04).	Aspartic Acid	126-129	nitric oxide synthase 3	Homo sapiens	59-63
12010932-6	2002	In comparison with subjects who had a Glu298 allele in the eNOS gene, the risk of coronary artery disease was increased among Asp/Asp carriers (odds ratio 2.9, 95% confidence interval 1.2 to 6.8, p = 0.01) and was independent of the other common risk factors (p = 0.04).	Aspartic Acid	130-133	nitric oxide synthase 3	Homo sapiens	59-63
12010932-8	2002	CONCLUSIONS: Glu298--&gt;Asp polymorphism of the eNOS gene appears to be associated with the presence, extent, and severity of angiographically assessed coronary artery disease.	Aspartic Acid	25-28	nitric oxide synthase 3	Homo sapiens	49-53
12110779-1	2002	BACKGROUND: Nitric oxide is synthesized by endothelial nitric oxide synthase and plays a key role in adequate endothelial function.	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	43-76
12076969-5	2002	The catalytic activity of eNOS is augmented by phosphorylation of a C-terminal serine residue (Ser-1177 of human eNOS) through the phosphatidyl-3 kinase (PI-3K)/Akt pathway.	Serine	79-85	nitric oxide synthase 3	Homo sapiens	26-30
12076969-5	2002	The catalytic activity of eNOS is augmented by phosphorylation of a C-terminal serine residue (Ser-1177 of human eNOS) through the phosphatidyl-3 kinase (PI-3K)/Akt pathway.	Serine	79-85	nitric oxide synthase 3	Homo sapiens	113-117
12076969-5	2002	The catalytic activity of eNOS is augmented by phosphorylation of a C-terminal serine residue (Ser-1177 of human eNOS) through the phosphatidyl-3 kinase (PI-3K)/Akt pathway.	Serine	95-98	nitric oxide synthase 3	Homo sapiens	26-30
12076969-5	2002	The catalytic activity of eNOS is augmented by phosphorylation of a C-terminal serine residue (Ser-1177 of human eNOS) through the phosphatidyl-3 kinase (PI-3K)/Akt pathway.	Serine	95-98	nitric oxide synthase 3	Homo sapiens	113-117
12363386-1	2002	To further understand the potential role of nitric oxide synthase (NOS) in schizophrenia and affective disorders, we determined the calcium-dependent constitutive NOS (cNOS) enzymatic activity and protein levels in the prefrontal cortex of postmortem brains of patients with unipolar, bipolar, and schizophrenic disorders and non-psychiatric controls (n = 15 for each group).	Calcium	132-139	nitric oxide synthase 3	Homo sapiens	150-166
12363386-1	2002	To further understand the potential role of nitric oxide synthase (NOS) in schizophrenia and affective disorders, we determined the calcium-dependent constitutive NOS (cNOS) enzymatic activity and protein levels in the prefrontal cortex of postmortem brains of patients with unipolar, bipolar, and schizophrenic disorders and non-psychiatric controls (n = 15 for each group).	Calcium	132-139	nitric oxide synthase 3	Homo sapiens	168-172
11980874-0	2002	PGE(2)-mediated eNOS induction in prolonged hypercapnia.	Dinoprostone	0-6	nitric oxide synthase 3	Homo sapiens	16-20
12045385-6	2002	Increased oxidative stress in patients with CHF is likely caused by decreased bioavailability of nitric oxide due to reduced expression of endothelial nitric oxide synthase and increased generation of reactive oxygen species.	Nitric Oxide	97-109	nitric oxide synthase 3	Homo sapiens	139-172
11980874-9	2002	The ex vivo time course of eNOS mRNA expression corresponded with the late-phase increase in RBF and was blocked by the transcription inhibitor actinomycin D and the receptor-operated Ca(2+) channel blocker SK&amp;F96365.	Dactinomycin	144-157	nitric oxide synthase 3	Homo sapiens	27-31
11980874-11	2002	CONCLUSIONS: This study discloses a previously unexplored mechanism for late retinal hyperemia during sustained hypercapnia that appears secondary to the induced expression of eNOS mediated by PGE(2).	Prostaglandins E	193-196	nitric oxide synthase 3	Homo sapiens	176-180
11920344-11	2002	CsA potently affected the placental ET-1/ecNOS vasoactive balance.	Cyclosporine	0-3	nitric oxide synthase 3	Homo sapiens	41-46
12162424-5	2002	H2O2 in turn enhanced endothelial nitric oxide synthase (eNOS) transcription in endothelial cells and myocytes.	Hydrogen Peroxide	0-4	nitric oxide synthase 3	Homo sapiens	22-55
12162424-5	2002	H2O2 in turn enhanced endothelial nitric oxide synthase (eNOS) transcription in endothelial cells and myocytes.	Hydrogen Peroxide	0-4	nitric oxide synthase 3	Homo sapiens	57-61
12162424-6	2002	Antisense eNOS depressed DOX-induced oxidative stress and apoptosis.	Doxorubicin	25-28	nitric oxide synthase 3	Homo sapiens	10-14
12059072-1	2002	NOS3 (endothelial nitric oxide (NO) synthase) and p22phox (subunit of NAD(P)H oxidase) are two genes whose products are involved in formation and degradation of NO, a ubiquitous signaling molecule largely responsible for the maintenance of normal endothelial function.	nitric	18-24	nitric oxide synthase 3	Homo sapiens	0-4
11934836-1	2002	We reported upregulation of endothelial nitric oxide synthase (eNOS) by PGE(2) in tissues and presence of perinuclear PGE(2) receptors (EP).	Prostaglandins E	72-75	nitric oxide synthase 3	Homo sapiens	28-61
11934836-1	2002	We reported upregulation of endothelial nitric oxide synthase (eNOS) by PGE(2) in tissues and presence of perinuclear PGE(2) receptors (EP).	Prostaglandins E	72-75	nitric oxide synthase 3	Homo sapiens	63-67
11934836-2	2002	We presently studied mechanisms by which PGE(2) induces eNOS expression in cerebral microvessel endothelial cells (ECs).	Prostaglandins E	41-44	nitric oxide synthase 3	Homo sapiens	56-60
11934836-3	2002	16,16-Dimethyl PGE(2) and selective EP(3) receptor agonist M&amp;B28767 increased eNOS expression in ECs and the NO-dependent vasorelaxant responses induced by substance P on cerebral microvessels.	16,16-dimethyl pge	0-18	nitric oxide synthase 3	Homo sapiens	82-86
11934836-3	2002	16,16-Dimethyl PGE(2) and selective EP(3) receptor agonist M&amp;B28767 increased eNOS expression in ECs and the NO-dependent vasorelaxant responses induced by substance P on cerebral microvessels.	Acebutolol	59-64	nitric oxide synthase 3	Homo sapiens	82-86
11934836-6	2002	M&amp;B28767 increased eNOS RNA expression in EC nuclei, and this effect was augmented by overexpression of EP(3) receptors.	Adenosine Monophosphate	2-5	nitric oxide synthase 3	Homo sapiens	23-27
11934836-9	2002	We describe for the first time that PGE(2) through its access into cell by prostaglandin transporters induces eNOS expression by activating perinuclear EP(3) receptors coupled to pertussis toxin-sensitive G proteins, a process that depends on nuclear envelope K(Ca) channels, protein kinases, and NF-kappaB; the roles for nuclear EP(3) receptors seem different from those on plasma membrane.	Prostaglandins E	36-39	nitric oxide synthase 3	Homo sapiens	110-114
11934843-7	2002	The dose-dependent promigratory and proangiogenic effects of atorvastatin on mature endothelial cells are correlated with the activation of the phosphatidylinositol 3-kinase-Akt pathway, as determined by the phosphorylation of Akt and endothelial NO synthase (eNOS) at Ser1177.	Atorvastatin	61-73	nitric oxide synthase 3	Homo sapiens	235-258
11934843-7	2002	The dose-dependent promigratory and proangiogenic effects of atorvastatin on mature endothelial cells are correlated with the activation of the phosphatidylinositol 3-kinase-Akt pathway, as determined by the phosphorylation of Akt and endothelial NO synthase (eNOS) at Ser1177.	Atorvastatin	61-73	nitric oxide synthase 3	Homo sapiens	260-264
11934843-9	2002	In contrast, the well-established stabilization of eNOS mRNA was achieved only at higher concentrations, suggesting that posttranscriptional activation rather than an increase in eNOS expression mediates the proangiogenic effect of atorvastatin.	Atorvastatin	232-244	nitric oxide synthase 3	Homo sapiens	51-55
11961297-7	2002	LY294002 was found to attenuate VEGF-stimulated eNOS expression.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	0-8	nitric oxide synthase 3	Homo sapiens	48-52
12003352-4	2002	Folate acts directly to produce antioxidant effects, interactions with enzyme endothelial NO synthase (eNOS) and effects on cofactor bioavailability of NO.	Folic Acid	0-6	nitric oxide synthase 3	Homo sapiens	103-107
11996210-17	2002	PYC antagonizes the vasoconstriction caused by epinephrine and norepinephrine by increasing the activity of endothelial nitric oxide synthase.	Epinephrine	47-58	nitric oxide synthase 3	Homo sapiens	108-141
11996210-17	2002	PYC antagonizes the vasoconstriction caused by epinephrine and norepinephrine by increasing the activity of endothelial nitric oxide synthase.	Norepinephrine	63-77	nitric oxide synthase 3	Homo sapiens	108-141
11961297-10	2002	Moreover, the VEGF-induced eNOS expression was reduced by the PD98059, MAPK pathway inhibitor.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	62-69	nitric oxide synthase 3	Homo sapiens	27-31
11879202-0	2002	The ratio between tetrahydrobiopterin and oxidized tetrahydrobiopterin analogues controls superoxide release from endothelial nitric oxide synthase: an EPR spin trapping study.	sapropterin	18-37	nitric oxide synthase 3	Homo sapiens	114-147
11792700-0	2002	High density lipoprotein binding to scavenger receptor, Class B, type I activates endothelial nitric-oxide synthase in a ceramide-dependent manner.	Ceramides	121-129	nitric oxide synthase 3	Homo sapiens	82-115
11901050-0	2002	Nongenomic mechanisms of endothelial nitric oxide synthase activation by the selective estrogen receptor modulator raloxifene.	Raloxifene Hydrochloride	115-125	nitric oxide synthase 3	Homo sapiens	25-58
11901050-3	2002	The selective estrogen receptor modulator (SERM) raloxifene is effective for the treatment of postmenopausal osteoporosis, but its ability to activate eNOS via PI3K is unknown.	Raloxifene Hydrochloride	49-59	nitric oxide synthase 3	Homo sapiens	151-155
11901050-5	2002	Raloxifene stimulated eNOS in a concentration- and time-dependent manner.	Raloxifene Hydrochloride	0-10	nitric oxide synthase 3	Homo sapiens	22-26
11901050-6	2002	Activation of eNOS by raloxifene was blocked by the PI3K inhibitor wortmannin and by the ER antagonist ICI 182,780 but not by transcriptional or translational inhibitors.	Raloxifene Hydrochloride	22-32	nitric oxide synthase 3	Homo sapiens	14-18
11901050-6	2002	Activation of eNOS by raloxifene was blocked by the PI3K inhibitor wortmannin and by the ER antagonist ICI 182,780 but not by transcriptional or translational inhibitors.	Wortmannin	67-77	nitric oxide synthase 3	Homo sapiens	14-18
11931846-4	2002	Since in vitro phosphorylation by ERK reduced the catalytic activity of eNOS, it was suggested that this mechanism may be an important determinant of nitric oxide signalling in endothelial cells.	Nitric Oxide	150-162	nitric oxide synthase 3	Homo sapiens	72-76
11879202-0	2002	The ratio between tetrahydrobiopterin and oxidized tetrahydrobiopterin analogues controls superoxide release from endothelial nitric oxide synthase: an EPR spin trapping study.	sapropterin	51-70	nitric oxide synthase 3	Homo sapiens	114-147
11879202-0	2002	The ratio between tetrahydrobiopterin and oxidized tetrahydrobiopterin analogues controls superoxide release from endothelial nitric oxide synthase: an EPR spin trapping study.	Superoxides	90-100	nitric oxide synthase 3	Homo sapiens	114-147
11879202-2	2002	Purified endothelial nitric oxide synthase (eNOS) generates superoxide under limited availability of 5,6,7,8-tetrahydrobiopterin (BH(4)).	Superoxides	60-70	nitric oxide synthase 3	Homo sapiens	9-42
11879202-2	2002	Purified endothelial nitric oxide synthase (eNOS) generates superoxide under limited availability of 5,6,7,8-tetrahydrobiopterin (BH(4)).	Superoxides	60-70	nitric oxide synthase 3	Homo sapiens	44-48
11879202-2	2002	Purified endothelial nitric oxide synthase (eNOS) generates superoxide under limited availability of 5,6,7,8-tetrahydrobiopterin (BH(4)).	sapropterin	101-128	nitric oxide synthase 3	Homo sapiens	9-42
11879202-2	2002	Purified endothelial nitric oxide synthase (eNOS) generates superoxide under limited availability of 5,6,7,8-tetrahydrobiopterin (BH(4)).	sapropterin	101-128	nitric oxide synthase 3	Homo sapiens	44-48
11879202-3	2002	Thus alterations in endothelial BH(4) levels have been postulated to stimulate superoxide production from eNOS.	Superoxides	79-89	nitric oxide synthase 3	Homo sapiens	106-110
11879202-4	2002	This possibility was examined by determining the concentration-dependent effects of BH(4), and its analogues, on superoxide formation by eNOS.	Superoxides	113-123	nitric oxide synthase 3	Homo sapiens	137-141
11879202-5	2002	Superoxide was quantified by EPR spin trapping, which is the only available technique to quantify superoxide from eNOS.	Superoxides	0-10	nitric oxide synthase 3	Homo sapiens	114-118
11879202-5	2002	Superoxide was quantified by EPR spin trapping, which is the only available technique to quantify superoxide from eNOS.	Superoxides	98-108	nitric oxide synthase 3	Homo sapiens	114-118
11879202-6	2002	Using 5-ethoxycarbonyl-5-methyl-pyrroline N-oxide, we show that only fully reduced BH(4) diminished superoxide release from eNOS, with efficiency BH(4)&gt;6-methyl-BH(4)&gt;5-methyl-BH(4).	SCHEMBL4020438	6-49	nitric oxide synthase 3	Homo sapiens	124-128
11879202-6	2002	Using 5-ethoxycarbonyl-5-methyl-pyrroline N-oxide, we show that only fully reduced BH(4) diminished superoxide release from eNOS, with efficiency BH(4)&gt;6-methyl-BH(4)&gt;5-methyl-BH(4).	Superoxides	100-110	nitric oxide synthase 3	Homo sapiens	124-128
11879202-11	2002	This role was verified by adding 7,8-BH(2) or sepiapterin to fully active eNOS.	7,8-bh	33-39	nitric oxide synthase 3	Homo sapiens	74-78
11879202-11	2002	This role was verified by adding 7,8-BH(2) or sepiapterin to fully active eNOS.	sepiapterin	46-57	nitric oxide synthase 3	Homo sapiens	74-78
11879202-14	2002	Collectively, these results indicate that the ratio between oxidized and reduced BH(4) metabolites tightly regulates superoxide formation from eNOS.	Superoxides	117-127	nitric oxide synthase 3	Homo sapiens	143-147
11719512-2	2002	Nitric oxide (NO) traffic within the reduced ferrous-nitrosyl complex of endothelial nitric-oxide synthase (eNOS) has been studied by ultrafast time-resolved absorption spectroscopy.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	73-106
11886397-8	2002	However, endothelial nitric oxide synthase inhibition caused a marked elevation of arterial blood pressure (P &lt; 0.01) that was restored to pretreatment values by l- but not d-arginine.	l- but	165-171	nitric oxide synthase 3	Homo sapiens	9-42
11926202-14	2002	The explanation remains speculative but probably relates to the known cyclosporine-induced upregulation of ecNOS gene and enzyme activity.	Cyclosporine	70-82	nitric oxide synthase 3	Homo sapiens	107-112
11986889-5	2002	These effects are reversed, or at least reduced, by lipid-lowering agents and (because LDL cholesterol down-regulates endothelial nitric oxide synthase) by the administration of L-arginine, the substrate for nitric oxide (NO) formation.	Cholesterol	91-102	nitric oxide synthase 3	Homo sapiens	118-151
11986889-5	2002	These effects are reversed, or at least reduced, by lipid-lowering agents and (because LDL cholesterol down-regulates endothelial nitric oxide synthase) by the administration of L-arginine, the substrate for nitric oxide (NO) formation.	Arginine	178-188	nitric oxide synthase 3	Homo sapiens	118-151
11744698-0	2002	Hydrogen peroxide activates endothelial nitric-oxide synthase through coordinated phosphorylation and dephosphorylation via a phosphoinositide 3-kinase-dependent signaling pathway.	Hydrogen Peroxide	0-17	nitric oxide synthase 3	Homo sapiens	28-61
11894144-0	2002	Effect of ecNOS polymorphisms and coronary artery disease upon exhaled nitric oxide.	Nitric Oxide	71-83	nitric oxide synthase 3	Homo sapiens	10-15
11870235-0	2002	Chemical stabilization of tetrahydrobiopterin by L-ascorbic acid: contribution to placental endothelial nitric oxide synthase activity.	sapropterin	26-45	nitric oxide synthase 3	Homo sapiens	92-125
11870235-0	2002	Chemical stabilization of tetrahydrobiopterin by L-ascorbic acid: contribution to placental endothelial nitric oxide synthase activity.	Ascorbic Acid	49-64	nitric oxide synthase 3	Homo sapiens	92-125
11870235-1	2002	The aim of this study was to characterize the mechanism of the chemical interaction between L-ascorbic acid (ASC) and tetrahydrobiopterin (BH(4)) in vitro and to examine its effect on the activity of endothelial nitric oxide synthase (eNOS) in first trimester human placentae.	Ascorbic Acid	92-107	nitric oxide synthase 3	Homo sapiens	200-233
11908569-6	2002	CONCLUSION: Our findings show that Glu-Asp298 polymorphism of eNOS gene is associated with BD susceptibility.	Glutamic Acid	35-38	nitric oxide synthase 3	Homo sapiens	62-66
11831907-9	2002	Recombinant NOS I and NOS III also oxidize several N-aryl N"-hydroxyguanidines with the formation of NO, with a clearly different substrate specificity.	n-aryl n"-hydroxyguanidines	51-78	nitric oxide synthase 3	Homo sapiens	22-29
11921705-3	2002	In this paper some of the characteristic molecular properties and certain evident or putative physiological roles of NO-synthase III (NOS III) as well as those experimental results of the author"s group that demonstrate the concept of dual regulation of placental NOS III activity by Ca2+ and tetrahydrobiopterin (BH4) are reviewed.	sapropterin	293-312	nitric oxide synthase 3	Homo sapiens	264-271
11921705-3	2002	In this paper some of the characteristic molecular properties and certain evident or putative physiological roles of NO-synthase III (NOS III) as well as those experimental results of the author"s group that demonstrate the concept of dual regulation of placental NOS III activity by Ca2+ and tetrahydrobiopterin (BH4) are reviewed.	sapropterin	314-317	nitric oxide synthase 3	Homo sapiens	264-271
11921705-4	2002	BH4 promotes the formation of the enzymatically active stable homodimeric structure of NOS III.	sapropterin	0-3	nitric oxide synthase 3	Homo sapiens	87-94
11921705-8	2002	In first trimester placentae NOS III exhibits 42-81% of the BH4-dependent maximal activity, whereas in terminal placentae this value falls to 16-59%.	sapropterin	60-63	nitric oxide synthase 3	Homo sapiens	29-36
11921705-10	2002	Studies of the author"s group indicate that in some of the preeclamptic pregnant women, activation of placental NOS III by physiological concentrations of BH4 is not detectable while the basal activity of the enzyme remains unchanged.	sapropterin	155-158	nitric oxide synthase 3	Homo sapiens	112-119
11729179-0	2002	Localization of endothelial nitric-oxide synthase phosphorylated on serine 1179 and nitric oxide in Golgi and plasma membrane defines the existence of two pools of active enzyme.	Serine	68-74	nitric oxide synthase 3	Homo sapiens	16-49
11729179-1	2002	The subcellular localization of endothelial nitric-oxide synthase (eNOS) is critical for optimal coupling of extracellular stimulation to nitric oxide production.	Nitric Oxide	138-150	nitric oxide synthase 3	Homo sapiens	32-65
11729179-1	2002	The subcellular localization of endothelial nitric-oxide synthase (eNOS) is critical for optimal coupling of extracellular stimulation to nitric oxide production.	Nitric Oxide	138-150	nitric oxide synthase 3	Homo sapiens	67-71
11729179-2	2002	Because eNOS is activated by Akt-dependent phosphorylation to produce nitric oxide (NO), we determined the subcellular distribution of eNOS phosphorylated on serine 1179 using a variety of methodologies.	Nitric Oxide	70-82	nitric oxide synthase 3	Homo sapiens	8-12
11729179-2	2002	Because eNOS is activated by Akt-dependent phosphorylation to produce nitric oxide (NO), we determined the subcellular distribution of eNOS phosphorylated on serine 1179 using a variety of methodologies.	Serine	158-164	nitric oxide synthase 3	Homo sapiens	8-12
11729179-2	2002	Because eNOS is activated by Akt-dependent phosphorylation to produce nitric oxide (NO), we determined the subcellular distribution of eNOS phosphorylated on serine 1179 using a variety of methodologies.	Serine	158-164	nitric oxide synthase 3	Homo sapiens	135-139
11729179-3	2002	Based on sucrose gradient fractionation, phosphorylated-eNOS (P-eNOS) was found in both caveolin-1-enriched membranes and intracellular domains.	Sucrose	9-16	nitric oxide synthase 3	Homo sapiens	56-60
11729179-3	2002	Based on sucrose gradient fractionation, phosphorylated-eNOS (P-eNOS) was found in both caveolin-1-enriched membranes and intracellular domains.	Sucrose	9-16	nitric oxide synthase 3	Homo sapiens	64-68
11729179-5	2002	The proper localization of eNOS to intracellular membranes was required for agonist-dependent phosphorylation on serine 1179, since VEGF did not increase eNOS phosphorylation in cells transfected with a non-acylated, mistargeted form of eNOS.	Serine	113-119	nitric oxide synthase 3	Homo sapiens	27-31
11882622-8	2002	Both eNOS and iNOS expression seemed to increase during perindopril treatment.	Perindopril	56-67	nitric oxide synthase 3	Homo sapiens	5-9
11826414-8	2002	In conclusion, these findings show that in PHT gastric mucosa, TNF-alpha stimulates eNOS phosphorylation at serine 1177 (required for its activation) via the PI 3-kinase-Akt signal transduction pathway.	Serine	108-114	nitric oxide synthase 3	Homo sapiens	84-88
11826414-3	2002	In PHT gastric mucosa we studied (1) eNOS phosphorylation (at serine 1177) required for its activation; (2) association of the phosphatidylinositol 3-kinase (PI 3-kinase), and its downstream effector Akt, with eNOS; and, (3) whether TNF-alpha neutralization affects eNOS phosphorylation and PI 3-kinase-Akt activation.	Serine	62-68	nitric oxide synthase 3	Homo sapiens	37-41
11779139-4	2002	On the contrary, activation by acetylcholine or endothelial nitric oxide synthase (eNOS), which produces NO while consuming oxygen, induces a significant decrease in PO(2), whose amplitude is dependent on the acetylcholine dose, i.e., the eNOS activity level.	Acetylcholine	31-44	nitric oxide synthase 3	Homo sapiens	48-81
11707433-3	2002	Inhibition of phosphatidylinositol 3-kinase with wortmannin blocked the ability of insulin to stimulate increased expression of endothelial nitric-oxide synthase, did not affect insulin-induced activation of MAP kinase, and increased the effects of insulin on prenylation of Ras and Rho proteins.	Wortmannin	49-59	nitric oxide synthase 3	Homo sapiens	128-161
12136949-1	2002	Nitric oxide (NO) is synthesised in the vascular endothelium by nitric oxide synthase (NOS3) and is an important factor in the regulation of blood pressure.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	87-91
11748067-10	2002	The results show that GA can attenuate NO-mediated dilation in human skin, suggesting a potential role for HSP90 in activation of eNOS in the microcirculation.	geldanamycin	22-24	nitric oxide synthase 3	Homo sapiens	130-134
11826287-1	2002	Endothelial nitric oxide synthase (eNOS) is expressed in vascular endothelium, airway epithelium, and certain other cell types where it generates the key signaling molecule nitric oxide (NO).	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	35-39
11826287-5	2002	This compartmentalization facilitates dynamic protein-protein interactions and calcium- and phosphorylation-dependent signal transduction events that modify eNOS activity.	Calcium	79-86	nitric oxide synthase 3	Homo sapiens	157-161
11779139-4	2002	On the contrary, activation by acetylcholine or endothelial nitric oxide synthase (eNOS), which produces NO while consuming oxygen, induces a significant decrease in PO(2), whose amplitude is dependent on the acetylcholine dose, i.e., the eNOS activity level.	Oxygen	124-130	nitric oxide synthase 3	Homo sapiens	48-81
11779139-4	2002	On the contrary, activation by acetylcholine or endothelial nitric oxide synthase (eNOS), which produces NO while consuming oxygen, induces a significant decrease in PO(2), whose amplitude is dependent on the acetylcholine dose, i.e., the eNOS activity level.	Acetylcholine	209-222	nitric oxide synthase 3	Homo sapiens	48-81
11579094-0	2001	Doxorubicin-induced apoptosis is associated with increased transcription of endothelial nitric-oxide synthase.	Doxorubicin	0-11	nitric oxide synthase 3	Homo sapiens	76-109
11862754-2	2002	Free intracellular L-NMMA and ADMA, but not SDMA, are inhibitors of all three isoforms of nitric oxide synthases (nNOS, eNOS and iNOS).	omega-N-Methylarginine	19-25	nitric oxide synthase 3	Homo sapiens	120-124
11862754-2	2002	Free intracellular L-NMMA and ADMA, but not SDMA, are inhibitors of all three isoforms of nitric oxide synthases (nNOS, eNOS and iNOS).	N,N-dimethylarginine	30-34	nitric oxide synthase 3	Homo sapiens	120-124
11812265-2	2002	The major cause of the endothelial dysfunction is decreased bioavailability of nitric oxide (NO), a potent biological vasodilator produced in vascular endothelium from L-arginine by the endothelial NO synthase (eNOS).	Nitric Oxide	79-91	nitric oxide synthase 3	Homo sapiens	211-215
11812265-2	2002	The major cause of the endothelial dysfunction is decreased bioavailability of nitric oxide (NO), a potent biological vasodilator produced in vascular endothelium from L-arginine by the endothelial NO synthase (eNOS).	Arginine	168-178	nitric oxide synthase 3	Homo sapiens	211-215
11812265-4	2002	The deactivation of eNOS is often associated with elevated plasma levels of its endogenous inhibitor, N(G) N(G)-dimethyl-L-arginine (ADMA).	N(G),N(G')-dimethylarginine	102-131	nitric oxide synthase 3	Homo sapiens	20-24
11812265-4	2002	The deactivation of eNOS is often associated with elevated plasma levels of its endogenous inhibitor, N(G) N(G)-dimethyl-L-arginine (ADMA).	N,N-dimethylarginine	133-137	nitric oxide synthase 3	Homo sapiens	20-24
11812265-8	2002	Promising results were also obtained in some, but not all, vascular diseases after treatment with antioxidant vitamins (C and E) and after administration of eNOS substrate, L-arginine, or its cofactor, tetrahydrobiopterin (BH(4)).	sapropterin	202-221	nitric oxide synthase 3	Homo sapiens	157-161
12494183-4	2002	In patients without left ventricular hypertrophy (LVH) genotypes frequencies of NOS3 (Glu298Asp) were: Glu/Glu - 34.4%; Glu/Asp - 62,5%; Asp/Asp - 3,1%.	Glutamic Acid	86-89	nitric oxide synthase 3	Homo sapiens	80-84
12494183-4	2002	In patients without left ventricular hypertrophy (LVH) genotypes frequencies of NOS3 (Glu298Asp) were: Glu/Glu - 34.4%; Glu/Asp - 62,5%; Asp/Asp - 3,1%.	Glutamic Acid	103-106	nitric oxide synthase 3	Homo sapiens	80-84
12494183-4	2002	In patients without left ventricular hypertrophy (LVH) genotypes frequencies of NOS3 (Glu298Asp) were: Glu/Glu - 34.4%; Glu/Asp - 62,5%; Asp/Asp - 3,1%.	Glutamic Acid	103-106	nitric oxide synthase 3	Homo sapiens	80-84
12494183-4	2002	In patients without left ventricular hypertrophy (LVH) genotypes frequencies of NOS3 (Glu298Asp) were: Glu/Glu - 34.4%; Glu/Asp - 62,5%; Asp/Asp - 3,1%.	Aspartic Acid	92-95	nitric oxide synthase 3	Homo sapiens	80-84
12494183-4	2002	In patients without left ventricular hypertrophy (LVH) genotypes frequencies of NOS3 (Glu298Asp) were: Glu/Glu - 34.4%; Glu/Asp - 62,5%; Asp/Asp - 3,1%.	Aspartic Acid	124-127	nitric oxide synthase 3	Homo sapiens	80-84
12494183-4	2002	In patients without left ventricular hypertrophy (LVH) genotypes frequencies of NOS3 (Glu298Asp) were: Glu/Glu - 34.4%; Glu/Asp - 62,5%; Asp/Asp - 3,1%.	Aspartic Acid	124-127	nitric oxide synthase 3	Homo sapiens	80-84
12494183-10	2002	Therefore, we show associations between Glu allele of NOS3 (Glu298Asp) and left ventricular hypertrophy and between 4a allele (ecNOS4a/4b) and diastolic dysfunction in patients with essential hypertension.	Glutamic Acid	40-43	nitric oxide synthase 3	Homo sapiens	54-58
12152104-10	2002	It is proposed that the elevated hemodynamic forces present in hypertension may themselves initiate these alterations, probably by enhancing the release of reactive oxygen species (ROS; produced by xanthine oxidase, NAD(P)H oxidoreductase, eNOS, etc.	Reactive Oxygen Species	156-179	nitric oxide synthase 3	Homo sapiens	240-244
12152104-10	2002	It is proposed that the elevated hemodynamic forces present in hypertension may themselves initiate these alterations, probably by enhancing the release of reactive oxygen species (ROS; produced by xanthine oxidase, NAD(P)H oxidoreductase, eNOS, etc.	Reactive Oxygen Species	181-184	nitric oxide synthase 3	Homo sapiens	240-244
11579094-4	2001	Previously, we showed that DOX undergoes a reductive activation at the reductase domain of endothelial nitric-oxide synthase (eNOS) forming the semiquinone and superoxide (Vasquez-Vivar, J., Martasek, P., Hogg, N., Masters, B. S. S., Pritchard, K. A., Jr., and Kalyanaraman, B.	Doxorubicin	27-30	nitric oxide synthase 3	Homo sapiens	91-124
11579094-4	2001	Previously, we showed that DOX undergoes a reductive activation at the reductase domain of endothelial nitric-oxide synthase (eNOS) forming the semiquinone and superoxide (Vasquez-Vivar, J., Martasek, P., Hogg, N., Masters, B. S. S., Pritchard, K. A., Jr., and Kalyanaraman, B.	Superoxides	160-170	nitric oxide synthase 3	Homo sapiens	91-124
11707586-2	2001	Here we show that in cells lacking caveolae, the dually acylated protein, endothelial nitric oxide synthase (eNOS), localizes to cholesterol-rich lipid raft domains of the plasma membrane.	Cholesterol	129-140	nitric oxide synthase 3	Homo sapiens	74-107
11730805-0	2001	Loss of heterozygosity of the NOS3 dinucleotide repeat marker in atherosclerotic plaques of human carotid arteries.	Dinucleoside Phosphates	35-47	nitric oxide synthase 3	Homo sapiens	30-34
11730805-4	2001	The percentages of LOH ranged between 3.8 and 14.3% and the highest involved polymorphic marker is the NOS3 internal dinucleotide repeat.	Dinucleoside Phosphates	117-129	nitric oxide synthase 3	Homo sapiens	103-107
11707586-2	2001	Here we show that in cells lacking caveolae, the dually acylated protein, endothelial nitric oxide synthase (eNOS), localizes to cholesterol-rich lipid raft domains of the plasma membrane.	Cholesterol	129-140	nitric oxide synthase 3	Homo sapiens	109-113
11696579-1	2001	Endothelial nitric oxide synthase (eNOS) is activated by phosphorylation of serine 1177 by the protein kinase Akt/PKB.	Serine	76-82	nitric oxide synthase 3	Homo sapiens	0-33
11717166-6	2001	Downstream of Ras, MEK1/2 and ERK1/2 are important in this pathway, as 2 inhibitors of MEK1/2, PD98059 and UO126, completely prevented this early increase in eNOS mRNA.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	95-102	nitric oxide synthase 3	Homo sapiens	158-162
11717166-6	2001	Downstream of Ras, MEK1/2 and ERK1/2 are important in this pathway, as 2 inhibitors of MEK1/2, PD98059 and UO126, completely prevented this early increase in eNOS mRNA.	U 0126	107-112	nitric oxide synthase 3	Homo sapiens	158-162
11668050-0	2001	eNOS 894T allele and coronary blood flow at rest and during adenosine-induced hyperemia.	Adenosine	60-69	nitric oxide synthase 3	Homo sapiens	0-4
11668066-4	2001	The results indicate that nNOS is more active than eNOS, both in unstimulated as well as calcium-stimulated cells.	Calcium	89-96	nitric oxide synthase 3	Homo sapiens	51-55
11668066-5	2001	Under basal conditions, the soluble mutant of eNOS appeared to be slightly more active than wild-type eNOS in terms of NO and cGMP formation, suggesting that membrane association may be crucial for inhibition of basal NO release but is not required for stimulation by Ca2+-mobilizing agents.	Cyclic GMP	126-130	nitric oxide synthase 3	Homo sapiens	46-50
11668066-5	2001	Under basal conditions, the soluble mutant of eNOS appeared to be slightly more active than wild-type eNOS in terms of NO and cGMP formation, suggesting that membrane association may be crucial for inhibition of basal NO release but is not required for stimulation by Ca2+-mobilizing agents.	Cyclic GMP	126-130	nitric oxide synthase 3	Homo sapiens	102-106
11711497-6	2001	DNA samples were screened for 4 NOS 3 gene polymorphisms: -786 T/C, -922 A/G, 894 G/T (which predicts a Glu(298)--&gt;Asp amino acid substitution in the mature protein), and a 27-bp tandem repeat in intron 4 (eNOS4a/4b).	Glutamic Acid	104-107	nitric oxide synthase 3	Homo sapiens	32-37
11711497-6	2001	DNA samples were screened for 4 NOS 3 gene polymorphisms: -786 T/C, -922 A/G, 894 G/T (which predicts a Glu(298)--&gt;Asp amino acid substitution in the mature protein), and a 27-bp tandem repeat in intron 4 (eNOS4a/4b).	Aspartic Acid	118-121	nitric oxide synthase 3	Homo sapiens	32-37
11802531-1	2001	BACKGROUND AND PURPOSE: Endothelial nitric oxide synthase (eNOS) plays a key role in atherosclerosis, because its product, nitric oxide, possesses antiatherogenic properties.	Nitric Oxide	36-48	nitric oxide synthase 3	Homo sapiens	59-63
11788791-4	2001	The objective of this study was to investigate the pathway leading to the activation of eNOS in response to arsenite using human keratinocytes.	arsenite	108-116	nitric oxide synthase 3	Homo sapiens	88-92
11788791-12	2001	PI-3-kinase inhibitors, Wortmannin and LY294002 inhibited arsenite-induced phosphorylation of AKT and eNOS but had no effect on phosphorylation of p38.	arsenite	58-66	nitric oxide synthase 3	Homo sapiens	102-106
11788791-10	2001	RESULTS: Arsenite induced the activation of AKT at both Ser473 and Thr308, and its downstream effector eNOS in cultured human keratinocytes.	arsenite	9-17	nitric oxide synthase 3	Homo sapiens	103-107
11788791-13	2001	Interestingly, however, SB203580, a known p38 inhibitor, completely inhibited arsenite-induced phosphorylation of AKT and eNOS.	SB 203580	24-32	nitric oxide synthase 3	Homo sapiens	122-126
11788791-12	2001	PI-3-kinase inhibitors, Wortmannin and LY294002 inhibited arsenite-induced phosphorylation of AKT and eNOS but had no effect on phosphorylation of p38.	Wortmannin	24-34	nitric oxide synthase 3	Homo sapiens	102-106
11788791-13	2001	Interestingly, however, SB203580, a known p38 inhibitor, completely inhibited arsenite-induced phosphorylation of AKT and eNOS.	arsenite	78-86	nitric oxide synthase 3	Homo sapiens	122-126
11788791-12	2001	PI-3-kinase inhibitors, Wortmannin and LY294002 inhibited arsenite-induced phosphorylation of AKT and eNOS but had no effect on phosphorylation of p38.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	39-47	nitric oxide synthase 3	Homo sapiens	102-106
11788791-15	2001	CONCLUSIONS: Collectively, our data indicate that arsenite induces activation of AKT and eNOS, via PI-3-kinase and p38 pathway, likely bypassing the activation of EGF receptor in cultured human keratinocytes.	arsenite	50-58	nitric oxide synthase 3	Homo sapiens	89-93
11692081-2	2001	A maldistribution of eNOS variants among ethnic groups may explain interethnic differences in nitric oxide (NO)-mediated vasodilation and response to drugs.	Nitric Oxide	94-106	nitric oxide synthase 3	Homo sapiens	21-25
11720085-0	2001	Hydrocortisone modulates the effect of estradiol on endothelial nitric oxide synthase expression in human endothelial cells.	Hydrocortisone	0-14	nitric oxide synthase 3	Homo sapiens	52-85
11747093-1	2001	Nitric oxide (NO) is a short-living free molecule synthesized by three different isoforms of nitric oxide synthases (NOS)-neuronal NOS, endothelial NOS, and inducible NOS-associated with neuromuscular transmission, muscle contractility, mitochondrial respiration, and carbohydrate metabolism in skeletal muscle.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	136-151
11720085-0	2001	Hydrocortisone modulates the effect of estradiol on endothelial nitric oxide synthase expression in human endothelial cells.	Estradiol	39-48	nitric oxide synthase 3	Homo sapiens	52-85
11720085-1	2001	The interaction between hydrocortisone and estradiol on the regulation of endothelial nitric oxide synthase (eNOS) expression was investigated in human umbilical vein endothelial cells (HUVECs).	Hydrocortisone	24-38	nitric oxide synthase 3	Homo sapiens	74-107
11720085-1	2001	The interaction between hydrocortisone and estradiol on the regulation of endothelial nitric oxide synthase (eNOS) expression was investigated in human umbilical vein endothelial cells (HUVECs).	Hydrocortisone	24-38	nitric oxide synthase 3	Homo sapiens	109-113
11720085-1	2001	The interaction between hydrocortisone and estradiol on the regulation of endothelial nitric oxide synthase (eNOS) expression was investigated in human umbilical vein endothelial cells (HUVECs).	Estradiol	43-52	nitric oxide synthase 3	Homo sapiens	74-107
11720085-1	2001	The interaction between hydrocortisone and estradiol on the regulation of endothelial nitric oxide synthase (eNOS) expression was investigated in human umbilical vein endothelial cells (HUVECs).	Estradiol	43-52	nitric oxide synthase 3	Homo sapiens	109-113
11720085-3	2001	2 microM hydrocortisone applied for 24 hr preceding and during estradiol application inhibited the estradiol-elicited increase in eNOS mRNA levels, reducing mRNA levels from 134% +/- 14% of control to 85% +/- 5% of control.	Hydrocortisone	9-23	nitric oxide synthase 3	Homo sapiens	130-134
11720085-3	2001	2 microM hydrocortisone applied for 24 hr preceding and during estradiol application inhibited the estradiol-elicited increase in eNOS mRNA levels, reducing mRNA levels from 134% +/- 14% of control to 85% +/- 5% of control.	Estradiol	63-72	nitric oxide synthase 3	Homo sapiens	130-134
11720085-3	2001	2 microM hydrocortisone applied for 24 hr preceding and during estradiol application inhibited the estradiol-elicited increase in eNOS mRNA levels, reducing mRNA levels from 134% +/- 14% of control to 85% +/- 5% of control.	Estradiol	99-108	nitric oxide synthase 3	Homo sapiens	130-134
11720085-5	2001	In the presence of 2 microM hydrocortisone, 10 nM estradiol significantly reduced eNOS mRNA levels to 59% +/- 3% of control.	Hydrocortisone	28-42	nitric oxide synthase 3	Homo sapiens	82-86
11720085-5	2001	In the presence of 2 microM hydrocortisone, 10 nM estradiol significantly reduced eNOS mRNA levels to 59% +/- 3% of control.	Estradiol	50-59	nitric oxide synthase 3	Homo sapiens	82-86
11720085-6	2001	The ability of hydrocortisone to block or reverse the estradiol-mediated increase in eNOS mRNA levels may provide a link between elevated hydrocortisone levels and decreased NO production, potentially contributing to the development of hypertension and cardiovascular disease in vivo and antagonizing cardioprotective effects of estrogens.	Hydrocortisone	15-29	nitric oxide synthase 3	Homo sapiens	85-89
11720085-6	2001	The ability of hydrocortisone to block or reverse the estradiol-mediated increase in eNOS mRNA levels may provide a link between elevated hydrocortisone levels and decreased NO production, potentially contributing to the development of hypertension and cardiovascular disease in vivo and antagonizing cardioprotective effects of estrogens.	Estradiol	54-63	nitric oxide synthase 3	Homo sapiens	85-89
11720085-6	2001	The ability of hydrocortisone to block or reverse the estradiol-mediated increase in eNOS mRNA levels may provide a link between elevated hydrocortisone levels and decreased NO production, potentially contributing to the development of hypertension and cardiovascular disease in vivo and antagonizing cardioprotective effects of estrogens.	Hydrocortisone	138-152	nitric oxide synthase 3	Homo sapiens	85-89
11694897-6	2001	Fourth, nitric oxide produced by endothelial nitric oxide synthase (eNOS) in the early seconds of ischemia induces reactive hyperemia.	Nitric Oxide	8-20	nitric oxide synthase 3	Homo sapiens	33-66
11562476-2	2001	To investigate the potential contribution of low steady state levels of nitric oxide generated by endothelial nitric oxide synthase (eNOS) and the mechanisms of protection against H(2)O(2), spontaneously transformed human ECV304 cells, which normally do not express eNOS, were stably transfected with a green fluorescent-tagged eNOS cDNA.	Nitric Oxide	72-84	nitric oxide synthase 3	Homo sapiens	98-131
11770418-2	2001	METHODS: RT-PCR was used to detect the expression of PKC alpha mRNA in PASMC of procine, and the effect of activator and inhibitor of PKC on the expression of cNOS mRNA in PASMC.	pasmc	172-177	nitric oxide synthase 3	Homo sapiens	159-163
11770418-5	2001	PMA, an agonist of PKC could reduce the expression of cNOS mNRA in hypoxia, while RO 31-8220, an inhibitor of PKC could inhibit it and enhance the expression of NOS mRNA(P &lt; 0.01).	Tetradecanoylphorbol Acetate	0-3	nitric oxide synthase 3	Homo sapiens	54-58
11562476-2	2001	To investigate the potential contribution of low steady state levels of nitric oxide generated by endothelial nitric oxide synthase (eNOS) and the mechanisms of protection against H(2)O(2), spontaneously transformed human ECV304 cells, which normally do not express eNOS, were stably transfected with a green fluorescent-tagged eNOS cDNA.	Nitric Oxide	72-84	nitric oxide synthase 3	Homo sapiens	133-137
11562476-3	2001	The eNOS-transfected cells were found to be resistant to injury and delayed death following a 2-h exposure to H(2)O(2) (50-150 microM).	h(2)	110-114	nitric oxide synthase 3	Homo sapiens	4-8
11562476-5	2001	The ability of nitric oxide to protect cells depended on the presence of respiring mitochondria as ECV304+eNOS cells with diminished mitochondria respiration (rho(-)) are injured to the same extent as nontransfected ECV304 cells and recovery of mitochondrial respiration restores the ability of nitric oxide to protect against H(2)O(2)-induced death.	Nitric Oxide	15-27	nitric oxide synthase 3	Homo sapiens	106-110
11562476-6	2001	Nitric oxide also found to have a profound effect in cell metabolism, because ECV304+eNOS cells had lower steady state levels of ATP and higher utilization of glucose via the glycolytic pathway than ECV304 cells.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	85-89
11562476-6	2001	Nitric oxide also found to have a profound effect in cell metabolism, because ECV304+eNOS cells had lower steady state levels of ATP and higher utilization of glucose via the glycolytic pathway than ECV304 cells.	Adenosine Triphosphate	129-132	nitric oxide synthase 3	Homo sapiens	85-89
11562476-6	2001	Nitric oxide also found to have a profound effect in cell metabolism, because ECV304+eNOS cells had lower steady state levels of ATP and higher utilization of glucose via the glycolytic pathway than ECV304 cells.	Glucose	159-166	nitric oxide synthase 3	Homo sapiens	85-89
11532083-1	2001	BACKGROUND: The constitutive endothelial isoform of nitric oxide synthase (ecNOS) and nitric oxide (NO) production are increased in patients with Bartter syndrome (BS) and Gitelman (GS) syndrome and may reduce vascular tone.	Nitric Oxide	52-64	nitric oxide synthase 3	Homo sapiens	75-80
11532247-1	2001	The nitric oxide-synthesizing enzyme nitric oxide synthase (NOS) is present in the mammalian brain in three different isoforms, two constitutive enzymes (i.e., neuronal, nNOS, and endothelial eNOS) and one inducible enzyme (iNOS).	Nitric Oxide	4-16	nitric oxide synthase 3	Homo sapiens	192-196
11678735-11	2001	We conclude that ANGII activates endothelial nitric oxide synthase to release nitric oxide which enhances gamma-amino butyric acid transmission destined for circuitry mediating the baroreflex.	gamma-Aminobutyric Acid	106-130	nitric oxide synthase 3	Homo sapiens	33-66
12604012-12	2001	These data demonstrate that morphine is capable of induction of both cNOS and iNOS coupled NO release that regulates the macrophage activation state.	Morphine	28-36	nitric oxide synthase 3	Homo sapiens	69-73
11577023-9	2001	Inhibition of Rho A by C3 exoenzyme (20 microgram/mL) and ROCK by Y-27632 (10 micromol/L) prevented the downregulation of eNOS expression by thrombin.	Y 27632	66-73	nitric oxide synthase 3	Homo sapiens	122-126
11470627-11	2001	The expression of endothelial NOS (eNOS) was scarce in both LC and IPH patients.	Phenol	67-70	nitric oxide synthase 3	Homo sapiens	18-33
11532083-9	2001	In BS/GS, PKC stimulation with PMA dose dependently reduced ecNOS gene expression (from 0.80 +/- 0.05 to 0.78 +/- 0.03 densitometric units; PMA 50 nmol/L, P = NS; to 0.55 +/- 0.07, PMA 100 nmol/L, P &lt; 0.001) to an undetectable expression (PMA 200 nmol/L).	Tetradecanoylphorbol Acetate	31-34	nitric oxide synthase 3	Homo sapiens	60-65
11532083-9	2001	In BS/GS, PKC stimulation with PMA dose dependently reduced ecNOS gene expression (from 0.80 +/- 0.05 to 0.78 +/- 0.03 densitometric units; PMA 50 nmol/L, P = NS; to 0.55 +/- 0.07, PMA 100 nmol/L, P &lt; 0.001) to an undetectable expression (PMA 200 nmol/L).	Tetradecanoylphorbol Acetate	140-143	nitric oxide synthase 3	Homo sapiens	60-65
11532083-9	2001	In BS/GS, PKC stimulation with PMA dose dependently reduced ecNOS gene expression (from 0.80 +/- 0.05 to 0.78 +/- 0.03 densitometric units; PMA 50 nmol/L, P = NS; to 0.55 +/- 0.07, PMA 100 nmol/L, P &lt; 0.001) to an undetectable expression (PMA 200 nmol/L).	Tetradecanoylphorbol Acetate	140-143	nitric oxide synthase 3	Homo sapiens	60-65
11532083-11	2001	Incubation of monocytes from patients and controls with the PKC inhibitor GF109203X increased ecNOS mRNA, with no difference between patients and controls.	bisindolylmaleimide I	74-83	nitric oxide synthase 3	Homo sapiens	94-99
11516104-3	2001	In endothelial cells, the VEGF/Flk-1/KDR signal system is a very important generator of nitric oxide (NO) through the activation of its downstream effectors phosphatidylinositol-3-OH-kinase (PI3-K), Akt kinase and endothelial NO synthase (eNOS).	Nitric Oxide	88-100	nitric oxide synthase 3	Homo sapiens	239-243
11509453-7	2001	Furthermore, cotreatment of cells with ET-1 and NO increased peroxynitrite levels by 26% (P&lt;0.05), whereas preincubation of purified human endothelial nitric oxide synthase (eNOS) protein with peroxynitrite generated a nitrated enzyme with 50% activity relative to control (P&lt;0.05).	Peroxynitrous Acid	196-209	nitric oxide synthase 3	Homo sapiens	142-175
11551532-6	2001	Endothelial nitric oxide synthase activity (eNOS) was suppressed by menadione.	Vitamin K 3	68-77	nitric oxide synthase 3	Homo sapiens	0-33
11589505-1	2001	17beta-estradiol up-regulates endothelial nitric oxide synthase (eNOS) expression in cultured endothelial cells.	Estradiol	0-16	nitric oxide synthase 3	Homo sapiens	30-63
11589505-1	2001	17beta-estradiol up-regulates endothelial nitric oxide synthase (eNOS) expression in cultured endothelial cells.	Estradiol	0-16	nitric oxide synthase 3	Homo sapiens	65-69
11589505-2	2001	To clarify the role of mRNA stabilization in upregulation of eNOS expression, endothelial cells were incubated with actinomycin D as transcriptional inhibitor.	Dactinomycin	116-129	nitric oxide synthase 3	Homo sapiens	61-65
11589505-4	2001	As tumor necrosis factor-alpha (TNF-alpha) is associated with the progression of atherosclerosis, we examined the effect of 17beta-estradiol on eNOS mRNA destabilization with TNF-alpha.	Estradiol	124-140	nitric oxide synthase 3	Homo sapiens	144-148
11589505-5	2001	After 10 hours co-incubation with TNF-alpha, relative intensity of eNOS mRNA decreased to 50% of the intensity at the start time of incubation, however, it remained significantly 1.6 times in the presence of 17beta-estradiol.	Estradiol	208-224	nitric oxide synthase 3	Homo sapiens	67-71
11589505-7	2001	This is the first finding that 17beta-estradiol stabilizes eNOS mRNA destabilized by TNF-alpha through estrogen receptor mediated mechanism.	Estradiol	31-47	nitric oxide synthase 3	Homo sapiens	59-63
11509453-7	2001	Furthermore, cotreatment of cells with ET-1 and NO increased peroxynitrite levels by 26% (P&lt;0.05), whereas preincubation of purified human endothelial nitric oxide synthase (eNOS) protein with peroxynitrite generated a nitrated enzyme with 50% activity relative to control (P&lt;0.05).	Peroxynitrous Acid	196-209	nitric oxide synthase 3	Homo sapiens	177-181
11443071-6	2001	Diamide treatment of either PAECs, PAEC membrane fractions, or purified endothelial nitric oxide synthase (eNOS) resulted in significant inhibition (approximately 75%) of eNOS catalytic activity measured as L-[(3)H]arginine-to-L-[(3)H]citrulline conversion.	Diamide	0-7	nitric oxide synthase 3	Homo sapiens	72-105
11443071-6	2001	Diamide treatment of either PAECs, PAEC membrane fractions, or purified endothelial nitric oxide synthase (eNOS) resulted in significant inhibition (approximately 75%) of eNOS catalytic activity measured as L-[(3)H]arginine-to-L-[(3)H]citrulline conversion.	Diamide	0-7	nitric oxide synthase 3	Homo sapiens	107-111
11443053-1	2001	Expression of endothelial nitric oxide synthase (eNOS) in transfected U-937 cells upregulates phorbol 12-myristate 13-acetate (PMA)-induced tumor necrosis factor-alpha (TNF-alpha) production through a superoxide (O(2)(-))-dependent mechanism.	Tetradecanoylphorbol Acetate	127-130	nitric oxide synthase 3	Homo sapiens	14-47
11443071-6	2001	Diamide treatment of either PAECs, PAEC membrane fractions, or purified endothelial nitric oxide synthase (eNOS) resulted in significant inhibition (approximately 75%) of eNOS catalytic activity measured as L-[(3)H]arginine-to-L-[(3)H]citrulline conversion.	Diamide	0-7	nitric oxide synthase 3	Homo sapiens	171-175
11443053-1	2001	Expression of endothelial nitric oxide synthase (eNOS) in transfected U-937 cells upregulates phorbol 12-myristate 13-acetate (PMA)-induced tumor necrosis factor-alpha (TNF-alpha) production through a superoxide (O(2)(-))-dependent mechanism.	Tetradecanoylphorbol Acetate	127-130	nitric oxide synthase 3	Homo sapiens	49-53
11443053-0	2001	Signaling by eNOS through a superoxide-dependent p42/44 mitogen-activated protein kinase pathway.	Superoxides	28-38	nitric oxide synthase 3	Homo sapiens	13-17
11443071-6	2001	Diamide treatment of either PAECs, PAEC membrane fractions, or purified endothelial nitric oxide synthase (eNOS) resulted in significant inhibition (approximately 75%) of eNOS catalytic activity measured as L-[(3)H]arginine-to-L-[(3)H]citrulline conversion.	paec	28-32	nitric oxide synthase 3	Homo sapiens	171-175
11443053-1	2001	Expression of endothelial nitric oxide synthase (eNOS) in transfected U-937 cells upregulates phorbol 12-myristate 13-acetate (PMA)-induced tumor necrosis factor-alpha (TNF-alpha) production through a superoxide (O(2)(-))-dependent mechanism.	Tetradecanoylphorbol Acetate	94-125	nitric oxide synthase 3	Homo sapiens	14-47
11443053-1	2001	Expression of endothelial nitric oxide synthase (eNOS) in transfected U-937 cells upregulates phorbol 12-myristate 13-acetate (PMA)-induced tumor necrosis factor-alpha (TNF-alpha) production through a superoxide (O(2)(-))-dependent mechanism.	Tetradecanoylphorbol Acetate	94-125	nitric oxide synthase 3	Homo sapiens	49-53
11443053-1	2001	Expression of endothelial nitric oxide synthase (eNOS) in transfected U-937 cells upregulates phorbol 12-myristate 13-acetate (PMA)-induced tumor necrosis factor-alpha (TNF-alpha) production through a superoxide (O(2)(-))-dependent mechanism.	Superoxides	201-211	nitric oxide synthase 3	Homo sapiens	14-47
11443053-1	2001	Expression of endothelial nitric oxide synthase (eNOS) in transfected U-937 cells upregulates phorbol 12-myristate 13-acetate (PMA)-induced tumor necrosis factor-alpha (TNF-alpha) production through a superoxide (O(2)(-))-dependent mechanism.	Superoxides	201-211	nitric oxide synthase 3	Homo sapiens	49-53
11443071-6	2001	Diamide treatment of either PAECs, PAEC membrane fractions, or purified endothelial nitric oxide synthase (eNOS) resulted in significant inhibition (approximately 75%) of eNOS catalytic activity measured as L-[(3)H]arginine-to-L-[(3)H]citrulline conversion.	Arginine	215-223	nitric oxide synthase 3	Homo sapiens	72-105
11443053-1	2001	Expression of endothelial nitric oxide synthase (eNOS) in transfected U-937 cells upregulates phorbol 12-myristate 13-acetate (PMA)-induced tumor necrosis factor-alpha (TNF-alpha) production through a superoxide (O(2)(-))-dependent mechanism.	Superoxides	213-217	nitric oxide synthase 3	Homo sapiens	14-47
11443053-1	2001	Expression of endothelial nitric oxide synthase (eNOS) in transfected U-937 cells upregulates phorbol 12-myristate 13-acetate (PMA)-induced tumor necrosis factor-alpha (TNF-alpha) production through a superoxide (O(2)(-))-dependent mechanism.	Superoxides	213-217	nitric oxide synthase 3	Homo sapiens	49-53
11443071-6	2001	Diamide treatment of either PAECs, PAEC membrane fractions, or purified endothelial nitric oxide synthase (eNOS) resulted in significant inhibition (approximately 75%) of eNOS catalytic activity measured as L-[(3)H]arginine-to-L-[(3)H]citrulline conversion.	Arginine	215-223	nitric oxide synthase 3	Homo sapiens	107-111
11443053-2	2001	Because mitogen-activated protein kinases (MAPK) have been shown to participate in both reactive oxygen species signaling and TNF-alpha regulation, their possible role in eNOS-derived O(2)(-) signal transduction was examined.	Superoxides	184-188	nitric oxide synthase 3	Homo sapiens	171-175
11443071-6	2001	Diamide treatment of either PAECs, PAEC membrane fractions, or purified endothelial nitric oxide synthase (eNOS) resulted in significant inhibition (approximately 75%) of eNOS catalytic activity measured as L-[(3)H]arginine-to-L-[(3)H]citrulline conversion.	Citrulline	235-245	nitric oxide synthase 3	Homo sapiens	72-105
11443053-7	2001	Expression of Gln(361)eNOS, a mutant that produces O(2)(-) but not NO, still resulted in p42/44 MAPK phosphorylation.	Glutamine	14-17	nitric oxide synthase 3	Homo sapiens	22-26
11443053-7	2001	Expression of Gln(361)eNOS, a mutant that produces O(2)(-) but not NO, still resulted in p42/44 MAPK phosphorylation.	Superoxides	51-55	nitric oxide synthase 3	Homo sapiens	22-26
11443071-6	2001	Diamide treatment of either PAECs, PAEC membrane fractions, or purified endothelial nitric oxide synthase (eNOS) resulted in significant inhibition (approximately 75%) of eNOS catalytic activity measured as L-[(3)H]arginine-to-L-[(3)H]citrulline conversion.	Citrulline	235-245	nitric oxide synthase 3	Homo sapiens	107-111
11443053-8	2001	In contrast, two NADPH binding site deletion mutants of eNOS that lack oxidase activity had no effect on p42/44 MAPK.	NADP	17-22	nitric oxide synthase 3	Homo sapiens	56-60
11443071-7	2001	This effect appeared related to oxidation of eNOS thiols as it was completely reversed by dithiothreitol.	Sulfhydryl Compounds	50-56	nitric oxide synthase 3	Homo sapiens	45-49
11443053-9	2001	Finally, PD-98059, a p42/44 MAPK pathway inhibitor, blocked TNF-alpha upregulation by eNOS (P = 0.02).	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	9-17	nitric oxide synthase 3	Homo sapiens	86-90
11443071-7	2001	This effect appeared related to oxidation of eNOS thiols as it was completely reversed by dithiothreitol.	Dithiothreitol	90-104	nitric oxide synthase 3	Homo sapiens	45-49
11443071-9	2001	Rather, CDNB treatment impaired eNOS catalytic activity in intact PAECs, and this effect was reversed by excess NADPH in isolated purified eNOS assays.	Dinitrochlorobenzene	8-12	nitric oxide synthase 3	Homo sapiens	32-36
11443071-9	2001	Rather, CDNB treatment impaired eNOS catalytic activity in intact PAECs, and this effect was reversed by excess NADPH in isolated purified eNOS assays.	Dinitrochlorobenzene	8-12	nitric oxide synthase 3	Homo sapiens	139-143
11443071-9	2001	Rather, CDNB treatment impaired eNOS catalytic activity in intact PAECs, and this effect was reversed by excess NADPH in isolated purified eNOS assays.	NADP	112-117	nitric oxide synthase 3	Homo sapiens	139-143
11443071-10	2001	Consistent with these results, we found spectral evidence that CDNB reacts with NADPH and renders it inactive as a cofactor for either eNOS or glutathione reductase.	Dinitrochlorobenzene	63-67	nitric oxide synthase 3	Homo sapiens	135-139
11382920-6	2001	Exposure to rotenone, DNP, and lactate increased the NAD(P)H/NAD(P) ratio, MTT-reduction, and eNOS mRNA also in parallel.	Rotenone	12-20	nitric oxide synthase 3	Homo sapiens	94-98
11463332-3	2001	The crystal structures of the oxygenase domains of inducible NOS (iNOS) and vascular endothelial NOS (eNOS) allow us to interpret other information in the context of this important part of the enzyme, with its binding sites for iron protoporphyrin IX (haem), biopterin, L-arginine, and the many inhibitors which interact with them.	Heme	252-256	nitric oxide synthase 3	Homo sapiens	85-100
11463332-3	2001	The crystal structures of the oxygenase domains of inducible NOS (iNOS) and vascular endothelial NOS (eNOS) allow us to interpret other information in the context of this important part of the enzyme, with its binding sites for iron protoporphyrin IX (haem), biopterin, L-arginine, and the many inhibitors which interact with them.	Biopterin	259-268	nitric oxide synthase 3	Homo sapiens	85-100
11463332-3	2001	The crystal structures of the oxygenase domains of inducible NOS (iNOS) and vascular endothelial NOS (eNOS) allow us to interpret other information in the context of this important part of the enzyme, with its binding sites for iron protoporphyrin IX (haem), biopterin, L-arginine, and the many inhibitors which interact with them.	Arginine	270-280	nitric oxide synthase 3	Homo sapiens	85-100
11529286-0	2001	Response of nitric oxide pathway to L-arginine infusion at the altitude of 4,350 m. It was hypothesized that hypoxia may inhibit nitric oxide (NO) production by reducing the availability of endothelial NO synthase (NOS III) substrate.	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	215-222
11529286-0	2001	Response of nitric oxide pathway to L-arginine infusion at the altitude of 4,350 m. It was hypothesized that hypoxia may inhibit nitric oxide (NO) production by reducing the availability of endothelial NO synthase (NOS III) substrate.	Arginine	36-46	nitric oxide synthase 3	Homo sapiens	215-222
11331290-0	2001	Implications for isoform-selective inhibitor design derived from the binding mode of bulky isothioureas to the heme domain of endothelial nitric-oxide synthase.	Thiourea	91-103	nitric oxide synthase 3	Homo sapiens	126-159
11331290-0	2001	Implications for isoform-selective inhibitor design derived from the binding mode of bulky isothioureas to the heme domain of endothelial nitric-oxide synthase.	Heme	111-115	nitric oxide synthase 3	Homo sapiens	126-159
11331296-0	2001	Acidic hydrolysis as a mechanism for the cleavage of the Glu(298)--&gt;Asp variant of human endothelial nitric-oxide synthase.	Glutamic Acid	57-60	nitric oxide synthase 3	Homo sapiens	92-125
11331296-0	2001	Acidic hydrolysis as a mechanism for the cleavage of the Glu(298)--&gt;Asp variant of human endothelial nitric-oxide synthase.	Aspartic Acid	71-74	nitric oxide synthase 3	Homo sapiens	92-125
11331296-1	2001	The 894G--&gt;T polymorphism within exon 7 of the human endothelial nitric-oxide synthase (eNOS) gene codes for glutamate or aspartate, respectively, at residue 298 and has been associated with several diseases of cardiovascular origin.	Glutamic Acid	112-121	nitric oxide synthase 3	Homo sapiens	56-89
11331296-1	2001	The 894G--&gt;T polymorphism within exon 7 of the human endothelial nitric-oxide synthase (eNOS) gene codes for glutamate or aspartate, respectively, at residue 298 and has been associated with several diseases of cardiovascular origin.	Glutamic Acid	112-121	nitric oxide synthase 3	Homo sapiens	91-95
11331296-1	2001	The 894G--&gt;T polymorphism within exon 7 of the human endothelial nitric-oxide synthase (eNOS) gene codes for glutamate or aspartate, respectively, at residue 298 and has been associated with several diseases of cardiovascular origin.	Aspartic Acid	125-134	nitric oxide synthase 3	Homo sapiens	56-89
11331296-1	2001	The 894G--&gt;T polymorphism within exon 7 of the human endothelial nitric-oxide synthase (eNOS) gene codes for glutamate or aspartate, respectively, at residue 298 and has been associated with several diseases of cardiovascular origin.	Aspartic Acid	125-134	nitric oxide synthase 3	Homo sapiens	91-95
11331296-2	2001	A recent report indicates that Asp(298)-eNOS (E298D) is cleaved intracellularly to 100- and 35-kDa fragments, suggesting a mechanism for reduced endothelial function.	Aspartic Acid	31-34	nitric oxide synthase 3	Homo sapiens	40-44
11454054-10	2001	eNOS also mediates the effects of mechanical loading on the skeleton where it acts along with prostaglandins, to promote bone formation and suppress bone resorption.	Prostaglandins	94-108	nitric oxide synthase 3	Homo sapiens	0-4
11463332-3	2001	The crystal structures of the oxygenase domains of inducible NOS (iNOS) and vascular endothelial NOS (eNOS) allow us to interpret other information in the context of this important part of the enzyme, with its binding sites for iron protoporphyrin IX (haem), biopterin, L-arginine, and the many inhibitors which interact with them.	iron protoporphyrin IX	228-250	nitric oxide synthase 3	Homo sapiens	85-100
11673056-2	2001	Recent studies demonstrate that endothelial nitric oxide synthase (eNOS), caveolin, hetero-trimeric G-protein coupled receptors, and a calcium channel form an activation complex that is associated with cholesterol-rich caveolae.	Cholesterol	202-213	nitric oxide synthase 3	Homo sapiens	32-65
11382920-6	2001	Exposure to rotenone, DNP, and lactate increased the NAD(P)H/NAD(P) ratio, MTT-reduction, and eNOS mRNA also in parallel.	Dinitrophenols	22-25	nitric oxide synthase 3	Homo sapiens	94-98
11382920-7	2001	In contrast, 2-deoxyglucose and nicotinic acid attenuated both MTT-reduction and eNOS mRNA expression.	Deoxyglucose	13-27	nitric oxide synthase 3	Homo sapiens	81-85
11382920-7	2001	In contrast, 2-deoxyglucose and nicotinic acid attenuated both MTT-reduction and eNOS mRNA expression.	Niacin	32-46	nitric oxide synthase 3	Homo sapiens	81-85
11382920-10	2001	Furthermore, in the presence of oligodeoxynucleotides corresponding to the AP-1 binding sites of the eNOS promoter, the hypoxia and chemically induced eNOS mRNA expression was completely abolished.	Oligodeoxyribonucleotides	32-53	nitric oxide synthase 3	Homo sapiens	101-105
11382920-10	2001	Furthermore, in the presence of oligodeoxynucleotides corresponding to the AP-1 binding sites of the eNOS promoter, the hypoxia and chemically induced eNOS mRNA expression was completely abolished.	Oligodeoxyribonucleotides	32-53	nitric oxide synthase 3	Homo sapiens	151-155
11382920-11	2001	We propose that hypoxia, by altering cellular metabolism, leads to an increase in the cellular NAD(P)H/NAD(P) ratio which favors enhanced eNOS expression by redox-sensitive AP-1 mediated transcriptional control.	nad(p)h	95-102	nitric oxide synthase 3	Homo sapiens	138-142
11382920-11	2001	We propose that hypoxia, by altering cellular metabolism, leads to an increase in the cellular NAD(P)H/NAD(P) ratio which favors enhanced eNOS expression by redox-sensitive AP-1 mediated transcriptional control.	NADP	95-101	nitric oxide synthase 3	Homo sapiens	138-142
11431031-2	2001	Production of nitric oxide via the endothelial isoform of nitric oxide synthase [eNOS (previously termed NOS3 or ecNOS)] is vital for a healthy endothelium; several polymorphic variations of the gene encoding eNOS (NOS3) are now known and have been investigated with respect to disease risk.	Nitric Oxide	14-26	nitric oxide synthase 3	Homo sapiens	81-85
11431031-2	2001	Production of nitric oxide via the endothelial isoform of nitric oxide synthase [eNOS (previously termed NOS3 or ecNOS)] is vital for a healthy endothelium; several polymorphic variations of the gene encoding eNOS (NOS3) are now known and have been investigated with respect to disease risk.	Nitric Oxide	14-26	nitric oxide synthase 3	Homo sapiens	105-109
11431031-2	2001	Production of nitric oxide via the endothelial isoform of nitric oxide synthase [eNOS (previously termed NOS3 or ecNOS)] is vital for a healthy endothelium; several polymorphic variations of the gene encoding eNOS (NOS3) are now known and have been investigated with respect to disease risk.	Nitric Oxide	14-26	nitric oxide synthase 3	Homo sapiens	113-118
11313363-1	2001	Neuronal nitric-oxide synthase (nNOS or NOS I) and endothelial NOS (eNOS or NOS III) differ widely in their reductase and nitric oxide (NO) synthesis activities, electron transfer rates, and propensities to form a heme-NO complex during catalysis.	Nitric Oxide	122-134	nitric oxide synthase 3	Homo sapiens	76-83
11431031-2	2001	Production of nitric oxide via the endothelial isoform of nitric oxide synthase [eNOS (previously termed NOS3 or ecNOS)] is vital for a healthy endothelium; several polymorphic variations of the gene encoding eNOS (NOS3) are now known and have been investigated with respect to disease risk.	Nitric Oxide	14-26	nitric oxide synthase 3	Homo sapiens	209-213
11431031-2	2001	Production of nitric oxide via the endothelial isoform of nitric oxide synthase [eNOS (previously termed NOS3 or ecNOS)] is vital for a healthy endothelium; several polymorphic variations of the gene encoding eNOS (NOS3) are now known and have been investigated with respect to disease risk.	Nitric Oxide	14-26	nitric oxide synthase 3	Homo sapiens	215-219
11394896-1	2001	Endothelial nitric oxide synthase (eNOS) produces nitric oxide (NO) which, after diffusing into vascular smooth muscle cells, activates guanylate cyclase leading to vasodilatation.	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	35-39
11313363-1	2001	Neuronal nitric-oxide synthase (nNOS or NOS I) and endothelial NOS (eNOS or NOS III) differ widely in their reductase and nitric oxide (NO) synthesis activities, electron transfer rates, and propensities to form a heme-NO complex during catalysis.	heme-no	214-221	nitric oxide synthase 3	Homo sapiens	76-83
11394896-3	2001	The recently described crystal structure of the heme domain of eNOS protein shows that Glu298 is fully solvent accessible and distant from regions integral to enzyme function.	Heme	48-52	nitric oxide synthase 3	Homo sapiens	63-67
11356602-0	2001	Tetrahydrobiopterin: a critical cofactor for eNOS and a strategy in the treatment of endothelial dysfunction?	sapropterin	0-19	nitric oxide synthase 3	Homo sapiens	45-49
11290515-5	2001	ecNOS antisense oligonucleotide decreased ecNOS protein, which prevented the increase in NO and albumin permeability at TNF-4 h. Spermine-NONOATE, the NO agonist, ablated the protective effect of ecNOS antisense oligonucleotide on albumin permeability in response to TNF-4 h. However, ecNOS antisense oligonucleotide had no effect on the TNF-induced increase in albumin permeability at 24 h despite prevention of the increase in NO.	Oligonucleotides	212-227	nitric oxide synthase 3	Homo sapiens	0-5
11397791-1	2001	The activity of the endothelial nitric oxide synthase (eNOS) can be regulated independently of an increase in Ca(2+) by the phosphorylation of Ser(1177) but results only in a low nitric oxide (NO) output.	Serine	143-146	nitric oxide synthase 3	Homo sapiens	20-53
11397791-1	2001	The activity of the endothelial nitric oxide synthase (eNOS) can be regulated independently of an increase in Ca(2+) by the phosphorylation of Ser(1177) but results only in a low nitric oxide (NO) output.	Serine	143-146	nitric oxide synthase 3	Homo sapiens	55-59
11397791-1	2001	The activity of the endothelial nitric oxide synthase (eNOS) can be regulated independently of an increase in Ca(2+) by the phosphorylation of Ser(1177) but results only in a low nitric oxide (NO) output.	Nitric Oxide	32-44	nitric oxide synthase 3	Homo sapiens	55-59
11397791-2	2001	In the present study, we assessed whether the agonist-induced (Ca(2+)-dependent, high-output) activation of eNOS is associated with changes in the phosphorylation of Thr(495) in the calmodulin (CaM)-binding domain.	Threonine	166-169	nitric oxide synthase 3	Homo sapiens	108-112
11397791-3	2001	eNOS Thr(495) was constitutively phosphorylated in porcine aortic endothelial cells and was rapidly dephosphorylated after bradykinin stimulation.	Threonine	5-8	nitric oxide synthase 3	Homo sapiens	0-4
11397791-11	2001	These results suggest that the dual phosphorylation of Ser(1177) and Thr(495) determines the activity of eNOS in agonist-stimulated endothelial cells.	Serine	55-58	nitric oxide synthase 3	Homo sapiens	105-109
11397791-11	2001	These results suggest that the dual phosphorylation of Ser(1177) and Thr(495) determines the activity of eNOS in agonist-stimulated endothelial cells.	Threonine	69-72	nitric oxide synthase 3	Homo sapiens	105-109
11384194-3	2001	Our experiments clearly showed that human fibroblasts with and without peroxisomal deficiencies only contain the constitutively expressed endothelial nitric oxide synthase (eNOS) isoform and that the eNOS is tyrosine-phosphorylated.	Tyrosine	208-216	nitric oxide synthase 3	Homo sapiens	200-204
11384194-6	2001	However the tyrosine-phosphorylated portion of eNOS is significantly lower in X-ALD and Zellweger cells.	Tyrosine	12-20	nitric oxide synthase 3	Homo sapiens	47-51
11411789-6	2001	Basal eNOS activity in HUVEC determined under "no flow" (static) conditions was significantly increased (approximately 1.8 fold) by 60 mM ethanol.	Ethanol	138-145	nitric oxide synthase 3	Homo sapiens	6-10
11411789-7	2001	These data are consistent with a stimulatory effect of ethanol on eNOS activity in both basal and flow-stimulated conditions, which may serve a protective role against its vasoconstrictive acute effect.	Ethanol	55-62	nitric oxide synthase 3	Homo sapiens	66-70
11290515-1	2001	We tested the hypothesis that endothelial cell nitric oxide synthase (ecNOS) mediates the tumor necrosis factor (TNF)-alpha-induced increase in nitric oxide (NO) and albumin permeability in pulmonary microvessel endothelial monolayers (PEM).	Nitric Oxide	47-59	nitric oxide synthase 3	Homo sapiens	70-75
11290515-5	2001	ecNOS antisense oligonucleotide decreased ecNOS protein, which prevented the increase in NO and albumin permeability at TNF-4 h. Spermine-NONOATE, the NO agonist, ablated the protective effect of ecNOS antisense oligonucleotide on albumin permeability in response to TNF-4 h. However, ecNOS antisense oligonucleotide had no effect on the TNF-induced increase in albumin permeability at 24 h despite prevention of the increase in NO.	Oligonucleotides	16-31	nitric oxide synthase 3	Homo sapiens	0-5
11290515-5	2001	ecNOS antisense oligonucleotide decreased ecNOS protein, which prevented the increase in NO and albumin permeability at TNF-4 h. Spermine-NONOATE, the NO agonist, ablated the protective effect of ecNOS antisense oligonucleotide on albumin permeability in response to TNF-4 h. However, ecNOS antisense oligonucleotide had no effect on the TNF-induced increase in albumin permeability at 24 h despite prevention of the increase in NO.	Oligonucleotides	16-31	nitric oxide synthase 3	Homo sapiens	42-47
11290515-5	2001	ecNOS antisense oligonucleotide decreased ecNOS protein, which prevented the increase in NO and albumin permeability at TNF-4 h. Spermine-NONOATE, the NO agonist, ablated the protective effect of ecNOS antisense oligonucleotide on albumin permeability in response to TNF-4 h. However, ecNOS antisense oligonucleotide had no effect on the TNF-induced increase in albumin permeability at 24 h despite prevention of the increase in NO.	Oligonucleotides	16-31	nitric oxide synthase 3	Homo sapiens	42-47
11290515-5	2001	ecNOS antisense oligonucleotide decreased ecNOS protein, which prevented the increase in NO and albumin permeability at TNF-4 h. Spermine-NONOATE, the NO agonist, ablated the protective effect of ecNOS antisense oligonucleotide on albumin permeability in response to TNF-4 h. However, ecNOS antisense oligonucleotide had no effect on the TNF-induced increase in albumin permeability at 24 h despite prevention of the increase in NO.	Oligonucleotides	16-31	nitric oxide synthase 3	Homo sapiens	42-47
11397791-0	2001	Phosphorylation of Thr(495) regulates Ca(2+)/calmodulin-dependent endothelial nitric oxide synthase activity.	Threonine	19-22	nitric oxide synthase 3	Homo sapiens	66-99
11434508-2	2001	We tested the hypothesis that the variability in venous response to acetylcholine may be associated with two recently identified genetic polymorphisms for proteins involved in the signal transduction pathway, i.e. the G-protein beta3-subunit (GNB3) and endothelial nitric oxide synthase (eNOS).	Acetylcholine	68-81	nitric oxide synthase 3	Homo sapiens	253-286
11434508-2	2001	We tested the hypothesis that the variability in venous response to acetylcholine may be associated with two recently identified genetic polymorphisms for proteins involved in the signal transduction pathway, i.e. the G-protein beta3-subunit (GNB3) and endothelial nitric oxide synthase (eNOS).	Acetylcholine	68-81	nitric oxide synthase 3	Homo sapiens	288-292
11292821-1	2001	Endothelial nitric-oxide synthase (eNOS) is an important regulatory enzyme in the cardiovascular system catalyzing the production of NO from arginine.	Arginine	141-149	nitric oxide synthase 3	Homo sapiens	0-33
11290515-5	2001	ecNOS antisense oligonucleotide decreased ecNOS protein, which prevented the increase in NO and albumin permeability at TNF-4 h. Spermine-NONOATE, the NO agonist, ablated the protective effect of ecNOS antisense oligonucleotide on albumin permeability in response to TNF-4 h. However, ecNOS antisense oligonucleotide had no effect on the TNF-induced increase in albumin permeability at 24 h despite prevention of the increase in NO.	spermine nitric oxide complex	129-145	nitric oxide synthase 3	Homo sapiens	0-5
11290515-5	2001	ecNOS antisense oligonucleotide decreased ecNOS protein, which prevented the increase in NO and albumin permeability at TNF-4 h. Spermine-NONOATE, the NO agonist, ablated the protective effect of ecNOS antisense oligonucleotide on albumin permeability in response to TNF-4 h. However, ecNOS antisense oligonucleotide had no effect on the TNF-induced increase in albumin permeability at 24 h despite prevention of the increase in NO.	spermine nitric oxide complex	129-145	nitric oxide synthase 3	Homo sapiens	42-47
11290515-5	2001	ecNOS antisense oligonucleotide decreased ecNOS protein, which prevented the increase in NO and albumin permeability at TNF-4 h. Spermine-NONOATE, the NO agonist, ablated the protective effect of ecNOS antisense oligonucleotide on albumin permeability in response to TNF-4 h. However, ecNOS antisense oligonucleotide had no effect on the TNF-induced increase in albumin permeability at 24 h despite prevention of the increase in NO.	spermine nitric oxide complex	129-145	nitric oxide synthase 3	Homo sapiens	42-47
11290515-5	2001	ecNOS antisense oligonucleotide decreased ecNOS protein, which prevented the increase in NO and albumin permeability at TNF-4 h. Spermine-NONOATE, the NO agonist, ablated the protective effect of ecNOS antisense oligonucleotide on albumin permeability in response to TNF-4 h. However, ecNOS antisense oligonucleotide had no effect on the TNF-induced increase in albumin permeability at 24 h despite prevention of the increase in NO.	spermine nitric oxide complex	129-145	nitric oxide synthase 3	Homo sapiens	42-47
11290515-5	2001	ecNOS antisense oligonucleotide decreased ecNOS protein, which prevented the increase in NO and albumin permeability at TNF-4 h. Spermine-NONOATE, the NO agonist, ablated the protective effect of ecNOS antisense oligonucleotide on albumin permeability in response to TNF-4 h. However, ecNOS antisense oligonucleotide had no effect on the TNF-induced increase in albumin permeability at 24 h despite prevention of the increase in NO.	Oligonucleotides	212-227	nitric oxide synthase 3	Homo sapiens	0-5
11290515-5	2001	ecNOS antisense oligonucleotide decreased ecNOS protein, which prevented the increase in NO and albumin permeability at TNF-4 h. Spermine-NONOATE, the NO agonist, ablated the protective effect of ecNOS antisense oligonucleotide on albumin permeability in response to TNF-4 h. However, ecNOS antisense oligonucleotide had no effect on the TNF-induced increase in albumin permeability at 24 h despite prevention of the increase in NO.	Oligonucleotides	212-227	nitric oxide synthase 3	Homo sapiens	42-47
11290515-5	2001	ecNOS antisense oligonucleotide decreased ecNOS protein, which prevented the increase in NO and albumin permeability at TNF-4 h. Spermine-NONOATE, the NO agonist, ablated the protective effect of ecNOS antisense oligonucleotide on albumin permeability in response to TNF-4 h. However, ecNOS antisense oligonucleotide had no effect on the TNF-induced increase in albumin permeability at 24 h despite prevention of the increase in NO.	Oligonucleotides	212-227	nitric oxide synthase 3	Homo sapiens	42-47
11290515-5	2001	ecNOS antisense oligonucleotide decreased ecNOS protein, which prevented the increase in NO and albumin permeability at TNF-4 h. Spermine-NONOATE, the NO agonist, ablated the protective effect of ecNOS antisense oligonucleotide on albumin permeability in response to TNF-4 h. However, ecNOS antisense oligonucleotide had no effect on the TNF-induced increase in albumin permeability at 24 h despite prevention of the increase in NO.	Oligonucleotides	212-227	nitric oxide synthase 3	Homo sapiens	42-47
11290515-5	2001	ecNOS antisense oligonucleotide decreased ecNOS protein, which prevented the increase in NO and albumin permeability at TNF-4 h. Spermine-NONOATE, the NO agonist, ablated the protective effect of ecNOS antisense oligonucleotide on albumin permeability in response to TNF-4 h. However, ecNOS antisense oligonucleotide had no effect on the TNF-induced increase in albumin permeability at 24 h despite prevention of the increase in NO.	Oligonucleotides	212-227	nitric oxide synthase 3	Homo sapiens	42-47
11290515-5	2001	ecNOS antisense oligonucleotide decreased ecNOS protein, which prevented the increase in NO and albumin permeability at TNF-4 h. Spermine-NONOATE, the NO agonist, ablated the protective effect of ecNOS antisense oligonucleotide on albumin permeability in response to TNF-4 h. However, ecNOS antisense oligonucleotide had no effect on the TNF-induced increase in albumin permeability at 24 h despite prevention of the increase in NO.	Oligonucleotides	212-227	nitric oxide synthase 3	Homo sapiens	42-47
11290515-5	2001	ecNOS antisense oligonucleotide decreased ecNOS protein, which prevented the increase in NO and albumin permeability at TNF-4 h. Spermine-NONOATE, the NO agonist, ablated the protective effect of ecNOS antisense oligonucleotide on albumin permeability in response to TNF-4 h. However, ecNOS antisense oligonucleotide had no effect on the TNF-induced increase in albumin permeability at 24 h despite prevention of the increase in NO.	Oligonucleotides	212-227	nitric oxide synthase 3	Homo sapiens	42-47
11278358-7	2001	Hypochlorite-modified LDL caused remarkable changes of intracellular eNOS distribution including translocation from the plasma membrane and disintegration of the Golgi location without altering myristoylation or palmitoylation of the enzyme.	Hypochlorous Acid	0-12	nitric oxide synthase 3	Homo sapiens	69-73
11319157-2	2001	We hypothesized that the expression of endothelial nitric oxide synthase (eNOS) in fetoplacental artery endothelium and the concentrations of nitric oxide (NO) and cyclic GMP (cGMP) in amniotic fluid (AF) are increased during the third trimester of ovine gestation.	Nitric Oxide	51-63	nitric oxide synthase 3	Homo sapiens	74-78
11120737-7	2001	Additionally, the calcium ionophore, a reagent that promotes nitric oxide release, enhances coprecipitation of dynamin with eNOS in BAEC, suggesting the interaction between the proteins can be regulated by intracellular signals.	Calcium	18-25	nitric oxide synthase 3	Homo sapiens	124-128
11120737-7	2001	Additionally, the calcium ionophore, a reagent that promotes nitric oxide release, enhances coprecipitation of dynamin with eNOS in BAEC, suggesting the interaction between the proteins can be regulated by intracellular signals.	Nitric Oxide	61-73	nitric oxide synthase 3	Homo sapiens	124-128
11348878-2	2001	Here, we show that simvastatin, a 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor, within the therapeutic range (0.01 to 1 micromol/L) prevented the downregulation of eNOS mRNA and protein promoted by nLDL (180 mg cholesterol/dL, 48 hours) in human umbilical vein endothelial cells.	Simvastatin	19-30	nitric oxide synthase 3	Homo sapiens	177-181
11348878-2	2001	Here, we show that simvastatin, a 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor, within the therapeutic range (0.01 to 1 micromol/L) prevented the downregulation of eNOS mRNA and protein promoted by nLDL (180 mg cholesterol/dL, 48 hours) in human umbilical vein endothelial cells.	Cholesterol	224-235	nitric oxide synthase 3	Homo sapiens	177-181
11348878-4	2001	Simvastatin significantly stabilized eNOS mRNA in cells treated with nLDL during 48 hours (eNOS mRNA half-life approximately 11 hours in controls versus &gt;24 hours in nLDL per 0.1 micromol/L simvastatin-treated cells).	Simvastatin	0-11	nitric oxide synthase 3	Homo sapiens	37-41
11348878-4	2001	Simvastatin significantly stabilized eNOS mRNA in cells treated with nLDL during 48 hours (eNOS mRNA half-life approximately 11 hours in controls versus &gt;24 hours in nLDL per 0.1 micromol/L simvastatin-treated cells).	Simvastatin	0-11	nitric oxide synthase 3	Homo sapiens	91-95
11348878-5	2001	The downregulation of eNOS by nLDL was abrogated by cycloheximide, an inhibitor of protein synthesis, and by N-acetyl-leucyl-leucyl-norleucinal, a protease inhibitor that reduces the catabolism of sterol regulatory element binding proteins.	Cycloheximide	52-65	nitric oxide synthase 3	Homo sapiens	22-26
11348878-5	2001	The downregulation of eNOS by nLDL was abrogated by cycloheximide, an inhibitor of protein synthesis, and by N-acetyl-leucyl-leucyl-norleucinal, a protease inhibitor that reduces the catabolism of sterol regulatory element binding proteins.	Sterols	197-203	nitric oxide synthase 3	Homo sapiens	22-26
11348878-6	2001	Sterol deprivation increased the downregulation produced by nLDL on eNOS and sterol regulatory element binding protein-2 expression levels.	Sterols	0-6	nitric oxide synthase 3	Homo sapiens	68-72
11378533-7	2001	HOCl-exposed cells had an increased production of NO, probably by an increased activity of cNOS, due to increased intracellular Ca2+.	Hypochlorous Acid	0-4	nitric oxide synthase 3	Homo sapiens	91-95
11378533-9	2001	The cNOS-inhibitor N-propyl-L-arginine inhibited HOCl-induced NO production.	n-propyl-l-arginine	19-38	nitric oxide synthase 3	Homo sapiens	4-8
11378533-9	2001	The cNOS-inhibitor N-propyl-L-arginine inhibited HOCl-induced NO production.	Hypochlorous Acid	49-53	nitric oxide synthase 3	Homo sapiens	4-8
11350569-15	2001	However, male diabetic patients with eNOS Asp298Asp genotype had higher plasma very-low density lipoprotein (VLDL) cholesterol and VLDL-triglyceride concentrations than those with the genotypes Glu298Glu or Glu298Asp (P &lt; 0.01 for trend).	Cholesterol	115-126	nitric oxide synthase 3	Homo sapiens	37-41
11350569-15	2001	However, male diabetic patients with eNOS Asp298Asp genotype had higher plasma very-low density lipoprotein (VLDL) cholesterol and VLDL-triglyceride concentrations than those with the genotypes Glu298Glu or Glu298Asp (P &lt; 0.01 for trend).	Triglycerides	136-148	nitric oxide synthase 3	Homo sapiens	37-41
11278358-0	2001	Hypochlorite-modified low density lipoprotein inhibits nitric oxide synthesis in endothelial cells via an intracellular dislocalization of endothelial nitric-oxide synthase.	Hypochlorous Acid	0-12	nitric oxide synthase 3	Homo sapiens	139-172
11278358-8	2001	In contrast, cyclodextrin known to deplete plasma membrane of cholesterol and to disrupt caveolae induced only a disappearance of eNOS from the plasma membrane that was not associated with decreased agonist-induced citrulline and cGMP formation.	Cyclodextrins	13-25	nitric oxide synthase 3	Homo sapiens	130-134
11319202-2	2001	Stimulating ECs with vascular endothelial growth factor (VEGF) leads to the activation of Akt/protein kinase B, which in turn activates endothelial nitric oxide synthase (eNOS) by phosphorylation on serine 1177.	Serine	199-205	nitric oxide synthase 3	Homo sapiens	136-169
11509922-7	2001	These isoforms of tocopherol did not affect cNOS protein expression, but enhanced cNOS phosphorylation in platelets.	Tocopherols	18-28	nitric oxide synthase 3	Homo sapiens	82-86
11298374-1	2001	Nitric oxide (NO), produced by endothelial nitric oxide synthase (eNOS), plays important roles in normal vascular homeostasis, and reduced endothelial NO bioactivity is an important feature of vascular disease states.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	31-64
11298374-1	2001	Nitric oxide (NO), produced by endothelial nitric oxide synthase (eNOS), plays important roles in normal vascular homeostasis, and reduced endothelial NO bioactivity is an important feature of vascular disease states.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	66-70
11352660-7	2001	The effects of VEGF on NO production and the expression of endothelial NOS (eNOS) were attenuated by treating BeWo cells with the selective inhibitor of MAPK kinase, PD98059.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	166-173	nitric oxide synthase 3	Homo sapiens	59-74
11306434-7	2001	Immunohistochemical studies on formalin-fixed, paraffin-embedded sections of surgical and autopsy material from lungs of individuals with LAM showed diffuse NO synthase III (NOSIII) expression in the lesional smooth muscle of LAM similar to that in the vascular endothelium.	Formaldehyde	31-39	nitric oxide synthase 3	Homo sapiens	157-172
11306434-7	2001	Immunohistochemical studies on formalin-fixed, paraffin-embedded sections of surgical and autopsy material from lungs of individuals with LAM showed diffuse NO synthase III (NOSIII) expression in the lesional smooth muscle of LAM similar to that in the vascular endothelium.	Formaldehyde	31-39	nitric oxide synthase 3	Homo sapiens	174-180
11306434-7	2001	Immunohistochemical studies on formalin-fixed, paraffin-embedded sections of surgical and autopsy material from lungs of individuals with LAM showed diffuse NO synthase III (NOSIII) expression in the lesional smooth muscle of LAM similar to that in the vascular endothelium.	Paraffin	47-55	nitric oxide synthase 3	Homo sapiens	157-172
11306434-7	2001	Immunohistochemical studies on formalin-fixed, paraffin-embedded sections of surgical and autopsy material from lungs of individuals with LAM showed diffuse NO synthase III (NOSIII) expression in the lesional smooth muscle of LAM similar to that in the vascular endothelium.	Paraffin	47-55	nitric oxide synthase 3	Homo sapiens	174-180
11292368-0	2001	Caveolar localization of arginine regeneration enzymes, argininosuccinate synthase, and lyase, with endothelial nitric oxide synthase.	Arginine	25-33	nitric oxide synthase 3	Homo sapiens	100-133
11339671-13	2001	We conclude that antenatal Dex therapy enhances the abundance of eNOS protein expression in the lung at birth and could be a factor in improving respiratory functions in infants who received antenatal steroid therapy.	Dexamethasone	27-30	nitric oxide synthase 3	Homo sapiens	65-69
11339671-13	2001	We conclude that antenatal Dex therapy enhances the abundance of eNOS protein expression in the lung at birth and could be a factor in improving respiratory functions in infants who received antenatal steroid therapy.	Steroids	201-208	nitric oxide synthase 3	Homo sapiens	65-69
11243424-4	2001	L-Citrulline formation (a measure of eNOS enzymatic activity) was significantly increased in cells treated for 24 h with vitamin C.	Citrulline	0-12	nitric oxide synthase 3	Homo sapiens	37-41
11159040-1	2001	Past studies have demonstrated that 17beta-estradiol (E(2)beta) increases endothelial nitric oxide (NO) synthase (eNOS) activity in uterine, heart, and skeletal muscle and in cultured human endothelial cells.	Estradiol	36-52	nitric oxide synthase 3	Homo sapiens	114-118
11181410-3	2001	Here we demonstrate that acute exposure of human endothelial cells to glucose, at levels found in plasma of diabetic patients, results in a significant blunting of NO responses to the endothelial nitric oxide synthase (eNOS) agonists bradykinin and A-23187.	Glucose	70-77	nitric oxide synthase 3	Homo sapiens	184-217
11181410-3	2001	Here we demonstrate that acute exposure of human endothelial cells to glucose, at levels found in plasma of diabetic patients, results in a significant blunting of NO responses to the endothelial nitric oxide synthase (eNOS) agonists bradykinin and A-23187.	Glucose	70-77	nitric oxide synthase 3	Homo sapiens	219-223
11243424-7	2001	Treatment with vitamin C for 24 h significantly increased levels of the eNOS co-factor tetrahydrobiopterin (BH4), whereas MnTBAP did not affect its levels.	sapropterin	108-111	nitric oxide synthase 3	Homo sapiens	72-76
11243424-8	2001	Sepiapterin (10(-4) M), a precursor of BH4, significantly increased eNOS activity, whereas addition of vitamin C to cells treated with sepiapterin did not cause any further increase in eNOS activity.	sepiapterin	0-11	nitric oxide synthase 3	Homo sapiens	68-72
11243424-8	2001	Sepiapterin (10(-4) M), a precursor of BH4, significantly increased eNOS activity, whereas addition of vitamin C to cells treated with sepiapterin did not cause any further increase in eNOS activity.	sapropterin	39-42	nitric oxide synthase 3	Homo sapiens	68-72
11243424-9	2001	Our results suggest that the beneficial effect of vitamin C on endothelial function is best explained by increased intracellular BH4 content and subsequent enhancement of eNOS activity.	Ascorbic Acid	50-59	nitric oxide synthase 3	Homo sapiens	171-175
11693755-9	2001	Simvastatin reduced the TNF-alpha-related binding activity of neutrophil cytosolic proteins to eNOS mRNA, which was associated with its protective effect on eNOS protein expression.	Simvastatin	0-11	nitric oxide synthase 3	Homo sapiens	95-99
11693755-9	2001	Simvastatin reduced the TNF-alpha-related binding activity of neutrophil cytosolic proteins to eNOS mRNA, which was associated with its protective effect on eNOS protein expression.	Simvastatin	0-11	nitric oxide synthase 3	Homo sapiens	157-161
11243424-4	2001	L-Citrulline formation (a measure of eNOS enzymatic activity) was significantly increased in cells treated for 24 h with vitamin C.	Ascorbic Acid	121-130	nitric oxide synthase 3	Homo sapiens	37-41
11243424-7	2001	Treatment with vitamin C for 24 h significantly increased levels of the eNOS co-factor tetrahydrobiopterin (BH4), whereas MnTBAP did not affect its levels.	Ascorbic Acid	15-24	nitric oxide synthase 3	Homo sapiens	72-76
11243424-7	2001	Treatment with vitamin C for 24 h significantly increased levels of the eNOS co-factor tetrahydrobiopterin (BH4), whereas MnTBAP did not affect its levels.	sapropterin	87-106	nitric oxide synthase 3	Homo sapiens	72-76
11208594-4	2001	eNOS-mediated NO generation is a highly regulated cellular event, which is induced by calcium-mobilizing agonists and fluid shear stress.	Calcium	86-93	nitric oxide synthase 3	Homo sapiens	0-4
11241423-8	2001	Because nitric oxide, after its production by eNOS, is believed to be degraded by superoxide radicals, the effect of eNOS expression on atherosclerosis remains controversial.	Nitric Oxide	8-20	nitric oxide synthase 3	Homo sapiens	46-50
11239195-1	2001	BACKGROUND AND PURPOSE: Endothelium-derived NO is formed from L-arginine by endothelial NO synthase (eNOS) encoded by the NOS 3 gene on chromosome 7.	Arginine	62-72	nitric oxide synthase 3	Homo sapiens	101-105
11239195-1	2001	BACKGROUND AND PURPOSE: Endothelium-derived NO is formed from L-arginine by endothelial NO synthase (eNOS) encoded by the NOS 3 gene on chromosome 7.	Arginine	62-72	nitric oxide synthase 3	Homo sapiens	122-127
11136695-2	2001	Increased uptake of cholesterol by endothelial cells (ECs) upregulates the abundance of the structural protein caveolin-1 and impairs NO release through the stabilization of the inhibitory heterocomplex between caveolin-1 and endothelial NO synthase (eNOS).	Cholesterol	20-31	nitric oxide synthase 3	Homo sapiens	226-249
11230275-6	2001	Cotreatment with either tempol or lazaroid abrogated the lead-induced upregulation of eNOS protein and NO(x) production.	tempol	24-30	nitric oxide synthase 3	Homo sapiens	86-90
11230275-6	2001	Cotreatment with either tempol or lazaroid abrogated the lead-induced upregulation of eNOS protein and NO(x) production.	lazaroid	34-42	nitric oxide synthase 3	Homo sapiens	86-90
11293408-0	2001	Formation of a protonated trihydrobiopterin radical cation in the first reaction cycle of neuronal and endothelial nitric oxide synthase detected by electron paramagnetic resonance spectroscopy.	trihydrobiopterin	26-43	nitric oxide synthase 3	Homo sapiens	103-136
11286396-0	2001	Regulation of endothelial nitric oxide synthase and endothelin-1 expression by fluvastatin in human vascular endothelial cells.	Fluvastatin	79-90	nitric oxide synthase 3	Homo sapiens	14-47
11286396-2	2001	Incubation of HUVECs with fluvastatin for 12 h increased endothelial nitric oxide synthase (eNOS) mRNA expression in a concentration-dependent manner (peak, 276 +/- 38%, mean +/- S.D., of the control, at 1.0 microM fluvastatin, P&lt;0.01).	Fluvastatin	26-37	nitric oxide synthase 3	Homo sapiens	57-90
11042169-1	2001	Our recent study indicates that lysophosphatidylcholine (LPC) enhances Sp1 binding and Sp1-dependent endothelial nitric oxide synthase (eNOS) promoter activity via the mitogen-activated protein kinase/extracellular signal-regulated kinase kinase 1 (MEK-1) signaling pathway (Cieslik, K., Lee, C.-M., Tang, J.-L., and Wu, K. K. (1999) J. Biol.	Lysophosphatidylcholines	32-55	nitric oxide synthase 3	Homo sapiens	101-134
11042169-1	2001	Our recent study indicates that lysophosphatidylcholine (LPC) enhances Sp1 binding and Sp1-dependent endothelial nitric oxide synthase (eNOS) promoter activity via the mitogen-activated protein kinase/extracellular signal-regulated kinase kinase 1 (MEK-1) signaling pathway (Cieslik, K., Lee, C.-M., Tang, J.-L., and Wu, K. K. (1999) J. Biol.	Lysophosphatidylcholines	57-60	nitric oxide synthase 3	Homo sapiens	101-134
11166759-3	2001	Treatment of primary human coronary artery endothelial cells with nicotine for 24 h at concentrations (10(-5) and 10(-7) M) similar to those in the blood of smokers resulted in increased mRNA levels of endothelial nitric oxide synthase, angiotensin-I converting enzyme, tissue-type plasminogen activator, plasminogen activator inhibitor-1, von Willebrand factor, and vascular cell adhesion molecule-1.	Nicotine	66-74	nitric oxide synthase 3	Homo sapiens	202-235
11136695-2	2001	Increased uptake of cholesterol by endothelial cells (ECs) upregulates the abundance of the structural protein caveolin-1 and impairs NO release through the stabilization of the inhibitory heterocomplex between caveolin-1 and endothelial NO synthase (eNOS).	Cholesterol	20-31	nitric oxide synthase 3	Homo sapiens	251-255
11136695-3	2001	Therefore, we examined whether the hydroxy-methylglutaryl-coenzyme A reductase inhibitor atorvastatin modulates caveolin abundance, eNOS activity, and NO release through a reduction in endogenous cholesterol levels.	Atorvastatin	89-101	nitric oxide synthase 3	Homo sapiens	132-136
11136695-8	2001	In the presence of LDL-Chol, atorvastatin also promoted the agonist-induced association of eNOS and the chaperone Hsp90, resulting in the potentiation of eNOS activation.	chol	23-27	nitric oxide synthase 3	Homo sapiens	91-95
11136695-8	2001	In the presence of LDL-Chol, atorvastatin also promoted the agonist-induced association of eNOS and the chaperone Hsp90, resulting in the potentiation of eNOS activation.	chol	23-27	nitric oxide synthase 3	Homo sapiens	154-158
11136695-8	2001	In the presence of LDL-Chol, atorvastatin also promoted the agonist-induced association of eNOS and the chaperone Hsp90, resulting in the potentiation of eNOS activation.	Atorvastatin	29-41	nitric oxide synthase 3	Homo sapiens	91-95
11136695-8	2001	In the presence of LDL-Chol, atorvastatin also promoted the agonist-induced association of eNOS and the chaperone Hsp90, resulting in the potentiation of eNOS activation.	Atorvastatin	29-41	nitric oxide synthase 3	Homo sapiens	154-158
11120631-12	2001	2 and a 24.1% reduction in eNOS expression for nicotine- and cotinine-treated vessels, respectively (P&lt;0.01).	Nicotine	47-55	nitric oxide synthase 3	Homo sapiens	27-31
11121998-1	2001	OBJECTIVE: To investigate how endothelial nitric oxide (eNOS) expression in the seminiferous tubules might be related to spermatogenesis, by examining eNOS expression in testicular tissue of patients infertile from various causes.	Nitric Oxide	42-54	nitric oxide synthase 3	Homo sapiens	56-60
11409302-1	2001	The effect of the synthetic statin fluvastatin was investigated on the concentrations of endothelial nitric oxide synthase (eNOS) and of soluble adhesion molecules in human vascular endothelial cell cultures.	Fluvastatin	35-46	nitric oxide synthase 3	Homo sapiens	89-122
11227730-4	2001	We tested the hypothesis that treatment with GSH may improve platelet constitutive NO sinthase (cNOS) activity in patients with T2DM.	Glutathione	45-48	nitric oxide synthase 3	Homo sapiens	96-100
11227730-10	2001	These data suggest that the administration of GSH, in patients with T2DM, is able to improve platelet cNOS activity together with a reduction of PAI-1.	Glutathione	46-49	nitric oxide synthase 3	Homo sapiens	102-106
11120631-12	2001	2 and a 24.1% reduction in eNOS expression for nicotine- and cotinine-treated vessels, respectively (P&lt;0.01).	Cotinine	61-69	nitric oxide synthase 3	Homo sapiens	27-31
11887863-6	2001	Anti-inflammatory doses of aspirin (1-10 mmol/L) restored eNOS expression in LPS-stimulated human peritoneal tissue samples.	Aspirin	27-34	nitric oxide synthase 3	Homo sapiens	58-62
11887863-10	2001	High doses of aspirin protected both eNOS protein expression and sGC in human peritoneum.	Aspirin	14-21	nitric oxide synthase 3	Homo sapiens	37-41
11120631-13	2001	Additionally, immunohistochemical staining for eNOS showed less dense staining on nicotine- and cotinine-treated vessels as compared to controls.	Nicotine	82-90	nitric oxide synthase 3	Homo sapiens	47-51
11120631-13	2001	Additionally, immunohistochemical staining for eNOS showed less dense staining on nicotine- and cotinine-treated vessels as compared to controls.	Cotinine	96-104	nitric oxide synthase 3	Homo sapiens	47-51
11120633-6	2001	Increases in diaminofluorescein fluorescence were used to measure bradykinin activation of endothelial nitric oxide synthase (eNOS) with or without N-nitro-l-arginine (L-NNA).	diaminofluorescein	13-31	nitric oxide synthase 3	Homo sapiens	91-124
11222026-4	2000	Activity of the constitutive endothelial nitric oxide synthase (eNOS) was measured by the conversion [3H]-l-arginine to [3H]-l-citrulline and eNOS protein expression by Western blotting.	3h]-l-arginine	102-116	nitric oxide synthase 3	Homo sapiens	29-62
11118505-7	2000	D-Glucose and PMA increased endothelial NOS (eNOS) activity, which was prevented by calphostin C or omission of extracellular Ca2+ and unaffected by PD-98059.	Glucose	0-9	nitric oxide synthase 3	Homo sapiens	28-43
11222026-4	2000	Activity of the constitutive endothelial nitric oxide synthase (eNOS) was measured by the conversion [3H]-l-arginine to [3H]-l-citrulline and eNOS protein expression by Western blotting.	3h]-l-arginine	102-116	nitric oxide synthase 3	Homo sapiens	64-68
11222026-4	2000	Activity of the constitutive endothelial nitric oxide synthase (eNOS) was measured by the conversion [3H]-l-arginine to [3H]-l-citrulline and eNOS protein expression by Western blotting.	3h]-l-citrulline	121-137	nitric oxide synthase 3	Homo sapiens	29-62
11222026-4	2000	Activity of the constitutive endothelial nitric oxide synthase (eNOS) was measured by the conversion [3H]-l-arginine to [3H]-l-citrulline and eNOS protein expression by Western blotting.	3h]-l-citrulline	121-137	nitric oxide synthase 3	Homo sapiens	64-68
11040050-9	2000	High iNOS versus eNOS selectivity was found for 1400W, whereas several isothiourea derivatives and 1400W displayed moderate n- versus eNOS selectivity.	Thiourea	71-82	nitric oxide synthase 3	Homo sapiens	134-138
11132600-13	2000	acetylcholine (average increase: + 554 +/- 371%), nitroprusside or L-NMMA infusion were found across the eNOS genotypes, neither for endothelium-dependent or endothelium-independent vasodilation, nor for basal NO production and release.	Acetylcholine	0-13	nitric oxide synthase 3	Homo sapiens	105-109
11132600-13	2000	acetylcholine (average increase: + 554 +/- 371%), nitroprusside or L-NMMA infusion were found across the eNOS genotypes, neither for endothelium-dependent or endothelium-independent vasodilation, nor for basal NO production and release.	Nitroprusside	50-63	nitric oxide synthase 3	Homo sapiens	105-109
11132600-13	2000	acetylcholine (average increase: + 554 +/- 371%), nitroprusside or L-NMMA infusion were found across the eNOS genotypes, neither for endothelium-dependent or endothelium-independent vasodilation, nor for basal NO production and release.	omega-N-Methylarginine	67-73	nitric oxide synthase 3	Homo sapiens	105-109
11029297-0	2000	Calcium regulates estrogen increase in permeability of cultured CaSki epithelium by eNOS-dependent mechanism.	Calcium	0-7	nitric oxide synthase 3	Homo sapiens	84-88
11029297-8	2000	These results indicate that cytosolic calcium mediates the responses to estrogen and suggest that the estrogen increase in permeability and the augmented increase in permeability in response to hypertonicity involve an increase in NO synthesis by upregulation of the calcium-dependent eNOS.	Calcium	38-45	nitric oxide synthase 3	Homo sapiens	285-289
11149042-3	2000	Within the liver, sinusoidal cells produce a basal level of nitric oxide from endothelial nitric oxide synthase activity.	Nitric Oxide	60-72	nitric oxide synthase 3	Homo sapiens	78-111
11079678-8	2000	RESULTS: Cerivastatin (10(-9) to 10(-6) mol/liter) enhanced eNOS protein expression and NO release (about two-fold) in EC in response to Ca2+ ionophore (10(-6) mol/liter).	cerivastatin	9-21	nitric oxide synthase 3	Homo sapiens	60-64
11079678-13	2000	CONCLUSIONS: In humans, SVEC inhibition of HMG-CoA/mevalonate pathway contributes to the enhanced eNOS expression and NO release by cerivastatin, whereas in SMC, inhibition of this pathway only partially explains cerivastatin-induced cell growth arrest.	3-hydroxy-3-methylglutaryl-coenzyme A	43-50	nitric oxide synthase 3	Homo sapiens	98-102
11079678-13	2000	CONCLUSIONS: In humans, SVEC inhibition of HMG-CoA/mevalonate pathway contributes to the enhanced eNOS expression and NO release by cerivastatin, whereas in SMC, inhibition of this pathway only partially explains cerivastatin-induced cell growth arrest.	Mevalonic Acid	51-61	nitric oxide synthase 3	Homo sapiens	98-102
11053225-0	2000	Endothelial nitric oxide synthase is a site of superoxide synthesis in endothelial cells treated with glyceryl trinitrate.	Superoxides	47-57	nitric oxide synthase 3	Homo sapiens	0-33
11053225-0	2000	Endothelial nitric oxide synthase is a site of superoxide synthesis in endothelial cells treated with glyceryl trinitrate.	Nitroglycerin	102-121	nitric oxide synthase 3	Homo sapiens	0-33
11053225-11	2000	In conclusion, endothelial NOS is a site of O(2)(*-) synthesis in endothelial cells activated by GTN.	Nitroglycerin	97-100	nitric oxide synthase 3	Homo sapiens	15-30
11063722-6	2000	The functional importance of the diminished eNOS expression was revealed by the finding that serum nitrite/nitrate levels among individuals carrying the -786T--&gt;C mutation were significantly lower than among those without the mutation.	Nitrites	99-106	nitric oxide synthase 3	Homo sapiens	44-48
11063722-6	2000	The functional importance of the diminished eNOS expression was revealed by the finding that serum nitrite/nitrate levels among individuals carrying the -786T--&gt;C mutation were significantly lower than among those without the mutation.	Nitrates	107-114	nitric oxide synthase 3	Homo sapiens	44-48
11040050-9	2000	High iNOS versus eNOS selectivity was found for 1400W, whereas several isothiourea derivatives and 1400W displayed moderate n- versus eNOS selectivity.	N-((3-(aminomethyl)phenyl)methyl)ethanimidamide	99-104	nitric oxide synthase 3	Homo sapiens	134-138
10997917-10	2000	In conclusion, electrochemical detection of NO release from cultured endothelial cells demonstrated that concentrations of Hcy &gt;20 microM produce a significant indirect suppression of eNOS activity without any discernible effects on its expression.	hcy &gt	123-130	nitric oxide synthase 3	Homo sapiens	187-191
11095925-1	2000	The possible regulatory role of tetrahydrobiopterin (BH(4)) in Type III nitric oxide synthase (NOS III) activity of human placentae from first trimester, term and pre-eclamptic pregnancies was investigated.	sapropterin	32-51	nitric oxide synthase 3	Homo sapiens	95-102
11030378-1	2000	BACKGROUND: Nitric oxide, including that produced by endothelial constitutive nitric oxide synthase (ecNOS), may regulate vascular and airway tone in the lungs and may influence various aspects of airway homeostasis.	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	53-99
11030378-1	2000	BACKGROUND: Nitric oxide, including that produced by endothelial constitutive nitric oxide synthase (ecNOS), may regulate vascular and airway tone in the lungs and may influence various aspects of airway homeostasis.	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	101-106
11029403-1	2000	17beta-Estradiol (E(2)) is a rapid activator of endothelial nitric oxide synthase (eNOS).	Estradiol	0-16	nitric oxide synthase 3	Homo sapiens	48-81
11029403-1	2000	17beta-Estradiol (E(2)) is a rapid activator of endothelial nitric oxide synthase (eNOS).	Estradiol	0-16	nitric oxide synthase 3	Homo sapiens	83-87
11029403-4	2000	Here we demonstrate for the first time, to our knowledge, that E(2) rapidly induces phosphorylation and activation of eNOS through the phosphatidylinositol 3 (PI3)-kinase-Akt pathway.	phosphatidylinositol 3	135-157	nitric oxide synthase 3	Homo sapiens	118-122
11029403-7	2000	As has been shown for vascular endothelial growth factor, eNOS is an E(2)-activated Akt substrate, demonstrated by rapid eNOS phosphorylation on serine 1177, a critical residue for eNOS activation and enhanced sensitivity to resting cellular Ca(2+) levels.	Serine	145-151	nitric oxide synthase 3	Homo sapiens	58-62
11029403-7	2000	As has been shown for vascular endothelial growth factor, eNOS is an E(2)-activated Akt substrate, demonstrated by rapid eNOS phosphorylation on serine 1177, a critical residue for eNOS activation and enhanced sensitivity to resting cellular Ca(2+) levels.	Serine	145-151	nitric oxide synthase 3	Homo sapiens	121-125
11029403-7	2000	As has been shown for vascular endothelial growth factor, eNOS is an E(2)-activated Akt substrate, demonstrated by rapid eNOS phosphorylation on serine 1177, a critical residue for eNOS activation and enhanced sensitivity to resting cellular Ca(2+) levels.	Serine	145-151	nitric oxide synthase 3	Homo sapiens	121-125
10997917-11	2000	Folates, superoxide ions, and peroxynitrite scavengers restore the NO-generating activity to eNOS, collectively suggesting that cellular redox state plays an important role in HCy-suppressed NO-generating function of this enzyme.	Folic Acid	0-7	nitric oxide synthase 3	Homo sapiens	93-97
10997917-11	2000	Folates, superoxide ions, and peroxynitrite scavengers restore the NO-generating activity to eNOS, collectively suggesting that cellular redox state plays an important role in HCy-suppressed NO-generating function of this enzyme.	Superoxides	9-19	nitric oxide synthase 3	Homo sapiens	93-97
10997917-11	2000	Folates, superoxide ions, and peroxynitrite scavengers restore the NO-generating activity to eNOS, collectively suggesting that cellular redox state plays an important role in HCy-suppressed NO-generating function of this enzyme.	Peroxynitrous Acid	30-43	nitric oxide synthase 3	Homo sapiens	93-97
10946913-0	2000	Raloxifene acutely stimulates nitric oxide release from human endothelial cells via an activation of endothelial nitric oxide synthase.	Raloxifene Hydrochloride	0-10	nitric oxide synthase 3	Homo sapiens	101-134
11017941-3	2000	The aims of this study were to examine plasma NOx in patients with coronary artery disease (CAD) and to assess the association between plasma NOx concentrations and the three ecNOS gene polymorphisms.	nicotine 1-N-oxide	142-145	nitric oxide synthase 3	Homo sapiens	175-180
10978247-6	2000	Western blots of immunoprecipitated eNOS showed the presence of a major tyrosine-phosphorylated protein band at a mass corresponding to approximately 125 kDa and 2 minor bands corresponding to approximately 105 and 75 kDa after treatment with vanadate/Bk.	Tyrosine	72-80	nitric oxide synthase 3	Homo sapiens	36-40
10978247-6	2000	Western blots of immunoprecipitated eNOS showed the presence of a major tyrosine-phosphorylated protein band at a mass corresponding to approximately 125 kDa and 2 minor bands corresponding to approximately 105 and 75 kDa after treatment with vanadate/Bk.	Vanadates	243-251	nitric oxide synthase 3	Homo sapiens	36-40
10978247-8	2000	Geldanamycin, an inhibitor of heat shock protein 90, also inhibited the enhancement of NO production by vanadate/Bk or vanadate/A23187, and there was an increase in the amount of heat shock protein 90 that coimmunoprecipitated with eNOS after treatment with vanadate/Bk.	geldanamycin	0-12	nitric oxide synthase 3	Homo sapiens	232-236
10978247-9	2000	These results show that there is a clear link between tyrosine phosphorylation and stimulation of eNO production, which does not appear to involve direct modification of eNOS, changes in eNOS levels, or compartmentation, but rather appears to be due to changes in proteins associating with eNOS, thereby enhancing the state of activation of eNOS.	Tyrosine	54-62	nitric oxide synthase 3	Homo sapiens	187-191
10978247-9	2000	These results show that there is a clear link between tyrosine phosphorylation and stimulation of eNO production, which does not appear to involve direct modification of eNOS, changes in eNOS levels, or compartmentation, but rather appears to be due to changes in proteins associating with eNOS, thereby enhancing the state of activation of eNOS.	Tyrosine	54-62	nitric oxide synthase 3	Homo sapiens	187-191
10978247-9	2000	These results show that there is a clear link between tyrosine phosphorylation and stimulation of eNO production, which does not appear to involve direct modification of eNOS, changes in eNOS levels, or compartmentation, but rather appears to be due to changes in proteins associating with eNOS, thereby enhancing the state of activation of eNOS.	Tyrosine	54-62	nitric oxide synthase 3	Homo sapiens	187-191
10974218-13	2000	cGMP levels were increased in eNOS-transduced compared to control cells.	Cyclic GMP	0-4	nitric oxide synthase 3	Homo sapiens	30-34
10944110-7	2000	Finally, repeated carbachol stimulations of mAchRs co-expressed in COS cells with endothelial nitric oxide synthase (eNOS) and wild-type, but not mutant, dynamin led to a progressive increase in mAchR sequestration and a concurrent stabilization of the inhibitory eNOS-caveolin complex.	Carbachol	18-27	nitric oxide synthase 3	Homo sapiens	82-115
11015297-3	2000	AmB used at concentrations of 0.6 to 1.25 microg ml(-1) led to increases in ecNOS mRNA and protein expression as well as NO production.	Amphotericin B	0-3	nitric oxide synthase 3	Homo sapiens	76-81
11015297-5	2000	In contrast, incubation of cells with higher albeit subtoxic concentrations of AmB (2.5 - 5.0 microg ml(-1)) resulted in a decrease or respectively in completely abolished ecNOS mRNA and protein expression with a strongly reduced or inhibited ecNOS activity, due to a decrease of ecNOS mRNA half-life.	Amphotericin B	79-82	nitric oxide synthase 3	Homo sapiens	172-177
11015297-5	2000	In contrast, incubation of cells with higher albeit subtoxic concentrations of AmB (2.5 - 5.0 microg ml(-1)) resulted in a decrease or respectively in completely abolished ecNOS mRNA and protein expression with a strongly reduced or inhibited ecNOS activity, due to a decrease of ecNOS mRNA half-life.	Amphotericin B	79-82	nitric oxide synthase 3	Homo sapiens	243-248
11015297-5	2000	In contrast, incubation of cells with higher albeit subtoxic concentrations of AmB (2.5 - 5.0 microg ml(-1)) resulted in a decrease or respectively in completely abolished ecNOS mRNA and protein expression with a strongly reduced or inhibited ecNOS activity, due to a decrease of ecNOS mRNA half-life.	Amphotericin B	79-82	nitric oxide synthase 3	Homo sapiens	243-248
10998082-6	2000	RESULTS: After treatment with triflusal, there was an increase in NO production by neutrophils and an increase in endothelial nitric oxide synthase (eNOS) protein expression in neutrophils.	triflusal	30-39	nitric oxide synthase 3	Homo sapiens	114-147
10998082-6	2000	RESULTS: After treatment with triflusal, there was an increase in NO production by neutrophils and an increase in endothelial nitric oxide synthase (eNOS) protein expression in neutrophils.	triflusal	30-39	nitric oxide synthase 3	Homo sapiens	149-153
10998082-11	2000	CONCLUSION: Oral treatment of healthy volunteers with triflusal stimulated NO production and eNOS protein expression in their neutrophils.	triflusal	54-63	nitric oxide synthase 3	Homo sapiens	93-97
10906046-1	2000	There is recent evidence that mouse and human spermatozoa contain constitutive nitric oxide synthase (cNOS) and can synthesize nitric oxide.	Nitric Oxide	79-91	nitric oxide synthase 3	Homo sapiens	102-106
10906046-3	2000	N(G)-nitro-L-arginine methyl ester (L-NAME) was used as cNOS inhibitor.	NG-Nitroarginine Methyl Ester	0-34	nitric oxide synthase 3	Homo sapiens	56-60
10906046-3	2000	N(G)-nitro-L-arginine methyl ester (L-NAME) was used as cNOS inhibitor.	NG-Nitroarginine Methyl Ester	36-42	nitric oxide synthase 3	Homo sapiens	56-60
10946913-0	2000	Raloxifene acutely stimulates nitric oxide release from human endothelial cells via an activation of endothelial nitric oxide synthase.	Nitric Oxide	30-42	nitric oxide synthase 3	Homo sapiens	101-134
10946913-7	2000	Indeed, raloxifene-induced NO production is due to an estrogen receptor-dependent acute stimulation of eNOS enzymatic activity.	Raloxifene Hydrochloride	8-18	nitric oxide synthase 3	Homo sapiens	103-107
10946913-8	2000	In conclusion, raloxifene activates eNOS in human endothelial cells, exerting a potentially important direct vasculo-protective effect stimulating endothelial NO production.	Raloxifene Hydrochloride	15-25	nitric oxide synthase 3	Homo sapiens	36-40
10908731-2	2000	The protein kinase Akt activates the endothelial NO synthase (eNOS) by phosphorylation of Ser-1177.	Serine	90-93	nitric oxide synthase 3	Homo sapiens	62-66
10993711-2	2000	Endothelial nitric oxide synthase (eNOS)-a key regulator of vascular nitric oxide production-has been investigated extensively to determine the relevance of DNA variants in the eNOS gene and vascular diseases.	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	35-39
10993711-2	2000	Endothelial nitric oxide synthase (eNOS)-a key regulator of vascular nitric oxide production-has been investigated extensively to determine the relevance of DNA variants in the eNOS gene and vascular diseases.	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	177-181
10899290-2	2000	[(3-Chlorophenyl)methyl]amino?ethyl)phenyl]-2-thiophenecarbo ximidamide dihydrochloride</compound-id> (ARL 17477) on recombinant human neuronal NOS (nNOS) and endothelial NOS (eNOS).	Levodopa	103-106	nitric oxide synthase 3	Homo sapiens	159-174
10908731-7	2000	Our data indicate that eNOS activation via phosphorylation of Ser-1177 by Akt is necessary and sufficient for VEGF-mediated EC migration.	Serine	62-65	nitric oxide synthase 3	Homo sapiens	23-27
10747895-0	2000	Superoxide production and reactive oxygen species signaling by endothelial nitric-oxide synthase.	Reactive Oxygen Species	26-49	nitric oxide synthase 3	Homo sapiens	63-96
10946853-4	2000	Furthermore, TMPZ concentration (50 and 200 microM)- and time (15 and 30 min)-dependently triggered endothelial-type constitutive nitric oxide synthase (ecNOS) protein expression in human platelets.	tetramethylpyrazine	13-17	nitric oxide synthase 3	Homo sapiens	100-151
10946853-4	2000	Furthermore, TMPZ concentration (50 and 200 microM)- and time (15 and 30 min)-dependently triggered endothelial-type constitutive nitric oxide synthase (ecNOS) protein expression in human platelets.	tetramethylpyrazine	13-17	nitric oxide synthase 3	Homo sapiens	153-158
10946853-5	2000	These results indicated that TMPZ at micromolar concentrations stimulated nitric oxide production in human platelets via a novel mechanism that activated ecNOS protein expression.	tetramethylpyrazine	29-33	nitric oxide synthase 3	Homo sapiens	154-159
10946853-5	2000	These results indicated that TMPZ at micromolar concentrations stimulated nitric oxide production in human platelets via a novel mechanism that activated ecNOS protein expression.	Nitric Oxide	74-86	nitric oxide synthase 3	Homo sapiens	154-159
10884465-2	2000	BACKGROUND AND PURPOSE: Nitric oxide (NO) synthesized by endothelial constitutive NO synthase (ecNOS) plays a key role in vascular regulation and atherosclerosis.	Nitric Oxide	24-36	nitric oxide synthase 3	Homo sapiens	95-100
10850963-0	2000	Folic acid reverts dysfunction of endothelial nitric oxide synthase.	Folic Acid	0-10	nitric oxide synthase 3	Homo sapiens	34-67
10747895-2	2000	Purified endothelial nitric-oxide synthase (eNOS) can generate superoxide (O(2)) under special conditions but is only known to participate in cell signaling through NO.	Superoxides	63-73	nitric oxide synthase 3	Homo sapiens	9-42
10747895-2	2000	Purified endothelial nitric-oxide synthase (eNOS) can generate superoxide (O(2)) under special conditions but is only known to participate in cell signaling through NO.	Superoxides	63-73	nitric oxide synthase 3	Homo sapiens	44-48
10747895-2	2000	Purified endothelial nitric-oxide synthase (eNOS) can generate superoxide (O(2)) under special conditions but is only known to participate in cell signaling through NO.	Superoxides	75-79	nitric oxide synthase 3	Homo sapiens	9-42
10747895-2	2000	Purified endothelial nitric-oxide synthase (eNOS) can generate superoxide (O(2)) under special conditions but is only known to participate in cell signaling through NO.	Superoxides	75-79	nitric oxide synthase 3	Homo sapiens	44-48
10747895-3	2000	Here we show that eNOS regulates tumor necrosis factor alpha (TNFalpha) through a mechanism dependent on the production of O(2) and completely independent of NO.	Superoxides	123-127	nitric oxide synthase 3	Homo sapiens	18-22
10747895-4	2000	Expression of eNOS in transfected U937 cells increased phorbol 12-myristate 13-acetate-induced TNFalpha promoter activity and TNFalpha production.	Tetradecanoylphorbol Acetate	55-86	nitric oxide synthase 3	Homo sapiens	14-18
10747895-5	2000	N(omega)-Methyl-l-arginine, an inhibitor of eNOS that blocks NO production but not its NADPH oxidase activity, did not prevent TNFalpha up-regulation.	omega-N-Methylarginine	0-26	nitric oxide synthase 3	Homo sapiens	44-48
10747895-6	2000	Likewise, Gln(361)eNOS, a competent NADPH oxidase that lacks NOS activity, retained the ability to increase TNFalpha.	Glutamine	10-13	nitric oxide synthase 3	Homo sapiens	18-22
10747895-7	2000	Similar to the effect of eNOS, a O(2) donor dose-dependently increased TNFalpha production in differentiated U937 cells.	Superoxides	33-37	nitric oxide synthase 3	Homo sapiens	25-29
10747895-8	2000	In contrast, cotransfection of superoxide dismutase with eNOS prevented TNFalpha up-regulation, as did partial deletion of the eNOS NADPH binding site, a mutation associated with loss of O(2) production.	NADP	132-137	nitric oxide synthase 3	Homo sapiens	57-61
10747895-8	2000	In contrast, cotransfection of superoxide dismutase with eNOS prevented TNFalpha up-regulation, as did partial deletion of the eNOS NADPH binding site, a mutation associated with loss of O(2) production.	NADP	132-137	nitric oxide synthase 3	Homo sapiens	127-131
10747895-8	2000	In contrast, cotransfection of superoxide dismutase with eNOS prevented TNFalpha up-regulation, as did partial deletion of the eNOS NADPH binding site, a mutation associated with loss of O(2) production.	Superoxides	187-191	nitric oxide synthase 3	Homo sapiens	57-61
10747895-8	2000	In contrast, cotransfection of superoxide dismutase with eNOS prevented TNFalpha up-regulation, as did partial deletion of the eNOS NADPH binding site, a mutation associated with loss of O(2) production.	Superoxides	187-191	nitric oxide synthase 3	Homo sapiens	127-131
10747895-9	2000	Thus, eNOS may straddle a bifurcating pathway that can lead to the formation of either NO or O(2), interrelated but often opposing free radical messengers.	Superoxides	93-97	nitric oxide synthase 3	Homo sapiens	6-10
10845872-15	2000	Because ADMA acts as a competitive inhibitor of endothelial nitric oxide synthase, these findings suggest a novel mechanism for impaired endothelial function in hyperhomocyst(e)inemia.	N,N-dimethylarginine	8-12	nitric oxide synthase 3	Homo sapiens	48-81
10828238-10	2000	Inclusion of the calcium channel blocker, nifedipine, abolished the arterial flow-induced changes in eNOS and VCAM-1 but increased the TF staining area ratio from 3.0+/-0.4 to 8.5+/-0.7%, p=0.01.	Nifedipine	42-52	nitric oxide synthase 3	Homo sapiens	101-105
10781649-2	2000	Genetic variants of methylene tetrahydrofolate reductase (MTHFR) and endothelial nitric oxide synthase (ecNOS) influence homocysteine metabolism and nitric oxide synthesis, respectively and might thus be determinants of the risk of atherosclerotic disease.	Nitric Oxide	81-93	nitric oxide synthase 3	Homo sapiens	104-109
10835326-7	2000	Incubation of PAEC with a specific inhibitor of HSP90 (geldanamycin) mimicked the hypoxic decrease of eNOS activity.	geldanamycin	55-67	nitric oxide synthase 3	Homo sapiens	102-106
10828238-11	2000	Inclusion of the stretch-activated cation-channel blocker, gadolinium, enhanced the arterial flow-induced increase in eNOS, but prevented the arterial flow-induced increase in ICAM-1.	Gadolinium	59-69	nitric oxide synthase 3	Homo sapiens	118-122
10828238-12	2000	CONCLUSIONS: perfusion of veins under arterial flow conditions with gadolinium was associated with low endothelial concentrations of ICAM-1, VCAM-1 and TF, but high levels of eNOS.	Gadolinium	68-78	nitric oxide synthase 3	Homo sapiens	175-179
10717002-0	2000	Intracellular processing of endothelial nitric oxide synthase isoforms associated with differences in severity of cardiopulmonary diseases: cleavage of proteins with aspartate vs. glutamate at position 298.	Aspartic Acid	166-175	nitric oxide synthase 3	Homo sapiens	28-61
10803574-12	2000	17beta-Estradiol up-regulated ecNOS messenger RNA, and tamoxifen blocked the effect.	Estradiol	0-16	nitric oxide synthase 3	Homo sapiens	30-35
10753680-2	2000	ONO-1714 was found to be 10-fold selective for human iNOS over human endothelial NOS (ecNOS).	7-chloro-3-imino-5-methyl-2-azabicyclo(4.1.0)heptane	0-8	nitric oxide synthase 3	Homo sapiens	86-91
10809426-3	2000	PATIENTS AND METHODS: Our study evaluates ecNOS gene status and NO metabolites in kidney transplanted patients under chronic CsA treatment with CsA-induced hypertension.	Cyclosporine	125-128	nitric oxide synthase 3	Homo sapiens	42-47
10809426-3	2000	PATIENTS AND METHODS: Our study evaluates ecNOS gene status and NO metabolites in kidney transplanted patients under chronic CsA treatment with CsA-induced hypertension.	Cyclosporine	144-147	nitric oxide synthase 3	Homo sapiens	42-47
10766457-5	2000	The ecNOS mRNA level was decreased by the ascitic fluids; ascitic fluids-induced expression of adhesion molecules and interleukin-8 as well as the nuclear translocation of NF-kappaB were attenuated by SNP, whereas L-NNA augmented them; and the effects on the endothelial activation were paralleled by the altered adhesion of U937 cells to endothelium.	Nitroarginine	214-219	nitric oxide synthase 3	Homo sapiens	4-9
10803574-13	2000	Based on these results we suggest that the effect of estradiol on permeability involves four signaling steps: 1) activation of estrogen receptors, 2) increase in ecNOS transcription and up-regulation of NO activity, 3) NO activation of guanylate cyclase and increase in cGMP, and 4) cGMP activation of cGMP-dependent protein kinase.	Estradiol	53-62	nitric oxide synthase 3	Homo sapiens	162-167
10739087-7	2000	Furthermore, naturally occurring signaling molecules such as morphine, anandamide, interleukin-10 and 17-beta-estradiol appear to exert, in part, their beneficial physiological actions, i.e., immune and endothelial down regulation by the stimulation of cNOS.	Morphine	61-69	nitric oxide synthase 3	Homo sapiens	253-257
10739087-7	2000	Furthermore, naturally occurring signaling molecules such as morphine, anandamide, interleukin-10 and 17-beta-estradiol appear to exert, in part, their beneficial physiological actions, i.e., immune and endothelial down regulation by the stimulation of cNOS.	anandamide	71-81	nitric oxide synthase 3	Homo sapiens	253-257
10739087-7	2000	Furthermore, naturally occurring signaling molecules such as morphine, anandamide, interleukin-10 and 17-beta-estradiol appear to exert, in part, their beneficial physiological actions, i.e., immune and endothelial down regulation by the stimulation of cNOS.	Estradiol	102-119	nitric oxide synthase 3	Homo sapiens	253-257
12000044-1	2000	In the endothelium, synthesis of nitric oxide (NO) from the amino acid L-arginine is catalyzed by the endothelial NO synthase (eNOS), and the continuously generated NO serves to maintain basal vascular tone.	Nitric Oxide	33-45	nitric oxide synthase 3	Homo sapiens	127-131
12000044-1	2000	In the endothelium, synthesis of nitric oxide (NO) from the amino acid L-arginine is catalyzed by the endothelial NO synthase (eNOS), and the continuously generated NO serves to maintain basal vascular tone.	amino acid l-arginine	60-81	nitric oxide synthase 3	Homo sapiens	127-131
10717002-5	2000	Immunoblotting after SDS/PAGE with a carboxyl-terminal antibody showed a single major protein band in the predicted position for eNOS at 135 kDa.	Sodium Dodecyl Sulfate	21-24	nitric oxide synthase 3	Homo sapiens	129-133
10717002-8	2000	Thus, eNOS with aspartate but not glutamate at position 298 is cleaved, resulting in the generation of N-terminal 35-kDa and C-terminal 100-kDa fragments.	Aspartic Acid	16-25	nitric oxide synthase 3	Homo sapiens	6-10
10717002-0	2000	Intracellular processing of endothelial nitric oxide synthase isoforms associated with differences in severity of cardiopulmonary diseases: cleavage of proteins with aspartate vs. glutamate at position 298.	Glutamic Acid	180-189	nitric oxide synthase 3	Homo sapiens	28-61
10717002-1	2000	An endothelial nitric oxide synthase (eNOS) polymorphism in exon 7 (894 G/T) resulting in glutamate or aspartate, respectively, at position 298 on the protein is correlated with severity of cardiopulmonary diseases.	Glutamic Acid	90-99	nitric oxide synthase 3	Homo sapiens	3-36
10717002-1	2000	An endothelial nitric oxide synthase (eNOS) polymorphism in exon 7 (894 G/T) resulting in glutamate or aspartate, respectively, at position 298 on the protein is correlated with severity of cardiopulmonary diseases.	Glutamic Acid	90-99	nitric oxide synthase 3	Homo sapiens	38-42
10717002-1	2000	An endothelial nitric oxide synthase (eNOS) polymorphism in exon 7 (894 G/T) resulting in glutamate or aspartate, respectively, at position 298 on the protein is correlated with severity of cardiopulmonary diseases.	Aspartic Acid	103-112	nitric oxide synthase 3	Homo sapiens	3-36
10717002-1	2000	An endothelial nitric oxide synthase (eNOS) polymorphism in exon 7 (894 G/T) resulting in glutamate or aspartate, respectively, at position 298 on the protein is correlated with severity of cardiopulmonary diseases.	Aspartic Acid	103-112	nitric oxide synthase 3	Homo sapiens	38-42
10717002-3	2000	We now show in transfected cells, primary human endothelial cells, and human hearts, that eNOS with aspartate, but not glutamate, at position 298 is cleaved, resulting in the generation of 100-kDa and 35-kDa products.	Aspartic Acid	100-109	nitric oxide synthase 3	Homo sapiens	90-94
10739530-10	2000	After ethanol exposure, eNOS protein expression increased 2.5- to 3.0-fold over that of the control.	Ethanol	6-13	nitric oxide synthase 3	Homo sapiens	24-28
10694495-2	2000	Under anesthesia, using intravital microscopy and a closed cranial window system, pial arteriolar diameter changes were monitored during sequential cortical suffusions of an eNOS-dependent dilator [acetylcholine (ACh)] and a direct NO donor [S-nitrosoacetylpenicillamine (SNAP)].	Acetylcholine	198-211	nitric oxide synthase 3	Homo sapiens	174-178
10739530-13	2000	Increased eNOS protein expression may be a response to the increased demand for nitric oxide.	Nitric Oxide	80-92	nitric oxide synthase 3	Homo sapiens	10-14
10758392-7	2000	NOS-III activity was determined using TV-densitometry (gray units) and cGMP content using a semiquantitative score.	Cyclic GMP	71-75	nitric oxide synthase 3	Homo sapiens	0-7
10879682-2	2000	Three enzyme systems produce reactive oxygen species in the vascular wall: NADH/NADPH oxidase, xanthine oxidoreductase, and endothelial nitric oxide synthase.	Reactive Oxygen Species	29-52	nitric oxide synthase 3	Homo sapiens	124-157
12501625-8	2000	We belive that the decreased expression of eNOS may be related with the deficiency of nitric oxide release and may be responsible for tissue damage during CPB.	Nitric Oxide	86-98	nitric oxide synthase 3	Homo sapiens	43-47
10653602-1	2000	Nitric oxide (NO) synthesized by endothelial cell nitric oxide synthase (eNOS) elicits vasodilation of resistance-sized coronary microvessels.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	73-77
10692481-0	2000	Structure-activity relationship of staurosporine analogs in regulating expression of endothelial nitric-oxide synthase gene.	Staurosporine	35-48	nitric oxide synthase 3	Homo sapiens	85-118
10762001-2	2000	Because its product, nitric oxide, possesses vasodilatory and antiatherogenic properties, an altered eNOS function might promote atherosclerosis.	Nitric Oxide	21-33	nitric oxide synthase 3	Homo sapiens	101-105
10671543-3	2000	We have previously shown that E(2)-induced activation of endothelial nitric oxide synthase (eNOS) reduces its calcium dependence.	Estradiol	30-34	nitric oxide synthase 3	Homo sapiens	57-90
10671543-3	2000	We have previously shown that E(2)-induced activation of endothelial nitric oxide synthase (eNOS) reduces its calcium dependence.	Calcium	110-117	nitric oxide synthase 3	Homo sapiens	57-90
10671564-2	2000	We demonstrate here that NOS-III, but neither NOS-I nor -II, is rapidly and strongly activated and phosphorylated on both Ser and Thr in the presence of cGMP-dependent protein kinase II (cGK II) and the catalytic subunit of cAMP-dependent protein kinase (cAK) in vitro.	Threonine	130-133	nitric oxide synthase 3	Homo sapiens	25-32
10671564-3	2000	Phosphopeptide analysis by mass spectrometry identified Ser(1177), as well as Ser(633) which is situated in a recently defined CaM autoinhibitory domain within the flavin-binding region of human NOS-III.	Serine	78-81	nitric oxide synthase 3	Homo sapiens	195-202
10671564-3	2000	Phosphopeptide analysis by mass spectrometry identified Ser(1177), as well as Ser(633) which is situated in a recently defined CaM autoinhibitory domain within the flavin-binding region of human NOS-III.	4,6-dinitro-o-cresol	164-170	nitric oxide synthase 3	Homo sapiens	195-202
10671564-7	2000	These data collectively provide new evidence for cAK and cGK stimulation of both Ca(2+)/CaM-independent and -dependent NOS-III activity, and suggest possible cross-talk between the NO and prostaglandin I(2) pathways and a positive feedback mechanism for NO/cGMP signaling.	Epoprostenol	188-206	nitric oxide synthase 3	Homo sapiens	119-126
10671564-0	2000	Endothelial nitric-oxide synthase (type III) is activated and becomes calcium independent upon phosphorylation by cyclic nucleotide-dependent protein kinases.	Calcium	70-77	nitric oxide synthase 3	Homo sapiens	0-33
10671564-2	2000	We demonstrate here that NOS-III, but neither NOS-I nor -II, is rapidly and strongly activated and phosphorylated on both Ser and Thr in the presence of cGMP-dependent protein kinase II (cGK II) and the catalytic subunit of cAMP-dependent protein kinase (cAK) in vitro.	Serine	122-125	nitric oxide synthase 3	Homo sapiens	25-32
10703689-4	2000	A number of studies have shown altered nitric oxide production by the endothelial constitutive isoform of nitric oxide synthase (NOS III), but there is little information on the role of NOS II.	Nitric Oxide	39-51	nitric oxide synthase 3	Homo sapiens	129-136
10666071-8	2000	However, in endothelium-denuded arteries transduced with recombinant eNOS, bradykinin and substance P caused relaxations that were abolished in the presence of the NOS inhibitor N(G)-nitro-L-arginine methyl ester.	NG-Nitroarginine Methyl Ester	178-212	nitric oxide synthase 3	Homo sapiens	69-73
10666071-11	2000	Our results suggest that, in small brain stem arteries, expression of recombinant eNOS increases biosynthesis of nitric oxide.	Nitric Oxide	113-125	nitric oxide synthase 3	Homo sapiens	82-86
10640297-0	2000	Nifedipine and diltiazem but not verapamil up-regulate endothelial nitric-oxide synthase expression.	Nifedipine	0-10	nitric oxide synthase 3	Homo sapiens	55-88
10640297-0	2000	Nifedipine and diltiazem but not verapamil up-regulate endothelial nitric-oxide synthase expression.	Diltiazem	15-24	nitric oxide synthase 3	Homo sapiens	55-88
10640297-1	2000	We have recently shown that felodipine, a long-acting dihydropyridine L-type calcium channel blocker (CCB), up-regulates nitric oxide (NO) production and endothelial NO synthase (eNOS) expression and activity in cultured endothelial cells as well as in animals with chronic renal failure.	Felodipine	28-38	nitric oxide synthase 3	Homo sapiens	179-183
10640297-7	2000	Similarly, eNOS protein abundance was increased significantly by nifedipine (P &lt;.05) and diltiazem (P &lt;.05).	Nifedipine	65-75	nitric oxide synthase 3	Homo sapiens	11-15
10640297-7	2000	Similarly, eNOS protein abundance was increased significantly by nifedipine (P &lt;.05) and diltiazem (P &lt;.05).	Diltiazem	92-101	nitric oxide synthase 3	Homo sapiens	11-15
11043380-1	2000	The endothelial nitric oxide synthase (eNOS) gene is responsible for constitutive nitric oxide synthesis and arterial vasodilatation.	Nitric Oxide	16-28	nitric oxide synthase 3	Homo sapiens	39-43
10653901-1	2000	OBJECTIVE: Endothelial nitric oxide synthase (ecNOS) catalyzes the NADPH and O(2) to nitric oxide(NO).	NADP	67-72	nitric oxide synthase 3	Homo sapiens	11-44
10653901-1	2000	OBJECTIVE: Endothelial nitric oxide synthase (ecNOS) catalyzes the NADPH and O(2) to nitric oxide(NO).	NADP	67-72	nitric oxide synthase 3	Homo sapiens	46-51
10653901-1	2000	OBJECTIVE: Endothelial nitric oxide synthase (ecNOS) catalyzes the NADPH and O(2) to nitric oxide(NO).	o(2)	77-81	nitric oxide synthase 3	Homo sapiens	11-44
10653901-1	2000	OBJECTIVE: Endothelial nitric oxide synthase (ecNOS) catalyzes the NADPH and O(2) to nitric oxide(NO).	o(2)	77-81	nitric oxide synthase 3	Homo sapiens	46-51
10653901-1	2000	OBJECTIVE: Endothelial nitric oxide synthase (ecNOS) catalyzes the NADPH and O(2) to nitric oxide(NO).	Nitric Oxide	23-35	nitric oxide synthase 3	Homo sapiens	46-51
11270506-8	2000	Quinaprilat could ameliorate both apoptosis and necrosis through the upregulation of constitutive endothelial nitric oxide synthase via an increase of bradykinin, with the resulting increase of nitric oxide.	quinaprilat	0-11	nitric oxide synthase 3	Homo sapiens	98-131
10733874-3	2000	This assay is at least 10-fold more sensitive than when Cd reduction is coupled with the spectrophotometric Greiss reaction and can be used to quantitate the small amounts of NO(-)(x) generated from the constitutive form of endothelial nitric oxide synthase (eNOS).	Cadmium	56-58	nitric oxide synthase 3	Homo sapiens	224-257
10691780-1	2000	NO production by the endothelial and neuronal isoforms of nitric oxide synthase (cNOS) is regulated on a moment-to-moment basis by calmodulin binding, triggered by transient elevations in intracellular-free calcium levels.	Calcium	207-214	nitric oxide synthase 3	Homo sapiens	81-85
11324314-1	2000	The endothelial isoform of nitric oxide synthase (eNOS) ensures enzymatic production of nitric oxide (NO) not only in endothelial cells but also in other cell types, such as neurons, platelets, and some epithelial cells.	Nitric Oxide	27-39	nitric oxide synthase 3	Homo sapiens	50-54
10604975-6	2000	The endothelial NOS gene transfer also inhibited thymidine incorporation into type A receptor-transfected cells in response to endothelin-1, which was abolished in the presence of the NOS inhibitor N(G)-monomethyl-L-arginine acetate.	Thymidine	49-58	nitric oxide synthase 3	Homo sapiens	4-19
10604975-6	2000	The endothelial NOS gene transfer also inhibited thymidine incorporation into type A receptor-transfected cells in response to endothelin-1, which was abolished in the presence of the NOS inhibitor N(G)-monomethyl-L-arginine acetate.	n(g)-monomethyl-l-arginine acetate	198-232	nitric oxide synthase 3	Homo sapiens	4-19
10574932-1	1999	We previously demonstrated that lysophosphatidylcholine up-regulated endothelial nitric-oxide synthase promoter activity by increasing Sp1 binding via the action of protein serine/threonine phosphatase 2A (Cieslik, K., Zembowicz, A., Tang, J.-L., and Wu, K.K.	Lysophosphatidylcholines	32-55	nitric oxide synthase 3	Homo sapiens	69-102
11112080-1	2000	Experiments were designed to study whether overexpression of nitric oxide (NO) from endothelial nitric oxide synthase (eNOS) affects acute rejection.	Nitric Oxide	61-73	nitric oxide synthase 3	Homo sapiens	84-117
11112080-1	2000	Experiments were designed to study whether overexpression of nitric oxide (NO) from endothelial nitric oxide synthase (eNOS) affects acute rejection.	Nitric Oxide	61-73	nitric oxide synthase 3	Homo sapiens	119-123
11112080-5	2000	Calcium-dependent NOS activity, reflecting eNOS, was greater in eNOS-transduced lungs (587 +/- 97 vs 2.1 +/- 1.4 pmol/mg protein per h, P &lt;0.001).	Calcium	0-7	nitric oxide synthase 3	Homo sapiens	43-47
11112080-5	2000	Calcium-dependent NOS activity, reflecting eNOS, was greater in eNOS-transduced lungs (587 +/- 97 vs 2.1 +/- 1.4 pmol/mg protein per h, P &lt;0.001).	Calcium	0-7	nitric oxide synthase 3	Homo sapiens	64-68
11112080-7	2000	Concentrations of cGMP were higher in eNOS-transduced lungs (13.2 +/- 2.3 vs 4.9 +/- 0.5 pmol/mg protein).	Cyclic GMP	18-22	nitric oxide synthase 3	Homo sapiens	38-42
10601500-5	1999	Immunoblotting of extracts from freshly isolated myometrial tissue, affinity-enriched for NOS proteins by precipitation with ADP-sepharose, revealed expression of endothelial NOS (eNOS or NOS3) in tissues from preterm, term non-labour and active labour at term.	Sepharose	129-138	nitric oxide synthase 3	Homo sapiens	180-184
10608822-17	1999	271, 11462-11467), the human eNOS appears to be markedly stabilized by H(4)biopterin.	sapropterin	71-84	nitric oxide synthase 3	Homo sapiens	29-33
10574932-5	1999	To characterize the regulation of basal endothelial nitric-oxide synthase promoter activity and the signaling pathway through which lysophosphatidylcholine augments endothelial nitric-oxide synthase transcription, we used a casein kinase 2 inhibitor coupled with immunoprecipitation to demonstrate that basal Sp1 binding and endothelial nitric-oxide synthase promoter activity were controlled by casein kinase 2 complexed with protein serine/threonine phosphatase 2A.	Lysophosphatidylcholines	132-155	nitric oxide synthase 3	Homo sapiens	165-198
10574932-5	1999	To characterize the regulation of basal endothelial nitric-oxide synthase promoter activity and the signaling pathway through which lysophosphatidylcholine augments endothelial nitric-oxide synthase transcription, we used a casein kinase 2 inhibitor coupled with immunoprecipitation to demonstrate that basal Sp1 binding and endothelial nitric-oxide synthase promoter activity were controlled by casein kinase 2 complexed with protein serine/threonine phosphatase 2A.	Lysophosphatidylcholines	132-155	nitric oxide synthase 3	Homo sapiens	165-198
10601124-1	1999	Earlier studies have demonstrated that nitric oxide (NO) exerts a fast-acting inhibitory influence on endothelial NO synthase (eNOS) enzymatic activity in isolated vascular tissue preparations.	Nitric Oxide	39-51	nitric oxide synthase 3	Homo sapiens	127-131
10601124-9	1999	Phosphodiesterase inhibitor and 8-Br-cGMP downregulated, whereas the guanylate cyclase inhibitor ODQ upregulated eNOS protein expression.	1H-(1,2,3)oxadiazolo(4,4-a)quinoxalin-1-one	97-100	nitric oxide synthase 3	Homo sapiens	113-117
10601124-12	1999	NO serves as a negative-feedback regulator of eNOS expression via a cGMP-mediated process.	Cyclic GMP	68-72	nitric oxide synthase 3	Homo sapiens	46-50
10551875-4	1999	The elevated eNOS protein level was sustained over the time course if VEGF was co-incubated with L-N(G)-nitroarginine methyl ester, a competitive eNOS inhibitor.	l-n(g)-nitroarginine methyl ester	97-130	nitric oxide synthase 3	Homo sapiens	13-17
10600473-1	1999	VEGF-A induces angiogenesis and regulates endothelial function via production and release of nitric oxide (NO), which is produced by endothelial nitric oxide synthase (eNOS).	Nitric Oxide	93-105	nitric oxide synthase 3	Homo sapiens	133-166
10551875-4	1999	The elevated eNOS protein level was sustained over the time course if VEGF was co-incubated with L-N(G)-nitroarginine methyl ester, a competitive eNOS inhibitor.	l-n(g)-nitroarginine methyl ester	97-130	nitric oxide synthase 3	Homo sapiens	146-150
10551875-5	1999	Addition of S-nitroso-N-acetylpenicillamine, a nitric oxide donor, prevented VEGF-induced eNOS up-regulation.	S-Nitroso-N-Acetylpenicillamine	12-43	nitric oxide synthase 3	Homo sapiens	90-94
10551875-5	1999	Addition of S-nitroso-N-acetylpenicillamine, a nitric oxide donor, prevented VEGF-induced eNOS up-regulation.	Nitric Oxide	47-59	nitric oxide synthase 3	Homo sapiens	90-94
10551875-6	1999	These data suggest that nitric oxide participates in a negative feedback mechanism regulating eNOS expression.	Nitric Oxide	24-36	nitric oxide synthase 3	Homo sapiens	94-98
10551875-10	1999	SU1498, a selective inhibitor of the KDR receptor tyrosine kinase, blocked eNOS up-regulation, thus providing further evidence that the KDR receptor signals for eNOS up-regulation.	SU 1498	0-6	nitric oxide synthase 3	Homo sapiens	75-79
10551875-10	1999	SU1498, a selective inhibitor of the KDR receptor tyrosine kinase, blocked eNOS up-regulation, thus providing further evidence that the KDR receptor signals for eNOS up-regulation.	SU 1498	0-6	nitric oxide synthase 3	Homo sapiens	161-165
10551875-11	1999	Finally, treatment of adrenal cortex endothelial cells with VEGF or phorbol ester resulted in protein kinase C activation and elevated eNOS expression, whereas inhibition of protein kinase C with isoform-specific inhibitors abolished VEGF-induced eNOS up-regulation.	Phorbol Esters	68-81	nitric oxide synthase 3	Homo sapiens	135-139
10551875-11	1999	Finally, treatment of adrenal cortex endothelial cells with VEGF or phorbol ester resulted in protein kinase C activation and elevated eNOS expression, whereas inhibition of protein kinase C with isoform-specific inhibitors abolished VEGF-induced eNOS up-regulation.	Phorbol Esters	68-81	nitric oxide synthase 3	Homo sapiens	247-251
10536122-1	1999	Endothelium-derived nitric oxide (NO) generated by endothelial NO synthase (eNOS) is critically involved in pulmonary vasodilation during cardiopulmonary transition at birth.	Nitric Oxide	20-32	nitric oxide synthase 3	Homo sapiens	76-80
10613097-2	1999	NO is normally produced in the endothelium from L-arginine by the constitutive isoform of the NO synthase (cNOS).	Arginine	48-58	nitric oxide synthase 3	Homo sapiens	107-111
10542298-5	1999	Treatment with oxLDL also inhibited acetylcholine-induced activation of eNOS but not prostacyclin production.	Acetylcholine	36-49	nitric oxide synthase 3	Homo sapiens	72-76
10542298-9	1999	Cyclodextrin also depleted caveolae of cholesterol and caused eNOS and caveolin to translocate from caveolae.	Cyclodextrins	0-12	nitric oxide synthase 3	Homo sapiens	62-66
10542298-11	1999	We conclude that oxLDL-induced depletion of caveola cholesterol causes eNOS to leave caveolae and inhibits acetylcholine-induced activation of the enzyme.	Cholesterol	52-63	nitric oxide synthase 3	Homo sapiens	71-75
10536122-6	1999	In contrast, the inhibition of endogenous NO production with nitro-L-arginine-methyl ester (L-NAME) caused a reduction in eNOS protein expression that was evident within 8 h. Paralleling the changes in eNOS protein, eNOS messenger RNA (mRNA) abundance was upregulated by exogenous NO and downregulated by L-NAME, suggesting that NO modulation of eNOS expression involves processes at the level of gene transcription or mRNA stability.	NG-Nitroarginine Methyl Ester	305-311	nitric oxide synthase 3	Homo sapiens	202-206
10536122-6	1999	In contrast, the inhibition of endogenous NO production with nitro-L-arginine-methyl ester (L-NAME) caused a reduction in eNOS protein expression that was evident within 8 h. Paralleling the changes in eNOS protein, eNOS messenger RNA (mRNA) abundance was upregulated by exogenous NO and downregulated by L-NAME, suggesting that NO modulation of eNOS expression involves processes at the level of gene transcription or mRNA stability.	nitro-l-arginine-methyl ester	61-90	nitric oxide synthase 3	Homo sapiens	122-126
10536122-6	1999	In contrast, the inhibition of endogenous NO production with nitro-L-arginine-methyl ester (L-NAME) caused a reduction in eNOS protein expression that was evident within 8 h. Paralleling the changes in eNOS protein, eNOS messenger RNA (mRNA) abundance was upregulated by exogenous NO and downregulated by L-NAME, suggesting that NO modulation of eNOS expression involves processes at the level of gene transcription or mRNA stability.	nitro-l-arginine-methyl ester	61-90	nitric oxide synthase 3	Homo sapiens	202-206
10536122-6	1999	In contrast, the inhibition of endogenous NO production with nitro-L-arginine-methyl ester (L-NAME) caused a reduction in eNOS protein expression that was evident within 8 h. Paralleling the changes in eNOS protein, eNOS messenger RNA (mRNA) abundance was upregulated by exogenous NO and downregulated by L-NAME, suggesting that NO modulation of eNOS expression involves processes at the level of gene transcription or mRNA stability.	nitro-l-arginine-methyl ester	61-90	nitric oxide synthase 3	Homo sapiens	202-206
10536122-6	1999	In contrast, the inhibition of endogenous NO production with nitro-L-arginine-methyl ester (L-NAME) caused a reduction in eNOS protein expression that was evident within 8 h. Paralleling the changes in eNOS protein, eNOS messenger RNA (mRNA) abundance was upregulated by exogenous NO and downregulated by L-NAME, suggesting that NO modulation of eNOS expression involves processes at the level of gene transcription or mRNA stability.	nitro-l-arginine-methyl ester	61-90	nitric oxide synthase 3	Homo sapiens	202-206
10536122-6	1999	In contrast, the inhibition of endogenous NO production with nitro-L-arginine-methyl ester (L-NAME) caused a reduction in eNOS protein expression that was evident within 8 h. Paralleling the changes in eNOS protein, eNOS messenger RNA (mRNA) abundance was upregulated by exogenous NO and downregulated by L-NAME, suggesting that NO modulation of eNOS expression involves processes at the level of gene transcription or mRNA stability.	NG-Nitroarginine Methyl Ester	92-98	nitric oxide synthase 3	Homo sapiens	122-126
10536122-6	1999	In contrast, the inhibition of endogenous NO production with nitro-L-arginine-methyl ester (L-NAME) caused a reduction in eNOS protein expression that was evident within 8 h. Paralleling the changes in eNOS protein, eNOS messenger RNA (mRNA) abundance was upregulated by exogenous NO and downregulated by L-NAME, suggesting that NO modulation of eNOS expression involves processes at the level of gene transcription or mRNA stability.	NG-Nitroarginine Methyl Ester	92-98	nitric oxide synthase 3	Homo sapiens	202-206
10536122-6	1999	In contrast, the inhibition of endogenous NO production with nitro-L-arginine-methyl ester (L-NAME) caused a reduction in eNOS protein expression that was evident within 8 h. Paralleling the changes in eNOS protein, eNOS messenger RNA (mRNA) abundance was upregulated by exogenous NO and downregulated by L-NAME, suggesting that NO modulation of eNOS expression involves processes at the level of gene transcription or mRNA stability.	NG-Nitroarginine Methyl Ester	92-98	nitric oxide synthase 3	Homo sapiens	202-206
10536122-6	1999	In contrast, the inhibition of endogenous NO production with nitro-L-arginine-methyl ester (L-NAME) caused a reduction in eNOS protein expression that was evident within 8 h. Paralleling the changes in eNOS protein, eNOS messenger RNA (mRNA) abundance was upregulated by exogenous NO and downregulated by L-NAME, suggesting that NO modulation of eNOS expression involves processes at the level of gene transcription or mRNA stability.	NG-Nitroarginine Methyl Ester	92-98	nitric oxide synthase 3	Homo sapiens	202-206
10536122-6	1999	In contrast, the inhibition of endogenous NO production with nitro-L-arginine-methyl ester (L-NAME) caused a reduction in eNOS protein expression that was evident within 8 h. Paralleling the changes in eNOS protein, eNOS messenger RNA (mRNA) abundance was upregulated by exogenous NO and downregulated by L-NAME, suggesting that NO modulation of eNOS expression involves processes at the level of gene transcription or mRNA stability.	NG-Nitroarginine Methyl Ester	305-311	nitric oxide synthase 3	Homo sapiens	122-126
10536122-6	1999	In contrast, the inhibition of endogenous NO production with nitro-L-arginine-methyl ester (L-NAME) caused a reduction in eNOS protein expression that was evident within 8 h. Paralleling the changes in eNOS protein, eNOS messenger RNA (mRNA) abundance was upregulated by exogenous NO and downregulated by L-NAME, suggesting that NO modulation of eNOS expression involves processes at the level of gene transcription or mRNA stability.	NG-Nitroarginine Methyl Ester	305-311	nitric oxide synthase 3	Homo sapiens	202-206
10536122-6	1999	In contrast, the inhibition of endogenous NO production with nitro-L-arginine-methyl ester (L-NAME) caused a reduction in eNOS protein expression that was evident within 8 h. Paralleling the changes in eNOS protein, eNOS messenger RNA (mRNA) abundance was upregulated by exogenous NO and downregulated by L-NAME, suggesting that NO modulation of eNOS expression involves processes at the level of gene transcription or mRNA stability.	NG-Nitroarginine Methyl Ester	305-311	nitric oxide synthase 3	Homo sapiens	202-206
10531147-1	1999	STUDY OBJECTIVES: To determine whether the polymorphic dinucleotide repeats found in intron 4 of the endothelial cell nitric oxide synthase (ecNOS) gene and the platelet GPIIIa PLA(1)/A(2) polymorphism are associated with myocardial infarction (MI) and venous thromboembolism (VTE) in African Americans.	Dinucleoside Phosphates	55-67	nitric oxide synthase 3	Homo sapiens	101-139
10541567-6	1999	Quantitative reverse transcription-polymerase chain reaction (RT-PCR) experiments revealed an induction of myometrial smooth muscle endothelial NOS (eNOS) expression by progesterone and 17beta-oestradiol, while myometrial iNOS expression was unaffected by steroid hormones.	Progesterone	169-181	nitric oxide synthase 3	Homo sapiens	132-147
10541567-6	1999	Quantitative reverse transcription-polymerase chain reaction (RT-PCR) experiments revealed an induction of myometrial smooth muscle endothelial NOS (eNOS) expression by progesterone and 17beta-oestradiol, while myometrial iNOS expression was unaffected by steroid hormones.	Estradiol	186-203	nitric oxide synthase 3	Homo sapiens	132-147
10510297-1	1999	The endothelial nitric oxide synthase (eNOS) is activated in response to stimulation of endothelial cells by a number of vasoactive substances including, bradykinin (BK), angiotensin II (Ang II), endothelin-1 (ET-1) and ATP.	Adenosine Triphosphate	220-223	nitric oxide synthase 3	Homo sapiens	4-37
10510054-1	1999	BACKGROUND: Endothelium-derived nitric oxide (NO) is synthesised from L-arginine by endothelial nitric oxide synthase (eNOS) encoded by the NOS 3 gene on chromosome 7.	Nitric Oxide	32-44	nitric oxide synthase 3	Homo sapiens	84-117
10510054-1	1999	BACKGROUND: Endothelium-derived nitric oxide (NO) is synthesised from L-arginine by endothelial nitric oxide synthase (eNOS) encoded by the NOS 3 gene on chromosome 7.	Nitric Oxide	32-44	nitric oxide synthase 3	Homo sapiens	140-145
10510054-1	1999	BACKGROUND: Endothelium-derived nitric oxide (NO) is synthesised from L-arginine by endothelial nitric oxide synthase (eNOS) encoded by the NOS 3 gene on chromosome 7.	Arginine	70-80	nitric oxide synthase 3	Homo sapiens	84-117
10510054-1	1999	BACKGROUND: Endothelium-derived nitric oxide (NO) is synthesised from L-arginine by endothelial nitric oxide synthase (eNOS) encoded by the NOS 3 gene on chromosome 7.	Arginine	70-80	nitric oxide synthase 3	Homo sapiens	140-145
10510054-3	1999	METHODS AND RESULTS: Single-strand conformation polymorphism analysis of NOS 3 identified a G--&gt;T polymorphism in exon 7 of the gene which encodes a Glu--&gt;Asp amino acid substitution at residue 298 of eNOS.	Glutamic Acid	152-155	nitric oxide synthase 3	Homo sapiens	73-78
10510054-3	1999	METHODS AND RESULTS: Single-strand conformation polymorphism analysis of NOS 3 identified a G--&gt;T polymorphism in exon 7 of the gene which encodes a Glu--&gt;Asp amino acid substitution at residue 298 of eNOS.	asp amino acid	161-175	nitric oxide synthase 3	Homo sapiens	73-78
10510054-9	1999	CONCLUSIONS: Homozygosity for a common NOS 3 polymorphism (894 G--&gt;T) which encodes a Glu298--&gt;Asp amino acid substitution in eNOS is a risk factor for angiographic CAD and recent MI in this population.	asp amino acid	101-115	nitric oxide synthase 3	Homo sapiens	39-44
10516221-3	1999	In contrast, ANG IV-mediated activation of ecNOS was abolished by the intracellular Ca(2+) chelator 1,2-bis(2-aminophenoxy)ethane-N,N,N",N"-tetraacetic acid-AM.	1,2-bis(2-aminophenoxy)ethane-n,n,n",n"-tetraacetic acid-am	100-159	nitric oxide synthase 3	Homo sapiens	43-48
10514107-6	1999	We have genotyped 122 cases of early-onset AD (EOAD) and 317 cases of late-onset AD (LOAD) as well as 392 controls for a common structural polymorphism Glu/Asp at codon 298 in the NOS3 gene.	Glutamic Acid	152-155	nitric oxide synthase 3	Homo sapiens	180-184
10506483-4	1999	The half-life of eNOS mRNA, measured after actinomycin D transcriptional arrest, was 3-fold greater in preconfluent compared with confluent endothelial cells.	Dactinomycin	43-56	nitric oxide synthase 3	Homo sapiens	17-21
10595624-0	1999	Atorvastatin increases ecNOS levels in human platelets of hyperlipidemic subjects.	Atorvastatin	0-12	nitric oxide synthase 3	Homo sapiens	23-28
10595624-4	1999	These studies indicate that with atrovastatin ecNOS levels increased on average by approximately approximately 1.7-fold (paired t-test p = 0.009).	atrovastatin	33-45	nitric oxide synthase 3	Homo sapiens	46-51
10595624-9	1999	Here, Atorvastatin is shown to significantly elevate intraplatelet ecNOS levels in hyperlipidemic subjects without affecting iNOS expression.	Atorvastatin	6-18	nitric oxide synthase 3	Homo sapiens	67-72
10531147-1	1999	STUDY OBJECTIVES: To determine whether the polymorphic dinucleotide repeats found in intron 4 of the endothelial cell nitric oxide synthase (ecNOS) gene and the platelet GPIIIa PLA(1)/A(2) polymorphism are associated with myocardial infarction (MI) and venous thromboembolism (VTE) in African Americans.	Dinucleoside Phosphates	55-67	nitric oxide synthase 3	Homo sapiens	141-146
10471612-7	1999	In contrast, L-NMMA infusion that inhibited endothelial NOS, as evidenced by an increase in blood pressure and a decrease in heart rate, had only a barely detectable effect on exhaled NO (-11 +/- 4% from baseline).	omega-N-Methylarginine	13-19	nitric oxide synthase 3	Homo sapiens	44-59
10543322-1	1999	BACKGROUND: Nitric oxide (NO) is synthesized by endothelial cell NO synthase (ecNOS) on vascular endothelium, and it plays a key role in the regulation of blood flow and pressure.	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	78-83
10520813-1	1999	OBJECTIVES: The purpose of the study was to investigate the role of nitric oxide (NO) in monocyte-endothelial interaction by augmenting NO release via transfection of human endothelial cells (ECs) with EC NO synthase (eNOS) DNA.	Nitric Oxide	68-80	nitric oxide synthase 3	Homo sapiens	202-216
10534441-7	1999	However, when l-arginine level is higher than 2 x 10(-4) M, as observed under in vivo conditions, NOS-III activity is essentially unaffected by temperature, the substrate concentration exceeding the value of K(m).	Arginine	14-24	nitric oxide synthase 3	Homo sapiens	98-105
10500231-5	1999	The increase in cavernosal pressure in response to cavernosal nerve stimulation was enhanced in animals transfected with eNOS, and erectile responses to acetylcholine and zaprinast were enhanced at a time when the erectile response to the NO donor sodium 1-(N,N-diethylamino)diazen-1-ium-1,2-diolate was not altered.	sodium 1-(n,n-diethylamino)diazen-1-ium-1,2-diolate	248-299	nitric oxide synthase 3	Homo sapiens	121-125
10519149-1	1999	In vascular endothelium, endothelium-derived relaxing factor, predominantly nitric oxide (NO), is synthesized by endothelial NO synthase (eNOS).	Nitric Oxide	76-88	nitric oxide synthase 3	Homo sapiens	138-142
10568338-2	1999	Careful dissection of the steps involved in regulating endothelial nitric oxide synthase (eNOS) activity has revealed that cholesterol-induced caveolin expression reduces NO production by stimulating the production of inhibitory caveolin eNOS complexes.	Cholesterol	123-134	nitric oxide synthase 3	Homo sapiens	55-88
10568338-2	1999	Careful dissection of the steps involved in regulating endothelial nitric oxide synthase (eNOS) activity has revealed that cholesterol-induced caveolin expression reduces NO production by stimulating the production of inhibitory caveolin eNOS complexes.	Cholesterol	123-134	nitric oxide synthase 3	Homo sapiens	90-94
10568338-2	1999	Careful dissection of the steps involved in regulating endothelial nitric oxide synthase (eNOS) activity has revealed that cholesterol-induced caveolin expression reduces NO production by stimulating the production of inhibitory caveolin eNOS complexes.	Cholesterol	123-134	nitric oxide synthase 3	Homo sapiens	238-242
10409685-4	1999	In the zinc-bound state, these same two cysteine residues form part of a zinc-tetrathiolate (ZnS(4)) center indistinguishable from that observed in the endothelial isoform (NOS-3).	Cysteine	40-48	nitric oxide synthase 3	Homo sapiens	173-178
10690325-2	1999	Additional post-translational mechanisms regulate the activity of eNOS, including the interaction of eNOS with caveolin-1, heat shock protein 90 (Hsp90), or membrane phospholipids, as well as enzyme translocation and phosphorylation.	Phospholipids	166-179	nitric oxide synthase 3	Homo sapiens	66-70
10419469-0	1999	Mutation of the five conserved histidines in the endothelial nitric-oxide synthase hemoprotein domain.	Histidine	31-41	nitric oxide synthase 3	Homo sapiens	49-82
10419469-2	1999	Five conserved histidine residues are found in the human endothelial nitric-oxide synthase (NOS) heme domain: His-420, His-421, and His-461 are close to the heme, whereas His-146 and His-214 are some distance away.	Histidine	15-24	nitric oxide synthase 3	Homo sapiens	57-90
10419469-2	1999	Five conserved histidine residues are found in the human endothelial nitric-oxide synthase (NOS) heme domain: His-420, His-421, and His-461 are close to the heme, whereas His-146 and His-214 are some distance away.	Heme	97-101	nitric oxide synthase 3	Homo sapiens	57-90
10419469-2	1999	Five conserved histidine residues are found in the human endothelial nitric-oxide synthase (NOS) heme domain: His-420, His-421, and His-461 are close to the heme, whereas His-146 and His-214 are some distance away.	Histidine	110-113	nitric oxide synthase 3	Homo sapiens	57-90
10419469-2	1999	Five conserved histidine residues are found in the human endothelial nitric-oxide synthase (NOS) heme domain: His-420, His-421, and His-461 are close to the heme, whereas His-146 and His-214 are some distance away.	Histidine	119-122	nitric oxide synthase 3	Homo sapiens	57-90
10419469-2	1999	Five conserved histidine residues are found in the human endothelial nitric-oxide synthase (NOS) heme domain: His-420, His-421, and His-461 are close to the heme, whereas His-146 and His-214 are some distance away.	Histidine	119-122	nitric oxide synthase 3	Homo sapiens	57-90
10419469-2	1999	Five conserved histidine residues are found in the human endothelial nitric-oxide synthase (NOS) heme domain: His-420, His-421, and His-461 are close to the heme, whereas His-146 and His-214 are some distance away.	Heme	157-161	nitric oxide synthase 3	Homo sapiens	57-90
10419469-2	1999	Five conserved histidine residues are found in the human endothelial nitric-oxide synthase (NOS) heme domain: His-420, His-421, and His-461 are close to the heme, whereas His-146 and His-214 are some distance away.	Histidine	119-122	nitric oxide synthase 3	Homo sapiens	57-90
10419469-2	1999	Five conserved histidine residues are found in the human endothelial nitric-oxide synthase (NOS) heme domain: His-420, His-421, and His-461 are close to the heme, whereas His-146 and His-214 are some distance away.	Histidine	119-122	nitric oxide synthase 3	Homo sapiens	57-90
10409685-4	1999	In the zinc-bound state, these same two cysteine residues form part of a zinc-tetrathiolate (ZnS(4)) center indistinguishable from that observed in the endothelial isoform (NOS-3).	zns(4)	93-99	nitric oxide synthase 3	Homo sapiens	173-178
10409685-5	1999	As in NOS-3, ZnS(4) plays a key role in stabilizing intersubunit contacts and in maintaining the integrity of the cofactor (tetrahydrobiopterin) binding site of NOS-2.	zns(4)	13-19	nitric oxide synthase 3	Homo sapiens	6-11
10409236-4	1999	Acetylcholine-stimulated eNOS activity was 218-255% above basal levels in immortalized cells, and this was comparable to the 250% increase seen in primary PAECs (passage 6).	Acetylcholine	0-13	nitric oxide synthase 3	Homo sapiens	25-29
10409236-5	1999	eNOS was also acutely activated by estradiol to levels 197-309% above basal, paralleling the stimulation obtained in primary cells.	Estradiol	35-44	nitric oxide synthase 3	Homo sapiens	0-4
10385691-0	1999	Modulation of expression of endothelial nitric oxide synthase by nordihydroguaiaretic acid, a phenolic antioxidant in cultured endothelial cells.	Masoprocol	65-90	nitric oxide synthase 3	Homo sapiens	28-61
10440125-12	1999	CONCLUSION/INTERPRETATION: Human VSMC express cNOS, which is rapidly activated by insulin with a consequent increase of both cGMP and cAMP, suggesting that insulin-induced vasodilation in vivo is not entirely endothelium-mediated.	Cyclic GMP	125-129	nitric oxide synthase 3	Homo sapiens	46-50
10440125-12	1999	CONCLUSION/INTERPRETATION: Human VSMC express cNOS, which is rapidly activated by insulin with a consequent increase of both cGMP and cAMP, suggesting that insulin-induced vasodilation in vivo is not entirely endothelium-mediated.	Cyclic AMP	134-138	nitric oxide synthase 3	Homo sapiens	46-50
10481258-5	1999	strongly suggesting that intracellular calcium levels regulate cNOS activity in invertebrate immunocytes.	Calcium	39-46	nitric oxide synthase 3	Homo sapiens	63-67
10385691-4	1999	NDGA seemed to be the most potent of the phenolic antioxidants, producing a 3-fold increase in eNOS mRNA.	Masoprocol	0-4	nitric oxide synthase 3	Homo sapiens	95-99
10377070-0	1999	G894T polymorphism in the endothelial nitric oxide synthase gene is associated with an enhanced vascular responsiveness to phenylephrine.	Phenylephrine	123-136	nitric oxide synthase 3	Homo sapiens	26-59
10377070-2	1999	Because nitric oxide (NO) strongly affects modulation of the vascular tone in response to vasopressor agents, we hypothesized that the G894T polymorphism of the endothelial NO synthase gene (eNOS) could be related to changes in the pressor response to PE.	Nitric Oxide	8-20	nitric oxide synthase 3	Homo sapiens	191-195
10377070-2	1999	Because nitric oxide (NO) strongly affects modulation of the vascular tone in response to vasopressor agents, we hypothesized that the G894T polymorphism of the endothelial NO synthase gene (eNOS) could be related to changes in the pressor response to PE.	Phenylephrine	252-254	nitric oxide synthase 3	Homo sapiens	191-195
10367598-1	1999	This study examined the occurrence of endothelial nitric oxide (NO)-synthase (NOS-III) in terminal mesenteric vessels and the involvement of NO in microvascular permeability.	Nitric Oxide	50-62	nitric oxide synthase 3	Homo sapiens	78-85
10376602-2	1999	eNOS is phosphorylated in response to various forms of cellular stimulation, but the role of phosphorylation in the regulation of nitric oxide (NO) production and the kinase(s) responsible are not known.	Nitric Oxide	130-142	nitric oxide synthase 3	Homo sapiens	0-4
10376602-3	1999	Here we show that the serine/threonine protein kinase Akt (protein kinase B) can directly phosphorylate eNOS on serine 1179 and activate the enzyme, leading to NO production, whereas mutant eNOS (S1179A) is resistant to phosphorylation and activation by Akt.	Serine	22-28	nitric oxide synthase 3	Homo sapiens	104-108
10376602-3	1999	Here we show that the serine/threonine protein kinase Akt (protein kinase B) can directly phosphorylate eNOS on serine 1179 and activate the enzyme, leading to NO production, whereas mutant eNOS (S1179A) is resistant to phosphorylation and activation by Akt.	Serine	22-28	nitric oxide synthase 3	Homo sapiens	190-194
11593517-1	1999	OBJECTIVE: To observe the effects of nerve growth factor (NGF) on nitric oxide (NO) release and constitutive nitric oxide synthase (cNOS) gene expression in oxygen/glucose deprived cortical neuron cultures.	Oxygen	157-163	nitric oxide synthase 3	Homo sapiens	132-136
10320673-3	1999	Brain ischemia triggers a cascade of events, possibly mediated by excitatory amino acids, yielding the activation of the Ca2+-dependent NOS isoforms, i.e. neuronal NOS (nNOS) and endothelial NOS (eNOS).	Excitatory Amino Acids	66-88	nitric oxide synthase 3	Homo sapiens	179-194
10330227-4	1999	Transfection of the eNOS gene (eNOS) into VSM cells significantly inhibited (P &lt; 0.05) [3H]thymidine incorporation into the DNA in response to PDGF-BB stimulation compared with lacZ-transfected control cells.	Tritium	91-93	nitric oxide synthase 3	Homo sapiens	20-24
10330227-4	1999	Transfection of the eNOS gene (eNOS) into VSM cells significantly inhibited (P &lt; 0.05) [3H]thymidine incorporation into the DNA in response to PDGF-BB stimulation compared with lacZ-transfected control cells.	Tritium	91-93	nitric oxide synthase 3	Homo sapiens	31-35
10475066-0	1999	The Glu-298--&gt;Asp (894G--&gt;T) mutation at exon 7 of the endothelial nitric oxide synthase gene and coronary artery disease.	Glutamic Acid	4-7	nitric oxide synthase 3	Homo sapiens	61-94
10475066-1	1999	We examined associations between the endothelial nitric oxide synthase (eNOS) gene Glu-298--&gt;Asp (894G--&gt;T) mutation and the occurrence and severity of angiographically defined coronary artery disease (CAD).	Glutamic Acid	83-86	nitric oxide synthase 3	Homo sapiens	37-70
10475066-1	1999	We examined associations between the endothelial nitric oxide synthase (eNOS) gene Glu-298--&gt;Asp (894G--&gt;T) mutation and the occurrence and severity of angiographically defined coronary artery disease (CAD).	Glutamic Acid	83-86	nitric oxide synthase 3	Homo sapiens	72-76
10475066-2	1999	eNOS mediates basal vascular wall nitric oxide production, and altered nitric oxide production has been implicated in atherosclerosis.	Nitric Oxide	34-46	nitric oxide synthase 3	Homo sapiens	0-4
10475066-3	1999	The newly identified eNOS Glu-298--&gt;Asp mutation in exon 7 is common and likely to be functional.	Glutamic Acid	26-29	nitric oxide synthase 3	Homo sapiens	21-25
10475066-3	1999	The newly identified eNOS Glu-298--&gt;Asp mutation in exon 7 is common and likely to be functional.	Aspartic Acid	39-42	nitric oxide synthase 3	Homo sapiens	21-25
10475066-5	1999	We genotyped 763 white Australians undergoing coronary angiography for the eNOS Glu-298--&gt;Asp mutation.	Glutamic Acid	80-83	nitric oxide synthase 3	Homo sapiens	75-79
10475066-5	1999	We genotyped 763 white Australians undergoing coronary angiography for the eNOS Glu-298--&gt;Asp mutation.	Aspartic Acid	93-96	nitric oxide synthase 3	Homo sapiens	75-79
10475066-9	1999	In conclusion, the eNOS Glu-298--&gt;Asp mutation is common, occurring with an allele frequency of 32.5%, but is not associated with either the occurrence or severity of CAD in the Australian population or with other established coronary risk factors assessed in our study.	Glutamic Acid	24-27	nitric oxide synthase 3	Homo sapiens	19-23
10475066-9	1999	In conclusion, the eNOS Glu-298--&gt;Asp mutation is common, occurring with an allele frequency of 32.5%, but is not associated with either the occurrence or severity of CAD in the Australian population or with other established coronary risk factors assessed in our study.	Aspartic Acid	37-40	nitric oxide synthase 3	Homo sapiens	19-23
11593517-1	1999	OBJECTIVE: To observe the effects of nerve growth factor (NGF) on nitric oxide (NO) release and constitutive nitric oxide synthase (cNOS) gene expression in oxygen/glucose deprived cortical neuron cultures.	Glucose	164-171	nitric oxide synthase 3	Homo sapiens	132-136
10205218-3	1999	METHODS: Activity of the calcium dependent constitutive and calcium independent inducible isoforms of NO synthase (cNOS and iNOS, respectively) was assayed biochemically in biopsy specimens of liver and a vascular portion of the greater omentum (representative of mesenteric vasculature) obtained from patients with cirrhosis undergoing liver transplantation (n=14) and non-cirrhotic control patients undergoing liver resection for metastases (n=9).	Calcium	25-32	nitric oxide synthase 3	Homo sapiens	115-119
10215736-0	1999	Expression of endothelial cell-derived nitric oxide synthase (eNOS) is increased during gastric adaptation to chronic aspirin intake in humans.	Aspirin	118-125	nitric oxide synthase 3	Homo sapiens	14-60
10329249-12	1999	Ca2+ is the principal activator of endothelial nitric oxide synthase (eNOS), which stimulates cyclic GMP production.	Cyclic GMP	94-104	nitric oxide synthase 3	Homo sapiens	35-68
10329249-12	1999	Ca2+ is the principal activator of endothelial nitric oxide synthase (eNOS), which stimulates cyclic GMP production.	Cyclic GMP	94-104	nitric oxide synthase 3	Homo sapiens	70-74
10329249-13	1999	The final result that the eNOS inhibitor L-NAME enhanced the histamine (100 microM) induced [Ca2+]i plateau suggests a negative feedback loop (via cGMP) of endothelial NO on its own synthesis in the regulation of endothelial [Ca2+]i signal.	NG-Nitroarginine Methyl Ester	41-47	nitric oxide synthase 3	Homo sapiens	26-30
10329249-13	1999	The final result that the eNOS inhibitor L-NAME enhanced the histamine (100 microM) induced [Ca2+]i plateau suggests a negative feedback loop (via cGMP) of endothelial NO on its own synthesis in the regulation of endothelial [Ca2+]i signal.	Histamine	61-70	nitric oxide synthase 3	Homo sapiens	26-30
10329249-13	1999	The final result that the eNOS inhibitor L-NAME enhanced the histamine (100 microM) induced [Ca2+]i plateau suggests a negative feedback loop (via cGMP) of endothelial NO on its own synthesis in the regulation of endothelial [Ca2+]i signal.	Cyclic GMP	147-151	nitric oxide synthase 3	Homo sapiens	26-30
10600037-6	1999	VSMC transfected with another plasmid, containing endothelial constitutive NO synthase (ecNOS) cDNA generated micromolar quantities of nitrite.	Nitrites	135-142	nitric oxide synthase 3	Homo sapiens	88-93
10215736-0	1999	Expression of endothelial cell-derived nitric oxide synthase (eNOS) is increased during gastric adaptation to chronic aspirin intake in humans.	Aspirin	118-125	nitric oxide synthase 3	Homo sapiens	62-66
10215736-10	1999	eNOS expression started to increase on day 7 in oxyntic mucosa and on day 3 in antral mucosa, reaching its highest values at the end of the consumption of aspirin.	Aspirin	155-162	nitric oxide synthase 3	Homo sapiens	0-4
10215736-12	1999	Increase of mucosal eNOS expression might compensate for reduced prostaglandin synthesis and be responsible for gastric adaptation to chronic aspirin intake in humans.	Prostaglandins	65-78	nitric oxide synthase 3	Homo sapiens	20-24
10215736-12	1999	Increase of mucosal eNOS expression might compensate for reduced prostaglandin synthesis and be responsible for gastric adaptation to chronic aspirin intake in humans.	Aspirin	142-149	nitric oxide synthase 3	Homo sapiens	20-24
10079196-1	1999	Cardiac myocytes express the calcium-responsive nitric oxide synthase (eNOS or NOS3).	Calcium	29-36	nitric oxide synthase 3	Homo sapiens	79-83
10100997-4	1999	eNOS activation was assessed by measuring conversion of [3H]L-arginine to [3H]L-citrulline in intact cells.	[3h]l-arginine	56-70	nitric oxide synthase 3	Homo sapiens	0-4
10100997-4	1999	eNOS activation was assessed by measuring conversion of [3H]L-arginine to [3H]L-citrulline in intact cells.	[3h]l-citrulline	74-90	nitric oxide synthase 3	Homo sapiens	0-4
10100997-8	1999	E2beta-stimulated eNOS activity was dependent on the influx of extracellular Ca2+, and was completely inhibited by the estrogen receptor (ER) antagonist ICI182,780.	ici182	153-159	nitric oxide synthase 3	Homo sapiens	18-22
10450377-0	1999	Dinucleotide repeat polymorphisms in EDN1 and NOS3 are not associated with severe diabetic retinopathy in type 1 or type 2 diabetes.	Dinucleoside Phosphates	0-12	nitric oxide synthase 3	Homo sapiens	46-50
11263184-5	1999	CONCLUSION: eNOS is present in syncytiotrophoblast and endothelium of stem villi vessels, and it can synthesize nitric oxide which results in the increase of nitric oxide in pregnancy.	Nitric Oxide	112-124	nitric oxide synthase 3	Homo sapiens	12-16
10235453-6	1999	eNOS mRNA increased two-fold within 3 h and gradually declined, but the increased levels of mRNA persisted for &gt;24 h. A similar increase of eNOS expression was observed in human umbilical endothelial cells exposed to ethanol.	Ethanol	220-227	nitric oxide synthase 3	Homo sapiens	0-4
10235453-6	1999	eNOS mRNA increased two-fold within 3 h and gradually declined, but the increased levels of mRNA persisted for &gt;24 h. A similar increase of eNOS expression was observed in human umbilical endothelial cells exposed to ethanol.	Ethanol	220-227	nitric oxide synthase 3	Homo sapiens	143-147
10235453-7	1999	These results demonstrate that ethanol augments both basal and stimulated NO production and that this effect is associated with increased eNOS protein and mRNA expression levels.	Ethanol	31-38	nitric oxide synthase 3	Homo sapiens	138-142
10074942-1	1999	Crystal structures of human endothelial nitric oxide synthase (eNOS) and human inducible NOS (iNOS) catalytic domains were solved in complex with the arginine substrate and an inhibitor S-ethylisothiourea (SEITU), respectively.	Arginine	150-158	nitric oxide synthase 3	Homo sapiens	28-61
10074942-1	1999	Crystal structures of human endothelial nitric oxide synthase (eNOS) and human inducible NOS (iNOS) catalytic domains were solved in complex with the arginine substrate and an inhibitor S-ethylisothiourea (SEITU), respectively.	etiron	186-204	nitric oxide synthase 3	Homo sapiens	28-61
10074942-1	1999	Crystal structures of human endothelial nitric oxide synthase (eNOS) and human inducible NOS (iNOS) catalytic domains were solved in complex with the arginine substrate and an inhibitor S-ethylisothiourea (SEITU), respectively.	etiron	206-211	nitric oxide synthase 3	Homo sapiens	28-61
10082505-7	1999	EPO resulted in a dose-dependent inhibition of basal and acetylcholine-stimulated NO production and eNOS protein expression and also led to a significant dose-dependent stimulation of DNA synthesis in endothelial cells.	Acetylcholine	57-70	nitric oxide synthase 3	Homo sapiens	100-104
10082505-8	1999	The inhibitory effects of EPO on NO production and eNOS expression were reversed by felodipine.	Felodipine	84-94	nitric oxide synthase 3	Homo sapiens	51-55
10086391-4	1999	This is supported by the observations that NOS3, the endothelial constitutive NOS, is expressed in normal cardiac myocytes from rodents and human, and NOS and/or guanylyl cyclase inhibitors antagonize the effect of muscarinic agonists on heart rate, atrio-ventricular conduction, contractility and L-type calcium current.	Calcium	305-312	nitric oxide synthase 3	Homo sapiens	43-47
11263184-5	1999	CONCLUSION: eNOS is present in syncytiotrophoblast and endothelium of stem villi vessels, and it can synthesize nitric oxide which results in the increase of nitric oxide in pregnancy.	Nitric Oxide	158-170	nitric oxide synthase 3	Homo sapiens	12-16
9989455-8	1999	However, the production of nitric oxide in blood vessels by NOS 3, which, like NOS 1, is Ca2+-dependent, causes vasodilatation and improves blood flow in the penumbral region of brain infarcts.	Nitric Oxide	27-39	nitric oxide synthase 3	Homo sapiens	60-65
9988806-3	1999	Expressions of inducible, calcium-independent nitric oxide synthase and constitutive, calcium-dependent endothelial nitric oxide synthase were determined by semiquantitative reverse transcriptase-polymerase chain reaction.	Calcium	86-93	nitric oxide synthase 3	Homo sapiens	104-137
9950855-8	1999	In contrast, U-73122 and BIM were able to inhibit VEGF-elicited serine phosphorylation of ecNOS.	1-(6-((3-methoxyestra-1,3,5(10)-trien-17-yl)amino)hexyl)-1H-pyrrole-2,5-dione	13-20	nitric oxide synthase 3	Homo sapiens	90-95
9950855-8	1999	In contrast, U-73122 and BIM were able to inhibit VEGF-elicited serine phosphorylation of ecNOS.	bisindolylmaleimide	25-28	nitric oxide synthase 3	Homo sapiens	90-95
9950855-8	1999	In contrast, U-73122 and BIM were able to inhibit VEGF-elicited serine phosphorylation of ecNOS.	Serine	64-70	nitric oxide synthase 3	Homo sapiens	90-95
9852077-0	1998	Effects of Asp-369 and Arg-372 mutations on heme environment and function in human endothelial nitric-oxide synthase.	Aspartic Acid	11-14	nitric oxide synthase 3	Homo sapiens	83-116
9914861-1	1999	Nitric oxide production by the Ca2+/calmodulin-dependent enzyme endothelial nitric oxide synthase primarily reflects changes in intracellular [Ca2+], increasing as Ca2+ rises and decreasing as Ca2+ falls.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	64-97
9914861-3	1999	Moreover, other endothelial nitric oxide synthase-associated proteins could account for a delayed Ca(2+)-independent activation of nitric oxide production, and may be involved with caveolin in the reversible trafficking of a large endothelial nitric oxide synthase-containing heterocomplex between the caveolae and cytosolic cell structures.	Nitric Oxide	28-40	nitric oxide synthase 3	Homo sapiens	231-264
9914865-7	1999	Induction of the enzyme GTP cyclohydrolase 1 and consequent production of tetrahydrobiopterin contributes to the increase in the activity of endothelial nitric oxide synthase.	sapropterin	74-93	nitric oxide synthase 3	Homo sapiens	141-174
10191369-1	1999	This study was done to determine the effects of the angioprotective agent dobesilate on expression and activity on the constitutive nitric oxide synthase (ecNOS) in resident endothelial cells, as well as of the inducible nitric oxide synthase (iNOS) in cytokine-activated endothelial cells, by recording, in culture supernatants, the concentrations of citrulline as a reaction product of both enzymes.	2,5-Dihydroxybenzenesulfonic Acid	74-84	nitric oxide synthase 3	Homo sapiens	155-160
10191369-2	1999	In capillary, microvascular, and macrovascular endothelial cells, Mg dobesilate incubation (0.25-1 mM) for 24 hours led to a highly significant concentration-correlating increase in ecNOS activities.	Magnesium	66-68	nitric oxide synthase 3	Homo sapiens	182-187
10191369-2	1999	In capillary, microvascular, and macrovascular endothelial cells, Mg dobesilate incubation (0.25-1 mM) for 24 hours led to a highly significant concentration-correlating increase in ecNOS activities.	2,5-Dihydroxybenzenesulfonic Acid	69-79	nitric oxide synthase 3	Homo sapiens	182-187
9857005-1	1998	It has been proposed that Cys99 of human endothelial nitric oxide synthase (eNOS) is responsible for tetrahydrobiopterin (BH4) binding.	sapropterin	101-120	nitric oxide synthase 3	Homo sapiens	41-74
9857005-1	1998	It has been proposed that Cys99 of human endothelial nitric oxide synthase (eNOS) is responsible for tetrahydrobiopterin (BH4) binding.	sapropterin	122-125	nitric oxide synthase 3	Homo sapiens	41-74
10442575-5	1999	In endothelial cells, NOS III is a constitutively expressed isoform of NOS which releases small amounts of NO in a calcium-dependent manner.	Calcium	115-122	nitric oxide synthase 3	Homo sapiens	22-29
10442576-2	1999	In normal blood vessels, NO is synthesized from L-arginine by a constitutively expressed NO synthase (NOS III) in endothelial cells.	Arginine	48-58	nitric oxide synthase 3	Homo sapiens	102-109
10072713-4	1999	Several intracellular mechanisms are involved in the synthesis of nitric oxide, including receptor-coupled G proteins, the availability of L-arginine, cofactors for endothelial nitric oxide synthase and the expression of the enzyme.	Nitric Oxide	66-78	nitric oxide synthase 3	Homo sapiens	165-198
10072713-7	1999	The reduced production of nitric oxide by the endothelium is caused by abnormalities in endothelial signal transduction, availability of L-arginine, cofactors for endothelial nitric oxide synthase and expression of the enzyme.	Nitric Oxide	26-38	nitric oxide synthase 3	Homo sapiens	163-196
9875848-0	1998	Crystal structure of constitutive endothelial nitric oxide synthase: a paradigm for pterin function involving a novel metal center.	Pterins	84-90	nitric oxide synthase 3	Homo sapiens	34-67
9875848-0	1998	Crystal structure of constitutive endothelial nitric oxide synthase: a paradigm for pterin function involving a novel metal center.	Metals	118-123	nitric oxide synthase 3	Homo sapiens	34-67
9852077-0	1998	Effects of Asp-369 and Arg-372 mutations on heme environment and function in human endothelial nitric-oxide synthase.	Arginine	23-26	nitric oxide synthase 3	Homo sapiens	83-116
9852077-0	1998	Effects of Asp-369 and Arg-372 mutations on heme environment and function in human endothelial nitric-oxide synthase.	Heme	44-48	nitric oxide synthase 3	Homo sapiens	83-116
9852077-1	1998	Eight polar amino acid residues in the putative substrate-binding region from Thr-360 to Val-379 in human endothelial nitric-oxide synthase (eNOS) (Thr-360, Arg-365, Cys-368, Asp-369, Arg-372, Tyr-373, Glu-377, and Asp-378) were individually mutated.	Threonine	78-81	nitric oxide synthase 3	Homo sapiens	106-139
9852077-1	1998	Eight polar amino acid residues in the putative substrate-binding region from Thr-360 to Val-379 in human endothelial nitric-oxide synthase (eNOS) (Thr-360, Arg-365, Cys-368, Asp-369, Arg-372, Tyr-373, Glu-377, and Asp-378) were individually mutated.	Arginine	157-160	nitric oxide synthase 3	Homo sapiens	106-139
9852077-1	1998	Eight polar amino acid residues in the putative substrate-binding region from Thr-360 to Val-379 in human endothelial nitric-oxide synthase (eNOS) (Thr-360, Arg-365, Cys-368, Asp-369, Arg-372, Tyr-373, Glu-377, and Asp-378) were individually mutated.	Cysteine	166-169	nitric oxide synthase 3	Homo sapiens	106-139
9852077-1	1998	Eight polar amino acid residues in the putative substrate-binding region from Thr-360 to Val-379 in human endothelial nitric-oxide synthase (eNOS) (Thr-360, Arg-365, Cys-368, Asp-369, Arg-372, Tyr-373, Glu-377, and Asp-378) were individually mutated.	Aspartic Acid	175-178	nitric oxide synthase 3	Homo sapiens	106-139
9852077-1	1998	Eight polar amino acid residues in the putative substrate-binding region from Thr-360 to Val-379 in human endothelial nitric-oxide synthase (eNOS) (Thr-360, Arg-365, Cys-368, Asp-369, Arg-372, Tyr-373, Glu-377, and Asp-378) were individually mutated.	Arginine	184-187	nitric oxide synthase 3	Homo sapiens	106-139
9852077-1	1998	Eight polar amino acid residues in the putative substrate-binding region from Thr-360 to Val-379 in human endothelial nitric-oxide synthase (eNOS) (Thr-360, Arg-365, Cys-368, Asp-369, Arg-372, Tyr-373, Glu-377, and Asp-378) were individually mutated.	Tyrosine	193-196	nitric oxide synthase 3	Homo sapiens	106-139
9852077-1	1998	Eight polar amino acid residues in the putative substrate-binding region from Thr-360 to Val-379 in human endothelial nitric-oxide synthase (eNOS) (Thr-360, Arg-365, Cys-368, Asp-369, Arg-372, Tyr-373, Glu-377, and Asp-378) were individually mutated.	Glutamic Acid	202-205	nitric oxide synthase 3	Homo sapiens	106-139
9852077-1	1998	Eight polar amino acid residues in the putative substrate-binding region from Thr-360 to Val-379 in human endothelial nitric-oxide synthase (eNOS) (Thr-360, Arg-365, Cys-368, Asp-369, Arg-372, Tyr-373, Glu-377, and Asp-378) were individually mutated.	Aspartic Acid	215-218	nitric oxide synthase 3	Homo sapiens	106-139
9837777-2	1998	Endothelial nitric oxide synthase (eNOS) is an essential molecule in mediating VEGF-A-induced angiogenesis and endothelial function via production of nitric oxide (NO).	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	35-39
9864293-6	1998	Several HMN-1180 derivatives were synthesized and analyzed for their inhibitory actions against nNOS, eNOS and iNOS to cast light on its structure-activity relationships.	HMN 1180	8-16	nitric oxide synthase 3	Homo sapiens	102-106
9872368-1	1998	The major enzyme isoform that synthesizes nitric oxide (NO) in first trimester human placentae is endothelial or type III NO-synthase (NOS III) which exhibits high specific activity in the microsomal fraction.	Nitric Oxide	42-54	nitric oxide synthase 3	Homo sapiens	135-142
9872368-4	1998	SDS (&gt; or =0.05% w/v) resulted in significant inhibition both of basal and BH4-stimulated activities of NOS III, but the latter responded more sensitively.	Sodium Dodecyl Sulfate	0-3	nitric oxide synthase 3	Homo sapiens	107-114
9872368-4	1998	SDS (&gt; or =0.05% w/v) resulted in significant inhibition both of basal and BH4-stimulated activities of NOS III, but the latter responded more sensitively.	sapropterin	78-81	nitric oxide synthase 3	Homo sapiens	107-114
9872368-7	1998	Considering that basal activity is due to the presence of endogenous BH4 tightly bound to the enzyme, this differential sensitivity of basal and BH4-stimulated enzyme activities to SDS may be related to a putative differential protective effect of BH4 on the two subunits of the NOS III dimer.	sapropterin	69-72	nitric oxide synthase 3	Homo sapiens	279-286
9872368-7	1998	Considering that basal activity is due to the presence of endogenous BH4 tightly bound to the enzyme, this differential sensitivity of basal and BH4-stimulated enzyme activities to SDS may be related to a putative differential protective effect of BH4 on the two subunits of the NOS III dimer.	sapropterin	145-148	nitric oxide synthase 3	Homo sapiens	279-286
9872368-7	1998	Considering that basal activity is due to the presence of endogenous BH4 tightly bound to the enzyme, this differential sensitivity of basal and BH4-stimulated enzyme activities to SDS may be related to a putative differential protective effect of BH4 on the two subunits of the NOS III dimer.	Sodium Dodecyl Sulfate	181-184	nitric oxide synthase 3	Homo sapiens	279-286
9872368-7	1998	Considering that basal activity is due to the presence of endogenous BH4 tightly bound to the enzyme, this differential sensitivity of basal and BH4-stimulated enzyme activities to SDS may be related to a putative differential protective effect of BH4 on the two subunits of the NOS III dimer.	sapropterin	145-148	nitric oxide synthase 3	Homo sapiens	279-286
9872368-9	1998	This finding confirms the view that SDS may affect NOS III activity without necessarily deteriorating quaternary protein structure.	Sodium Dodecyl Sulfate	36-39	nitric oxide synthase 3	Homo sapiens	51-58
9872368-11	1998	A model describing the interaction between BH4 and NOS III, and its implications on the physiology and pathology of the human placenta, is discussed.	sapropterin	43-46	nitric oxide synthase 3	Homo sapiens	51-58
9837744-5	1998	Moreover, the astroglial NOS-III-like protein is constitutively tyrosine-phosphorylated and associated with caveolin-1.	Tyrosine	64-72	nitric oxide synthase 3	Homo sapiens	25-32
9881104-4	1998	Of this series of compounds, 2-amino-5-(imidazol-1-yl)pentanoic acid was identified as the most potent member against rat iNOS, rat nNOS and a human-derived cNOS.	2-amino-5-(imidazol-1-yl)pentanoic acid	29-68	nitric oxide synthase 3	Homo sapiens	157-161
9859864-6	1998	Compared to controls, the amount of eNOS transcripts was found to be elevated at low-oxygen tension, however, cNOS protein was downregulated after 24 h in the hypoxic environment, as shown by immunocytochemistry and Western blot analysis.	Oxygen	85-91	nitric oxide synthase 3	Homo sapiens	36-40
9859864-7	1998	Forskolin and methotrexate, which induce biochemical differentiation/ growth arrest in choriocarcinoma cells, stimulate eNOS mRNA and protein synthesis, but cannot overcome the decline of eNOS polypeptide levels during hypoxic incubation.	Colforsin	0-9	nitric oxide synthase 3	Homo sapiens	120-124
9859864-7	1998	Forskolin and methotrexate, which induce biochemical differentiation/ growth arrest in choriocarcinoma cells, stimulate eNOS mRNA and protein synthesis, but cannot overcome the decline of eNOS polypeptide levels during hypoxic incubation.	Methotrexate	14-26	nitric oxide synthase 3	Homo sapiens	120-124
9748253-6	1998	With the spin trap 5,5-dimethyl-1-pyrroline-N-oxide (DMPO), prominent signals of O-2 adduct, DMPO-OOH, were detected from eNOS in the absence of added tetrahydrobiopterin (BH4), and these were quenched by superoxide dismutase.	5,5-dimethyl-1-pyrroline-1-oxide	19-51	nitric oxide synthase 3	Homo sapiens	122-126
9769300-2	1998	Recently, constitutive nitric oxide synthase (cNOS) has been identified in human platelets, and platelet-derived nitric oxide has been shown to inhibit platelet recruitment after aggregation.	Nitric Oxide	23-35	nitric oxide synthase 3	Homo sapiens	46-50
9748253-6	1998	With the spin trap 5,5-dimethyl-1-pyrroline-N-oxide (DMPO), prominent signals of O-2 adduct, DMPO-OOH, were detected from eNOS in the absence of added tetrahydrobiopterin (BH4), and these were quenched by superoxide dismutase.	5,5-dimethyl-1-pyrroline-1-oxide	53-57	nitric oxide synthase 3	Homo sapiens	122-126
9748253-6	1998	With the spin trap 5,5-dimethyl-1-pyrroline-N-oxide (DMPO), prominent signals of O-2 adduct, DMPO-OOH, were detected from eNOS in the absence of added tetrahydrobiopterin (BH4), and these were quenched by superoxide dismutase.	5,5-dimethyl-1-pyrroline-1-oxide	93-97	nitric oxide synthase 3	Homo sapiens	122-126
9748253-6	1998	With the spin trap 5,5-dimethyl-1-pyrroline-N-oxide (DMPO), prominent signals of O-2 adduct, DMPO-OOH, were detected from eNOS in the absence of added tetrahydrobiopterin (BH4), and these were quenched by superoxide dismutase.	OOH	98-101	nitric oxide synthase 3	Homo sapiens	122-126
9748253-6	1998	With the spin trap 5,5-dimethyl-1-pyrroline-N-oxide (DMPO), prominent signals of O-2 adduct, DMPO-OOH, were detected from eNOS in the absence of added tetrahydrobiopterin (BH4), and these were quenched by superoxide dismutase.	sapropterin	172-175	nitric oxide synthase 3	Homo sapiens	122-126
9748253-10	1998	BH4 exerted dose-dependent inhibition of the O-2 signals generated by eNOS.	sapropterin	0-3	nitric oxide synthase 3	Homo sapiens	70-74
9748253-12	1998	Thus, eNOS can also catalyze O-2 formation, and this appears to occur primarily at the heme center of its oxygenase domain.	Heme	87-91	nitric oxide synthase 3	Homo sapiens	6-10
9748253-13	1998	O-2 synthesis from eNOS requires Ca2+/calmodulin and is primarily regulated by BH4 rather than L-arginine.	sapropterin	79-82	nitric oxide synthase 3	Homo sapiens	19-23
9748253-13	1998	O-2 synthesis from eNOS requires Ca2+/calmodulin and is primarily regulated by BH4 rather than L-arginine.	Arginine	95-105	nitric oxide synthase 3	Homo sapiens	19-23
9733492-1	1998	A series of substituted 2-iminopyrrolidines has been prepared and shown to be potent and selective inhibitors of the human inducible nitric oxide synthase (hiNOS) isoform versus the human endothelial nitric oxide synthase (heNOS) and the human neuronal nitric oxide synthase (hnNOS).	2-iminopyrrolidines	24-43	nitric oxide synthase 3	Homo sapiens	188-221
9811394-1	1998	Vascular endothelium releases nitric oxide (NO), an important vasodilator that is continuously synthesised by the constitutive enzyme, endothelial nitric oxide synthase (NOS).	Nitric Oxide	30-42	nitric oxide synthase 3	Homo sapiens	135-168
9735341-0	1998	Nitric oxide response to shear stress by human bone cell cultures is endothelial nitric oxide synthase dependent.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	69-102
9735341-8	1998	PFF also leads to an increase in ecNOS mRNA which is likely related to the shear stress responsive element in the promoter of ecNOS.	p-Fluorophenylalanine	0-3	nitric oxide synthase 3	Homo sapiens	33-38
9735341-8	1998	PFF also leads to an increase in ecNOS mRNA which is likely related to the shear stress responsive element in the promoter of ecNOS.	p-Fluorophenylalanine	0-3	nitric oxide synthase 3	Homo sapiens	126-131
9725818-1	1998	Nitric oxide (NO) produced by islet constitutive NO synthase (cNOS) is a putative modulator of islet hormone secretion.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	62-66
9725818-4	1998	Biochemical determination of islet cNOS activity revealed that the NO production with L-homoarginine as substrate was only approximately 40% of that of L-arginine.	Homoarginine	86-100	nitric oxide synthase 3	Homo sapiens	35-39
9740620-1	1998	Recently a point mutation of guanine to thymine at nucleotide position 1917 in the endothelial nitric oxide synthase (eNOS) gene has been reported to be associated with coronary artery spasm.	Guanine	29-36	nitric oxide synthase 3	Homo sapiens	83-116
9725818-6	1998	Moreover, inhibition of cNOS suppressed glucagon release, more so with L-arginine than with L-homoarginine as secretagogue, reflecting the relative rates of their NO production.	Glucagon	40-48	nitric oxide synthase 3	Homo sapiens	24-28
9725818-6	1998	Moreover, inhibition of cNOS suppressed glucagon release, more so with L-arginine than with L-homoarginine as secretagogue, reflecting the relative rates of their NO production.	Arginine	71-81	nitric oxide synthase 3	Homo sapiens	24-28
9725818-7	1998	In K+-depolarized islets, inhibition of cNOS enhanced the insulin response to L-arginine by 50% and that to L-homoarginine by 23%, largely corresponding to their relative NO production.	Arginine	78-88	nitric oxide synthase 3	Homo sapiens	40-44
9740620-1	1998	Recently a point mutation of guanine to thymine at nucleotide position 1917 in the endothelial nitric oxide synthase (eNOS) gene has been reported to be associated with coronary artery spasm.	Guanine	29-36	nitric oxide synthase 3	Homo sapiens	118-122
9740620-1	1998	Recently a point mutation of guanine to thymine at nucleotide position 1917 in the endothelial nitric oxide synthase (eNOS) gene has been reported to be associated with coronary artery spasm.	Thymine	40-47	nitric oxide synthase 3	Homo sapiens	83-116
9740620-1	1998	Recently a point mutation of guanine to thymine at nucleotide position 1917 in the endothelial nitric oxide synthase (eNOS) gene has been reported to be associated with coronary artery spasm.	Thymine	40-47	nitric oxide synthase 3	Homo sapiens	118-122
9689061-12	1998	Our data indicate that modulation of BH4 concentration may regulate the ratio of superoxide to nitric oxide generated by eNOS.	sapropterin	37-40	nitric oxide synthase 3	Homo sapiens	121-125
9712842-3	1998	cav-1 binding to a consensus site in the eNOS oxygenase domain is proposed to antagonize calmodulin (CaM) binding and thereby inhibit eNOS nitric oxide (NO) synthesis.	Nitric Oxide	139-151	nitric oxide synthase 3	Homo sapiens	41-45
9712842-3	1998	cav-1 binding to a consensus site in the eNOS oxygenase domain is proposed to antagonize calmodulin (CaM) binding and thereby inhibit eNOS nitric oxide (NO) synthesis.	Nitric Oxide	139-151	nitric oxide synthase 3	Homo sapiens	134-138
9712842-8	1998	Immunoblotting showed that full-length eNOS, eNOS oxygenase, and eNOS reductase all bound to an immobilized glutathione S-transferase-cav-1 fusion protein.	Glutathione	108-119	nitric oxide synthase 3	Homo sapiens	39-43
9712842-8	1998	Immunoblotting showed that full-length eNOS, eNOS oxygenase, and eNOS reductase all bound to an immobilized glutathione S-transferase-cav-1 fusion protein.	Glutathione	108-119	nitric oxide synthase 3	Homo sapiens	45-49
9712842-8	1998	Immunoblotting showed that full-length eNOS, eNOS oxygenase, and eNOS reductase all bound to an immobilized glutathione S-transferase-cav-1 fusion protein.	Glutathione	108-119	nitric oxide synthase 3	Homo sapiens	45-49
9712842-11	1998	We propose that cav-1 binding to eNOS reductase compromises its ability to bind CaM and to donate electrons to the eNOS heme, thereby inhibiting NO synthesis.	Heme	120-124	nitric oxide synthase 3	Homo sapiens	33-37
9712842-11	1998	We propose that cav-1 binding to eNOS reductase compromises its ability to bind CaM and to donate electrons to the eNOS heme, thereby inhibiting NO synthesis.	Heme	120-124	nitric oxide synthase 3	Homo sapiens	115-119
9689061-0	1998	Superoxide generation by endothelial nitric oxide synthase: the influence of cofactors.	Superoxides	0-10	nitric oxide synthase 3	Homo sapiens	25-58
9689061-1	1998	The mechanism of superoxide generation by endothelial nitric oxide synthase (eNOS) was investigated by the electron spin resonance spin-trapping technique using 5-diethoxyphosphoryl-5-methyl-1-pyrroline N-oxide.	Superoxides	17-27	nitric oxide synthase 3	Homo sapiens	42-75
9689061-1	1998	The mechanism of superoxide generation by endothelial nitric oxide synthase (eNOS) was investigated by the electron spin resonance spin-trapping technique using 5-diethoxyphosphoryl-5-methyl-1-pyrroline N-oxide.	Superoxides	17-27	nitric oxide synthase 3	Homo sapiens	77-81
10806726-2	1998	METHODS: Dot blot, using DIG-labeled human eNOS cDNA probe, had been used to examine the expression of eNOS gene in placental tissues of 9 normotensive pregnancy and 9 preeclampsia women.	digitoxose	25-28	nitric oxide synthase 3	Homo sapiens	43-47
10806726-2	1998	METHODS: Dot blot, using DIG-labeled human eNOS cDNA probe, had been used to examine the expression of eNOS gene in placental tissues of 9 normotensive pregnancy and 9 preeclampsia women.	digitoxose	25-28	nitric oxide synthase 3	Homo sapiens	103-107
9689061-12	1998	Our data indicate that modulation of BH4 concentration may regulate the ratio of superoxide to nitric oxide generated by eNOS.	Superoxides	81-91	nitric oxide synthase 3	Homo sapiens	121-125
9700089-1	1998	We recently reported that nitric oxide (NO) induces posttranscriptional modulation of lung endothelial cell NO synthase (ecNOS) that results in loss of activity.	Nitric Oxide	26-38	nitric oxide synthase 3	Homo sapiens	121-126
9689061-1	1998	The mechanism of superoxide generation by endothelial nitric oxide synthase (eNOS) was investigated by the electron spin resonance spin-trapping technique using 5-diethoxyphosphoryl-5-methyl-1-pyrroline N-oxide.	5-diethoxyphosphoryl-5-methyl-1-pyrroline N-oxide	161-210	nitric oxide synthase 3	Homo sapiens	42-75
9689061-1	1998	The mechanism of superoxide generation by endothelial nitric oxide synthase (eNOS) was investigated by the electron spin resonance spin-trapping technique using 5-diethoxyphosphoryl-5-methyl-1-pyrroline N-oxide.	5-diethoxyphosphoryl-5-methyl-1-pyrroline N-oxide	161-210	nitric oxide synthase 3	Homo sapiens	77-81
9689061-2	1998	In the absence of calcium/calmodulin, eNOS produces low amounts of superoxide.	Superoxides	67-77	nitric oxide synthase 3	Homo sapiens	38-42
9689061-3	1998	Upon activating eNOS electron transfer reactions by calcium/calmodulin binding, superoxide formation is increased.	Superoxides	80-90	nitric oxide synthase 3	Homo sapiens	16-20
9689061-5	1998	No inhibition is observed after addition of L-arginine, NG-hydroxy-L-arginine, L-thiocitrulline, and L-NG-monomethyl arginine to activated eNOS.	omega-N-Methylarginine	101-125	nitric oxide synthase 3	Homo sapiens	139-143
9689061-7	1998	However, the concomitant addition of L-arginine and tetrahydrobiopterin (BH4) abolishes superoxide generation by eNOS.	Arginine	37-47	nitric oxide synthase 3	Homo sapiens	113-117
9689061-7	1998	However, the concomitant addition of L-arginine and tetrahydrobiopterin (BH4) abolishes superoxide generation by eNOS.	sapropterin	52-71	nitric oxide synthase 3	Homo sapiens	113-117
9689061-7	1998	However, the concomitant addition of L-arginine and tetrahydrobiopterin (BH4) abolishes superoxide generation by eNOS.	sapropterin	73-76	nitric oxide synthase 3	Homo sapiens	113-117
9689061-7	1998	However, the concomitant addition of L-arginine and tetrahydrobiopterin (BH4) abolishes superoxide generation by eNOS.	Superoxides	88-98	nitric oxide synthase 3	Homo sapiens	113-117
9689061-12	1998	Our data indicate that modulation of BH4 concentration may regulate the ratio of superoxide to nitric oxide generated by eNOS.	Nitric Oxide	95-107	nitric oxide synthase 3	Homo sapiens	121-125
9707923-5	1998	At least, three kinds of enzymes NOS have been described: two of them are calcium-dependent and continuously present in select cells (constitutive NOS, cNOS).	Calcium	74-81	nitric oxide synthase 3	Homo sapiens	152-156
9727648-1	1998	This study reviews the putative mechanism of ethanol (ETOH)-mediated downregulation of inducible nitric oxide synthase (iNOS) messenger RNA (mRNA) and protein and upregulation of constitutive NOS activity (ecNOS) in immunocompetent cells and endothelium, in vivo.	Ethanol	45-52	nitric oxide synthase 3	Homo sapiens	206-211
9727648-1	1998	This study reviews the putative mechanism of ethanol (ETOH)-mediated downregulation of inducible nitric oxide synthase (iNOS) messenger RNA (mRNA) and protein and upregulation of constitutive NOS activity (ecNOS) in immunocompetent cells and endothelium, in vivo.	Ethanol	54-58	nitric oxide synthase 3	Homo sapiens	206-211
9727648-5	1998	ETOH-mediated inhibition of tyrosine kinase activity may also explain the ability of ETOH to upregulate ecNOS enzymatic activity, because tyrosine kinase activity suppresses ecNOS enzymatic activity.	Ethanol	0-4	nitric oxide synthase 3	Homo sapiens	104-109
9727648-5	1998	ETOH-mediated inhibition of tyrosine kinase activity may also explain the ability of ETOH to upregulate ecNOS enzymatic activity, because tyrosine kinase activity suppresses ecNOS enzymatic activity.	Ethanol	0-4	nitric oxide synthase 3	Homo sapiens	174-179
9727648-5	1998	ETOH-mediated inhibition of tyrosine kinase activity may also explain the ability of ETOH to upregulate ecNOS enzymatic activity, because tyrosine kinase activity suppresses ecNOS enzymatic activity.	Ethanol	85-89	nitric oxide synthase 3	Homo sapiens	104-109
9727648-5	1998	ETOH-mediated inhibition of tyrosine kinase activity may also explain the ability of ETOH to upregulate ecNOS enzymatic activity, because tyrosine kinase activity suppresses ecNOS enzymatic activity.	Ethanol	85-89	nitric oxide synthase 3	Homo sapiens	174-179
9680177-0	1998	The activation of eNOS by copper ion (Cu2+) in human pulmonary arterial endothelial cells (HPAEC).	Copper	26-32	nitric oxide synthase 3	Homo sapiens	18-22
9680177-0	1998	The activation of eNOS by copper ion (Cu2+) in human pulmonary arterial endothelial cells (HPAEC).	cupric ion	38-42	nitric oxide synthase 3	Homo sapiens	18-22
9680177-7	1998	All the divalent cations tested suppressed the NOS activity in crude cell extract by about 50% at 1 x 10(-4) M, but only Cu2+ from 10(-6) M increased eNOS activation dose dependently with a significant elevation in whole-cell assay.	cupric ion	121-125	nitric oxide synthase 3	Homo sapiens	150-154
9680177-8	1998	Extracellular Ca2+ was prerequisite to the eNOS activation by Cu2+ in intact cells.	cupric ion	62-66	nitric oxide synthase 3	Homo sapiens	43-47
9680177-13	1998	These results indicated that Cu2+, but not Mn2+, Zn2+, and Fe2+, causes the activation of eNOS, while Cu2+, Mn2+, Zn2+, and Fe2+ directly suppressed eNOS activity extracted from HPAEC.	cupric ion	29-33	nitric oxide synthase 3	Homo sapiens	90-94
9680177-13	1998	These results indicated that Cu2+, but not Mn2+, Zn2+, and Fe2+, causes the activation of eNOS, while Cu2+, Mn2+, Zn2+, and Fe2+ directly suppressed eNOS activity extracted from HPAEC.	cupric ion	29-33	nitric oxide synthase 3	Homo sapiens	149-153
9680177-13	1998	These results indicated that Cu2+, but not Mn2+, Zn2+, and Fe2+, causes the activation of eNOS, while Cu2+, Mn2+, Zn2+, and Fe2+ directly suppressed eNOS activity extracted from HPAEC.	Zinc	49-53	nitric oxide synthase 3	Homo sapiens	90-94
9680177-13	1998	These results indicated that Cu2+, but not Mn2+, Zn2+, and Fe2+, causes the activation of eNOS, while Cu2+, Mn2+, Zn2+, and Fe2+ directly suppressed eNOS activity extracted from HPAEC.	cupric ion	102-106	nitric oxide synthase 3	Homo sapiens	149-153
9680177-13	1998	These results indicated that Cu2+, but not Mn2+, Zn2+, and Fe2+, causes the activation of eNOS, while Cu2+, Mn2+, Zn2+, and Fe2+ directly suppressed eNOS activity extracted from HPAEC.	Manganese(2+)	108-112	nitric oxide synthase 3	Homo sapiens	90-94
9680177-13	1998	These results indicated that Cu2+, but not Mn2+, Zn2+, and Fe2+, causes the activation of eNOS, while Cu2+, Mn2+, Zn2+, and Fe2+ directly suppressed eNOS activity extracted from HPAEC.	Manganese(2+)	108-112	nitric oxide synthase 3	Homo sapiens	149-153
9680177-13	1998	These results indicated that Cu2+, but not Mn2+, Zn2+, and Fe2+, causes the activation of eNOS, while Cu2+, Mn2+, Zn2+, and Fe2+ directly suppressed eNOS activity extracted from HPAEC.	Zinc	114-118	nitric oxide synthase 3	Homo sapiens	90-94
9680177-13	1998	These results indicated that Cu2+, but not Mn2+, Zn2+, and Fe2+, causes the activation of eNOS, while Cu2+, Mn2+, Zn2+, and Fe2+ directly suppressed eNOS activity extracted from HPAEC.	Zinc	114-118	nitric oxide synthase 3	Homo sapiens	149-153
9680177-13	1998	These results indicated that Cu2+, but not Mn2+, Zn2+, and Fe2+, causes the activation of eNOS, while Cu2+, Mn2+, Zn2+, and Fe2+ directly suppressed eNOS activity extracted from HPAEC.	ammonium ferrous sulfate	124-128	nitric oxide synthase 3	Homo sapiens	90-94
9680177-13	1998	These results indicated that Cu2+, but not Mn2+, Zn2+, and Fe2+, causes the activation of eNOS, while Cu2+, Mn2+, Zn2+, and Fe2+ directly suppressed eNOS activity extracted from HPAEC.	ammonium ferrous sulfate	124-128	nitric oxide synthase 3	Homo sapiens	149-153
9680177-14	1998	Further, our study showed that extracellular Ca2+ was essential for eNOS activation by Cu2+.	cupric ion	87-91	nitric oxide synthase 3	Homo sapiens	68-72
9723371-0	1998	ecNOS overexpression in CsA-treated renal transplant patients: implications for CsA-induced hypertension.	Cyclosporine	24-27	nitric oxide synthase 3	Homo sapiens	0-5
9712288-1	1998	Endothelium-derived nitric oxide formed by endothelial constitutive nitric oxide synthase (ecNOS) mediates endothelium-dependent vasodilation and antithrombotic action.	Nitric Oxide	20-32	nitric oxide synthase 3	Homo sapiens	43-89
9712288-1	1998	Endothelium-derived nitric oxide formed by endothelial constitutive nitric oxide synthase (ecNOS) mediates endothelium-dependent vasodilation and antithrombotic action.	Nitric Oxide	20-32	nitric oxide synthase 3	Homo sapiens	91-96
9669257-3	1998	We hypothesized that the nature of endothelial injury associated with individual cardiovascular risk factors might be different and that this might affect the response to L-arginine, the substrate for endothelial nitric oxide synthase.	Arginine	171-181	nitric oxide synthase 3	Homo sapiens	201-234
9614091-0	1998	Transcriptional regulation of endothelial nitric-oxide synthase by lysophosphatidylcholine.	Lysophosphatidylcholines	67-90	nitric oxide synthase 3	Homo sapiens	30-63
9614091-1	1998	We have shown that lysophosphatidylcholine (lyso-PC) increases endothelial nitric-oxide synthase (eNOS) expression at the transcriptional level (Zembowicz, A., Tang, J.-L., and Wu, K. K. (1995) J. Biol.	Lysophosphatidylcholines	19-42	nitric oxide synthase 3	Homo sapiens	63-96
9614091-1	1998	We have shown that lysophosphatidylcholine (lyso-PC) increases endothelial nitric-oxide synthase (eNOS) expression at the transcriptional level (Zembowicz, A., Tang, J.-L., and Wu, K. K. (1995) J. Biol.	Lysophosphatidylcholines	19-42	nitric oxide synthase 3	Homo sapiens	98-102
9614091-1	1998	We have shown that lysophosphatidylcholine (lyso-PC) increases endothelial nitric-oxide synthase (eNOS) expression at the transcriptional level (Zembowicz, A., Tang, J.-L., and Wu, K. K. (1995) J. Biol.	Lysophosphatidylcholines	44-51	nitric oxide synthase 3	Homo sapiens	63-96
9614091-1	1998	We have shown that lysophosphatidylcholine (lyso-PC) increases endothelial nitric-oxide synthase (eNOS) expression at the transcriptional level (Zembowicz, A., Tang, J.-L., and Wu, K. K. (1995) J. Biol.	Lysophosphatidylcholines	44-51	nitric oxide synthase 3	Homo sapiens	98-102
9641464-6	1998	Activation of human ECs, obtained from the saphenous vein, with morphine- or anandamide-stimulated NO release (35 nM and 28 nM, respectively) that peaked within 5 min and returned to basal levels within 10 min of agonist stimulation, consistent with constitutive NO synthase (cNOS) activation.	Morphine	64-72	nitric oxide synthase 3	Homo sapiens	276-280
9641464-6	1998	Activation of human ECs, obtained from the saphenous vein, with morphine- or anandamide-stimulated NO release (35 nM and 28 nM, respectively) that peaked within 5 min and returned to basal levels within 10 min of agonist stimulation, consistent with constitutive NO synthase (cNOS) activation.	anandamide	77-87	nitric oxide synthase 3	Homo sapiens	276-280
9725363-6	1998	Calcium-dependent nitric oxide synthase activity was increased in ecNOS- compared with betaGal-transduced lungs (2,139+/-756 versus 47+/-28 pmol x mg protein(-1) x h(-1); p &lt; 0.05).	Calcium	0-7	nitric oxide synthase 3	Homo sapiens	66-71
9580552-2	1998	Here we show that Hsp90 associates with endothelial nitric oxide synthase (eNOS) and is rapidly recruited to the eNOS complex by agonists that stimulate production of nitric oxide, namely vascular endothelial growth factor, histamine and fluid shear stress.	Nitric Oxide	52-64	nitric oxide synthase 3	Homo sapiens	75-79
9771440-2	1998	METHODS: The immunoperoxidase technique with an antibody directed against eNOS was applied to paraffin sections from first and second trimester placentas, placenta accreta, partial and complete hydatidiform moles, and choriocarcinoma.	Paraffin	94-102	nitric oxide synthase 3	Homo sapiens	74-78
9612300-6	1998	When the xanthine oxidase inhibitor allopurinol or the superoxide scavenger 4,5-dihydroxy-1-benzene-disulfonic acid were co-incubated with SNP, the inhibitory effects on eNOS activity could be partially alleviated.	4,5-dihydroxy-1-benzene-disulfonic acid	76-115	nitric oxide synthase 3	Homo sapiens	170-174
9612300-9	1998	A reaction between NO and superoxide would produce peroxynitrite, which could then react with the eNOS protein, resulting in enzyme inactivation.	Superoxides	26-36	nitric oxide synthase 3	Homo sapiens	98-102
9612300-9	1998	A reaction between NO and superoxide would produce peroxynitrite, which could then react with the eNOS protein, resulting in enzyme inactivation.	Peroxynitrous Acid	51-64	nitric oxide synthase 3	Homo sapiens	98-102
9580552-2	1998	Here we show that Hsp90 associates with endothelial nitric oxide synthase (eNOS) and is rapidly recruited to the eNOS complex by agonists that stimulate production of nitric oxide, namely vascular endothelial growth factor, histamine and fluid shear stress.	Nitric Oxide	52-64	nitric oxide synthase 3	Homo sapiens	113-117
9580552-2	1998	Here we show that Hsp90 associates with endothelial nitric oxide synthase (eNOS) and is rapidly recruited to the eNOS complex by agonists that stimulate production of nitric oxide, namely vascular endothelial growth factor, histamine and fluid shear stress.	Histamine	224-233	nitric oxide synthase 3	Homo sapiens	40-73
9580552-2	1998	Here we show that Hsp90 associates with endothelial nitric oxide synthase (eNOS) and is rapidly recruited to the eNOS complex by agonists that stimulate production of nitric oxide, namely vascular endothelial growth factor, histamine and fluid shear stress.	Histamine	224-233	nitric oxide synthase 3	Homo sapiens	75-79
9580552-2	1998	Here we show that Hsp90 associates with endothelial nitric oxide synthase (eNOS) and is rapidly recruited to the eNOS complex by agonists that stimulate production of nitric oxide, namely vascular endothelial growth factor, histamine and fluid shear stress.	Histamine	224-233	nitric oxide synthase 3	Homo sapiens	113-117
9562252-7	1998	In addition, constitutive NO synthase (cNOS) protein expression of endothelial cells was dose-dependently enhanced by treatment with erythromycin, which might also contribute to the enhancement of NO release from endothelial cells by erythromycin.	Erythromycin	133-145	nitric oxide synthase 3	Homo sapiens	39-43
9594510-1	1998	The continuous release of nitric oxide (NO) from the constitutive, endothelial isoform of nitric oxide synthase (e-NOS) serves mainly to keep the vasculature in a continuous state of active vasodilation.	Nitric Oxide	26-38	nitric oxide synthase 3	Homo sapiens	113-118
9562252-7	1998	In addition, constitutive NO synthase (cNOS) protein expression of endothelial cells was dose-dependently enhanced by treatment with erythromycin, which might also contribute to the enhancement of NO release from endothelial cells by erythromycin.	Erythromycin	234-246	nitric oxide synthase 3	Homo sapiens	39-43
9558353-0	1998	Effects of various imidazole ligands on heme conformation in endothelial nitric oxide synthase.	imidazole	19-28	nitric oxide synthase 3	Homo sapiens	61-94
9558353-0	1998	Effects of various imidazole ligands on heme conformation in endothelial nitric oxide synthase.	Heme	40-44	nitric oxide synthase 3	Homo sapiens	61-94
9558353-1	1998	We have evaluated the influence of a series of substituted imidazoles on the heme structure of endothelial nitric oxide synthase (eNOS).	Imidazoles	59-69	nitric oxide synthase 3	Homo sapiens	95-128
9558353-1	1998	We have evaluated the influence of a series of substituted imidazoles on the heme structure of endothelial nitric oxide synthase (eNOS).	Imidazoles	59-69	nitric oxide synthase 3	Homo sapiens	130-134
9558353-1	1998	We have evaluated the influence of a series of substituted imidazoles on the heme structure of endothelial nitric oxide synthase (eNOS).	Heme	77-81	nitric oxide synthase 3	Homo sapiens	95-128
9558353-1	1998	We have evaluated the influence of a series of substituted imidazoles on the heme structure of endothelial nitric oxide synthase (eNOS).	Heme	77-81	nitric oxide synthase 3	Homo sapiens	130-134
9558353-8	1998	MCD spectra also imply that an O-ligand is present in the low-spin resting eNOS, while EPR data reveal the presence of two low-spin heme complexes in resting eNOS and its imidazole complexes.	Heme	132-136	nitric oxide synthase 3	Homo sapiens	158-162
9558353-8	1998	MCD spectra also imply that an O-ligand is present in the low-spin resting eNOS, while EPR data reveal the presence of two low-spin heme complexes in resting eNOS and its imidazole complexes.	imidazole	171-180	nitric oxide synthase 3	Homo sapiens	158-162
9558353-9	1998	EPR also distinguishes four different high-spin forms of eNOS generated by different imidazole analogues.	imidazole	85-94	nitric oxide synthase 3	Homo sapiens	57-61
9547352-2	1998	In the HUVEC-derived cell line EA.hy 926, PMA and phorbol-12,13-dibutyrate stimulated endothelial nitric oxide synthase (NOS III) mRNA expression in a concentration- and time-dependent manner.	Phorbol 12,13-Dibutyrate	50-74	nitric oxide synthase 3	Homo sapiens	86-119
9547352-2	1998	In the HUVEC-derived cell line EA.hy 926, PMA and phorbol-12,13-dibutyrate stimulated endothelial nitric oxide synthase (NOS III) mRNA expression in a concentration- and time-dependent manner.	Phorbol 12,13-Dibutyrate	50-74	nitric oxide synthase 3	Homo sapiens	121-128
9547352-9	1998	The time course of activation and down-regulation of these two PKC isoforms correlated well with the PMA-stimulated increase in NOS III expression.	Tetradecanoylphorbol Acetate	101-104	nitric oxide synthase 3	Homo sapiens	128-135
9547352-12	1998	These data indicate that stimulation of PKC alpha, PKC epsilon, or both by active phorbol esters represents an efficacious pathway activating the human NOS III promoter in human endothelium.	Phorbol Esters	82-96	nitric oxide synthase 3	Homo sapiens	152-159
9562252-8	1998	The effect of erythromycin as an anti-inflammatory agent might be partially mediated through the enhancement of NO release from endothelial cells and the drug might be a useful tool for the investigation of cNOS of endothelial cells.	Erythromycin	14-26	nitric oxide synthase 3	Homo sapiens	207-211
9537338-5	1998	Both simvastatin (1 micromol/L) and lovastatin (10 micromol/L) upregulated ecNOS expression by 3.8-fold and 3.6-fold, respectively, and completely prevented its downregulation by ox-LDL.	Simvastatin	5-16	nitric oxide synthase 3	Homo sapiens	75-80
9537338-5	1998	Both simvastatin (1 micromol/L) and lovastatin (10 micromol/L) upregulated ecNOS expression by 3.8-fold and 3.6-fold, respectively, and completely prevented its downregulation by ox-LDL.	Lovastatin	36-46	nitric oxide synthase 3	Homo sapiens	75-80
9537338-6	1998	These effects of simvastatin on ecNOS expression correlated with changes in ecNOS activity.	Simvastatin	17-28	nitric oxide synthase 3	Homo sapiens	32-37
9537338-6	1998	These effects of simvastatin on ecNOS expression correlated with changes in ecNOS activity.	Simvastatin	17-28	nitric oxide synthase 3	Homo sapiens	76-81
9537338-7	1998	Although L-mevalonate alone did not affect ecNOS expression, cotreatment with L-mevalonate completely reversed ecNOS upregulation by simvastatin.	l-mevalonate	78-90	nitric oxide synthase 3	Homo sapiens	111-116
9537338-7	1998	Although L-mevalonate alone did not affect ecNOS expression, cotreatment with L-mevalonate completely reversed ecNOS upregulation by simvastatin.	Simvastatin	133-144	nitric oxide synthase 3	Homo sapiens	111-116
9537338-8	1998	Actinomycin D studies revealed that simvastatin stabilized ecNOS mRNA (tau1/2, 43 versus 35 hours).	Simvastatin	36-47	nitric oxide synthase 3	Homo sapiens	59-64
9518867-1	1998	UNLABELLED: Platelet cyclic guanosine monophosphate (cGMP) is produced by soluble guanylate cyclase (sGC), the activity of which is modulated by the activity of nitric oxide (NO) constitutive synthase (cNOS) which, in turn, is activated by a calcium/calmodulin complex.	Cyclic GMP	21-51	nitric oxide synthase 3	Homo sapiens	202-206
9452418-1	1998	Nitric oxide production in the vascular endothelium is promoted by diverse agonists that transiently increase intracellular Ca2+ concentration and activate the endothelial nitric-oxide synthase (eNOS), a Ca2+/calmodulin-dependent enzyme.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	160-193
9461225-4	1998	Incubation of EA.hy 926 cells with 17beta-estradiol or the more stable 17alpha-ethinyl estradiol enhanced NOS III mRNA and protein expression up to 1.8-fold, without changing the stability of the NOS III mRNA.	Estradiol	35-51	nitric oxide synthase 3	Homo sapiens	106-113
9461225-4	1998	Incubation of EA.hy 926 cells with 17beta-estradiol or the more stable 17alpha-ethinyl estradiol enhanced NOS III mRNA and protein expression up to 1.8-fold, without changing the stability of the NOS III mRNA.	Estradiol	35-51	nitric oxide synthase 3	Homo sapiens	196-203
9461225-4	1998	Incubation of EA.hy 926 cells with 17beta-estradiol or the more stable 17alpha-ethinyl estradiol enhanced NOS III mRNA and protein expression up to 1.8-fold, without changing the stability of the NOS III mRNA.	Ethinyl Estradiol	71-96	nitric oxide synthase 3	Homo sapiens	106-113
9461225-4	1998	Incubation of EA.hy 926 cells with 17beta-estradiol or the more stable 17alpha-ethinyl estradiol enhanced NOS III mRNA and protein expression up to 1.8-fold, without changing the stability of the NOS III mRNA.	Ethinyl Estradiol	71-96	nitric oxide synthase 3	Homo sapiens	196-203
9461225-7	1998	In transient transfection experiments using a 1.6 kb human NOS III promoter fragment (which contains no bona fide estrogen-responsive element, ERE), basal promoter activity was enhanced 1.7-fold by 17alpha-ethinyl estradiol.	Ethinyl Estradiol	198-223	nitric oxide synthase 3	Homo sapiens	59-66
9449657-5	1998	Further studies using RT/PCR indicated that only the endothelial nitric oxide synthase (ecNOS) isoform was expressed and RNase protection assays showed that 17beta-Estradiol treatment resulted in a 2.2 fold increase in ecNOS mRNA levels.	Estradiol	157-173	nitric oxide synthase 3	Homo sapiens	53-86
9449657-5	1998	Further studies using RT/PCR indicated that only the endothelial nitric oxide synthase (ecNOS) isoform was expressed and RNase protection assays showed that 17beta-Estradiol treatment resulted in a 2.2 fold increase in ecNOS mRNA levels.	Estradiol	157-173	nitric oxide synthase 3	Homo sapiens	88-93
9449657-5	1998	Further studies using RT/PCR indicated that only the endothelial nitric oxide synthase (ecNOS) isoform was expressed and RNase protection assays showed that 17beta-Estradiol treatment resulted in a 2.2 fold increase in ecNOS mRNA levels.	Estradiol	157-173	nitric oxide synthase 3	Homo sapiens	219-224
9518867-9	1998	As IBMXcGMP expresses basal cGMP and IONOcGMP expresses the cGMP after cNOS stimulation, it can be speculated that the increase in NO production could be a mechanism to downregulate the vasoconstriction which may be caused by the high calcium levels in smooth muscle cells.	ionocgmp	37-45	nitric oxide synthase 3	Homo sapiens	71-75
9518867-1	1998	UNLABELLED: Platelet cyclic guanosine monophosphate (cGMP) is produced by soluble guanylate cyclase (sGC), the activity of which is modulated by the activity of nitric oxide (NO) constitutive synthase (cNOS) which, in turn, is activated by a calcium/calmodulin complex.	Cyclic GMP	53-57	nitric oxide synthase 3	Homo sapiens	202-206
9518867-1	1998	UNLABELLED: Platelet cyclic guanosine monophosphate (cGMP) is produced by soluble guanylate cyclase (sGC), the activity of which is modulated by the activity of nitric oxide (NO) constitutive synthase (cNOS) which, in turn, is activated by a calcium/calmodulin complex.	Nitric Oxide	161-173	nitric oxide synthase 3	Homo sapiens	202-206
9481550-9	1998	In contrast, the increased concentrations of NO metabolites in amniotic fluid and the positive immunostaining of endothelial nitric oxide synthase in the placental villi suggest that the placental L-arginine-NO system is up-regulated in preeclampsia.	Arginine	197-207	nitric oxide synthase 3	Homo sapiens	113-146
9395443-0	1997	A caveolar complex between the cationic amino acid transporter 1 and endothelial nitric-oxide synthase may explain the "arginine paradox".	Arginine	120-128	nitric oxide synthase 3	Homo sapiens	69-102
9428309-0	1998	Cerebral ischemia/reperfusion increases endothelial nitric oxide synthase levels by an indomethacin-sensitive mechanism.	Indomethacin	87-99	nitric oxide synthase 3	Homo sapiens	40-73
9428309-10	1998	Pretreatment with the cyclooxygenase inhibitor indomethacin (5 mg/kg intravenously) abolished the ischemia-induced eNOS increase in parietal cortex and hippocampus (n = 7).	Indomethacin	47-59	nitric oxide synthase 3	Homo sapiens	115-119
9428309-11	1998	Thus, we conclude that the eNOS response is rapid, specific to vessels, and involves an indomethacin-sensitive mechanism.	Indomethacin	88-100	nitric oxide synthase 3	Homo sapiens	27-31
9883742-0	1998	Oxygen radical stress in vascular disease: the role of endothelial nitric oxide synthase.	Reactive Oxygen Species	0-14	nitric oxide synthase 3	Homo sapiens	55-88
9395516-5	1997	In a concentration-dependent manner, simvastatin, and to a lesser extent, lovastatin, prevented the down-regulation of ecNOS expression by hypoxia.	Simvastatin	37-48	nitric oxide synthase 3	Homo sapiens	119-124
9395443-2	1997	When incubated with solubilized PAEC plasma membrane proteins, eNOS-specific antibody immunoprecipitates CAT1-mediated arginine transport.	Arginine	119-127	nitric oxide synthase 3	Homo sapiens	63-67
9395516-5	1997	In a concentration-dependent manner, simvastatin, and to a lesser extent, lovastatin, prevented the down-regulation of ecNOS expression by hypoxia.	Lovastatin	74-84	nitric oxide synthase 3	Homo sapiens	119-124
9395516-6	1997	Simvastatin-induced changes in ecNOS expression correlated with changes in endothelial NO production and were reversed by treatment with L-mevalonate.	Simvastatin	0-11	nitric oxide synthase 3	Homo sapiens	31-36
9395516-6	1997	Simvastatin-induced changes in ecNOS expression correlated with changes in endothelial NO production and were reversed by treatment with L-mevalonate.	l-mevalonate	137-149	nitric oxide synthase 3	Homo sapiens	31-36
9395516-7	1997	Actinomycin D studies revealed that under hypoxic conditions, simvastatin increased ecNOS mRNA half-life from 13 to 38 h. Nuclear run-on studies showed that simvastatin had no effect on repression of ecNOS gene transcription by hypoxia.	Simvastatin	62-73	nitric oxide synthase 3	Homo sapiens	84-89
9395443-3	1997	These results document the existence of a caveolar complex between CAT1 and eNOS in PAEC that provides a mechanism for the directed delivery of substrate arginine to eNOS.	Arginine	154-162	nitric oxide synthase 3	Homo sapiens	76-80
9395443-3	1997	These results document the existence of a caveolar complex between CAT1 and eNOS in PAEC that provides a mechanism for the directed delivery of substrate arginine to eNOS.	Arginine	154-162	nitric oxide synthase 3	Homo sapiens	166-170
9395443-4	1997	Direct transfer of extracellular arginine to membrane-bound eNOS accounts for the "arginine paradox" and explains why caveolar localization of eNOS is required for optimal nitric oxide production by endothelial cells.	Arginine	33-41	nitric oxide synthase 3	Homo sapiens	60-64
9395443-4	1997	Direct transfer of extracellular arginine to membrane-bound eNOS accounts for the "arginine paradox" and explains why caveolar localization of eNOS is required for optimal nitric oxide production by endothelial cells.	Arginine	33-41	nitric oxide synthase 3	Homo sapiens	143-147
9395443-4	1997	Direct transfer of extracellular arginine to membrane-bound eNOS accounts for the "arginine paradox" and explains why caveolar localization of eNOS is required for optimal nitric oxide production by endothelial cells.	Arginine	83-91	nitric oxide synthase 3	Homo sapiens	60-64
9395443-4	1997	Direct transfer of extracellular arginine to membrane-bound eNOS accounts for the "arginine paradox" and explains why caveolar localization of eNOS is required for optimal nitric oxide production by endothelial cells.	Nitric Oxide	172-184	nitric oxide synthase 3	Homo sapiens	60-64
9395443-4	1997	Direct transfer of extracellular arginine to membrane-bound eNOS accounts for the "arginine paradox" and explains why caveolar localization of eNOS is required for optimal nitric oxide production by endothelial cells.	Nitric Oxide	172-184	nitric oxide synthase 3	Homo sapiens	143-147
9288162-2	1997	All of the dipeptides and dipeptide esters are competitive inhibitors of nNOS, macrophage nitric oxide synthase (iNOS), and endothelial nitric oxide synthase (eNOS), except for the ones that contain D-ArgNO2 (8-10, 12, 13), which are uncompetitive inhibitors of iNOS but competitive inhibitors of nNOS and eNOS.	Dipeptides	11-21	nitric oxide synthase 3	Homo sapiens	124-157
9409304-6	1997	The results of the variance component linkage analysis were consistent with linkage of a quantitative trait locus in or near the ecNOS gene to variation in plasma NOx levels (P = .0066).	nicotine 1-N-oxide	163-166	nitric oxide synthase 3	Homo sapiens	129-134
9409304-7	1997	While many environmental factors have been shown to alter transiently plasma NOx levels, our study is the first to identify a substantial effect of the ecNOS locus on the variance of plasma NOx, i.e. basal NO production.	nicotine 1-N-oxide	77-80	nitric oxide synthase 3	Homo sapiens	152-157
9409304-7	1997	While many environmental factors have been shown to alter transiently plasma NOx levels, our study is the first to identify a substantial effect of the ecNOS locus on the variance of plasma NOx, i.e. basal NO production.	nicotine 1-N-oxide	190-193	nitric oxide synthase 3	Homo sapiens	152-157
9409208-5	1997	cGMP production by AdeNOS-transduced cells was augmented by increasing intracellular levels of the eNOS cofactor tetrahydrobiopterin.	Cyclic GMP	0-4	nitric oxide synthase 3	Homo sapiens	21-25
9409208-5	1997	cGMP production by AdeNOS-transduced cells was augmented by increasing intracellular levels of the eNOS cofactor tetrahydrobiopterin.	sapropterin	113-132	nitric oxide synthase 3	Homo sapiens	21-25
9409208-8	1997	The present study demonstrates that adenovirus-mediated gene transfer of eNOS to CSMCs results in the expression of a functional enzyme whose activity can be augmented by increasing intracellular levels of tetrahydrobiopterin.	sapropterin	206-225	nitric oxide synthase 3	Homo sapiens	73-77
9370127-4	1997	In spontaneous hypertension, the production of nitric oxide, which in endothelial cells is formed from L-arginine via the constitutively expressed enzyme endothelial nitric oxide synthase, represents the main mediator of endothelium-dependent vasodilation and seems to be enhanced.	Nitric Oxide	47-59	nitric oxide synthase 3	Homo sapiens	154-187
9370127-4	1997	In spontaneous hypertension, the production of nitric oxide, which in endothelial cells is formed from L-arginine via the constitutively expressed enzyme endothelial nitric oxide synthase, represents the main mediator of endothelium-dependent vasodilation and seems to be enhanced.	Arginine	103-113	nitric oxide synthase 3	Homo sapiens	154-187
9305973-1	1997	The binding of arginine analogs to endothelial nitric oxide synthase (eNOS, NOSIII) perturbs the environment of the high-spin ferriheme in a highly ligand-specific manner.	Arginine	15-23	nitric oxide synthase 3	Homo sapiens	35-68
9305973-1	1997	The binding of arginine analogs to endothelial nitric oxide synthase (eNOS, NOSIII) perturbs the environment of the high-spin ferriheme in a highly ligand-specific manner.	Arginine	15-23	nitric oxide synthase 3	Homo sapiens	76-82
9305973-1	1997	The binding of arginine analogs to endothelial nitric oxide synthase (eNOS, NOSIII) perturbs the environment of the high-spin ferriheme in a highly ligand-specific manner.	Hemin	126-135	nitric oxide synthase 3	Homo sapiens	35-68
9305973-1	1997	The binding of arginine analogs to endothelial nitric oxide synthase (eNOS, NOSIII) perturbs the environment of the high-spin ferriheme in a highly ligand-specific manner.	Hemin	126-135	nitric oxide synthase 3	Homo sapiens	76-82
9305973-7	1997	Endothelial nitric oxide synthase readily forms such lower rhombicity complexes, which correlates with the tight binding of NNA to this isoform.	Nitroarginine	124-127	nitric oxide synthase 3	Homo sapiens	0-33
9333325-0	1997	Endothelial nitric oxide synthase-dependent superoxide generation from adriamycin.	Superoxides	44-54	nitric oxide synthase 3	Homo sapiens	0-33
9333325-0	1997	Endothelial nitric oxide synthase-dependent superoxide generation from adriamycin.	Doxorubicin	71-81	nitric oxide synthase 3	Homo sapiens	0-33
9333325-5	1997	We demonstrate here that the endothelial isoform of nitric oxide synthase (eNOS) reduces adriamycin to the semiquinone radical.	Doxorubicin	89-99	nitric oxide synthase 3	Homo sapiens	75-79
9333325-5	1997	We demonstrate here that the endothelial isoform of nitric oxide synthase (eNOS) reduces adriamycin to the semiquinone radical.	semiquinone radicals	107-126	nitric oxide synthase 3	Homo sapiens	75-79
9333325-7	1997	Adriamycin binds to eNOS with a Km of approximately 5 microM, as calculated from both eNOS-dependent NADPH consumption and superoxide generation.	Doxorubicin	0-10	nitric oxide synthase 3	Homo sapiens	20-24
9333325-7	1997	Adriamycin binds to eNOS with a Km of approximately 5 microM, as calculated from both eNOS-dependent NADPH consumption and superoxide generation.	Doxorubicin	0-10	nitric oxide synthase 3	Homo sapiens	86-90
9333325-7	1997	Adriamycin binds to eNOS with a Km of approximately 5 microM, as calculated from both eNOS-dependent NADPH consumption and superoxide generation.	NADP	101-106	nitric oxide synthase 3	Homo sapiens	20-24
9333325-7	1997	Adriamycin binds to eNOS with a Km of approximately 5 microM, as calculated from both eNOS-dependent NADPH consumption and superoxide generation.	NADP	101-106	nitric oxide synthase 3	Homo sapiens	86-90
9333325-7	1997	Adriamycin binds to eNOS with a Km of approximately 5 microM, as calculated from both eNOS-dependent NADPH consumption and superoxide generation.	Superoxides	123-133	nitric oxide synthase 3	Homo sapiens	20-24
9333325-9	1997	This strongly suggests that adriamycin undergoes reduction at the reductase domain of eNOS.	Doxorubicin	28-38	nitric oxide synthase 3	Homo sapiens	86-90
9333325-10	1997	A consequence of eNOS-mediated reductive activation of adriamycin is the disruption of the balance between nitric oxide and superoxide.	Doxorubicin	55-65	nitric oxide synthase 3	Homo sapiens	17-21
9333325-10	1997	A consequence of eNOS-mediated reductive activation of adriamycin is the disruption of the balance between nitric oxide and superoxide.	Nitric Oxide	107-119	nitric oxide synthase 3	Homo sapiens	17-21
9333325-10	1997	A consequence of eNOS-mediated reductive activation of adriamycin is the disruption of the balance between nitric oxide and superoxide.	Superoxides	124-134	nitric oxide synthase 3	Homo sapiens	17-21
9333325-11	1997	This may lead eNOS to generate peroxynitrite and hydrogen peroxide, potent oxidants implicated in several vascular pathologies.	Peroxynitrous Acid	31-44	nitric oxide synthase 3	Homo sapiens	14-18
9333325-11	1997	This may lead eNOS to generate peroxynitrite and hydrogen peroxide, potent oxidants implicated in several vascular pathologies.	Hydrogen Peroxide	49-66	nitric oxide synthase 3	Homo sapiens	14-18
9314409-6	1997	In a separate experiment, L-arginine, the substrate of eNOS, was supplied in drinking water at a concentration of 7.5 g/L for 11 weeks after eNOS gene delivery.	Arginine	26-36	nitric oxide synthase 3	Homo sapiens	55-59
9314409-6	1997	In a separate experiment, L-arginine, the substrate of eNOS, was supplied in drinking water at a concentration of 7.5 g/L for 11 weeks after eNOS gene delivery.	Arginine	26-36	nitric oxide synthase 3	Homo sapiens	141-145
9314409-6	1997	In a separate experiment, L-arginine, the substrate of eNOS, was supplied in drinking water at a concentration of 7.5 g/L for 11 weeks after eNOS gene delivery.	Drinking Water	77-91	nitric oxide synthase 3	Homo sapiens	55-59
9314409-8	1997	Human eNOS gene delivery induces significant increases in urinary and aortic cGMP levels and urinary and serum nitrite/nitrate content (P&lt;.05), while no significant differences in body weight, heart rate, water intake, food consumption, or urine excretion were observed.	Cyclic GMP	77-81	nitric oxide synthase 3	Homo sapiens	6-10
9314409-8	1997	Human eNOS gene delivery induces significant increases in urinary and aortic cGMP levels and urinary and serum nitrite/nitrate content (P&lt;.05), while no significant differences in body weight, heart rate, water intake, food consumption, or urine excretion were observed.	Nitrites	111-118	nitric oxide synthase 3	Homo sapiens	6-10
9314409-8	1997	Human eNOS gene delivery induces significant increases in urinary and aortic cGMP levels and urinary and serum nitrite/nitrate content (P&lt;.05), while no significant differences in body weight, heart rate, water intake, food consumption, or urine excretion were observed.	Nitrates	119-126	nitric oxide synthase 3	Homo sapiens	6-10
9268712-0	1997	Tetrahydrobiopterin regulates superoxide and nitric oxide generation by recombinant endothelial nitric oxide synthase.	sapropterin	0-19	nitric oxide synthase 3	Homo sapiens	84-117
9268712-0	1997	Tetrahydrobiopterin regulates superoxide and nitric oxide generation by recombinant endothelial nitric oxide synthase.	Superoxides	30-40	nitric oxide synthase 3	Homo sapiens	84-117
9268712-0	1997	Tetrahydrobiopterin regulates superoxide and nitric oxide generation by recombinant endothelial nitric oxide synthase.	Nitric Oxide	45-57	nitric oxide synthase 3	Homo sapiens	84-117
9268712-1	1997	Nitric oxide (NO) produced by the endothelial isoform of nitric oxide synthase (NOS III) is a key determinant of the anti-atherosclerotic properties of the endothelium.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	80-87
9268712-2	1997	Recent in vivo studies suggest that NOS III may also be a source of superoxide production, which would limit its role as a NO-producing enzyme.	Superoxides	68-78	nitric oxide synthase 3	Homo sapiens	36-43
9268712-3	1997	In the current study we examined both the NO and the superoxide generating potential of recombinant NOS III obtained from a baculovirus/Sf9 expression system.	Superoxides	53-63	nitric oxide synthase 3	Homo sapiens	100-107
9268712-4	1997	Using lucigenin chemiluminesence we could indeed demonstrate (superoxide dismutase inhibitable) superoxide production by NOS III.	10,10'-dimethyl-9,9'-biacridinium	6-15	nitric oxide synthase 3	Homo sapiens	121-128
9268712-4	1997	Using lucigenin chemiluminesence we could indeed demonstrate (superoxide dismutase inhibitable) superoxide production by NOS III.	Superoxides	62-72	nitric oxide synthase 3	Homo sapiens	121-128
9268712-7	1997	Superoxide generation by NOS III could be completely inhibited by diphenyleneiodonium (DPI), an inhibitor of the flavin moiety of the enzyme, indicating that this group is a main source of superoxide production by the enzyme.	Superoxides	0-10	nitric oxide synthase 3	Homo sapiens	25-32
9268712-7	1997	Superoxide generation by NOS III could be completely inhibited by diphenyleneiodonium (DPI), an inhibitor of the flavin moiety of the enzyme, indicating that this group is a main source of superoxide production by the enzyme.	diphenyleneiodonium	66-85	nitric oxide synthase 3	Homo sapiens	25-32
9268712-7	1997	Superoxide generation by NOS III could be completely inhibited by diphenyleneiodonium (DPI), an inhibitor of the flavin moiety of the enzyme, indicating that this group is a main source of superoxide production by the enzyme.	diphenyleneiodonium	87-90	nitric oxide synthase 3	Homo sapiens	25-32
9268712-7	1997	Superoxide generation by NOS III could be completely inhibited by diphenyleneiodonium (DPI), an inhibitor of the flavin moiety of the enzyme, indicating that this group is a main source of superoxide production by the enzyme.	4,6-dinitro-o-cresol	113-119	nitric oxide synthase 3	Homo sapiens	25-32
9268712-7	1997	Superoxide generation by NOS III could be completely inhibited by diphenyleneiodonium (DPI), an inhibitor of the flavin moiety of the enzyme, indicating that this group is a main source of superoxide production by the enzyme.	Superoxides	189-199	nitric oxide synthase 3	Homo sapiens	25-32
9268712-8	1997	Using measurement of [3H-L-arginine] conversion to [3H-L-citrulline], it appeared that BH4 directly increased the production of NO by NOS III.	3h-l-citrulline	52-67	nitric oxide synthase 3	Homo sapiens	134-141
9268712-8	1997	Using measurement of [3H-L-arginine] conversion to [3H-L-citrulline], it appeared that BH4 directly increased the production of NO by NOS III.	sapropterin	87-90	nitric oxide synthase 3	Homo sapiens	134-141
9268712-9	1997	In addition, we observed that BH4 stablized the NOS III in its dimeric form, suggesting that an effect on allosteric conformation could be involved in this effect on NO production.	sapropterin	30-33	nitric oxide synthase 3	Homo sapiens	48-55
9268712-10	1997	NOS III thus appears to be a superoxide generating enzyme probably through its flavin moiety, as well as a BH4-dependent NO producing enzyme.	Superoxides	29-39	nitric oxide synthase 3	Homo sapiens	0-7
9268712-10	1997	NOS III thus appears to be a superoxide generating enzyme probably through its flavin moiety, as well as a BH4-dependent NO producing enzyme.	4,6-dinitro-o-cresol	79-85	nitric oxide synthase 3	Homo sapiens	0-7
9268712-10	1997	NOS III thus appears to be a superoxide generating enzyme probably through its flavin moiety, as well as a BH4-dependent NO producing enzyme.	sapropterin	107-110	nitric oxide synthase 3	Homo sapiens	0-7
9288162-2	1997	All of the dipeptides and dipeptide esters are competitive inhibitors of nNOS, macrophage nitric oxide synthase (iNOS), and endothelial nitric oxide synthase (eNOS), except for the ones that contain D-ArgNO2 (8-10, 12, 13), which are uncompetitive inhibitors of iNOS but competitive inhibitors of nNOS and eNOS.	dipeptide esters	26-42	nitric oxide synthase 3	Homo sapiens	124-157
9378507-1	1997	The soluble cleavage fragment of the low-affinity immunoglobulin E (IgE) receptor/CD23 (sCD23 25000 MW) and antibodies directed against their receptors on monocytes, CD11b and CD11c, stimulate the production of nitric oxide (NO) by these cells and we have suggested that the enzyme involved could be related to the endothelial constitutive type III nitric oxide synthase (ecNOS).	Nitric Oxide	211-223	nitric oxide synthase 3	Homo sapiens	372-377
9277445-1	1997	In a previous study, we reported that nitric oxide (.NO) affects surfactant synthesis and ATP levels in alveolar type II cells and suggested that there is constitutive nitric oxide synthase (cNOS) activity in the cells.	Nitric Oxide	38-50	nitric oxide synthase 3	Homo sapiens	191-195
9277445-1	1997	In a previous study, we reported that nitric oxide (.NO) affects surfactant synthesis and ATP levels in alveolar type II cells and suggested that there is constitutive nitric oxide synthase (cNOS) activity in the cells.	Adenosine Triphosphate	90-93	nitric oxide synthase 3	Homo sapiens	191-195
9276767-3	1997	This study examines the effect of ibuprofen and its stereoeisomeric components on the activation of iNOS and cNOS as well as on the NO production by human umbilical vein endothelial cells.	Ibuprofen	34-43	nitric oxide synthase 3	Homo sapiens	109-113
9277445-5	1997	.NO formation is inhibited by 28-46% by three inhibitors of cNOS and inducible NOS (iNOS), NG-monomethyl-L-arginine (L-NMMA), L-N5-(1-iminoethyl)ornithine hydrochloride, and NG-nitro-L-arginine methyl ester, but a specific inhibitor of iNOS, aminoguanidine, has no effect.	NG-Nitroarginine Methyl Ester	174-206	nitric oxide synthase 3	Homo sapiens	60-64
9277445-5	1997	.NO formation is inhibited by 28-46% by three inhibitors of cNOS and inducible NOS (iNOS), NG-monomethyl-L-arginine (L-NMMA), L-N5-(1-iminoethyl)ornithine hydrochloride, and NG-nitro-L-arginine methyl ester, but a specific inhibitor of iNOS, aminoguanidine, has no effect.	pimagedine	242-256	nitric oxide synthase 3	Homo sapiens	60-64
9242548-6	1997	The eNOS transfectants were shown to contain functional enzyme by the conversion of L-arginine to L-citrulline in fractionated cells (P = .0001) and by exposing intact cells to calcium ionophore using the cGMP reporter cell assay (P = .0001).	Arginine	84-94	nitric oxide synthase 3	Homo sapiens	4-8
9242548-6	1997	The eNOS transfectants were shown to contain functional enzyme by the conversion of L-arginine to L-citrulline in fractionated cells (P = .0001) and by exposing intact cells to calcium ionophore using the cGMP reporter cell assay (P = .0001).	Citrulline	98-110	nitric oxide synthase 3	Homo sapiens	4-8
9242548-6	1997	The eNOS transfectants were shown to contain functional enzyme by the conversion of L-arginine to L-citrulline in fractionated cells (P = .0001) and by exposing intact cells to calcium ionophore using the cGMP reporter cell assay (P = .0001).	Calcium	177-184	nitric oxide synthase 3	Homo sapiens	4-8
9242548-6	1997	The eNOS transfectants were shown to contain functional enzyme by the conversion of L-arginine to L-citrulline in fractionated cells (P = .0001) and by exposing intact cells to calcium ionophore using the cGMP reporter cell assay (P = .0001).	Cyclic GMP	205-209	nitric oxide synthase 3	Homo sapiens	4-8
9194854-3	1997	Herein we report that human trophoblast and endothelial cells contain functional Flt-1 receptors for VEGF that trigger the synthesis and release of nitric oxide (NO) by the activation of constitutive NO synthase (cNOS).	Nitric Oxide	148-160	nitric oxide synthase 3	Homo sapiens	213-217
9225730-15	1997	NOSIII expression in thyroid follicular cells and the variations in its immunoreactivity suggest a possible role for nitric oxide in thyrocyte function and/or growth.	Nitric Oxide	117-129	nitric oxide synthase 3	Homo sapiens	0-6
9236411-10	1997	CONCLUSIONS: The present study demonstrates that prolonged exposure to high glucose increases eNOS gene expression, protein expression, and NO release.	Glucose	76-83	nitric oxide synthase 3	Homo sapiens	94-98
9236411-11	1997	However, upregulation of eNOS and NO release is associated with a marked concomitant increase of O2- production.	Superoxides	97-99	nitric oxide synthase 3	Homo sapiens	25-29
9256088-2	1997	We determined whether human myometrial endothelial and smooth muscle cells express estrogen receptors (ERs) and whether endothelial NO synthase (eNOS) expression in these cells was affected by 17beta-estradiol (10[-13]-10[-6]M).	Estradiol	193-209	nitric oxide synthase 3	Homo sapiens	120-143
9704584-1	1997	Constitutively expressed endothelial nitric oxide synthase (ecNOS) produces nitric oxide (NO) from L-arginine and is important for the maintenance of cardiovascular homeostasis.	Nitric Oxide	37-49	nitric oxide synthase 3	Homo sapiens	60-65
9704584-1	1997	Constitutively expressed endothelial nitric oxide synthase (ecNOS) produces nitric oxide (NO) from L-arginine and is important for the maintenance of cardiovascular homeostasis.	Arginine	99-109	nitric oxide synthase 3	Homo sapiens	25-58
9704584-1	1997	Constitutively expressed endothelial nitric oxide synthase (ecNOS) produces nitric oxide (NO) from L-arginine and is important for the maintenance of cardiovascular homeostasis.	Arginine	99-109	nitric oxide synthase 3	Homo sapiens	60-65
9115269-2	1997	The activity of the enzyme is regulated in vivo by calcium signaling involving the binding of calmodulin (CAM), which triggers the activation of eNOS.	Calcium	51-58	nitric oxide synthase 3	Homo sapiens	145-149
9115269-3	1997	We have examined the possible role of calcium-mediated CAM binding in promoting dimerization of eNOS through the oxygenase domain of the enzyme.	Calcium	38-45	nitric oxide synthase 3	Homo sapiens	96-100
9202399-3	1997	NO synthase (NOS) inhibitors with affinity for the inducible (iNOS) and the constitutive (cNOS) isoform such as N(G)-monomethyl-L-arginine (L-NMMA) and S-methyl-L-thiocitrulline (SMLT) dose-dependently blocked the inhibitory action of IFN-gamma on GHRH-stimulated GH secretion, and partially reversed the inhibitory effect on basal prolactin (PRL) release.	omega-N-Methylarginine	112-138	nitric oxide synthase 3	Homo sapiens	90-94
9149402-5	1997	A mammalian expression vector (pcDNA3) containing this cDNA was transfected into COS-7 cells, and ecNOS activity was detected by monitoring the formation of [3H]-citrulline from [3H]-L-arginine.	[3h]-citrulline	157-172	nitric oxide synthase 3	Homo sapiens	98-103
9202399-3	1997	NO synthase (NOS) inhibitors with affinity for the inducible (iNOS) and the constitutive (cNOS) isoform such as N(G)-monomethyl-L-arginine (L-NMMA) and S-methyl-L-thiocitrulline (SMLT) dose-dependently blocked the inhibitory action of IFN-gamma on GHRH-stimulated GH secretion, and partially reversed the inhibitory effect on basal prolactin (PRL) release.	omega-N-Methylarginine	140-146	nitric oxide synthase 3	Homo sapiens	90-94
9165669-10	1997	Hyperoxia significantly decreased ecNOS activity as measured by the conversion of L-[3H]arginine to L-[3H]citrulline.	l-[3h]arginine	82-96	nitric oxide synthase 3	Homo sapiens	34-39
9165669-10	1997	Hyperoxia significantly decreased ecNOS activity as measured by the conversion of L-[3H]arginine to L-[3H]citrulline.	l-[3h]citrulline	100-116	nitric oxide synthase 3	Homo sapiens	34-39
9226298-1	1997	Largely assumed to be a Ca2(+)-/calmodulin-dependent enzyme, the endothelial constitutive nitric oxide (NO) synthase (NOS III) can be activated by agonists as a consequence of an increase in the intracellular concentration of free Ca2+ ([Ca2+]i).	Nitric Oxide	90-102	nitric oxide synthase 3	Homo sapiens	118-125
9226298-6	1997	A pharmacologically identical activation of NOS III can be induced by protein phosphatase inhibitors suggesting that the tyrosine phosphorylation of NOS III or an associated regulatory protein is crucial for its Ca2(+)-independent activation.	Tyrosine	121-129	nitric oxide synthase 3	Homo sapiens	44-51
9226298-6	1997	A pharmacologically identical activation of NOS III can be induced by protein phosphatase inhibitors suggesting that the tyrosine phosphorylation of NOS III or an associated regulatory protein is crucial for its Ca2(+)-independent activation.	Tyrosine	121-129	nitric oxide synthase 3	Homo sapiens	149-156
9149402-5	1997	A mammalian expression vector (pcDNA3) containing this cDNA was transfected into COS-7 cells, and ecNOS activity was detected by monitoring the formation of [3H]-citrulline from [3H]-L-arginine.	3h]-l-arginine	179-193	nitric oxide synthase 3	Homo sapiens	98-103
9149402-7	1997	The deduced amino acid sequence of porcine ecNOS cDNA, containing binding sites for NADPH, flavin adenine dinucleotide and bound flavin mononucleotide, shows 94% identity to human ecNOS.	NADP	84-89	nitric oxide synthase 3	Homo sapiens	43-48
9149402-7	1997	The deduced amino acid sequence of porcine ecNOS cDNA, containing binding sites for NADPH, flavin adenine dinucleotide and bound flavin mononucleotide, shows 94% identity to human ecNOS.	Flavin-Adenine Dinucleotide	91-118	nitric oxide synthase 3	Homo sapiens	43-48
9149402-7	1997	The deduced amino acid sequence of porcine ecNOS cDNA, containing binding sites for NADPH, flavin adenine dinucleotide and bound flavin mononucleotide, shows 94% identity to human ecNOS.	Flavin Mononucleotide	129-150	nitric oxide synthase 3	Homo sapiens	43-48
9149402-7	1997	The deduced amino acid sequence of porcine ecNOS cDNA, containing binding sites for NADPH, flavin adenine dinucleotide and bound flavin mononucleotide, shows 94% identity to human ecNOS.	Flavin Mononucleotide	129-150	nitric oxide synthase 3	Homo sapiens	180-185
9030556-6	1997	In contrast, inhibition of human neuronal NOS and endothelial NOS (eNOS) was relatively weaker, rapidly reversible, and competitive with L-arginine, with Ki values of 2 microM and 50 microM, respectively.	Arginine	137-147	nitric oxide synthase 3	Homo sapiens	50-65
9077471-6	1997	The Ca2+-dependent NOS (cNOS) activity in the cytosol of HSc fibroblasts (1.43 pmol/min/g of protein) was significantly lower than that in normal fibroblasts (2.60 pmol/min/g of protein), as determined by citrulline assay (p &lt; 0.01, n = 4).	Citrulline	205-215	nitric oxide synthase 3	Homo sapiens	4-22
9077471-6	1997	The Ca2+-dependent NOS (cNOS) activity in the cytosol of HSc fibroblasts (1.43 pmol/min/g of protein) was significantly lower than that in normal fibroblasts (2.60 pmol/min/g of protein), as determined by citrulline assay (p &lt; 0.01, n = 4).	Citrulline	205-215	nitric oxide synthase 3	Homo sapiens	24-28
9237256-1	1997	Type III nitric oxide synthase (NOS III) is responsible for &gt; 90% of nitric oxide (NO) synthesizing activity in first trimester placentae.	Nitric Oxide	9-21	nitric oxide synthase 3	Homo sapiens	32-39
9237256-3	1997	In the present study, the effect of tetrahydrobiopterin (BH4) on subunit structure and activity of microsomal and cytosolic NOS III was compared.	sapropterin	36-55	nitric oxide synthase 3	Homo sapiens	124-131
9237256-3	1997	In the present study, the effect of tetrahydrobiopterin (BH4) on subunit structure and activity of microsomal and cytosolic NOS III was compared.	sapropterin	57-60	nitric oxide synthase 3	Homo sapiens	124-131
9237256-4	1997	As revealed by immunoblot analysis, incubation of microsomal membranes with 50 microM final concentration BH4 for 10 min at 37 degrees C resulted in a striking conversion of monomeric NOS III into a protein having the characteristics (electrophoretic mobility, resistance to sodium dodecyl sulphate) of the homodimeric form.	sapropterin	106-109	nitric oxide synthase 3	Homo sapiens	184-191
9237256-4	1997	As revealed by immunoblot analysis, incubation of microsomal membranes with 50 microM final concentration BH4 for 10 min at 37 degrees C resulted in a striking conversion of monomeric NOS III into a protein having the characteristics (electrophoretic mobility, resistance to sodium dodecyl sulphate) of the homodimeric form.	Sodium Dodecyl Sulfate	275-298	nitric oxide synthase 3	Homo sapiens	184-191
9237256-5	1997	In contrast, BH4 induced significantly less marked changes in the NOS III dimer content of cytosolic fractions.	sapropterin	13-16	nitric oxide synthase 3	Homo sapiens	66-73
9237256-7	1997	Taken together, the observations suggest that BH4 activates NOS III in the primordial human placenta by promoting its subunit assembly in the membrane, while cytosolic NOS III is relatively insensitive to BH4.	sapropterin	46-49	nitric oxide synthase 3	Homo sapiens	60-67
9065411-4	1997	In fact, a 30-min treatment of T67 cells with the combination of lipopolysaccharide plus interferon-gamma (MIX) strongly inhibits the cNOS activity, as determined by measuring [3H]citrulline production.	Tritium	177-179	nitric oxide synthase 3	Homo sapiens	134-138
9065411-4	1997	In fact, a 30-min treatment of T67 cells with the combination of lipopolysaccharide plus interferon-gamma (MIX) strongly inhibits the cNOS activity, as determined by measuring [3H]citrulline production.	Citrulline	180-190	nitric oxide synthase 3	Homo sapiens	134-138
9089781-7	1997	Thirdly, immunoblot analysis combined with laser densitometric evaluation demonstrated that BH4 efficiently promoted the aggregation of microsomal NOS type III isozyme into a protein having the characteristics (electrophoretic mobility, resistance of SDS) of the dimeric form.	sapropterin	92-95	nitric oxide synthase 3	Homo sapiens	147-159
9089781-9	1997	This is the first time that BH4-induced dimerization of a NOS type III isoform has been demonstrated.	sapropterin	28-31	nitric oxide synthase 3	Homo sapiens	58-70
9030556-6	1997	In contrast, inhibition of human neuronal NOS and endothelial NOS (eNOS) was relatively weaker, rapidly reversible, and competitive with L-arginine, with Ki values of 2 microM and 50 microM, respectively.	Arginine	137-147	nitric oxide synthase 3	Homo sapiens	67-71
9030556-7	1997	Thus, 1400W was at least 5000-fold selective for iNOS versus eNOS.	N-((3-(aminomethyl)phenyl)methyl)ethanimidamide	6-11	nitric oxide synthase 3	Homo sapiens	61-65
9042951-3	1997	We show, using the phosphorylated spin trap 5-diethoxyphosphoryl-5-methyl-1-pyrroline N-oxide (DEPMPO), that lucigenin stimulates NADPH-dependent superoxide production by endothelial nitric oxide synthase (eNOS).	10,10'-dimethyl-9,9'-biacridinium	109-118	nitric oxide synthase 3	Homo sapiens	171-204
9042951-3	1997	We show, using the phosphorylated spin trap 5-diethoxyphosphoryl-5-methyl-1-pyrroline N-oxide (DEPMPO), that lucigenin stimulates NADPH-dependent superoxide production by endothelial nitric oxide synthase (eNOS).	NADP	130-135	nitric oxide synthase 3	Homo sapiens	171-204
9065701-2	1997	NO is generated from L-arginine by nitric oxide synthase (NOS), which has three isoforms; endothelial-type NOS (eNOS) and brain-type NOS (bNOS) are constitutive enzymes, and inducible-type NOS (iNOS) is expressed after stimulation.	Arginine	21-31	nitric oxide synthase 3	Homo sapiens	90-110
9065701-2	1997	NO is generated from L-arginine by nitric oxide synthase (NOS), which has three isoforms; endothelial-type NOS (eNOS) and brain-type NOS (bNOS) are constitutive enzymes, and inducible-type NOS (iNOS) is expressed after stimulation.	Arginine	21-31	nitric oxide synthase 3	Homo sapiens	112-116
9027718-6	1997	Hypoxia, however, has opposite effects on the vasodilator nitric oxide (NO); hypoxia suppresses both the transcriptional rate of the endothelial nitric oxide synthase gene and the stability of its mRNA.	Nitric Oxide	58-70	nitric oxide synthase 3	Homo sapiens	133-166
8995432-5	1997	In this study, wild-type and mutant forms of eNOS have been expressed in a baculovirus system, and the quaternary structure of the purified enzymes has been analyzed by low temperature SDS-PAGE.	Sodium Dodecyl Sulfate	185-188	nitric oxide synthase 3	Homo sapiens	45-49
8995432-6	1997	eNOS dimer formation requires incorporation of the heme prosthetic group but does not require myristoylation or CaM or BH4 binding.	Heme	51-55	nitric oxide synthase 3	Homo sapiens	0-4
9064730-9	1997	Estrogens modulate vascular function by increasing nitric oxide production via stimulation of endothelial nitric oxide synthase (eNOS) and decreasing endothelin-1 levels in vivo.	Nitric Oxide	51-63	nitric oxide synthase 3	Homo sapiens	94-127
9415517-3	1997	The aim of this study was to examine the mRNA expression of the vasoconstrictor endothelin-1 (ET-1), its receptor ET-A and the endothelial constitutive nitric oxide synthase (ecNOS), forming the vasodilator nitric oxide, in hydatidiform moles.	Nitric Oxide	152-164	nitric oxide synthase 3	Homo sapiens	175-180
9187936-6	1997	Preincubation with a physiologic concentration of 17 beta-estradiol (10(-12) to 10(-8) M) over 8 h significantly enhanced the activity of NOS-3 in the endothelial cells of cultured human umbilical vein and bovine aortas.	Estradiol	50-67	nitric oxide synthase 3	Homo sapiens	138-143
18472828-1	1997	Atherosclerosis is a chronic inflammatory process in the intima of conduit arteries, which disturbs the endothelium-dependent regulation of the vascular tone by the labile liposoluble radical nitric oxide (NO) formed by the constitutive endothelial nitric oxide synthase (eNOS).	Nitric Oxide	192-204	nitric oxide synthase 3	Homo sapiens	237-270
8955082-14	1996	The ligands resulting in the low spin complexes bind directly to the heme iron, while their cognate ligands induce the formation of high spin complexes by indirectly perturbing the heme structure and excluding the original axial heme ligand in the resting eNOS (V. Berka, P.-F. Chen, and A.	Heme	69-73	nitric oxide synthase 3	Homo sapiens	256-260
8969188-0	1996	Spatial relationship between L-arginine and heme binding sites of endothelial nitric-oxide synthase.	Arginine	29-39	nitric oxide synthase 3	Homo sapiens	66-99
8969188-0	1996	Spatial relationship between L-arginine and heme binding sites of endothelial nitric-oxide synthase.	Heme	44-48	nitric oxide synthase 3	Homo sapiens	66-99
8969188-1	1996	Binding of L-arginine and imidazole to the endothelial nitric-oxide synthase (eNOS) was characterized by direct heme spectral perturbation.	Arginine	11-21	nitric oxide synthase 3	Homo sapiens	43-76
8969188-1	1996	Binding of L-arginine and imidazole to the endothelial nitric-oxide synthase (eNOS) was characterized by direct heme spectral perturbation.	imidazole	26-35	nitric oxide synthase 3	Homo sapiens	43-76
8969188-1	1996	Binding of L-arginine and imidazole to the endothelial nitric-oxide synthase (eNOS) was characterized by direct heme spectral perturbation.	Heme	112-116	nitric oxide synthase 3	Homo sapiens	43-76
8955082-2	1996	Resting eNOS and the G2A mutant have a mixture of low spin and high spin P450-heme with widely different relaxation behavior and a stable flavin semiquinone radical identified by EPR as a neutral radical.	Heme	78-82	nitric oxide synthase 3	Homo sapiens	8-12
8955082-2	1996	Resting eNOS and the G2A mutant have a mixture of low spin and high spin P450-heme with widely different relaxation behavior and a stable flavin semiquinone radical identified by EPR as a neutral radical.	flavin semiquinone	138-156	nitric oxide synthase 3	Homo sapiens	8-12
8955082-11	1996	As eNOS and chloroperoxidase lie closer than do eNOS and P450cam on the truth diagram, it implies that the distal heme environment in eNOS resembles chloroperoxidase more than P450cam.	Heme	114-118	nitric oxide synthase 3	Homo sapiens	3-7
8955082-11	1996	As eNOS and chloroperoxidase lie closer than do eNOS and P450cam on the truth diagram, it implies that the distal heme environment in eNOS resembles chloroperoxidase more than P450cam.	Heme	114-118	nitric oxide synthase 3	Homo sapiens	48-52
8955082-11	1996	As eNOS and chloroperoxidase lie closer than do eNOS and P450cam on the truth diagram, it implies that the distal heme environment in eNOS resembles chloroperoxidase more than P450cam.	Heme	114-118	nitric oxide synthase 3	Homo sapiens	48-52
8955082-14	1996	The ligands resulting in the low spin complexes bind directly to the heme iron, while their cognate ligands induce the formation of high spin complexes by indirectly perturbing the heme structure and excluding the original axial heme ligand in the resting eNOS (V. Berka, P.-F. Chen, and A.	Iron	74-78	nitric oxide synthase 3	Homo sapiens	256-260
8955082-14	1996	The ligands resulting in the low spin complexes bind directly to the heme iron, while their cognate ligands induce the formation of high spin complexes by indirectly perturbing the heme structure and excluding the original axial heme ligand in the resting eNOS (V. Berka, P.-F. Chen, and A.	Heme	181-185	nitric oxide synthase 3	Homo sapiens	256-260
8955082-14	1996	The ligands resulting in the low spin complexes bind directly to the heme iron, while their cognate ligands induce the formation of high spin complexes by indirectly perturbing the heme structure and excluding the original axial heme ligand in the resting eNOS (V. Berka, P.-F. Chen, and A.	Heme	181-185	nitric oxide synthase 3	Homo sapiens	256-260
8937711-6	1996	2-Amino-4-methylpyridine was less potent on human recombinant NOS II (IC50 = 40 nM) and was still less potent on human recombinant NOS I and NOS III (IC50 = 100 nM).	2-amino-4-picoline	0-24	nitric oxide synthase 3	Homo sapiens	141-148
8931564-3	1996	In this study, we have synthesized a 20-amino acid peptide corresponding to the putative calmodulin-binding domain of human eNOS and studied the interaction of the peptide with calmodulin and with various membrane phospholipids.	Phospholipids	214-227	nitric oxide synthase 3	Homo sapiens	124-128
8931564-6	1996	These results suggest that the same domain of eNOS binds both calmodulin and membrane phospholipids.	Phospholipids	86-99	nitric oxide synthase 3	Homo sapiens	46-50
8937711-19	1996	Larger doses of 2-amino-4-methylpyridine were required to raise mean arterial pressure in untreated conscious rats (ED50 = 0.060 mg kg-1 min-1) indicating 6.9 x selectivity for NOS II over NOS III in vivo.	2-amino-4-picoline	16-40	nitric oxide synthase 3	Homo sapiens	189-196
8806629-1	1996	We examined whether highly conserved cysteine residues in the reductase domain of the constitutive isoform of nitric oxide synthase in human endothelial cells (ecNOS) are crucial for catalytic activity of the enzyme.	Cysteine	37-45	nitric oxide synthase 3	Homo sapiens	160-165
8873592-1	1996	Endothelial nitric oxide synthase (eNOS) is dually acylated by N-myristoylation and cysteine palmitoylation and resides in Golgi and caveolae membranes.	Nitrogen	36-37	nitric oxide synthase 3	Homo sapiens	0-33
8873592-1	1996	Endothelial nitric oxide synthase (eNOS) is dually acylated by N-myristoylation and cysteine palmitoylation and resides in Golgi and caveolae membranes.	Cysteine	84-92	nitric oxide synthase 3	Homo sapiens	0-33
8873592-1	1996	Endothelial nitric oxide synthase (eNOS) is dually acylated by N-myristoylation and cysteine palmitoylation and resides in Golgi and caveolae membranes.	Cysteine	84-92	nitric oxide synthase 3	Homo sapiens	35-39
8966507-7	1996	Estrogens can modulate vascular function by increasing nitric oxide production via stimulation of endothelial nitric oxide synthase (eNOS) and decreasing endothelin-1 levels in vivo.	Nitric Oxide	55-67	nitric oxide synthase 3	Homo sapiens	98-131
8806629-2	1996	Substitution of alanine for cysteines 976 (Cys-976), 991 (Cys-991), 1048 (Cys-1048), or 1114 (Cys-1114), located in the reductase domain of human ecNOS, was achieved by oligonucleotide-directed mutagenesis and expression in COS-7 cells.	Alanine	16-23	nitric oxide synthase 3	Homo sapiens	146-151
8806629-3	1996	The specific activity of ecNOS was &gt; 7-fold increased in wild-type and in mutants Cys-976 and Cys-991, but not in mutants Cys-1048 and Cys-1114.	Cysteine	85-88	nitric oxide synthase 3	Homo sapiens	25-30
8806629-3	1996	The specific activity of ecNOS was &gt; 7-fold increased in wild-type and in mutants Cys-976 and Cys-991, but not in mutants Cys-1048 and Cys-1114.	Cysteine	97-100	nitric oxide synthase 3	Homo sapiens	25-30
8806629-3	1996	The specific activity of ecNOS was &gt; 7-fold increased in wild-type and in mutants Cys-976 and Cys-991, but not in mutants Cys-1048 and Cys-1114.	Cysteine	97-100	nitric oxide synthase 3	Homo sapiens	25-30
8806629-3	1996	The specific activity of ecNOS was &gt; 7-fold increased in wild-type and in mutants Cys-976 and Cys-991, but not in mutants Cys-1048 and Cys-1114.	Cysteine	97-100	nitric oxide synthase 3	Homo sapiens	25-30
8806629-7	1996	These results indicate that Cys-1048 and Cys-1114 residues in the NADPH binding site of the reductase domain are critical for human ecNOS activity.	Cysteine	28-31	nitric oxide synthase 3	Homo sapiens	132-137
8806629-7	1996	These results indicate that Cys-1048 and Cys-1114 residues in the NADPH binding site of the reductase domain are critical for human ecNOS activity.	Cysteine	41-44	nitric oxide synthase 3	Homo sapiens	132-137
8806629-7	1996	These results indicate that Cys-1048 and Cys-1114 residues in the NADPH binding site of the reductase domain are critical for human ecNOS activity.	NADP	66-71	nitric oxide synthase 3	Homo sapiens	132-137
8806629-8	1996	The lack of utilization of NADPH in L-arginine metabolism and in cytochrome c reduction suggests that these active site cysteine residues may be responsible for binding of NADPH and/or for electron transfer in human ecNOS.	Cysteine	120-128	nitric oxide synthase 3	Homo sapiens	216-221
8806629-8	1996	The lack of utilization of NADPH in L-arginine metabolism and in cytochrome c reduction suggests that these active site cysteine residues may be responsible for binding of NADPH and/or for electron transfer in human ecNOS.	NADP	172-177	nitric oxide synthase 3	Homo sapiens	216-221
8760128-8	1996	Production of .NO by type II cells is inhibited by L-NAME, a better inhibitor of constitutive NOS (cNOS) than inducible NOS (iNOS), and is reduced in the absence of external calcium.	NG-Nitroarginine Methyl Ester	51-57	nitric oxide synthase 3	Homo sapiens	81-97
8816908-8	1996	cNOS enzyme activity assessed by cGMP production in reporter cell fibroblasts was also lower in resistance arteries compared to conduit arteries (0.17 +/- 0.03 vs. 0.33 +/- 0.05 fmol cGMP/microgram protein, respectively; P &lt; 0.05 resistance artery endothelium vs. conduit artery endothelium).	Cyclic GMP	33-37	nitric oxide synthase 3	Homo sapiens	0-4
8816908-8	1996	cNOS enzyme activity assessed by cGMP production in reporter cell fibroblasts was also lower in resistance arteries compared to conduit arteries (0.17 +/- 0.03 vs. 0.33 +/- 0.05 fmol cGMP/microgram protein, respectively; P &lt; 0.05 resistance artery endothelium vs. conduit artery endothelium).	Cyclic GMP	183-187	nitric oxide synthase 3	Homo sapiens	0-4
8704216-4	1996	Constitutive NOS expression was detected by Western blotting of cell lysates and by the accumulation of nitrite in the culture media.	Nitrites	104-111	nitric oxide synthase 3	Homo sapiens	0-16
8760128-8	1996	Production of .NO by type II cells is inhibited by L-NAME, a better inhibitor of constitutive NOS (cNOS) than inducible NOS (iNOS), and is reduced in the absence of external calcium.	NG-Nitroarginine Methyl Ester	51-57	nitric oxide synthase 3	Homo sapiens	99-103
8687488-2	1996	In the present study, we demonstrated that NO synthase (cNOS) and xanthine oxidase (XO) of human keratinocytes can be activated to release NO, superoxide (O2-) and peroxynitrite (ONOO-) following exposure to ultraviolet B (UVB) radiation.	Superoxides	143-153	nitric oxide synthase 3	Homo sapiens	56-60
8687488-2	1996	In the present study, we demonstrated that NO synthase (cNOS) and xanthine oxidase (XO) of human keratinocytes can be activated to release NO, superoxide (O2-) and peroxynitrite (ONOO-) following exposure to ultraviolet B (UVB) radiation.	Superoxides	155-158	nitric oxide synthase 3	Homo sapiens	56-60
8687488-2	1996	In the present study, we demonstrated that NO synthase (cNOS) and xanthine oxidase (XO) of human keratinocytes can be activated to release NO, superoxide (O2-) and peroxynitrite (ONOO-) following exposure to ultraviolet B (UVB) radiation.	Peroxynitrous Acid	164-177	nitric oxide synthase 3	Homo sapiens	56-60
8687488-2	1996	In the present study, we demonstrated that NO synthase (cNOS) and xanthine oxidase (XO) of human keratinocytes can be activated to release NO, superoxide (O2-) and peroxynitrite (ONOO-) following exposure to ultraviolet B (UVB) radiation.	oxido nitrite	179-184	nitric oxide synthase 3	Homo sapiens	56-60
8687488-9	1996	ONOO- synthesized by NO and O2- following UVB radiation of cNOS and XO was inhibited by oxypurinol (100 microM).	onoo	0-4	nitric oxide synthase 3	Homo sapiens	59-63
8687488-9	1996	ONOO- synthesized by NO and O2- following UVB radiation of cNOS and XO was inhibited by oxypurinol (100 microM).	Superoxides	28-30	nitric oxide synthase 3	Homo sapiens	59-63
8687488-9	1996	ONOO- synthesized by NO and O2- following UVB radiation of cNOS and XO was inhibited by oxypurinol (100 microM).	Oxypurinol	88-98	nitric oxide synthase 3	Homo sapiens	59-63
8743501-5	1996	Endothelial NOS and neuronal NOS are constitutively present and activated by increases in intracellular calcium triggered by endogenous chemicals.	Calcium	104-111	nitric oxide synthase 3	Homo sapiens	0-15
8764145-4	1996	We observed that cNOS activity could be quantitated in islet homogenates by monitoring the formation of L-citrulline from L-arginine using an Amprep CBA cation-exhange minicolumn before derivatization with o-phthaldialdehyde and subsequent high-performance liquid chromatography analysis.	Citrulline	104-116	nitric oxide synthase 3	Homo sapiens	17-21
8764145-4	1996	We observed that cNOS activity could be quantitated in islet homogenates by monitoring the formation of L-citrulline from L-arginine using an Amprep CBA cation-exhange minicolumn before derivatization with o-phthaldialdehyde and subsequent high-performance liquid chromatography analysis.	Arginine	122-132	nitric oxide synthase 3	Homo sapiens	17-21
8764145-4	1996	We observed that cNOS activity could be quantitated in islet homogenates by monitoring the formation of L-citrulline from L-arginine using an Amprep CBA cation-exhange minicolumn before derivatization with o-phthaldialdehyde and subsequent high-performance liquid chromatography analysis.	o-Phthalaldehyde	206-224	nitric oxide synthase 3	Homo sapiens	17-21
8621055-2	1996	The nitric oxide synthases (NOS-I, neuronal, NOS-II, inducible, and NOS-III, endothelial) are the most recent additions to the large number of heme proteins that contain cysteine thiolate-liganded protoporphyrin IX heme prosthetic groups.	cysteine thiolate	170-187	nitric oxide synthase 3	Homo sapiens	68-75
8655601-6	1996	Cobalt inhibited the expression of cNOS transcripts, suggesting a mechanism comparable to that by which oxygen tension regulates expression of other vasoregulatory genes.	Cobalt	0-6	nitric oxide synthase 3	Homo sapiens	35-39
8655601-6	1996	Cobalt inhibited the expression of cNOS transcripts, suggesting a mechanism comparable to that by which oxygen tension regulates expression of other vasoregulatory genes.	Oxygen	104-110	nitric oxide synthase 3	Homo sapiens	35-39
8928825-4	1996	eNOS protein expression was 2.7-fold greater at higher oxygen tension; eNOS upregulation was also evident after 24 h. Inducible NOS protein was not detectable by immunoblot at either level of oxygenation.	Oxygen	55-61	nitric oxide synthase 3	Homo sapiens	0-4
8928825-5	1996	In the lung, the effect of oxygen on eNOS expression may be specific to the endothelium, as eNOS expression in bronchiolar epithelial cells of Clara cell lineage was not altered by varying oxygen tension.	Oxygen	27-33	nitric oxide synthase 3	Homo sapiens	37-41
8928825-6	1996	The oxygen-related increase in eNOS protein in the fetal PAEC was associated with 2.5-fold greater NOS enzymatic activity.	Oxygen	4-10	nitric oxide synthase 3	Homo sapiens	31-35
8928825-8	1996	Thus eNOS gene expression in ovine fetal PAEC is upregulated by oxygen, and this is mediated at the level of gene transcription or mRNA stability.	Oxygen	64-70	nitric oxide synthase 3	Homo sapiens	5-9
8621055-2	1996	The nitric oxide synthases (NOS-I, neuronal, NOS-II, inducible, and NOS-III, endothelial) are the most recent additions to the large number of heme proteins that contain cysteine thiolate-liganded protoporphyrin IX heme prosthetic groups.	protoporphyrin IX	197-214	nitric oxide synthase 3	Homo sapiens	68-75
8621055-2	1996	The nitric oxide synthases (NOS-I, neuronal, NOS-II, inducible, and NOS-III, endothelial) are the most recent additions to the large number of heme proteins that contain cysteine thiolate-liganded protoporphyrin IX heme prosthetic groups.	Heme	143-147	nitric oxide synthase 3	Homo sapiens	68-75
8796805-21	1996	This observation suggests that regulation of eNOS may be a physiologic response to steroid hormones and locally produced peptide hormones in the endometrial environment.	Steroids	83-99	nitric oxide synthase 3	Homo sapiens	45-49
8618000-1	1996	Nitric oxide is a potent mediator of endothelium-dependent vasodilation, the synthesis of which is catalyzed by the constitutively expressed enzyme endothelial nitric oxide synthase.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	148-181
8619882-1	1996	Nitric oxide (NO) is produced in physiological and pathophysiological conditions by three distinct isoforms of NO synthase (NOS): endothelial NOS (ecNOS), inducible NOS (iNOS), and brain NOS (bNOS).	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	130-145
8619882-1	1996	Nitric oxide (NO) is produced in physiological and pathophysiological conditions by three distinct isoforms of NO synthase (NOS): endothelial NOS (ecNOS), inducible NOS (iNOS), and brain NOS (bNOS).	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	147-152
8619882-5	1996	The amino acid-based NOS inhibitor, NG-nitro-L-arginine, shows a preference for ecNOS and bNOS over iNOS, whereas L-N6-(1-iminoethyl)lysine is selective for iNOS over bNOS.	Nitroarginine	36-55	nitric oxide synthase 3	Homo sapiens	80-85
8564837-1	1996	Endothelium-dependent vasodilatation is mediated by release of nitric oxide formed by constitutively expressed endothelial nitric oxide synthase (ecNOS).	Nitric Oxide	63-75	nitric oxide synthase 3	Homo sapiens	111-144
8564837-1	1996	Endothelium-dependent vasodilatation is mediated by release of nitric oxide formed by constitutively expressed endothelial nitric oxide synthase (ecNOS).	Nitric Oxide	63-75	nitric oxide synthase 3	Homo sapiens	146-151
8524847-7	1995	Immunoprecipitation of ecNOS mutants following cDNA transfection and biosynthetic labeling with [3H]palmitate revealed that mutagenesis of either cysteine residue attenuated palmitoylation, whereas replacement of both residues completely eliminated palmitoylation.	Cysteine	146-154	nitric oxide synthase 3	Homo sapiens	23-28
8524847-8	1995	Analysis of N-terminal deletion mutations of ecNOS demonstrated that the region containing these two cysteine residues is both necessary and sufficient for enzyme palmitoylation.	Cysteine	101-109	nitric oxide synthase 3	Homo sapiens	45-50
8524847-9	1995	The cysteines thus identified as the palmitoylation sites for ecNOS are separated by an unusual (Gly-Leu)5 sequence and appear to define a sequence motif for dual acylation.	Cysteine	4-13	nitric oxide synthase 3	Homo sapiens	62-67
8524847-9	1995	The cysteines thus identified as the palmitoylation sites for ecNOS are separated by an unusual (Gly-Leu)5 sequence and appear to define a sequence motif for dual acylation.	(gly-leu)5	96-106	nitric oxide synthase 3	Homo sapiens	62-67
8746197-2	1995	The objective of this study was to test the hypothesis that constitutive nitric oxide synthase (cNOS) is sensitive to oxygen tension and that hypoxia increases the activity of cNOS and nitric oxide production in the porcine coronary microcirculation.	Oxygen	118-124	nitric oxide synthase 3	Homo sapiens	96-100
8572165-6	1995	In BAEC, this induction in ecNOS mRNA was prevented by coincubation with actinomycin D (10 micrograms/ml).	Dactinomycin	73-86	nitric oxide synthase 3	Homo sapiens	27-32
8572165-7	1995	The K+ channel antagonist tetraethylammonium chloride (3 mM) prevented increase in ecNOS mRNA in response to shear stress.	Tetraethylammonium	26-53	nitric oxide synthase 3	Homo sapiens	83-88
8746197-2	1995	The objective of this study was to test the hypothesis that constitutive nitric oxide synthase (cNOS) is sensitive to oxygen tension and that hypoxia increases the activity of cNOS and nitric oxide production in the porcine coronary microcirculation.	Nitric Oxide	73-85	nitric oxide synthase 3	Homo sapiens	96-100
8746197-13	1995	CONCLUSIONS: These experiments demonstrated that the regulation of cNOS is sensitive to oxygen tension.	Oxygen	88-94	nitric oxide synthase 3	Homo sapiens	67-71
7488171-1	1995	Endothelial nitric oxide synthase (eNOS) is an important oxygenase which catalyzes the conversion of L-arginine to L-citrulline to form nitric oxide (NO), a potent important factor for vasodilation and inhibition of platelet aggregation.	Arginine	101-111	nitric oxide synthase 3	Homo sapiens	0-33
7488171-1	1995	Endothelial nitric oxide synthase (eNOS) is an important oxygenase which catalyzes the conversion of L-arginine to L-citrulline to form nitric oxide (NO), a potent important factor for vasodilation and inhibition of platelet aggregation.	Arginine	101-111	nitric oxide synthase 3	Homo sapiens	35-39
7488171-1	1995	Endothelial nitric oxide synthase (eNOS) is an important oxygenase which catalyzes the conversion of L-arginine to L-citrulline to form nitric oxide (NO), a potent important factor for vasodilation and inhibition of platelet aggregation.	Citrulline	115-127	nitric oxide synthase 3	Homo sapiens	0-33
7488171-1	1995	Endothelial nitric oxide synthase (eNOS) is an important oxygenase which catalyzes the conversion of L-arginine to L-citrulline to form nitric oxide (NO), a potent important factor for vasodilation and inhibition of platelet aggregation.	Citrulline	115-127	nitric oxide synthase 3	Homo sapiens	35-39
7488171-1	1995	Endothelial nitric oxide synthase (eNOS) is an important oxygenase which catalyzes the conversion of L-arginine to L-citrulline to form nitric oxide (NO), a potent important factor for vasodilation and inhibition of platelet aggregation.	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	35-39
7543089-1	1995	The particulate enzyme, endothelial nitric oxide synthase (eNOS), produces nitric oxide to maintain normal vasodilator tone in blood vessels.	Nitric Oxide	36-48	nitric oxide synthase 3	Homo sapiens	59-63
7488039-0	1995	Cysteine 99 of endothelial nitric oxide synthase (NOS-III) is critical for tetrahydrobiopterin-dependent NOS-III stability and activity.	Cysteine	0-8	nitric oxide synthase 3	Homo sapiens	15-48
7488039-0	1995	Cysteine 99 of endothelial nitric oxide synthase (NOS-III) is critical for tetrahydrobiopterin-dependent NOS-III stability and activity.	Cysteine	0-8	nitric oxide synthase 3	Homo sapiens	50-57
7488039-0	1995	Cysteine 99 of endothelial nitric oxide synthase (NOS-III) is critical for tetrahydrobiopterin-dependent NOS-III stability and activity.	sapropterin	75-94	nitric oxide synthase 3	Homo sapiens	15-48
7488039-0	1995	Cysteine 99 of endothelial nitric oxide synthase (NOS-III) is critical for tetrahydrobiopterin-dependent NOS-III stability and activity.	sapropterin	75-94	nitric oxide synthase 3	Homo sapiens	50-57
7488039-3	1995	Here, we demonstrated that cys-99 of human endothelial NOS (ecNOS) is critical for BH4 involvement in NOS catalytic activity and stability.	Cysteine	27-30	nitric oxide synthase 3	Homo sapiens	43-58
7488039-3	1995	Here, we demonstrated that cys-99 of human endothelial NOS (ecNOS) is critical for BH4 involvement in NOS catalytic activity and stability.	Cysteine	27-30	nitric oxide synthase 3	Homo sapiens	60-65
7488039-3	1995	Here, we demonstrated that cys-99 of human endothelial NOS (ecNOS) is critical for BH4 involvement in NOS catalytic activity and stability.	sapropterin	83-86	nitric oxide synthase 3	Homo sapiens	43-58
7488039-3	1995	Here, we demonstrated that cys-99 of human endothelial NOS (ecNOS) is critical for BH4 involvement in NOS catalytic activity and stability.	sapropterin	83-86	nitric oxide synthase 3	Homo sapiens	60-65
7488039-4	1995	Mutation of cys-99 to alanine in ecNOS resulted in loss of catalytic activity which could be restored to the level of wild type by adding a high concentration of exogenous BH4 to the crude extract.	Cysteine	12-15	nitric oxide synthase 3	Homo sapiens	33-38
7488039-4	1995	Mutation of cys-99 to alanine in ecNOS resulted in loss of catalytic activity which could be restored to the level of wild type by adding a high concentration of exogenous BH4 to the crude extract.	Alanine	22-29	nitric oxide synthase 3	Homo sapiens	33-38
7488039-4	1995	Mutation of cys-99 to alanine in ecNOS resulted in loss of catalytic activity which could be restored to the level of wild type by adding a high concentration of exogenous BH4 to the crude extract.	sapropterin	172-175	nitric oxide synthase 3	Homo sapiens	33-38
7488459-1	1995	OBJECTIVE: To determine the activity of the calcium-dependent constitutive (cNOS) and calcium-independent inducible nitric oxide (iNOS) synthases in heart tissue from patients with different cardiac diseases.	Calcium	44-51	nitric oxide synthase 3	Homo sapiens	76-80
8532063-13	1995	Expression is enhanced by e.g. estrogens (for NOS I and III), shear stress, TGF-beta 1, and (in certain endothelial cells) high glucose (for NOS III).	Glucose	128-135	nitric oxide synthase 3	Homo sapiens	141-148
7544542-4	1995	Shear stress exposure for 6 h caused a 2.2 +/- 0.3- and 2.8 +/- 0.3-fold elevation of cNOS protein levels in BAEC (n = 3, P &lt; 0.01) and HUVEC (n = 3, P &lt; 0.01), respectively, in the presence or absence of 1 microM dexamethasone.	Dexamethasone	220-233	nitric oxide synthase 3	Homo sapiens	86-90
7544542-5	1995	Dexamethasone suppresses induction of the inducible NOS gene, indicating that cNOS was elevated by fluid shear stress.	Dexamethasone	0-13	nitric oxide synthase 3	Homo sapiens	78-82
7544542-9	1995	The cNOS mRNA levels were found to be elevated by two- to threefold in BAEC after 6 or 12 h of flow exposure at either 4 or 25 dyn/cm2, and this induction of NOS mRNA occurred in the presence of dexamethasone.	Dexamethasone	195-208	nitric oxide synthase 3	Homo sapiens	4-8
7583282-12	1995	These results support an astroglial location of the alpha 1-adrenoceptors and the cNOS that mediate NA stimulation of cGMP formation in cerebellum.	Cyclic GMP	118-122	nitric oxide synthase 3	Homo sapiens	82-86
7591016-0	1995	Oleic acid inhibits endothelial nitric oxide synthase by a protein kinase C-independent mechanism.	Oleic Acid	0-10	nitric oxide synthase 3	Homo sapiens	20-53
7575554-2	1995	Preincubation with a physiologic concentration of 17 beta-estradiol (10(-12)-10(-8) M) over 8 hours significantly enhanced the activity of NOS-3 in endothelial cells of cultured human umblical vein (HUVEC) and of bovine aortas (BAEC).	Estradiol	50-67	nitric oxide synthase 3	Homo sapiens	139-144
7575554-4	1995	Western blot showed a similar effect of 17 beta-estradiol on NOS-3.	Estradiol	40-57	nitric oxide synthase 3	Homo sapiens	61-66
7568904-1	1995	Nitric oxide (NO), produced by either constitutive or inducible isoforms of NO synthase (cNOS or iNOS), influences myocardial inotropic and chronotropic responses.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	89-93
7476056-2	1995	The primary stimulus for the production of nitric oxide by the constitutive endothelial nitric oxide synthase (ECNOS, Type II) found in blood vessels is most likely the shear stress, the frictional force, caused by blood flowing through blood vessels.	Nitric Oxide	43-55	nitric oxide synthase 3	Homo sapiens	76-109
7476056-2	1995	The primary stimulus for the production of nitric oxide by the constitutive endothelial nitric oxide synthase (ECNOS, Type II) found in blood vessels is most likely the shear stress, the frictional force, caused by blood flowing through blood vessels.	Nitric Oxide	43-55	nitric oxide synthase 3	Homo sapiens	111-116
7530714-6	1995	Biosynthetic labeling of endothelial cells with [3H]palmitic acid followed by immunoprecipitation of ecNOS revealed that the enzyme is palmitoylated; the label is released by hydroxylamine, consistent with formation of a fatty acyl thioester, and authentic palmitate can be recovered from labeled ecNOS following acid hydrolysis.	fatty acyl thioester	221-241	nitric oxide synthase 3	Homo sapiens	101-106
7542654-2	1995	NOS-III has been thought to be regulated mainly at the level of enzyme activity by intracellular calcium.	Calcium	97-104	nitric oxide synthase 3	Homo sapiens	0-7
7542654-3	1995	We report that in human umbilical vein endothelial cells lysophosphatidylcholine (lyso-PC), a component of atherogenic lipoproteins and atherosclerotic lesions, increases NOS-III mRNA and protein levels.	Lysophosphatidylcholines	57-80	nitric oxide synthase 3	Homo sapiens	171-178
7542654-3	1995	We report that in human umbilical vein endothelial cells lysophosphatidylcholine (lyso-PC), a component of atherogenic lipoproteins and atherosclerotic lesions, increases NOS-III mRNA and protein levels.	Lysophosphatidylcholines	82-89	nitric oxide synthase 3	Homo sapiens	171-178
7542654-5	1995	Importantly, nuclear run-off experiments demonstrate a transcriptional mechanism of regulation of NOS-III expression by lysophosphatidylcholine.	Lysophosphatidylcholines	120-143	nitric oxide synthase 3	Homo sapiens	98-105
7542654-6	1995	As endothelium-derived NO appears to be an anti-atherogenic molecule, induction of NOS-III by lyso-PC may be a protective response that limits the progress of the atherosclerotic lesion and promotes its regression.	Lysophosphatidylcholines	94-101	nitric oxide synthase 3	Homo sapiens	83-90
7534070-0	1995	Heme requirement for production of active endothelial nitric oxide synthase in baculovirus-infected insect cells.	Heme	0-4	nitric oxide synthase 3	Homo sapiens	42-75
7534070-4	1995	While a precursor for heme biosynthesis increased the activity, inhibitors of heme biosynthesis reduced the ecNOS activity to 50% without affecting the level of enzyme.	Heme	78-82	nitric oxide synthase 3	Homo sapiens	108-113
7530714-6	1995	Biosynthetic labeling of endothelial cells with [3H]palmitic acid followed by immunoprecipitation of ecNOS revealed that the enzyme is palmitoylated; the label is released by hydroxylamine, consistent with formation of a fatty acyl thioester, and authentic palmitate can be recovered from labeled ecNOS following acid hydrolysis.	Palmitates	257-266	nitric oxide synthase 3	Homo sapiens	101-106
7546631-5	1995	NO production may be pharmacologically decreased by inhibition of expression of iNOS by glucocorticoids while both cNOS and iNOS derived NO production is inhibited by administration of false substrates, for example L-NAME.	NG-Nitroarginine Methyl Ester	215-221	nitric oxide synthase 3	Homo sapiens	115-119
7535933-9	1995	Thus, osteoclast function may require intermittent calcium-stimulated increases in NO production by cNOS against a basal inhibitory background activity of the iNOS isoform.	Calcium	51-58	nitric oxide synthase 3	Homo sapiens	100-104
7530714-7	1995	Importantly, pulse-chase experiments in endothelial cells biosynthetically labeled with [3H]palmitate show that bradykinin treatment promotes ecNOS depalmitoylation.	[3h]palmitate	88-101	nitric oxide synthase 3	Homo sapiens	142-147
7526714-5	1994	Exposing human endothelial cells to low PO2 results in 40-60% reduction in the steady-state mRNA levels of endothelial constitutive NO synthase (eNOS), the major enzyme responsible for NO production in these cells.	PO-2	40-43	nitric oxide synthase 3	Homo sapiens	107-143
7536382-1	1995	During the past two years, the enzyme responsible for production of endothelium-derived nitric oxide, the endothelial cell NO synthase (ecNOS) has been cloned and the gene encoding this enzyme isolated, cloned and its structure characterized.	Nitric Oxide	88-100	nitric oxide synthase 3	Homo sapiens	136-141
7536383-4	1995	The inhibition of cNOS was specific, since to some degree NADPH (0.5-4 mM) and more effectively L-arginine (0.1-1 mM), but not D-arginine, reversed the inhibition.	NADP	58-63	nitric oxide synthase 3	Homo sapiens	18-22
7536383-4	1995	The inhibition of cNOS was specific, since to some degree NADPH (0.5-4 mM) and more effectively L-arginine (0.1-1 mM), but not D-arginine, reversed the inhibition.	Arginine	96-106	nitric oxide synthase 3	Homo sapiens	18-22
7536383-4	1995	The inhibition of cNOS was specific, since to some degree NADPH (0.5-4 mM) and more effectively L-arginine (0.1-1 mM), but not D-arginine, reversed the inhibition.	D-Arginine	127-137	nitric oxide synthase 3	Homo sapiens	18-22
7538424-6	1995	Under control conditions, cNOS and PAI-1 mRNA were stable after treatment with actinomycin D for periods greater than 24 hours, whereas endothelin-1 message was rapidly degraded (half-life, &lt; 1 hour).	Dactinomycin	79-92	nitric oxide synthase 3	Homo sapiens	26-30
7538424-8	1995	TNF-alpha-induced destabilization of cNOS mRNA could be partially prevented by coincubation with cycloheximide (1 mumol/L) but was not reproduced by addition of sodium nitroprusside.	Cycloheximide	97-110	nitric oxide synthase 3	Homo sapiens	37-41
7999072-1	1994	Endotoxin and inflammatory cytokines downregulate expression of constitutive nitric oxide synthase (cNOS) in human vascular endothelial cells with concomitant increase of tetrahydrobiopterin synthesis in these cells and parallel upregulation of inducible NOS expression in smooth muscle cells, indicating compartmentalized nitric oxide (NO) production under septic conditions in man.	nitric	77-83	nitric oxide synthase 3	Homo sapiens	100-104
7999072-1	1994	Endotoxin and inflammatory cytokines downregulate expression of constitutive nitric oxide synthase (cNOS) in human vascular endothelial cells with concomitant increase of tetrahydrobiopterin synthesis in these cells and parallel upregulation of inducible NOS expression in smooth muscle cells, indicating compartmentalized nitric oxide (NO) production under septic conditions in man.	Nitric Oxide	77-89	nitric oxide synthase 3	Homo sapiens	100-104
7526714-5	1994	Exposing human endothelial cells to low PO2 results in 40-60% reduction in the steady-state mRNA levels of endothelial constitutive NO synthase (eNOS), the major enzyme responsible for NO production in these cells.	PO-2	40-43	nitric oxide synthase 3	Homo sapiens	145-149
7882138-3	1994	In addition, this cGMP generation was abrogated in the presence of either a Ca2+ chelator, EGTA, or a calcium/calmodulin inhibitor, W7, suggesting that IL-4 stimulates the constitutive NOS (cNOS).	Cyclic GMP	18-22	nitric oxide synthase 3	Homo sapiens	172-188
7882138-3	1994	In addition, this cGMP generation was abrogated in the presence of either a Ca2+ chelator, EGTA, or a calcium/calmodulin inhibitor, W7, suggesting that IL-4 stimulates the constitutive NOS (cNOS).	Cyclic GMP	18-22	nitric oxide synthase 3	Homo sapiens	190-194
7882138-3	1994	In addition, this cGMP generation was abrogated in the presence of either a Ca2+ chelator, EGTA, or a calcium/calmodulin inhibitor, W7, suggesting that IL-4 stimulates the constitutive NOS (cNOS).	Egtazic Acid	91-95	nitric oxide synthase 3	Homo sapiens	172-188
7523378-0	1994	Cysteine 184 of endothelial nitric oxide synthase is involved in heme coordination and catalytic activity.	Cysteine	0-8	nitric oxide synthase 3	Homo sapiens	16-49
7882138-3	1994	In addition, this cGMP generation was abrogated in the presence of either a Ca2+ chelator, EGTA, or a calcium/calmodulin inhibitor, W7, suggesting that IL-4 stimulates the constitutive NOS (cNOS).	Egtazic Acid	91-95	nitric oxide synthase 3	Homo sapiens	190-194
7523410-11	1994	Me-TC and Et-TC were less potent inhibitors of human iNOS (Ki values of 34 and 17 nM, respectively) and human eNOS (Ki values of 11 and 24 nM).	S-methylthiocitrulline	0-5	nitric oxide synthase 3	Homo sapiens	110-114
7523410-11	1994	Me-TC and Et-TC were less potent inhibitors of human iNOS (Ki values of 34 and 17 nM, respectively) and human eNOS (Ki values of 11 and 24 nM).	S-ethylthiocitrulline	10-15	nitric oxide synthase 3	Homo sapiens	110-114
7523410-12	1994	Thus, Me-TC and Et-TC were 10- and 50-fold, respectively, more potent inhibitors of nNOS than eNOS.	S-methylthiocitrulline	6-11	nitric oxide synthase 3	Homo sapiens	94-98
7523410-12	1994	Thus, Me-TC and Et-TC were 10- and 50-fold, respectively, more potent inhibitors of nNOS than eNOS.	S-ethylthiocitrulline	16-21	nitric oxide synthase 3	Homo sapiens	94-98
7523378-3	1994	To locate this specific cysteine, we altered three potential cysteine residues (Cys-99, Cys-184, and Cys-441) to alanine residues in human endothelial nitric oxide synthase (eNOS) by oligonucleotide-directed mutagenesis and expressed the wild-type and mutant eNOSs in COS-1 and the baculovirus expression system.	Cysteine	24-32	nitric oxide synthase 3	Homo sapiens	139-172
7523378-3	1994	To locate this specific cysteine, we altered three potential cysteine residues (Cys-99, Cys-184, and Cys-441) to alanine residues in human endothelial nitric oxide synthase (eNOS) by oligonucleotide-directed mutagenesis and expressed the wild-type and mutant eNOSs in COS-1 and the baculovirus expression system.	Cysteine	24-32	nitric oxide synthase 3	Homo sapiens	174-178
7523378-3	1994	To locate this specific cysteine, we altered three potential cysteine residues (Cys-99, Cys-184, and Cys-441) to alanine residues in human endothelial nitric oxide synthase (eNOS) by oligonucleotide-directed mutagenesis and expressed the wild-type and mutant eNOSs in COS-1 and the baculovirus expression system.	Cysteine	61-69	nitric oxide synthase 3	Homo sapiens	139-172
7523378-3	1994	To locate this specific cysteine, we altered three potential cysteine residues (Cys-99, Cys-184, and Cys-441) to alanine residues in human endothelial nitric oxide synthase (eNOS) by oligonucleotide-directed mutagenesis and expressed the wild-type and mutant eNOSs in COS-1 and the baculovirus expression system.	Cysteine	80-83	nitric oxide synthase 3	Homo sapiens	139-172
7523378-3	1994	To locate this specific cysteine, we altered three potential cysteine residues (Cys-99, Cys-184, and Cys-441) to alanine residues in human endothelial nitric oxide synthase (eNOS) by oligonucleotide-directed mutagenesis and expressed the wild-type and mutant eNOSs in COS-1 and the baculovirus expression system.	Cysteine	88-91	nitric oxide synthase 3	Homo sapiens	139-172
7523378-3	1994	To locate this specific cysteine, we altered three potential cysteine residues (Cys-99, Cys-184, and Cys-441) to alanine residues in human endothelial nitric oxide synthase (eNOS) by oligonucleotide-directed mutagenesis and expressed the wild-type and mutant eNOSs in COS-1 and the baculovirus expression system.	Oligonucleotides	183-198	nitric oxide synthase 3	Homo sapiens	139-172
7523378-3	1994	To locate this specific cysteine, we altered three potential cysteine residues (Cys-99, Cys-184, and Cys-441) to alanine residues in human endothelial nitric oxide synthase (eNOS) by oligonucleotide-directed mutagenesis and expressed the wild-type and mutant eNOSs in COS-1 and the baculovirus expression system.	Oligonucleotides	183-198	nitric oxide synthase 3	Homo sapiens	174-178
7523378-3	1994	To locate this specific cysteine, we altered three potential cysteine residues (Cys-99, Cys-184, and Cys-441) to alanine residues in human endothelial nitric oxide synthase (eNOS) by oligonucleotide-directed mutagenesis and expressed the wild-type and mutant eNOSs in COS-1 and the baculovirus expression system.	Carbon Monoxide	268-271	nitric oxide synthase 3	Homo sapiens	139-172
7523378-3	1994	To locate this specific cysteine, we altered three potential cysteine residues (Cys-99, Cys-184, and Cys-441) to alanine residues in human endothelial nitric oxide synthase (eNOS) by oligonucleotide-directed mutagenesis and expressed the wild-type and mutant eNOSs in COS-1 and the baculovirus expression system.	Carbon Monoxide	268-271	nitric oxide synthase 3	Homo sapiens	174-178
7523378-5	1994	Mutation of Cys-184 resulted in a complete loss of NOS catalytic activity and abrogation of the formation of carbon monoxide (CO)-heme ferrous complex, which was detected on CO difference spectra as a distinct peak centered on 444-446 nm, without reduction in the quantity of eNOS protein.	Cysteine	12-15	nitric oxide synthase 3	Homo sapiens	276-280
7523378-5	1994	Mutation of Cys-184 resulted in a complete loss of NOS catalytic activity and abrogation of the formation of carbon monoxide (CO)-heme ferrous complex, which was detected on CO difference spectra as a distinct peak centered on 444-446 nm, without reduction in the quantity of eNOS protein.	Carbon Monoxide	109-129	nitric oxide synthase 3	Homo sapiens	276-280
7523378-8	1994	These results indicate that the cysteine 184 of human eNOS is most likely the proximal heme ligand.	Cysteine	32-40	nitric oxide synthase 3	Homo sapiens	54-58
7523378-8	1994	These results indicate that the cysteine 184 of human eNOS is most likely the proximal heme ligand.	Heme	87-91	nitric oxide synthase 3	Homo sapiens	54-58
7680438-5	1993	These findings suggest that suppression of endothelial nitric oxide synthase in the porcine isolated splenic artery results in activation of arachidonic metabolism and production of vasoconstrictor eicosanoids.	Eicosanoids	198-209	nitric oxide synthase 3	Homo sapiens	43-76
7530816-3	1994	By contrast, endothelial nitric oxide synthase and neuronal nitric oxide synthase are thought to be constitutive with activation induced by calcium entry into cells in the absence of new protein synthesis.	Calcium	140-147	nitric oxide synthase 3	Homo sapiens	13-46
7537167-2	1994	Hemorrhagic shock leads to an inhibition of NO production by the calcium-dependent, endothelial NOS (ecNOS), which may lead to maldistribution of blood flow leading to, e.g., coronary, renal, and cerebral ischemia and may enhance the adhesion of neutrophil granulocytes and platelets to the endothelial surface.	Calcium	65-72	nitric oxide synthase 3	Homo sapiens	84-99
7537167-2	1994	Hemorrhagic shock leads to an inhibition of NO production by the calcium-dependent, endothelial NOS (ecNOS), which may lead to maldistribution of blood flow leading to, e.g., coronary, renal, and cerebral ischemia and may enhance the adhesion of neutrophil granulocytes and platelets to the endothelial surface.	Calcium	65-72	nitric oxide synthase 3	Homo sapiens	101-106
7514511-2	1994	Therefore, we investigated whether this sustained activation of the constitutive NO synthase (cNOS) could be mediated by an increase in pHi, which is induced by an activation of the Na(+)-H+ exchanger rather than an increase in [Ca2+]i. Cultured human endothelial cells grown on coverslips were loaded with either C.SNAFL-2 or fura 2-AM for fluorometric analysis of either pHi or [Ca2+]i.	SNAFL-2	316-323	nitric oxide synthase 3	Homo sapiens	94-98
7514511-2	1994	Therefore, we investigated whether this sustained activation of the constitutive NO synthase (cNOS) could be mediated by an increase in pHi, which is induced by an activation of the Na(+)-H+ exchanger rather than an increase in [Ca2+]i. Cultured human endothelial cells grown on coverslips were loaded with either C.SNAFL-2 or fura 2-AM for fluorometric analysis of either pHi or [Ca2+]i.	fura-2-am	327-336	nitric oxide synthase 3	Homo sapiens	94-98
7514511-4	1994	The pH dependence of a microsomal cNOS preparation was determined by assay of L-[3H]citrulline formation from L-[3H]arginine.	l-[3h]citrulline	78-94	nitric oxide synthase 3	Homo sapiens	34-38
7514511-4	1994	The pH dependence of a microsomal cNOS preparation was determined by assay of L-[3H]citrulline formation from L-[3H]arginine.	l-[3h]arginine	110-124	nitric oxide synthase 3	Homo sapiens	34-38
7514511-7	1994	The L-citrulline assay revealed a twofold increase in cNOS activity on increasing pH from 6.7 to 7.4, an optimum at pH 7.5, and a complete abolition of activity at pH 8.6.	Citrulline	4-16	nitric oxide synthase 3	Homo sapiens	54-58
7522050-5	1994	Upon complex formation, the amide I bands of the CaM-binding domains of MLCK and cNOS shift 4 cm-1 toward higher frequency (to approximately 1648 cm-1), and have a narrower bandwidth compared to the peptide in aqueous solution.	Amides	28-33	nitric oxide synthase 3	Homo sapiens	81-85
7685252-8	1993	This reduction in cNOS message in response to TNF-alpha depended on protein synthesis as it was blocked by cycloheximide.	Cycloheximide	107-120	nitric oxide synthase 3	Homo sapiens	18-22
33809023-0	2021	The Role of Single-Nucleotide Variants of NOS1, NOS2, and NOS3 Genes in the Comorbidity of Arterial Hypertension and Tension-Type Headache.	single-nucleotide	12-29	nitric oxide synthase 3	Homo sapiens	58-62
33777959-9	2021	In addition, crocin enhanced CD31, thrombomodulin (TM), and p-/t-endothelial nitric oxide synthase (eNOS) expressions as well as NO generation and decreased vascular tone.	crocin	13-19	nitric oxide synthase 3	Homo sapiens	60-98
33777959-9	2021	In addition, crocin enhanced CD31, thrombomodulin (TM), and p-/t-endothelial nitric oxide synthase (eNOS) expressions as well as NO generation and decreased vascular tone.	crocin	13-19	nitric oxide synthase 3	Homo sapiens	100-104
1719954-4	1991	The results indicate that Ca(2+)-calmodulin directly activates the endothelial nitric oxide synthase, thereby transducing agonist-induced increases in intracellular free Ca2+ concentration to nitric oxide formation from L-arginine, K(+)-induced depolarization of the endothelial cells markedly inhibited the sustained, but not initial phase of the intracellular Ca2+ response to bradykinin, indicating that K(+)-induced depolarization depresses the transmembrane Ca2+ influx.	Arginine	220-230	nitric oxide synthase 3	Homo sapiens	67-100
33806108-3	2021	The secretion of nitric oxide (NO), which is responsible for adequate regulation of the endothelium, is impaired due to a decrease in endothelial nitric oxide synthetase (eNOS) expression and an increase in endogenous eNOS inhibitors.	Nitric Oxide	17-29	nitric oxide synthase 3	Homo sapiens	134-169
33806108-3	2021	The secretion of nitric oxide (NO), which is responsible for adequate regulation of the endothelium, is impaired due to a decrease in endothelial nitric oxide synthetase (eNOS) expression and an increase in endogenous eNOS inhibitors.	Nitric Oxide	17-29	nitric oxide synthase 3	Homo sapiens	171-175
33806108-3	2021	The secretion of nitric oxide (NO), which is responsible for adequate regulation of the endothelium, is impaired due to a decrease in endothelial nitric oxide synthetase (eNOS) expression and an increase in endogenous eNOS inhibitors.	Nitric Oxide	17-29	nitric oxide synthase 3	Homo sapiens	218-222
31499544-7	2019	The aorta fails to relax completely after the addition of acetylcholine indicates the deranged eNOS signaling in the endothelium.	Acetylcholine	58-71	nitric oxide synthase 3	Homo sapiens	95-99
33232606-0	2020	Betulinic Acid Induces eNOS Expression via the AMPK-Dependent KLF2 Signaling Pathway.	betulinic acid	0-14	nitric oxide synthase 3	Homo sapiens	23-27
33232606-2	2020	We have previously shown that BA prevents endothelial dysfunction by increasing nitric oxide (NO) synthesis through activating endothelial nitric oxide synthase (eNOS) in human endothelial cells.	betulinic acid	30-32	nitric oxide synthase 3	Homo sapiens	127-160
33232606-2	2020	We have previously shown that BA prevents endothelial dysfunction by increasing nitric oxide (NO) synthesis through activating endothelial nitric oxide synthase (eNOS) in human endothelial cells.	betulinic acid	30-32	nitric oxide synthase 3	Homo sapiens	162-166
33232606-3	2020	However, the effect of BA on eNOS expression remains unclear.	betulinic acid	23-25	nitric oxide synthase 3	Homo sapiens	29-33
33232606-4	2020	Thus, the aim of our study was to investigate the intracellular pathways associated with the effect of BA to regulate eNOS expression in human endothelial cells.	betulinic acid	103-105	nitric oxide synthase 3	Homo sapiens	118-122
33232606-5	2020	BA significantly increased eNOS expression in a time- and concentration-dependent manner.	betulinic acid	0-2	nitric oxide synthase 3	Homo sapiens	27-31
33232606-6	2020	Additionally, BA upregulated the expression of the transcription factor KLF2, which is known to regulate eNOS expression.	betulinic acid	14-16	nitric oxide synthase 3	Homo sapiens	105-109
33232606-7	2020	KLF2 silencing in human endothelial cells attenuated the ability of BA to upregulate eNOS.	betulinic acid	68-70	nitric oxide synthase 3	Homo sapiens	85-89
31499544-8	2019	CONCLUSION: From the experimental findings, it was concluded that clozapine could depress the eNOS regulation and thereby perhaps initiates cardiovascular complications through subsequent vascular events.	Clozapine	66-75	nitric oxide synthase 3	Homo sapiens	94-98
22538734-1	2012	INTRODUCTION:  Asymmetric dimethylarginin (ADMA) is an endogenous inhibitor of endothelial nitric oxide synthase, considered an effector of endothelial dysfunction.	dimethylarginin	26-41	nitric oxide synthase 3	Homo sapiens	79-112
22538734-1	2012	INTRODUCTION:  Asymmetric dimethylarginin (ADMA) is an endogenous inhibitor of endothelial nitric oxide synthase, considered an effector of endothelial dysfunction.	N,N-dimethylarginine	43-47	nitric oxide synthase 3	Homo sapiens	79-112
23214142-6	2012	These molecules lead to further enhancement of oxidative stress, through uncoupling of endothelial nitric oxide synthase (eNOS) and production of peroxynitrite radical instead of nitric oxide which further disrupts eNOS function.	peroxynitrite radical	146-167	nitric oxide synthase 3	Homo sapiens	215-219
23214142-6	2012	These molecules lead to further enhancement of oxidative stress, through uncoupling of endothelial nitric oxide synthase (eNOS) and production of peroxynitrite radical instead of nitric oxide which further disrupts eNOS function.	Nitric Oxide	99-111	nitric oxide synthase 3	Homo sapiens	215-219
23214142-6	2012	These molecules lead to further enhancement of oxidative stress, through uncoupling of endothelial nitric oxide synthase (eNOS) and production of peroxynitrite radical instead of nitric oxide which further disrupts eNOS function.	Nitric Oxide	99-111	nitric oxide synthase 3	Homo sapiens	122-126
34953892-9	2022	Western blotting showed a higher level of SREBP2, iNOS, and VEGF and a lower eNOS level in the higher glucose groups.	Glucose	102-109	nitric oxide synthase 3	Homo sapiens	77-81
11701613-6	2001	We found that in macro- but not microvascular ECs, atorvastatin stabilized tube formation through a decrease in caveolin abundance and its inhibitory interaction with eNOS.	Atorvastatin	51-63	nitric oxide synthase 3	Homo sapiens	167-171
11701613-8	2001	Using geldanamycin, an inhibitor of hsp90 function, and overexpression of recombinant hsp90, we documented that the statin-induced phosphorylation of eNOS on Ser1177 was directly dependent on the ability of hsp90 to recruit Akt in the eNOS complex.	geldanamycin	6-18	nitric oxide synthase 3	Homo sapiens	150-154
34825477-0	2022	Gene-gene interactions in the protein kinase C/endothelial nitric oxide synthase axis impact the hypotensive effects of propofol.	Propofol	120-128	nitric oxide synthase 3	Homo sapiens	47-80
34825477-1	2022	Anaesthesia with propofol is frequently associated with hypotension, which is at least partially attributable to increased nitric oxide (NO) formation derived from the activation of protein kinase C (PKC)/endothelial NO synthase (NOS3) axis.	Propofol	17-25	nitric oxide synthase 3	Homo sapiens	230-234
34825477-1	2022	Anaesthesia with propofol is frequently associated with hypotension, which is at least partially attributable to increased nitric oxide (NO) formation derived from the activation of protein kinase C (PKC)/endothelial NO synthase (NOS3) axis.	Nitric Oxide	123-135	nitric oxide synthase 3	Homo sapiens	230-234
34825477-8	2022	Moreover, genotypes for the rs1010544 PRKCA polymorphism were associated with higher or lower blood pressure decreases in response to propofol depending on the genotypes for the rs2070744 NOS3 polymorphism.	Propofol	134-142	nitric oxide synthase 3	Homo sapiens	188-192
34825477-9	2022	Our findings suggest that PRKCA genotypes and haplotypes impact the hypotensive responses to propofol, possibly by modifying NO bioavailability, and that PRKCA-NOS3 interactions modify the blood pressure-lowering effects of propofol.	Propofol	224-232	nitric oxide synthase 3	Homo sapiens	160-164
24578389-12	2015	Reactive oxygen species excess, via NAD(P)H oxidase activation, induces the endothelial nitric oxide synthase uncoupling, which in turn generates superoxide and impairs NO production.	Reactive Oxygen Species	0-23	nitric oxide synthase 3	Homo sapiens	76-109
24578389-12	2015	Reactive oxygen species excess, via NAD(P)H oxidase activation, induces the endothelial nitric oxide synthase uncoupling, which in turn generates superoxide and impairs NO production.	Superoxides	146-156	nitric oxide synthase 3	Homo sapiens	76-109
24801072-5	2015	In this setting, Pin1 recognizes Ser-116 inhibitory phosphorylation of endothelial nitric oxide synthase (eNOS) leading to eNOS-caveolin-1 interaction and reduced NO availability.	Serine	33-36	nitric oxide synthase 3	Homo sapiens	71-104
34555857-0	2022	Anti-SARS-CoV-2 Action of Fluvoxamine may be Mediated by Endothelial Nitric Oxide Synthase.	Fluvoxamine	26-37	nitric oxide synthase 3	Homo sapiens	57-90
34634151-17	2022	While maternal treatment of normoxic or pair-fed pregnancies with melatonin on the offspring cardiovascular system was unremarkable, treatment of hypoxic pregnancies with melatonin in doses lower than those recommended for overcoming jet lag in humans enhanced fetal cardiac eNOS expression and prevented all alterations in cardiovascular structure and function in fetal and adult offspring.	Melatonin	171-180	nitric oxide synthase 3	Homo sapiens	275-279
34313822-6	2022	At the distal level, high UA concentrations impair endothelial NO synthase (eNOS)-NO system by decreasing eNOS expression and activity as well as by direct inactivation of NO.	Uric Acid	26-28	nitric oxide synthase 3	Homo sapiens	76-80
34986125-9	2021	Finally, the binding modes of EGFR, IL1B, NOS3 and TP53 with quercetin were visualized.	Quercetin	61-70	nitric oxide synthase 3	Homo sapiens	42-46
34313822-6	2022	At the distal level, high UA concentrations impair endothelial NO synthase (eNOS)-NO system by decreasing eNOS expression and activity as well as by direct inactivation of NO.	Uric Acid	26-28	nitric oxide synthase 3	Homo sapiens	106-110
34951375-6	2021	Variants in BDKRB2, NOS3, PRKCA, and VEGFA influenced the response to enalapril in patients with primary hypertension.	Enalapril	70-79	nitric oxide synthase 3	Homo sapiens	20-24
34986125-10	2021	DISCUSSION AND CONCLUSION: Quercetin of Baiying Qinghou decoction showed therapeutic effect against laryngeal squamous cell carcinoma by regulating TP53, EGFR, NOS3 and IL1B involved with drug resistance and PI3K-AKT signaling pathway.	Quercetin	27-36	nitric oxide synthase 3	Homo sapiens	160-164
34946563-7	2021	Moreover, some of them enhanced the activation of Akt (TYR, HT metabolites) and eNOS (HT, HVA, TYR-S, HT-3S).	4-hydroxyphenylethanol	95-98	nitric oxide synthase 3	Homo sapiens	80-84
34923902-3	2021	While the beneficial effects of eNOS are often thought to be mediated through the generation of nitric oxide, some protection is theorized to be through eNOS binding to regulatory pathways via a pentabasic RRKRK motif.	Nitric Oxide	96-108	nitric oxide synthase 3	Homo sapiens	32-36
34923902-8	2021	When TAT was coupled to the eNOS-RRKRK sequence, protection against LPS-induced permeability was still demonstrated, however cytokine production was not reduced.	Triethylenemelamine	5-8	nitric oxide synthase 3	Homo sapiens	28-32
34517018-8	2021	High levels of the phosphorylated monomeric superoxide anion-generating endothelial nitric oxide synthase (eNOS), decreased nitric oxide (NO) bioavailability, decreased soluble guanylyl cyclase (sGC) activity, and high levels of 3-nitrotyrosine were observed in HCM.	Superoxides	44-60	nitric oxide synthase 3	Homo sapiens	72-105
34871190-11	2022	Moreover, sPE-EVs significantly downregulated endothelial nitric oxide synthase (eNOS and p-eNOS) when compared to normotensive-EV.	spe-evs	10-17	nitric oxide synthase 3	Homo sapiens	46-79
34871190-11	2022	Moreover, sPE-EVs significantly downregulated endothelial nitric oxide synthase (eNOS and p-eNOS) when compared to normotensive-EV.	spe-evs	10-17	nitric oxide synthase 3	Homo sapiens	81-85
34871190-11	2022	Moreover, sPE-EVs significantly downregulated endothelial nitric oxide synthase (eNOS and p-eNOS) when compared to normotensive-EV.	spe-evs	10-17	nitric oxide synthase 3	Homo sapiens	92-96
34768128-10	2021	RESULTS: CS resulted in shrinkage of endothelial cells, impaired aorta relaxation, reduced eNOS expression, and induced expression of iNOS, NLRP3, caspase-1p20 and IL-1beta, which could be prevented by knockdown of iNOS and NLRP3.	Cesium	9-11	nitric oxide synthase 3	Homo sapiens	91-95
34773716-10	2021	Finally, miconazole and niacin were predicted as potential therapeutic drugs for gastric adenocarcinoma that bond stably with NOS3 and NNMT through hydrogen interactions.	Miconazole	9-19	nitric oxide synthase 3	Homo sapiens	126-130
34946286-5	2021	We have genotyped 4 single nucleotide polymorphisms (SNP) from 3 genes involved in the nitric oxide synthesis (NOS1, NOS2 and NOS3).	Nitric Oxide	87-99	nitric oxide synthase 3	Homo sapiens	126-130
34917264-9	2021	Moreover, KYP-2047 significantly reduced vascular-endothelial-growth-factor (VEGF) and endothelial-nitric-oxide-synthase (eNOS) expression.	3-hydroxy-2-({4-[4-(pyrimidin-2-yl)piperazine-1-carbonyl]phenyl}methyl)-1-benzofuran-7-carboxamide	10-13	nitric oxide synthase 3	Homo sapiens	87-120
34917264-9	2021	Moreover, KYP-2047 significantly reduced vascular-endothelial-growth-factor (VEGF) and endothelial-nitric-oxide-synthase (eNOS) expression.	3-hydroxy-2-({4-[4-(pyrimidin-2-yl)piperazine-1-carbonyl]phenyl}methyl)-1-benzofuran-7-carboxamide	10-13	nitric oxide synthase 3	Homo sapiens	122-126
34917264-10	2021	In the vivo xenograft model, KYP-2047 at doses of 1 and 5 mg/kg significantly reduced tumor burden and tumor weight, decreasing also angiogenesis markers VEGF and eNOS.	3-hydroxy-2-({4-[4-(pyrimidin-2-yl)piperazine-1-carbonyl]phenyl}methyl)-1-benzofuran-7-carboxamide	29-32	nitric oxide synthase 3	Homo sapiens	163-167
34860335-8	2021	In the candidate gene analysis, rs7830 (NOS3) was associated with both ADP aggregation rate and 18- and 30-month ISR, and rs 62,275,847 (AGTR1) was associated with both ADP aggregation rate and 30-month ISR.	Adenosine Diphosphate	71-74	nitric oxide synthase 3	Homo sapiens	40-44
34900182-12	2021	In conclusion, astragaloside IV can reverse the low level of eNOS caused by OxLDL by regulating HDAC activity to protect myocardial cells from oxide damage, which is manifested by the decrease of BNP concentration.	astragaloside	15-28	nitric oxide synthase 3	Homo sapiens	61-65
34652985-1	2021	Nitric oxide (NO) is a key factor in inflammation produced by endothelial nitric oxide synthase (eNOS) in endothelium, whose activity increases after stimulation with pro-inflammatory cytokines.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	62-95
34652985-1	2021	Nitric oxide (NO) is a key factor in inflammation produced by endothelial nitric oxide synthase (eNOS) in endothelium, whose activity increases after stimulation with pro-inflammatory cytokines.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	97-101
33896376-10	2021	RAGE inhibitor also increased the levels of NO and eNOS while decreasing the level of ET-1 in M-HSA-stimulated HUVECs.	Altretamine	96-99	nitric oxide synthase 3	Homo sapiens	51-55
34121195-6	2021	Recent and compelling evidence has reinforced that eNOS regulation results from a complex network of processes, with novel data concerning mechanisms such as mechano-sensing, epigenetic, posttranslational modifications, and the expression of NO- and l-arginine-related pathways.	Arginine	250-260	nitric oxide synthase 3	Homo sapiens	51-55
34773716-10	2021	Finally, miconazole and niacin were predicted as potential therapeutic drugs for gastric adenocarcinoma that bond stably with NOS3 and NNMT through hydrogen interactions.	Niacin	24-30	nitric oxide synthase 3	Homo sapiens	126-130
34773716-10	2021	Finally, miconazole and niacin were predicted as potential therapeutic drugs for gastric adenocarcinoma that bond stably with NOS3 and NNMT through hydrogen interactions.	Hydrogen	148-156	nitric oxide synthase 3	Homo sapiens	126-130
34517018-8	2021	High levels of the phosphorylated monomeric superoxide anion-generating endothelial nitric oxide synthase (eNOS), decreased nitric oxide (NO) bioavailability, decreased soluble guanylyl cyclase (sGC) activity, and high levels of 3-nitrotyrosine were observed in HCM.	Superoxides	44-60	nitric oxide synthase 3	Homo sapiens	107-111
34840664-2	2021	Uncoupling of endothelial nitric oxide synthase (eNOS) leads to a decrease in nitric oxide (NO) production, an increase in reactive oxygen species (ROS) production, NO consumption, and NO synthesis.	Nitric Oxide	78-90	nitric oxide synthase 3	Homo sapiens	14-47
34592471-0	2021	Endocan alters nitric oxide production in endothelial cells by targeting AKT/eNOS and NFkB/iNOS signaling.	Nitric Oxide	15-27	nitric oxide synthase 3	Homo sapiens	77-81
34638028-3	2021	Herein we focus on two enzymes that are key to the biosynthesis of superoxide and nitric oxide, NADPH oxidase 5 (NOX5) and endothelial nitric oxide synthase (eNOS), respectively.	Superoxides	67-77	nitric oxide synthase 3	Homo sapiens	123-156
34638028-3	2021	Herein we focus on two enzymes that are key to the biosynthesis of superoxide and nitric oxide, NADPH oxidase 5 (NOX5) and endothelial nitric oxide synthase (eNOS), respectively.	Superoxides	67-77	nitric oxide synthase 3	Homo sapiens	158-162
34638028-3	2021	Herein we focus on two enzymes that are key to the biosynthesis of superoxide and nitric oxide, NADPH oxidase 5 (NOX5) and endothelial nitric oxide synthase (eNOS), respectively.	Nitric Oxide	82-94	nitric oxide synthase 3	Homo sapiens	123-156
34638028-3	2021	Herein we focus on two enzymes that are key to the biosynthesis of superoxide and nitric oxide, NADPH oxidase 5 (NOX5) and endothelial nitric oxide synthase (eNOS), respectively.	Nitric Oxide	82-94	nitric oxide synthase 3	Homo sapiens	158-162
34818604-3	2022	AIM: To investigate whether Tetrathiomolybdate (TM) supplementation could ameliorate DMED by activation of eNOS.	tetrathiomolybdate	28-46	nitric oxide synthase 3	Homo sapiens	107-111
34818604-3	2022	AIM: To investigate whether Tetrathiomolybdate (TM) supplementation could ameliorate DMED by activation of eNOS.	tetrathiomolybdate	48-50	nitric oxide synthase 3	Homo sapiens	107-111
34818604-3	2022	AIM: To investigate whether Tetrathiomolybdate (TM) supplementation could ameliorate DMED by activation of eNOS.	dmed	85-89	nitric oxide synthase 3	Homo sapiens	107-111
34797313-1	2021	ABSTRACT: This study investigates the association of 5 single nucleotide polymorphisms (SNPs) in selected genes (ABO, VEGFA, BDKRB2, NOS3, and ADRB2) with blood pressure (BP) response to enalapril.	Enalapril	187-196	nitric oxide synthase 3	Homo sapiens	133-137
34797313-9	2021	A significant interaction between rs699947, rs495828, and rs2070744 (cross-validation consistency = 10/10; P = .0005) in response to enalapril was observed.We confirmed the association of rs1042714 (ADRB2) and rs1799722 (BDKRB2) with controlled hypertension and established an interaction between rs699947 (VEGFA), rs495828 (ABO), and rs2070744 (NOS3) with BP response to enalapril.	Enalapril	133-142	nitric oxide synthase 3	Homo sapiens	346-350
34716863-6	2021	UA uptake was concentration- and time-dependent, and UA treatment significantly reduced nitric oxide (NO) levels and eNOS activity.	Uric Acid	0-2	nitric oxide synthase 3	Homo sapiens	117-121
34716863-6	2021	UA uptake was concentration- and time-dependent, and UA treatment significantly reduced nitric oxide (NO) levels and eNOS activity.	Uric Acid	53-55	nitric oxide synthase 3	Homo sapiens	117-121
34716863-11	2021	CONCLUSIONS: GLUT9 mediated the effects of high UA levels on HUVECs by increasing the cellular uptake of UA, activating JAK2/STAT3 signaling, and reduced the production of active eNOS and NO in HUVECs.	Uric Acid	48-50	nitric oxide synthase 3	Homo sapiens	179-183
34536586-1	2021	Nitric oxide (NO) is omnipresent in the body and synthesized by 3 isoenzymes (nNOS, eNOS and iNOS), all detected in human skin.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	84-88
34900089-7	2021	Laboratory findings showed that SBP enhanced the endothelial nitric oxide synthase (eNOS) activity and regulated laboratory indexes especially for homocysteine.	Homocysteine	147-159	nitric oxide synthase 3	Homo sapiens	49-82
34840664-2	2021	Uncoupling of endothelial nitric oxide synthase (eNOS) leads to a decrease in nitric oxide (NO) production, an increase in reactive oxygen species (ROS) production, NO consumption, and NO synthesis.	Nitric Oxide	78-90	nitric oxide synthase 3	Homo sapiens	49-53
34840664-2	2021	Uncoupling of endothelial nitric oxide synthase (eNOS) leads to a decrease in nitric oxide (NO) production, an increase in reactive oxygen species (ROS) production, NO consumption, and NO synthesis.	Reactive Oxygen Species	123-146	nitric oxide synthase 3	Homo sapiens	14-47
34840664-2	2021	Uncoupling of endothelial nitric oxide synthase (eNOS) leads to a decrease in nitric oxide (NO) production, an increase in reactive oxygen species (ROS) production, NO consumption, and NO synthesis.	Reactive Oxygen Species	123-146	nitric oxide synthase 3	Homo sapiens	49-53
34840664-2	2021	Uncoupling of endothelial nitric oxide synthase (eNOS) leads to a decrease in nitric oxide (NO) production, an increase in reactive oxygen species (ROS) production, NO consumption, and NO synthesis.	Reactive Oxygen Species	148-151	nitric oxide synthase 3	Homo sapiens	14-47
34840664-2	2021	Uncoupling of endothelial nitric oxide synthase (eNOS) leads to a decrease in nitric oxide (NO) production, an increase in reactive oxygen species (ROS) production, NO consumption, and NO synthesis.	Reactive Oxygen Species	148-151	nitric oxide synthase 3	Homo sapiens	49-53
34840664-5	2021	The findings showed that the astragaloside IV can prevent or reverse the uncoupling of eNOS, increase eNOS and NO, and enhance several activating enzymes to activate the antioxidant system.	astragaloside	29-42	nitric oxide synthase 3	Homo sapiens	87-91
34840664-5	2021	The findings showed that the astragaloside IV can prevent or reverse the uncoupling of eNOS, increase eNOS and NO, and enhance several activating enzymes to activate the antioxidant system.	astragaloside	29-42	nitric oxide synthase 3	Homo sapiens	102-106
34720094-4	2021	The authors showed that PKN2 was activated by fluid shear stress and contributed to eNOS activation via a double play - indirect phosphorylation at serine 1177 (S1177) via AKT and direct phosphorylation of the S1179 site.	Serine	148-154	nitric oxide synthase 3	Homo sapiens	84-88
34798584-7	2021	BPC 157 activated endothelial nitric oxide synthase (eNOS) is associated with nitric oxide (NO) release, tissue repair and angiomodulatory properties which can lead to improved vascular integrity and immune response, reduced proinflammatory profile, and reduced critical levels of the disease.	Nitric Oxide	78-90	nitric oxide synthase 3	Homo sapiens	18-51
34798584-7	2021	BPC 157 activated endothelial nitric oxide synthase (eNOS) is associated with nitric oxide (NO) release, tissue repair and angiomodulatory properties which can lead to improved vascular integrity and immune response, reduced proinflammatory profile, and reduced critical levels of the disease.	Nitric Oxide	78-90	nitric oxide synthase 3	Homo sapiens	53-57
34750450-4	2021	Phosphorylation of eNOS and NO production were also increased in human umbilical vein endothelial cells cultured in medium containing NBIW, and NBIW showed reactive oxygen species scavenging activity.	nbiw	134-138	nitric oxide synthase 3	Homo sapiens	19-23
34750450-4	2021	Phosphorylation of eNOS and NO production were also increased in human umbilical vein endothelial cells cultured in medium containing NBIW, and NBIW showed reactive oxygen species scavenging activity.	Reactive Oxygen Species	156-179	nitric oxide synthase 3	Homo sapiens	19-23
34750450-6	2021	Taken together, our results show that percutaneously absorbed carbon dioxide changes to bicarbonate ions, which act directly on endothelial cells to increase NO production by phosphorylation of eNOS and thus improve blood flow.	Carbon Dioxide	62-76	nitric oxide synthase 3	Homo sapiens	194-198
34750450-6	2021	Taken together, our results show that percutaneously absorbed carbon dioxide changes to bicarbonate ions, which act directly on endothelial cells to increase NO production by phosphorylation of eNOS and thus improve blood flow.	Bicarbonates	88-99	nitric oxide synthase 3	Homo sapiens	194-198
34609050-1	2021	The balance between endothelial nitric oxide (NO) synthase (eNOS) activation and production of reactive oxygen species (ROS) is very important for NO homeostasis in liver sinusoidal endothelial cells (LSECs).	Nitric Oxide	32-44	nitric oxide synthase 3	Homo sapiens	60-64
34543641-4	2021	Recent evidence demonstrates testosterone activates androgen receptors (AR) and generates nitric oxide (NO) through the Akt-endothelial NO synthase (eNOS) pathway; however, it remains unknown how castration impacts this signaling pathway.	Testosterone	29-41	nitric oxide synthase 3	Homo sapiens	120-147
34543641-4	2021	Recent evidence demonstrates testosterone activates androgen receptors (AR) and generates nitric oxide (NO) through the Akt-endothelial NO synthase (eNOS) pathway; however, it remains unknown how castration impacts this signaling pathway.	Testosterone	29-41	nitric oxide synthase 3	Homo sapiens	149-153
34543641-4	2021	Recent evidence demonstrates testosterone activates androgen receptors (AR) and generates nitric oxide (NO) through the Akt-endothelial NO synthase (eNOS) pathway; however, it remains unknown how castration impacts this signaling pathway.	Nitric Oxide	90-102	nitric oxide synthase 3	Homo sapiens	120-147
34543641-4	2021	Recent evidence demonstrates testosterone activates androgen receptors (AR) and generates nitric oxide (NO) through the Akt-endothelial NO synthase (eNOS) pathway; however, it remains unknown how castration impacts this signaling pathway.	Nitric Oxide	90-102	nitric oxide synthase 3	Homo sapiens	149-153
34605247-0	2021	Laminar Flow on Endothelial Cells Suppresses eNOS O-GlcNAcylation to Promote eNOS Activity.	o-glcnacylation	50-65	nitric oxide synthase 3	Homo sapiens	45-49
34605247-0	2021	Laminar Flow on Endothelial Cells Suppresses eNOS O-GlcNAcylation to Promote eNOS Activity.	o-glcnacylation	50-65	nitric oxide synthase 3	Homo sapiens	77-81
34605247-1	2021	Rationale: In diabetic animals as well as high glucose cell culture conditions, endothelial nitric oxide synthase (eNOS) is heavily O-GlcNAcylated, which inhibits its phosphorylation and nitric oxide (NO) production.	Glucose	47-54	nitric oxide synthase 3	Homo sapiens	80-113
34605247-1	2021	Rationale: In diabetic animals as well as high glucose cell culture conditions, endothelial nitric oxide synthase (eNOS) is heavily O-GlcNAcylated, which inhibits its phosphorylation and nitric oxide (NO) production.	Glucose	47-54	nitric oxide synthase 3	Homo sapiens	115-119
34605247-1	2021	Rationale: In diabetic animals as well as high glucose cell culture conditions, endothelial nitric oxide synthase (eNOS) is heavily O-GlcNAcylated, which inhibits its phosphorylation and nitric oxide (NO) production.	Nitric Oxide	187-199	nitric oxide synthase 3	Homo sapiens	80-113
34605247-1	2021	Rationale: In diabetic animals as well as high glucose cell culture conditions, endothelial nitric oxide synthase (eNOS) is heavily O-GlcNAcylated, which inhibits its phosphorylation and nitric oxide (NO) production.	Nitric Oxide	187-199	nitric oxide synthase 3	Homo sapiens	115-119
34605247-8	2021	Inhibition of glycolysis via 2-deoxy-2-glucose (2-DG) in cells exposed to disturbed flow efficiently decreased eNOS O-GlcNAcylation, thereby increasing eNOS phosphorylation and NO production.	Glucose	39-46	nitric oxide synthase 3	Homo sapiens	111-115
34605247-8	2021	Inhibition of glycolysis via 2-deoxy-2-glucose (2-DG) in cells exposed to disturbed flow efficiently decreased eNOS O-GlcNAcylation, thereby increasing eNOS phosphorylation and NO production.	Glucose	39-46	nitric oxide synthase 3	Homo sapiens	152-156
34605247-8	2021	Inhibition of glycolysis via 2-deoxy-2-glucose (2-DG) in cells exposed to disturbed flow efficiently decreased eNOS O-GlcNAcylation, thereby increasing eNOS phosphorylation and NO production.	Deoxyglucose	48-52	nitric oxide synthase 3	Homo sapiens	111-115
34605247-8	2021	Inhibition of glycolysis via 2-deoxy-2-glucose (2-DG) in cells exposed to disturbed flow efficiently decreased eNOS O-GlcNAcylation, thereby increasing eNOS phosphorylation and NO production.	Deoxyglucose	48-52	nitric oxide synthase 3	Homo sapiens	152-156
34585422-6	2021	Treatment with EtOH alone or stimulation of Notch signaling by DLL4 increased eNOS activity and enhanced HCAEC barrier function as assessed by trans-endothelial electrical resistance.	Ethanol	15-19	nitric oxide synthase 3	Homo sapiens	78-82
34380696-2	2021	In this study, we show genetic deletion and viral knockdown of hepatocyte-specific eNOS exacerbated hepatic steatosis and inflammation, decreased hepatic mitochondrial fatty acid oxidation and respiration, increased mitochondrial H2O2 emission, and impaired the hepatic mitophagic (BNIP3 and LC3II) response.	Fatty Acids	168-178	nitric oxide synthase 3	Homo sapiens	83-87
34380696-2	2021	In this study, we show genetic deletion and viral knockdown of hepatocyte-specific eNOS exacerbated hepatic steatosis and inflammation, decreased hepatic mitochondrial fatty acid oxidation and respiration, increased mitochondrial H2O2 emission, and impaired the hepatic mitophagic (BNIP3 and LC3II) response.	Hydrogen Peroxide	230-234	nitric oxide synthase 3	Homo sapiens	83-87
34380696-4	2021	Moreover, patients with elevated NAFLD activity score (histology score of worsening steatosis, hepatocyte ballooning, and inflammation) exhibited reduced hepatic eNOS expression which correlated with reduced hepatic mitochondrial fatty acid oxidation and lower hepatic protein expression of mitophagy protein BNIP3.	Fatty Acids	230-240	nitric oxide synthase 3	Homo sapiens	162-166
34499618-1	2021	Formation of nitric oxide (NO) by the endothelial NO-synthase (eNOS) is a central process in the homeostatic regulation of vascular functions including blood pressure regulation and fluid shear stress exerted by the flowing blood is a main stimulus of eNOS activity.	Nitric Oxide	13-25	nitric oxide synthase 3	Homo sapiens	38-61
34499618-1	2021	Formation of nitric oxide (NO) by the endothelial NO-synthase (eNOS) is a central process in the homeostatic regulation of vascular functions including blood pressure regulation and fluid shear stress exerted by the flowing blood is a main stimulus of eNOS activity.	Nitric Oxide	13-25	nitric oxide synthase 3	Homo sapiens	63-67
34499618-1	2021	Formation of nitric oxide (NO) by the endothelial NO-synthase (eNOS) is a central process in the homeostatic regulation of vascular functions including blood pressure regulation and fluid shear stress exerted by the flowing blood is a main stimulus of eNOS activity.	Nitric Oxide	13-25	nitric oxide synthase 3	Homo sapiens	252-256
34499618-5	2021	Active PKN2 promoted phosphorylation of human eNOS at serine 1177 and at a newly identified site, serine 1179.	Serine	54-60	nitric oxide synthase 3	Homo sapiens	46-50
34499618-7	2021	PKN2-mediated eNOS phosphorylation at serine 1177 involved phosphorylation of AKT synergistically with mTORC2-mediated AKT phosphorylation while active PKN2 directly phosphorylated human eNOS at serine 1179.	Serine	38-44	nitric oxide synthase 3	Homo sapiens	14-18
34499618-7	2021	PKN2-mediated eNOS phosphorylation at serine 1177 involved phosphorylation of AKT synergistically with mTORC2-mediated AKT phosphorylation while active PKN2 directly phosphorylated human eNOS at serine 1179.	Serine	195-201	nitric oxide synthase 3	Homo sapiens	14-18
34499618-7	2021	PKN2-mediated eNOS phosphorylation at serine 1177 involved phosphorylation of AKT synergistically with mTORC2-mediated AKT phosphorylation while active PKN2 directly phosphorylated human eNOS at serine 1179.	Serine	195-201	nitric oxide synthase 3	Homo sapiens	187-191
34237174-2	2021	Increased arginase 1 activity leads to reduced nitric oxide (NO) production and increased formation of reactive oxygen species due to uncoupling of the NO-producing enzyme endothelial NO synthase (eNOS).	Oxygen	112-118	nitric oxide synthase 3	Homo sapiens	197-201
34724738-0	2021	Letter to the Editor Regarding "Pregabalin Protects Brain Tissue from Subarachnoid Hemorrhage by Enhancing HIF-1alpha/eNOS Signaling and VEGF Production".	Pregabalin	32-42	nitric oxide synthase 3	Homo sapiens	118-122
34507631-6	2021	Endothelial nitric oxide synthase activity was reduced by nicotine- and tar-free CSE of IQOS and hi-lite (IQOS < hi-lite), but not Ploom S and glo.	Nicotine	58-66	nitric oxide synthase 3	Homo sapiens	0-33
34547902-14	2021	CMA of SG-eNOS terminates O2 - generation preventing further tissue damage but causes irreversible loss of eNOS and NO availability.	Oxygen	26-28	nitric oxide synthase 3	Homo sapiens	10-14
34666758-2	2021	In some tissues, Akt phosphorylates and activates endothelial nitric oxide synthase (eNOS) to produce nitric oxide (NO) that has anti-inflammatory effects.	Nitric Oxide	102-114	nitric oxide synthase 3	Homo sapiens	50-83
34708887-7	2022	However, administration of NOX1/4 inhibitor GKT137831 alleviated PM2.5 -induced elevated endothelial dysfunction biomarkers (NO, ET-1, ADMA, iNOS, and tPA/PAI-1), inflammatory factors (IL-1beta, IL-10, and IL-18), and adhesion molecules (ICAM-1, VCAM-1, and P-selectin) and also passivated NOX-dependent AKT and eNOS phosphorylation that involved in endothelial activation.	setanaxib	44-53	nitric oxide synthase 3	Homo sapiens	312-316
34708887-8	2022	In summary, PM2.5 -induced NOX up-regulation is the source of ROS in EA.hy926, which activated AKT/eNOS/NO signal response leading to endothelial dysfunction and inflammatory damage in EA.hy926 cells.	ros	62-65	nitric oxide synthase 3	Homo sapiens	99-103
34698745-2	2022	Nitric oxide (NO) is mainly produced by endothelial nitric oxide synthase (eNOS) on the membrane of endothelial cells (ECs) in the cardiovascular system and plays an important role in vasomotor function.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	40-73
34698745-2	2022	Nitric oxide (NO) is mainly produced by endothelial nitric oxide synthase (eNOS) on the membrane of endothelial cells (ECs) in the cardiovascular system and plays an important role in vasomotor function.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	75-79
34601865-9	2021	Moreover, LH increased the expressions of eNOS, IL-10, and TNF-alpha in serum, which were all reversed by a single dose of MH at 2 h, similar to ketamine.	mh	123-125	nitric oxide synthase 3	Homo sapiens	42-46
34601865-9	2021	Moreover, LH increased the expressions of eNOS, IL-10, and TNF-alpha in serum, which were all reversed by a single dose of MH at 2 h, similar to ketamine.	Ketamine	145-153	nitric oxide synthase 3	Homo sapiens	42-46
34666758-2	2021	In some tissues, Akt phosphorylates and activates endothelial nitric oxide synthase (eNOS) to produce nitric oxide (NO) that has anti-inflammatory effects.	Nitric Oxide	102-114	nitric oxide synthase 3	Homo sapiens	85-89
34666758-9	2021	RESULTS: SC79 induced a ~ twofold induction of p-eNOS and Nrf-2 protein levels blocked by PI3K inhibitor LY294002.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	105-113	nitric oxide synthase 3	Homo sapiens	49-53
34419618-5	2021	Activating TRPA1 with cinnamaldehyde prevented downregulation of eNOS, Nrf2, and UCP2, inhibited superoxide production and apoptosis, and preserved nitric oxide bioavailability in senescent HUVECs.	cinnamaldehyde	22-36	nitric oxide synthase 3	Homo sapiens	65-69
34419618-7	2021	Dietary administration of cinnamaldehyde for 12 months prevented mitochondrial dysfunction, improved endothelium-dependent relaxation, and increased expression of eNOS, Nrf2, and UCP2 in aged aortas.	cinnamaldehyde	26-40	nitric oxide synthase 3	Homo sapiens	163-167
34620931-5	2021	Non-aspirin NSAID users who carry e-NOS intron 4 VNTR polymorphism have lower odds of UGIH (OR: 4.02 (95% CI 1.85, 8.75) than those users with wild type genotype (OR: 6.52 (95% CI 4.09, 10.38)); though the interaction estimates are not statistically significant (RERI: -2.68 (95% CI -6.67, 1.31); S: 0.53 (95% CI 0.18, 1.55)).	Aspirin	4-11	nitric oxide synthase 3	Homo sapiens	34-39
34635055-2	2021	There are multiple forms of cross-talk between the RhoA/ROCK pathway and the eNOS/NO/cGMP pathway, but previous work has not studied their interplay at a systems level.	Cyclic GMP	85-89	nitric oxide synthase 3	Homo sapiens	77-81
34692789-8	2021	Lower level of reactive oxygen species (ROS) after EDI treatment was correlated with a reduction of hypoxic damage (eNOS and Caveolin-1) and significant increase of oxidation-reduction potential.	Reactive Oxygen Species	15-38	nitric oxide synthase 3	Homo sapiens	116-120
34156316-0	2021	Association between endothelial nitric oxide synthase and the renin-angiotensin-aldosterone system polymorphisms, blood pressure and training status in normotensive/pre-hypertension and hypertensive older adults: a pilot study.	Aldosterone	80-91	nitric oxide synthase 3	Homo sapiens	20-53
34156316-1	2021	Introduction:Variations in blood pressure (BP) are, in part, genetically determined and some polymorphisms of renin-angiotensin- aldosterone system (RAAS) and synthase of endothelial nitric oxide (eNOS) have been related to hypertension (HT).	Nitric Oxide	183-195	nitric oxide synthase 3	Homo sapiens	197-201
34692789-8	2021	Lower level of reactive oxygen species (ROS) after EDI treatment was correlated with a reduction of hypoxic damage (eNOS and Caveolin-1) and significant increase of oxidation-reduction potential.	Reactive Oxygen Species	40-43	nitric oxide synthase 3	Homo sapiens	116-120
34332276-9	2021	However, the protective effect of U50,488H was abolished by kappa-OR antagonist, nor-BNI, and inhibitors of PI3K, Akt and eNOS.	u50	34-37	nitric oxide synthase 3	Homo sapiens	122-126
34363795-2	2021	It has been reported that G-1, an agonist of GPER, increases nitric oxide (NO) production through the phosphorylation of endothelial nitric oxide synthase (eNOS).	Nitric Oxide	61-73	nitric oxide synthase 3	Homo sapiens	121-154
34363795-2	2021	It has been reported that G-1, an agonist of GPER, increases nitric oxide (NO) production through the phosphorylation of endothelial nitric oxide synthase (eNOS).	Nitric Oxide	61-73	nitric oxide synthase 3	Homo sapiens	156-160
34363795-6	2021	In addition, inhibition of the Galphaq and Gbetagamma suppressed G-1-induced the expression of eNOS and KLF2 in EA.hy926 cells.	gbetagamma	43-53	nitric oxide synthase 3	Homo sapiens	95-99
34332276-6	2021	RESULTS: The SP-induced hyperlipidemic cell model demonstrated increased expression of NLRP3 and caspase-1 proteins (P < 0.05) and elevated ROS levels (P < 0.01), and decreased phosphorylated-Akt and phosphorylated-eNOS expression (P < 0.05).	Palmitic Acid	13-15	nitric oxide synthase 3	Homo sapiens	215-219
34332276-10	2021	CONCLUSION: Our findings suggest that kappa-OR activation inhibits SP-induced inflammation by activating the PI3K/Akt/eNOS signaling pathway.	Palmitic Acid	67-69	nitric oxide synthase 3	Homo sapiens	118-122
34368873-5	2021	The present study aimed to investigate whether SAL exerted its effects on Hcy-induced EndMT via the Kruppel-like factor 4 (KLF4)/endothelial nitric oxide (NO) synthase (eNOS) signaling pathway.	rhodioloside	47-50	nitric oxide synthase 3	Homo sapiens	169-173
34368873-0	2021	Salidroside inhibits endothelial-mesenchymal transition via the KLF4/eNOS signaling pathway.	rhodioloside	0-11	nitric oxide synthase 3	Homo sapiens	69-73
34346156-3	2021	It has been previously shown that polyphenols from wine and grape extracts possess vasodilator activities, due to the increased expression and phosphorylation of the endothelial nitric oxide synthase (eNOS), and consequent vasodilator nitric oxide (NO) production.	Polyphenols	34-45	nitric oxide synthase 3	Homo sapiens	166-199
34346156-3	2021	It has been previously shown that polyphenols from wine and grape extracts possess vasodilator activities, due to the increased expression and phosphorylation of the endothelial nitric oxide synthase (eNOS), and consequent vasodilator nitric oxide (NO) production.	Polyphenols	34-45	nitric oxide synthase 3	Homo sapiens	201-205
34346156-3	2021	It has been previously shown that polyphenols from wine and grape extracts possess vasodilator activities, due to the increased expression and phosphorylation of the endothelial nitric oxide synthase (eNOS), and consequent vasodilator nitric oxide (NO) production.	Nitric Oxide	235-247	nitric oxide synthase 3	Homo sapiens	166-199
34368873-5	2021	The present study aimed to investigate whether SAL exerted its effects on Hcy-induced EndMT via the Kruppel-like factor 4 (KLF4)/endothelial nitric oxide (NO) synthase (eNOS) signaling pathway.	Homocysteine	74-77	nitric oxide synthase 3	Homo sapiens	169-173
34346156-3	2021	It has been previously shown that polyphenols from wine and grape extracts possess vasodilator activities, due to the increased expression and phosphorylation of the endothelial nitric oxide synthase (eNOS), and consequent vasodilator nitric oxide (NO) production.	Nitric Oxide	235-247	nitric oxide synthase 3	Homo sapiens	201-205
34368873-5	2021	The present study aimed to investigate whether SAL exerted its effects on Hcy-induced EndMT via the Kruppel-like factor 4 (KLF4)/endothelial nitric oxide (NO) synthase (eNOS) signaling pathway.	Nitric Oxide	141-153	nitric oxide synthase 3	Homo sapiens	169-173
34368873-11	2021	The results of the present study revealed that treatment with SAL upregulated the expression levels of VE-cadherin, downregulated the expression levels of alpha-SMA, reduced cell migration and activated the eNOS/NO signaling axis, as well as downregulated KLF4 expression and translocation to the nucleus.	rhodioloside	62-65	nitric oxide synthase 3	Homo sapiens	207-211
34368873-13	2021	In conclusion, the findings of the present study revealed that SAL may inhibit Hcy-induced EndMT via regulation of the KLF4/eNOS signaling pathway.	rhodioloside	63-66	nitric oxide synthase 3	Homo sapiens	124-128
34368873-13	2021	In conclusion, the findings of the present study revealed that SAL may inhibit Hcy-induced EndMT via regulation of the KLF4/eNOS signaling pathway.	Homocysteine	79-82	nitric oxide synthase 3	Homo sapiens	124-128
34546460-8	2021	We also showed that the miR-182/Myadm relate BMP-TGF-beta pathway is associated with NOS3/NO/cGMP via the crosstalk between endothelial cells and smooth muscle cells.	Cyclic GMP	93-97	nitric oxide synthase 3	Homo sapiens	85-89
34638713-2	2021	In a cirrhotic liver, the key enzymes endothelial NO synthase (eNOS), soluble guanylate cyclase (sGC), and phosphodiesterase-5 (PDE-5) are overexpressed, leading to decreased cyclic guanosine-monophosphate (cGMP).	Cyclic GMP	175-205	nitric oxide synthase 3	Homo sapiens	38-61
34638713-2	2021	In a cirrhotic liver, the key enzymes endothelial NO synthase (eNOS), soluble guanylate cyclase (sGC), and phosphodiesterase-5 (PDE-5) are overexpressed, leading to decreased cyclic guanosine-monophosphate (cGMP).	Cyclic GMP	175-205	nitric oxide synthase 3	Homo sapiens	63-67
34638713-2	2021	In a cirrhotic liver, the key enzymes endothelial NO synthase (eNOS), soluble guanylate cyclase (sGC), and phosphodiesterase-5 (PDE-5) are overexpressed, leading to decreased cyclic guanosine-monophosphate (cGMP).	Cyclic GMP	207-211	nitric oxide synthase 3	Homo sapiens	38-61
34638713-2	2021	In a cirrhotic liver, the key enzymes endothelial NO synthase (eNOS), soluble guanylate cyclase (sGC), and phosphodiesterase-5 (PDE-5) are overexpressed, leading to decreased cyclic guanosine-monophosphate (cGMP).	Cyclic GMP	207-211	nitric oxide synthase 3	Homo sapiens	63-67
34638626-0	2021	Cilostazol Induces eNOS and TM Expression via Activation with Sirtuin 1/Kruppel-like Factor 2 Pathway in Endothelial Cells.	Cilostazol	0-10	nitric oxide synthase 3	Homo sapiens	19-23
34638626-6	2021	We found cilostazol significantly activated KLF2 expression and KLF2-related endothelial function, including eNOS activation, Nitric oxide (NO) production, and TM secretion.	Cilostazol	9-19	nitric oxide synthase 3	Homo sapiens	109-113
34553653-0	2021	Harnessing polyphenol power by targeting eNOS for vascular diseases.	Polyphenols	11-21	nitric oxide synthase 3	Homo sapiens	41-45
34553653-3	2021	Decreased nitric oxide (NO) bioavailability was found to be associated with anomalous endothelial function because of either its reduced production level by endothelial NO synthase (eNOS) which synthesize this potent endogenous vasodilator from L-arginine or its enhanced breakdown due to severe oxidative stress and eNOS uncoupling.	Nitric Oxide	10-22	nitric oxide synthase 3	Homo sapiens	157-180
34553653-3	2021	Decreased nitric oxide (NO) bioavailability was found to be associated with anomalous endothelial function because of either its reduced production level by endothelial NO synthase (eNOS) which synthesize this potent endogenous vasodilator from L-arginine or its enhanced breakdown due to severe oxidative stress and eNOS uncoupling.	Nitric Oxide	10-22	nitric oxide synthase 3	Homo sapiens	182-186
34553653-3	2021	Decreased nitric oxide (NO) bioavailability was found to be associated with anomalous endothelial function because of either its reduced production level by endothelial NO synthase (eNOS) which synthesize this potent endogenous vasodilator from L-arginine or its enhanced breakdown due to severe oxidative stress and eNOS uncoupling.	Nitric Oxide	10-22	nitric oxide synthase 3	Homo sapiens	317-321
34553653-3	2021	Decreased nitric oxide (NO) bioavailability was found to be associated with anomalous endothelial function because of either its reduced production level by endothelial NO synthase (eNOS) which synthesize this potent endogenous vasodilator from L-arginine or its enhanced breakdown due to severe oxidative stress and eNOS uncoupling.	Arginine	245-255	nitric oxide synthase 3	Homo sapiens	157-180
34553653-3	2021	Decreased nitric oxide (NO) bioavailability was found to be associated with anomalous endothelial function because of either its reduced production level by endothelial NO synthase (eNOS) which synthesize this potent endogenous vasodilator from L-arginine or its enhanced breakdown due to severe oxidative stress and eNOS uncoupling.	Arginine	245-255	nitric oxide synthase 3	Homo sapiens	182-186
34553653-7	2021	This article will focus on in vitro as well as in vivo and clinical studies evidences of the polyphenols with eNOS modulating activity against vascular disease condition while their molecular mechanism will also be discussed.	Polyphenols	93-104	nitric oxide synthase 3	Homo sapiens	110-114
34552142-5	2021	CTEPH-EC displayed a hyperproliferative phenotype with an increase expression of adhesion molecules and a decreased apoptosis, eNOS activity, migration capacity and reduced angiogenic capacity in vitro and in vivo compared to healthy endothelial cells.	cteph-ec	0-8	nitric oxide synthase 3	Homo sapiens	127-131
34536182-12	2022	Expression of eNOS and UCP2 mRNA and NO production were decreased after DOX exposure, and PBMT preconditioning before the DOX challenge reversed these changes.	Doxorubicin	72-75	nitric oxide synthase 3	Homo sapiens	14-18
34533033-9	2021	Pathway analysis suggested gene expression changes, driven by a network of inflammatory cytokines centered on IL-1beta (interleukin 1beta), lead to repression of reno-protective eNOS (endothelial nitric oxide synthase) signaling during ADHF development, and following recovery, activation of glomerulosclerosis and reno-protective pathways and repression of proinflammatory/fibrotic pathways.	adhf	236-240	nitric oxide synthase 3	Homo sapiens	178-182
34533033-9	2021	Pathway analysis suggested gene expression changes, driven by a network of inflammatory cytokines centered on IL-1beta (interleukin 1beta), lead to repression of reno-protective eNOS (endothelial nitric oxide synthase) signaling during ADHF development, and following recovery, activation of glomerulosclerosis and reno-protective pathways and repression of proinflammatory/fibrotic pathways.	adhf	236-240	nitric oxide synthase 3	Homo sapiens	184-217
34536182-12	2022	Expression of eNOS and UCP2 mRNA and NO production were decreased after DOX exposure, and PBMT preconditioning before the DOX challenge reversed these changes.	Doxorubicin	122-125	nitric oxide synthase 3	Homo sapiens	14-18
34496169-0	2021	The serum levels of testosterone in coronary artery disease patients; relation to NO, eNOS, endothelin-1, and disease severity.	Testosterone	20-32	nitric oxide synthase 3	Homo sapiens	86-90
34432981-7	2021	Moreover, the GL13K-coated titanium surface demonstrated significant promotion of angiogenesis differentiation of HUVECs as indicated by the upregulated expression of essential angiogenesis function genes, including hypoxia-inducible factor-1alpha, endothelial nitric oxide synthase, kinase insert domain receptor, and vascular endothelial growth factor A (HIF-1alpha, eNOS, KDR, and VEGF-A).	GL13K	14-19	nitric oxide synthase 3	Homo sapiens	249-282
34432981-7	2021	Moreover, the GL13K-coated titanium surface demonstrated significant promotion of angiogenesis differentiation of HUVECs as indicated by the upregulated expression of essential angiogenesis function genes, including hypoxia-inducible factor-1alpha, endothelial nitric oxide synthase, kinase insert domain receptor, and vascular endothelial growth factor A (HIF-1alpha, eNOS, KDR, and VEGF-A).	GL13K	14-19	nitric oxide synthase 3	Homo sapiens	369-373
34542035-1	2022	BACKGROUND: Our objective in this study was to assess the association between eNOS gene, that achieves synthesis of nitric oxide especially in the endothelial cells known to have an important role in angiogenesis and vasculogenesis, G894T, intron 4 VNTR (27-bp repeat) and T786C functional polymorphisms and retinopathy of prematurity (ROP), which is an important cause of morbidity in premature or low birth weight babies.	Nitric Oxide	116-128	nitric oxide synthase 3	Homo sapiens	78-82
34502464-0	2021	Metastatic Melanoma Progression Is Associated with Endothelial Nitric Oxide Synthase Uncoupling Induced by Loss of eNOS:BH4 Stoichiometry.	sapropterin	120-123	nitric oxide synthase 3	Homo sapiens	51-84
34502464-0	2021	Metastatic Melanoma Progression Is Associated with Endothelial Nitric Oxide Synthase Uncoupling Induced by Loss of eNOS:BH4 Stoichiometry.	sapropterin	120-123	nitric oxide synthase 3	Homo sapiens	115-119
34502464-3	2021	Dysfunctional endothelial nitric oxide synthase (eNOS) produces superoxide anion (O2- ) and contributes to the establishment of a pro-oxidant environment in melanoma.	Superoxides	64-80	nitric oxide synthase 3	Homo sapiens	14-47
34171447-7	2021	Of the few requirements of AMPK-SIRT1 activation, increased eNOS is essential for NED by elevating Nitric oxide (NO) levels.	Nitric Oxide	99-111	nitric oxide synthase 3	Homo sapiens	60-64
34502464-3	2021	Dysfunctional endothelial nitric oxide synthase (eNOS) produces superoxide anion (O2- ) and contributes to the establishment of a pro-oxidant environment in melanoma.	Superoxides	64-80	nitric oxide synthase 3	Homo sapiens	49-53
34502464-3	2021	Dysfunctional endothelial nitric oxide synthase (eNOS) produces superoxide anion (O2- ) and contributes to the establishment of a pro-oxidant environment in melanoma.	Oxygen	82-85	nitric oxide synthase 3	Homo sapiens	14-47
34502464-3	2021	Dysfunctional endothelial nitric oxide synthase (eNOS) produces superoxide anion (O2- ) and contributes to the establishment of a pro-oxidant environment in melanoma.	Oxygen	82-85	nitric oxide synthase 3	Homo sapiens	49-53
34502464-4	2021	Although decreased tetrahydrobiopterin (BH4) bioavailability is associated with eNOS uncoupling in endothelial and human melanoma cells, in the present work we show that eNOS uncoupling in metastatic melanoma cells expressing the genes from de novo biopterin synthesis pathway Gch1, Pts, and Spr, and high BH4 concentration and BH4:BH2 ratio.	sapropterin	19-38	nitric oxide synthase 3	Homo sapiens	80-84
34502464-4	2021	Although decreased tetrahydrobiopterin (BH4) bioavailability is associated with eNOS uncoupling in endothelial and human melanoma cells, in the present work we show that eNOS uncoupling in metastatic melanoma cells expressing the genes from de novo biopterin synthesis pathway Gch1, Pts, and Spr, and high BH4 concentration and BH4:BH2 ratio.	sapropterin	40-43	nitric oxide synthase 3	Homo sapiens	80-84
34502464-4	2021	Although decreased tetrahydrobiopterin (BH4) bioavailability is associated with eNOS uncoupling in endothelial and human melanoma cells, in the present work we show that eNOS uncoupling in metastatic melanoma cells expressing the genes from de novo biopterin synthesis pathway Gch1, Pts, and Spr, and high BH4 concentration and BH4:BH2 ratio.	Biopterin	249-258	nitric oxide synthase 3	Homo sapiens	170-174
34502464-5	2021	Western blot analysis showed increased expression of Nos3, altering the stoichiometry balance between eNOS and BH4, contributing to NOS uncoupling.	sapropterin	111-114	nitric oxide synthase 3	Homo sapiens	53-57
34502464-6	2021	Both treatment with L-sepiapterin and eNOS downregulation induced increased nitric oxide (NO) and decreased O2  levels, triggering NOS coupling and reducing cell growth and resistance to anoikis and dacarbazine chemotherapy.	Nitric Oxide	76-88	nitric oxide synthase 3	Homo sapiens	38-42
34502464-6	2021	Both treatment with L-sepiapterin and eNOS downregulation induced increased nitric oxide (NO) and decreased O2  levels, triggering NOS coupling and reducing cell growth and resistance to anoikis and dacarbazine chemotherapy.	Oxygen	108-110	nitric oxide synthase 3	Homo sapiens	38-42
34502464-6	2021	Both treatment with L-sepiapterin and eNOS downregulation induced increased nitric oxide (NO) and decreased O2  levels, triggering NOS coupling and reducing cell growth and resistance to anoikis and dacarbazine chemotherapy.	Dacarbazine	199-210	nitric oxide synthase 3	Homo sapiens	38-42
34573361-9	2021	In addition, BPME treatment of HUVECs for 48 h reduced mRNA expression of lipid peroxide (LPO) and increased NOS-3, Nrf-2, GSK-3beta, GPX, endothelial nitric oxide synthase (eNOS) and vascular cell growth factor (VEGF) mRNA expression levels.	bpme	13-17	nitric oxide synthase 3	Homo sapiens	109-114
34502308-0	2021	Rutaecarpine Increases Nitric Oxide Synthesis via eNOS Phosphorylation by TRPV1-Dependent CaMKII and CaMKKbeta/AMPK Signaling Pathway in Human Endothelial Cells.	rutecarpine	0-12	nitric oxide synthase 3	Homo sapiens	50-54
34502308-3	2021	In this study, we demonstrated the effects of RUT on nitric oxide (NO) synthesis via endothelial nitric oxide synthase (eNOS) phosphorylation in endothelial cells and the underlying molecular mechanisms.	Nitric Oxide	53-65	nitric oxide synthase 3	Homo sapiens	85-118
34502308-3	2021	In this study, we demonstrated the effects of RUT on nitric oxide (NO) synthesis via endothelial nitric oxide synthase (eNOS) phosphorylation in endothelial cells and the underlying molecular mechanisms.	Nitric Oxide	53-65	nitric oxide synthase 3	Homo sapiens	120-124
34502308-7	2021	Treatment with KN-62 (a CaMKII inhibitor), Compound C (an AMPK inhibitor), and STO-609 (a CaMKKbeta inhibitor) suppressed RUT-induced eNOS phosphorylation and NO generation.	KN 62	15-20	nitric oxide synthase 3	Homo sapiens	134-138
34502308-7	2021	Treatment with KN-62 (a CaMKII inhibitor), Compound C (an AMPK inhibitor), and STO-609 (a CaMKKbeta inhibitor) suppressed RUT-induced eNOS phosphorylation and NO generation.	STO 609	79-86	nitric oxide synthase 3	Homo sapiens	134-138
34564325-1	2021	Endothelial vasodilatory function is dependent on the NO synthesis from L-arginine by endothelial NO-synthetase (eNOS).	Arginine	72-82	nitric oxide synthase 3	Homo sapiens	86-111
34564325-1	2021	Endothelial vasodilatory function is dependent on the NO synthesis from L-arginine by endothelial NO-synthetase (eNOS).	Arginine	72-82	nitric oxide synthase 3	Homo sapiens	113-117
34564325-2	2021	eNOS can be inhibited by asymmetric dimethylarginine (ADMA) by competitive inhibition on the binding site, and symmetric dimethylarginine (SDMA) can reduce the L-arginine availability intracellularly through competing for transport over the cellular membrane.	dimethylarginine	36-52	nitric oxide synthase 3	Homo sapiens	0-4
34564325-2	2021	eNOS can be inhibited by asymmetric dimethylarginine (ADMA) by competitive inhibition on the binding site, and symmetric dimethylarginine (SDMA) can reduce the L-arginine availability intracellularly through competing for transport over the cellular membrane.	N,N-dimethylarginine	54-58	nitric oxide synthase 3	Homo sapiens	0-4
34564325-2	2021	eNOS can be inhibited by asymmetric dimethylarginine (ADMA) by competitive inhibition on the binding site, and symmetric dimethylarginine (SDMA) can reduce the L-arginine availability intracellularly through competing for transport over the cellular membrane.	dimethylarginine	121-137	nitric oxide synthase 3	Homo sapiens	0-4
34564325-2	2021	eNOS can be inhibited by asymmetric dimethylarginine (ADMA) by competitive inhibition on the binding site, and symmetric dimethylarginine (SDMA) can reduce the L-arginine availability intracellularly through competing for transport over the cellular membrane.	symmetric dimethylarginine	139-143	nitric oxide synthase 3	Homo sapiens	0-4
34564325-2	2021	eNOS can be inhibited by asymmetric dimethylarginine (ADMA) by competitive inhibition on the binding site, and symmetric dimethylarginine (SDMA) can reduce the L-arginine availability intracellularly through competing for transport over the cellular membrane.	Arginine	160-170	nitric oxide synthase 3	Homo sapiens	0-4
34573361-9	2021	In addition, BPME treatment of HUVECs for 48 h reduced mRNA expression of lipid peroxide (LPO) and increased NOS-3, Nrf-2, GSK-3beta, GPX, endothelial nitric oxide synthase (eNOS) and vascular cell growth factor (VEGF) mRNA expression levels.	bpme	13-17	nitric oxide synthase 3	Homo sapiens	139-172
34573361-9	2021	In addition, BPME treatment of HUVECs for 48 h reduced mRNA expression of lipid peroxide (LPO) and increased NOS-3, Nrf-2, GSK-3beta, GPX, endothelial nitric oxide synthase (eNOS) and vascular cell growth factor (VEGF) mRNA expression levels.	bpme	13-17	nitric oxide synthase 3	Homo sapiens	174-178
34438265-8	2021	Significant associations of BPA exposure with increased hypertension risk were suggested in individuals with the major allele of rs1256049 in ESR2, rs769214 in CAT, and rs1799983 in eNOS.	bisphenol A	28-31	nitric oxide synthase 3	Homo sapiens	182-186
34438265-10	2021	Individuals with specific genotypes in ESR1/2, CAT, and eNOS might be more susceptible to the hypertensive effects of BPA.	bisphenol A	118-121	nitric oxide synthase 3	Homo sapiens	56-60
34549711-3	2021	RESULTS: We identified 80 quercetin-HF intersectional targets (AKT1, CASP3, MAPK1, MMP9, and MAPK8) and 5 core targets of quercetin for treatment of HF.GO analysis suggested that the therapeutic effect of quercetin for HF was mediated mainly by such biological processes as responses to peptide hormones, phosphatidylinositol-mediated signalling, responses to lipopolysaccharides, responses to molecules of bacterial origin and regulation of inflammatory responses.KEGG pathway enrichment analysis identified lipid and atherosclerosis pathway, proteoglycans in cancer, PI3K-AKT signaling pathway, diabetic cardiomyopathy and MAPK signaling pathway as the most significantly enriched signaling pathways.Molecular docking showed a good binding activity of quercetin to the 5 core targets.The results of protein immunoblotting showed that 100 mumol/L quercetin significantly reduced AKT1, phospho-AKT (Ser473), eNOS, MMP9 and caspase-3 levels in the cell models of HF (P < 0.01).	Quercetin	205-214	nitric oxide synthase 3	Homo sapiens	908-912
34297017-9	2021	Furthermore, the expressions of angiogenesis-specific markers, PDGFR-beta, p-PI3K, p-Akt, and p-eNOS, were obviously increased in the PDGF-BB/SA/Dex/BMSCs group.	Alginates	142-144	nitric oxide synthase 3	Homo sapiens	96-100
34297017-9	2021	Furthermore, the expressions of angiogenesis-specific markers, PDGFR-beta, p-PI3K, p-Akt, and p-eNOS, were obviously increased in the PDGF-BB/SA/Dex/BMSCs group.	Dextrans	145-148	nitric oxide synthase 3	Homo sapiens	96-100
34297017-10	2021	In conclusion, the PDGF-BB/SA/Dex injectable hydrogels could accelerate BMSC-mediated skin wound healing by promoting angiogenesis via the activation of the PDGF-BB/PDGFR-beta-mediated PI3K/Akt/eNOS pathway, which may provide a new therapeutic strategy for stem cell therapy in wound healing.	Alginates	27-29	nitric oxide synthase 3	Homo sapiens	194-198
34297017-10	2021	In conclusion, the PDGF-BB/SA/Dex injectable hydrogels could accelerate BMSC-mediated skin wound healing by promoting angiogenesis via the activation of the PDGF-BB/PDGFR-beta-mediated PI3K/Akt/eNOS pathway, which may provide a new therapeutic strategy for stem cell therapy in wound healing.	Dextrans	30-33	nitric oxide synthase 3	Homo sapiens	194-198
34549711-2	2021	METHODS: Quercetin and HF-related targets were obtained using TCMSP, PharmMapper, CTD and GeneCards databases, and quercetin-HF intersection targets were obtained through the online website Venn; the protein interaction network was constructed and imported into Cytoscape 3.7.2 to identify the core targets of quercetin in the treatment of HF.GO and KEGG pathway enrichment analyses were performed using R package, and molecular docking was performed using Auto Dock Vina.The protein levels of AKT1, phospho-AKT(Ser473), eNOS, MMP9, and caspase-3 in quercetin-treated HF cell models were detected using protein immunoblotting.	Quercetin	310-319	nitric oxide synthase 3	Homo sapiens	521-525
34549711-4	2021	CONCLUSION: Quercetin improves the pathological changes in HF possibly by regulating the AKT1-eNOS-MMP9 pathway to inhibit cell apoptosis.	Quercetin	12-21	nitric oxide synthase 3	Homo sapiens	94-98
34264302-6	2021	Further exploration indicated that LINC01088 decreased the production of nitric oxide (NO) by binding and increasing Arginase-1 and decreasing eNOS protein levels.	Nitric Oxide	73-85	nitric oxide synthase 3	Homo sapiens	143-147
34394836-0	2021	Leonurine Ameliorates Oxidative Stress and Insufficient Angiogenesis by Regulating the PI3K/Akt-eNOS Signaling Pathway in H2O2-Induced HUVECs.	leonurine	0-9	nitric oxide synthase 3	Homo sapiens	96-100
34458695-0	2021	Alzheimer"s Abeta assembly binds sodium pump and blocks endothelial NOS activity via ROS-PKC pathway in brain vascular endothelial cells.	ros	85-88	nitric oxide synthase 3	Homo sapiens	56-71
34458695-4	2021	ASPD-NAKalpha3 interaction elicits neurodegeneration through calcium overload in neurons, while the same interaction suppresses vasorelaxation by increasing the inactive form of endothelial nitric oxide synthase (eNOS) in endothelial cells via mitochondrial ROS and protein kinase C, independently of the physiological relaxation system.	4-aminospiroperidol	0-4	nitric oxide synthase 3	Homo sapiens	178-211
34458695-4	2021	ASPD-NAKalpha3 interaction elicits neurodegeneration through calcium overload in neurons, while the same interaction suppresses vasorelaxation by increasing the inactive form of endothelial nitric oxide synthase (eNOS) in endothelial cells via mitochondrial ROS and protein kinase C, independently of the physiological relaxation system.	4-aminospiroperidol	0-4	nitric oxide synthase 3	Homo sapiens	213-217
34458695-4	2021	ASPD-NAKalpha3 interaction elicits neurodegeneration through calcium overload in neurons, while the same interaction suppresses vasorelaxation by increasing the inactive form of endothelial nitric oxide synthase (eNOS) in endothelial cells via mitochondrial ROS and protein kinase C, independently of the physiological relaxation system.	nakalpha3	5-14	nitric oxide synthase 3	Homo sapiens	178-211
34458695-4	2021	ASPD-NAKalpha3 interaction elicits neurodegeneration through calcium overload in neurons, while the same interaction suppresses vasorelaxation by increasing the inactive form of endothelial nitric oxide synthase (eNOS) in endothelial cells via mitochondrial ROS and protein kinase C, independently of the physiological relaxation system.	nakalpha3	5-14	nitric oxide synthase 3	Homo sapiens	213-217
34458695-4	2021	ASPD-NAKalpha3 interaction elicits neurodegeneration through calcium overload in neurons, while the same interaction suppresses vasorelaxation by increasing the inactive form of endothelial nitric oxide synthase (eNOS) in endothelial cells via mitochondrial ROS and protein kinase C, independently of the physiological relaxation system.	ros	258-261	nitric oxide synthase 3	Homo sapiens	178-211
34458695-4	2021	ASPD-NAKalpha3 interaction elicits neurodegeneration through calcium overload in neurons, while the same interaction suppresses vasorelaxation by increasing the inactive form of endothelial nitric oxide synthase (eNOS) in endothelial cells via mitochondrial ROS and protein kinase C, independently of the physiological relaxation system.	ros	258-261	nitric oxide synthase 3	Homo sapiens	213-217
34394836-8	2021	At the same time, LEO treatment significantly promoted the phosphorylation level of angiogenic protein PI3K, Akt, and eNOS and the expression level of survival factor Bcl2 and decreased the expression level of death factor Bax and caspase3.	leonurine	18-21	nitric oxide synthase 3	Homo sapiens	118-122
34394836-9	2021	In conclusion, our findings suggested that LEO can ameliorate the oxidative stress damage and insufficient angiogenesis of HUVECs induced by H2O2 through activating the PI3K/Akt-eNOS signaling pathway.	leonurine	43-46	nitric oxide synthase 3	Homo sapiens	178-182
34422545-1	2021	Reactive oxygen species by uncoupled eNOS is linked to endothelial dysfunction.	Reactive Oxygen Species	0-23	nitric oxide synthase 3	Homo sapiens	37-41
34394836-9	2021	In conclusion, our findings suggested that LEO can ameliorate the oxidative stress damage and insufficient angiogenesis of HUVECs induced by H2O2 through activating the PI3K/Akt-eNOS signaling pathway.	Hydrogen Peroxide	141-145	nitric oxide synthase 3	Homo sapiens	178-182
34119624-3	2021	According to experimental studies, RSV modulates several events involved in endothelial dysfunction such as impaired vasorelaxation, eNOS uncoupling, leukocyte adhesion, endothelial senescence, and EndoMT.	Resveratrol	35-38	nitric oxide synthase 3	Homo sapiens	133-137
34422545-9	2021	EA and caffeine acid are the strongest candidates for eNOS protein functional norms.	caffeine acid	7-20	nitric oxide synthase 3	Homo sapiens	54-58
34422545-11	2021	Predicting interaction of ellagic acid with eNOS protein by molecular docking in endothelial dysfunction.	Ellagic Acid	26-38	nitric oxide synthase 3	Homo sapiens	44-48
34119624-4	2021	Also, the endothelial protective effects of Resveratrol are found to be mediated by numerous molecular targets (e.g. Silent Information Regulator 1 (SIRT1), 5 " AMP-activated protein kinase (AMPK), endothelial nitric oxide synthase (eNOS), nuclear factor-erythroid-derived 2-related factor-2 (Nrf2), Kruppel-like factor-2 ( KLF2), and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kB).	Resveratrol	44-55	nitric oxide synthase 3	Homo sapiens	198-231
34119624-4	2021	Also, the endothelial protective effects of Resveratrol are found to be mediated by numerous molecular targets (e.g. Silent Information Regulator 1 (SIRT1), 5 " AMP-activated protein kinase (AMPK), endothelial nitric oxide synthase (eNOS), nuclear factor-erythroid-derived 2-related factor-2 (Nrf2), Kruppel-like factor-2 ( KLF2), and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kB).	Resveratrol	44-55	nitric oxide synthase 3	Homo sapiens	233-237
34233447-9	2022	Atorvastatin, but not resveratrol, largely restored eNOS expression, NO biosynthesis and neoangiogenesis in GATA2-deficient BOEC by a mechanism involving increased expression of the eNOS transcription factor AP-1/c-JUN, replacing GATA2 when the latter is inactive.	Atorvastatin	0-12	nitric oxide synthase 3	Homo sapiens	52-56
34105058-8	2021	In addition, CGP significantly attenuated LPS-induced oxidative injury, and improved Cav-3 expression and eNOS activation, similar effects were shown by the treatment of autophagy inhibitor 3-MA.	3-methyladenine	190-194	nitric oxide synthase 3	Homo sapiens	106-110
34360751-14	2021	Thus, ALA improves endothelial function by restoring the endothelial nitric oxide synthase activity and presents an anti-inflammatory effect dependent or independent of its antioxidant properties.	Thioctic Acid	6-9	nitric oxide synthase 3	Homo sapiens	57-90
34358119-9	2021	Our results might support the notion of two distinct defense mechanisms in COVID-19-derived ARDS; eNOS-derived nitric oxide could be one of them, while the dramatic rise in sACE2 may also represent an endogenous mechanism involved in severe COVID-19 complications, such as ARDS.	Nitric Oxide	111-123	nitric oxide synthase 3	Homo sapiens	98-102
34264338-9	2021	HDAC1 decreases antioxidant enzyme expression through the deacetylation of histones and transcription factors, and also regulates nitric oxide production through regulating both the expression and activity of nitric oxide synthase 3.	Nitric Oxide	130-142	nitric oxide synthase 3	Homo sapiens	209-232
34129987-0	2021	Pregabalin protects brain tissue from subarachnoid hemorrhage by enhancing HIF-1alpha/eNOS signaling and VEGF production.	Pregabalin	0-10	nitric oxide synthase 3	Homo sapiens	86-90
34233447-9	2022	Atorvastatin, but not resveratrol, largely restored eNOS expression, NO biosynthesis and neoangiogenesis in GATA2-deficient BOEC by a mechanism involving increased expression of the eNOS transcription factor AP-1/c-JUN, replacing GATA2 when the latter is inactive.	Atorvastatin	0-12	nitric oxide synthase 3	Homo sapiens	182-186
34356605-5	2021	In endothelial cells, NO is produced by endothelial nitric oxide synthase (eNOS) from L-Arg, with tetrahydrobiopterin (BH4) as an essential cofactor.	Arginine	86-91	nitric oxide synthase 3	Homo sapiens	40-73
34327240-6	2021	Our data showed that 100 mg/L ox-LDL significantly decreased the expression of GPX4 and eNOS, which was associated with increases in ROS levels and impairments of VEC viability and migration.	Reactive Oxygen Species	133-136	nitric oxide synthase 3	Homo sapiens	88-92
34298658-7	2021	Moreover, KYP-2047 significantly reduced vascular endothelial-growth-factor (VEGF), angiopoietins (Ang) and endothelial-nitric-oxide synthase (eNOS) expression.	3-hydroxy-2-({4-[4-(pyrimidin-2-yl)piperazine-1-carbonyl]phenyl}methyl)-1-benzofuran-7-carboxamide	10-13	nitric oxide synthase 3	Homo sapiens	108-141
34298658-7	2021	Moreover, KYP-2047 significantly reduced vascular endothelial-growth-factor (VEGF), angiopoietins (Ang) and endothelial-nitric-oxide synthase (eNOS) expression.	3-hydroxy-2-({4-[4-(pyrimidin-2-yl)piperazine-1-carbonyl]phenyl}methyl)-1-benzofuran-7-carboxamide	10-13	nitric oxide synthase 3	Homo sapiens	143-147
34356605-5	2021	In endothelial cells, NO is produced by endothelial nitric oxide synthase (eNOS) from L-Arg, with tetrahydrobiopterin (BH4) as an essential cofactor.	Arginine	86-91	nitric oxide synthase 3	Homo sapiens	75-79
34356605-5	2021	In endothelial cells, NO is produced by endothelial nitric oxide synthase (eNOS) from L-Arg, with tetrahydrobiopterin (BH4) as an essential cofactor.	sapropterin	98-117	nitric oxide synthase 3	Homo sapiens	40-73
34356605-5	2021	In endothelial cells, NO is produced by endothelial nitric oxide synthase (eNOS) from L-Arg, with tetrahydrobiopterin (BH4) as an essential cofactor.	sapropterin	98-117	nitric oxide synthase 3	Homo sapiens	75-79
34356605-7	2021	What is particularly important is the fact that hypoxia contributes to the depletion of cofactor BH4 and deficiency of substrate L-Arg, and thus elicits eNOS uncoupling-a state in which the enzyme produces superoxide instead of NO.	sapropterin	97-100	nitric oxide synthase 3	Homo sapiens	153-157
34356605-7	2021	What is particularly important is the fact that hypoxia contributes to the depletion of cofactor BH4 and deficiency of substrate L-Arg, and thus elicits eNOS uncoupling-a state in which the enzyme produces superoxide instead of NO.	Arginine	129-134	nitric oxide synthase 3	Homo sapiens	153-157
34356605-7	2021	What is particularly important is the fact that hypoxia contributes to the depletion of cofactor BH4 and deficiency of substrate L-Arg, and thus elicits eNOS uncoupling-a state in which the enzyme produces superoxide instead of NO.	Superoxides	206-216	nitric oxide synthase 3	Homo sapiens	153-157
34291395-0	2021	Omeprazole suppresses endothelial calcium response and eNOS Ser1177 phosphorylation in porcine aortic endothelial cells.	Omeprazole	0-10	nitric oxide synthase 3	Homo sapiens	55-59
34118596-0	2021	Apolipoprotein A-I mimetic peptide inhibits atherosclerosis by increasing tetrahydrobiopterin via regulation of GTP-cyclohydrolase 1 and reducing uncoupled endothelial nitric oxide synthase activity.	sapropterin	74-93	nitric oxide synthase 3	Homo sapiens	156-189
34118596-9	2021	CONCLUSIONS: Hypercholesterolemia enhanced uncoupled eNOS activity by decreasing GCH-1 concentration, thereby reducing BH4 levels.	sapropterin	119-122	nitric oxide synthase 3	Homo sapiens	53-57
34118596-10	2021	D-4F reduced uncoupled eNOS activity by increasing BH4 levels through GCH-1 expression and decreasing eNOS phosphorylation and eNOS-HSP90 association.	sapropterin	51-54	nitric oxide synthase 3	Homo sapiens	23-27
34291395-8	2021	CONCLUSION: Our results are the first to indicate that high doses of omeprazole may suppress both store-operated Ca2+ channels and partially the G protein-coupled receptor/phospholipase C/inositol 1,4,5-triphosphate pathway, and decreased BK-induced, Ca2+-dependent phosphorylation of eNOS(Ser1177).	Omeprazole	69-79	nitric oxide synthase 3	Homo sapiens	285-289
34291395-6	2021	Omeprazole decreased BK-induced phosphorylation of endothelial nitric oxide synthase (eNOS) at Ser1177 and tended to decrease BK-induced nitric oxide production.	Omeprazole	0-10	nitric oxide synthase 3	Homo sapiens	51-84
34291395-6	2021	Omeprazole decreased BK-induced phosphorylation of endothelial nitric oxide synthase (eNOS) at Ser1177 and tended to decrease BK-induced nitric oxide production.	Omeprazole	0-10	nitric oxide synthase 3	Homo sapiens	86-90
34169869-6	2021	The eNOS (Glu298Asp) polymorphism was identified in EDTA blood by PCR amplification of the target region followed by restriction enzyme digestion, and genotyping on Agarose gel.	Sepharose	165-172	nitric oxide synthase 3	Homo sapiens	4-8
33929389-10	2021	Following metformin treatment, p-AMPK and p-eNOS expression increased, while p-mTOR expression decreased.	Metformin	10-19	nitric oxide synthase 3	Homo sapiens	44-48
34257681-8	2021	The molecular docking results showed that the binding energies of beta sitosterol with AR, FOS, AKT1, VEGFA, NR3C1, and NOS3 were less than -7.0 kcal mol-1, indicating a good docking effect.	gamma-sitosterol	66-81	nitric oxide synthase 3	Homo sapiens	120-124
34206393-4	2021	However, IL-6 and the JAK1/2 inhibitor Ruxolitinib significantly increased angiogenic factors-endothelial nitric oxide synthase (eNOS), VEGF, and hypoxia-inducible factor-1 alpha (HIF-1alpha)-in patients with polycythemia vera (PV).	ruxolitinib	39-50	nitric oxide synthase 3	Homo sapiens	86-127
34206393-4	2021	However, IL-6 and the JAK1/2 inhibitor Ruxolitinib significantly increased angiogenic factors-endothelial nitric oxide synthase (eNOS), VEGF, and hypoxia-inducible factor-1 alpha (HIF-1alpha)-in patients with polycythemia vera (PV).	ruxolitinib	39-50	nitric oxide synthase 3	Homo sapiens	129-133
34095122-5	2021	Endothelial nitric oxide synthase (eNOS), argininosuccinate synthetase and ornithine decarboxylase (ODC) are the main enzymes for arginine metabolism.	Arginine	130-138	nitric oxide synthase 3	Homo sapiens	0-33
34095122-5	2021	Endothelial nitric oxide synthase (eNOS), argininosuccinate synthetase and ornithine decarboxylase (ODC) are the main enzymes for arginine metabolism.	Arginine	130-138	nitric oxide synthase 3	Homo sapiens	35-39
35617030-7	2022	Mechanistic studies showed that NACT increased inhibitory eNOS phosphorylation of threonine 495 in a ROCK-dependent manner and augmented vascular superoxide and hydrogen peroxide production and NADPH oxidase activity.	Threonine	82-91	nitric oxide synthase 3	Homo sapiens	58-62
34302694-4	2021	Endogenous NO is produced from L-arginine under catalysis of three isoforms of NOS (eNOS, iNOS, and nNOS).	Arginine	31-41	nitric oxide synthase 3	Homo sapiens	84-88
34218226-5	2021	In addition, we found that TSG not only increased the expression of Bcl-2, while decreasing Bax expression, but also activated phosphorylation of Akt and endothelial nitric oxide synthase (eNOS) with subsequent nitric oxide production and ultimately reduced high glucose-induced apoptosis.	Glucose	263-270	nitric oxide synthase 3	Homo sapiens	154-187
34218226-6	2021	However, the antiapoptotic effects of TSG were abrogated by pretreatment of the cells with PI3K inhibitor (LY294002) or eNOS inhibitor NG-L-nitro-arginine methyl ester, respectively.	ng-l-nitro-arginine methyl ester	135-167	nitric oxide synthase 3	Homo sapiens	120-124
34567165-6	2021	In this study, we found that taxifolin could decrease the expression of hypoxia-inducible factor-1alpha (HIF-1alpha) while increasing the expression of endothelial nitric oxide synthase (eNOS), presented a protective role.	taxifolin	29-38	nitric oxide synthase 3	Homo sapiens	152-185
34567165-6	2021	In this study, we found that taxifolin could decrease the expression of hypoxia-inducible factor-1alpha (HIF-1alpha) while increasing the expression of endothelial nitric oxide synthase (eNOS), presented a protective role.	taxifolin	29-38	nitric oxide synthase 3	Homo sapiens	187-191
34218226-5	2021	In addition, we found that TSG not only increased the expression of Bcl-2, while decreasing Bax expression, but also activated phosphorylation of Akt and endothelial nitric oxide synthase (eNOS) with subsequent nitric oxide production and ultimately reduced high glucose-induced apoptosis.	Nitric Oxide	211-223	nitric oxide synthase 3	Homo sapiens	154-187
34218226-5	2021	In addition, we found that TSG not only increased the expression of Bcl-2, while decreasing Bax expression, but also activated phosphorylation of Akt and endothelial nitric oxide synthase (eNOS) with subsequent nitric oxide production and ultimately reduced high glucose-induced apoptosis.	Nitric Oxide	211-223	nitric oxide synthase 3	Homo sapiens	189-193
35607381-0	2022	Naringenin upregulates GTPCH1/eNOS to ameliorate high glucose-induced retinal endothelial cell injury.	naringenin	0-10	nitric oxide synthase 3	Homo sapiens	30-34
35607381-6	2022	Reactive oxygen species (ROS) levels and concentration of tetrahydrobiopterin (BH4), the essential cofactor of endothelial nitric oxide synthase (eNOS), were measured using a ROS detection kit and ELISA, respectively.	sapropterin	58-77	nitric oxide synthase 3	Homo sapiens	111-144
35607381-6	2022	Reactive oxygen species (ROS) levels and concentration of tetrahydrobiopterin (BH4), the essential cofactor of endothelial nitric oxide synthase (eNOS), were measured using a ROS detection kit and ELISA, respectively.	sapropterin	58-77	nitric oxide synthase 3	Homo sapiens	146-150
35607381-10	2022	Furthermore, naringenin upregulated GTPCH1/eNOS signaling and promoted release of BH4.	naringenin	13-23	nitric oxide synthase 3	Homo sapiens	43-47
35607381-12	2022	In summary, the present study suggested that naringenin effectively inhibited HG-induced HREC apoptosis and intracellular oxidative stress, which may be associated with naringenin-mediated GTPCH1/eNOS upregulation.	naringenin	45-55	nitric oxide synthase 3	Homo sapiens	196-200
35607381-12	2022	In summary, the present study suggested that naringenin effectively inhibited HG-induced HREC apoptosis and intracellular oxidative stress, which may be associated with naringenin-mediated GTPCH1/eNOS upregulation.	naringenin	169-179	nitric oxide synthase 3	Homo sapiens	196-200
35617030-11	2022	These were prevented in Nox4-/- and by pharmacological inhibition of Nox4 or Rock.Commonly used chemotherapeutic agents, and in particular, docetaxel, alter vascular function by promoting inhibitory phosphorylation of eNOS and enhancing ROS production by NADPH oxidases.	Docetaxel	140-149	nitric oxide synthase 3	Homo sapiens	218-222
35617030-11	2022	These were prevented in Nox4-/- and by pharmacological inhibition of Nox4 or Rock.Commonly used chemotherapeutic agents, and in particular, docetaxel, alter vascular function by promoting inhibitory phosphorylation of eNOS and enhancing ROS production by NADPH oxidases.	ros	237-240	nitric oxide synthase 3	Homo sapiens	218-222
35609778-7	2022	The adipokine may have an athero-protective role by increasing nitric oxide level in the vascular endothelium by enhancing endothelial nitric oxide synthase phosphorylation, enhancing reverse cholesterol transport, and exerting an antithrombotic effect.	Nitric Oxide	63-75	nitric oxide synthase 3	Homo sapiens	123-156
35296150-7	2022	Conversely, FTO overexpression significantly upregulated the mRNA and protein levels of VCAM-1 and ICAM-1, downregulated those of KLF2 and eNOS, and strongly attenuated the atorvastatin-mediated induction of KLF2 and eNOS expression.	Atorvastatin	173-185	nitric oxide synthase 3	Homo sapiens	217-221
35602302-11	2022	Sihax-1 treatment remarkably decreased the phosphonation of phosphatidylinositol 3-kinase (PI3K)/AKT/mammalian target of rapamycin (mTOR)/endothelial NO synthase (eNOS) in mum-2B and C918.	sihax-1	0-7	nitric oxide synthase 3	Homo sapiens	163-167
35602302-12	2022	Pretreatment with LY294002 significantly restored iHAX-1-induced decline in PI3K/AKT/mTOR/eNOS phosphorylation.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	18-26	nitric oxide synthase 3	Homo sapiens	90-94
35602302-12	2022	Pretreatment with LY294002 significantly restored iHAX-1-induced decline in PI3K/AKT/mTOR/eNOS phosphorylation.	ihax-1	50-56	nitric oxide synthase 3	Homo sapiens	90-94
35180005-4	2022	The enzyme cofactor tetrahydrobiopterin (BH4) stabilizes the catalytic active state of eNOS.	sapropterin	20-39	nitric oxide synthase 3	Homo sapiens	87-91
35180005-4	2022	The enzyme cofactor tetrahydrobiopterin (BH4) stabilizes the catalytic active state of eNOS.	sapropterin	41-44	nitric oxide synthase 3	Homo sapiens	87-91
35179568-4	2022	Inhibition of autophagic flux by chloroquine or bafilomycin A1 were sufficient to induce eNOS monomerization and lowers nitric oxide bioavailability through raising mitochondrial reactive oxygen species (mtROS).	Chloroquine	33-44	nitric oxide synthase 3	Homo sapiens	89-93
35179568-4	2022	Inhibition of autophagic flux by chloroquine or bafilomycin A1 were sufficient to induce eNOS monomerization and lowers nitric oxide bioavailability through raising mitochondrial reactive oxygen species (mtROS).	bafilomycin A1	48-62	nitric oxide synthase 3	Homo sapiens	89-93
35179568-4	2022	Inhibition of autophagic flux by chloroquine or bafilomycin A1 were sufficient to induce eNOS monomerization and lowers nitric oxide bioavailability through raising mitochondrial reactive oxygen species (mtROS).	Reactive Oxygen Species	179-202	nitric oxide synthase 3	Homo sapiens	89-93
35143872-17	2022	Besides, the improvement of skeletal muscle function affected by TMZ was associated with reducing NOS3 expression in senescent myoblasts.	Trimetazidine	65-68	nitric oxide synthase 3	Homo sapiens	98-102
35182051-1	2022	Nitric oxide synthase 3 (NOS3) is a major vasoprotective enzyme that catalyzes the conversion of L-arginine to nitric oxide (NO) in response to a significant number of signaling pathways.	Arginine	97-107	nitric oxide synthase 3	Homo sapiens	0-23
35182051-1	2022	Nitric oxide synthase 3 (NOS3) is a major vasoprotective enzyme that catalyzes the conversion of L-arginine to nitric oxide (NO) in response to a significant number of signaling pathways.	Arginine	97-107	nitric oxide synthase 3	Homo sapiens	25-29
35182051-1	2022	Nitric oxide synthase 3 (NOS3) is a major vasoprotective enzyme that catalyzes the conversion of L-arginine to nitric oxide (NO) in response to a significant number of signaling pathways.	Nitric Oxide	111-123	nitric oxide synthase 3	Homo sapiens	0-23
35182051-1	2022	Nitric oxide synthase 3 (NOS3) is a major vasoprotective enzyme that catalyzes the conversion of L-arginine to nitric oxide (NO) in response to a significant number of signaling pathways.	Nitric Oxide	111-123	nitric oxide synthase 3	Homo sapiens	25-29
35182051-9	2022	However, NOS3 peptides with a phosphate at either S114 or S633 did not meaningfully interact with the kinases.	Phosphates	30-39	nitric oxide synthase 3	Homo sapiens	9-13
35379328-15	2022	They improved the morphology and biofunctions of the mitochondria and Golgi apparatus, thereby elevating the levels of SOD, T-AOC and production of CoQ10, endothelial nitric oxide synthase (eNOS)-regulated nitric oxide (NO) generation as well as suppressed MDA generation.	Nitric Oxide	206-218	nitric oxide synthase 3	Homo sapiens	155-188
35378380-4	2022	We show that the strong deleterious effect of miR-142-3p may be due in part to its ability to block the activation of ERK1/2 and eNOS-mediated signals in ECs.	mir-142-3p	46-56	nitric oxide synthase 3	Homo sapiens	129-133
35563784-2	2022	T2Rs in these two innate immune cell types are activated by bitter products, including those secreted by Pseudomonas aeruginosa, leading to Ca2+-dependent activation of endothelial nitric oxide (NO) synthase (eNOS).	Nitric Oxide	181-193	nitric oxide synthase 3	Homo sapiens	209-213
35389901-8	2022	The signal transduction of CD44-ankyrin-Akt-eNOS was significantly repressed in the ONFH group as compared with the control group after hyaluronic acid treatment.	Hyaluronic Acid	136-151	nitric oxide synthase 3	Homo sapiens	44-48
35466583-11	2022	CONCLUSION: Low androgen status up-regulated the expressions of patients in MAMs (FACL-4, PACS-2 and IP3R1) in the corpus cavernosum and inhibited the eNOS/NO/cGMP signaling pathway, resulting in impaired erectile function in rats.	Cyclic GMP	159-163	nitric oxide synthase 3	Homo sapiens	151-155
35449538-7	2022	Protein expression analyses also showed that Mg-L-theanine complexes decrease inducible nitric oxide synthase (iNOS) and endothelial nitric oxide synthase (eNOS) levels significantly.	mg-l-theanine	45-58	nitric oxide synthase 3	Homo sapiens	121-154
35449538-7	2022	Protein expression analyses also showed that Mg-L-theanine complexes decrease inducible nitric oxide synthase (iNOS) and endothelial nitric oxide synthase (eNOS) levels significantly.	mg-l-theanine	45-58	nitric oxide synthase 3	Homo sapiens	156-160
35379328-15	2022	They improved the morphology and biofunctions of the mitochondria and Golgi apparatus, thereby elevating the levels of SOD, T-AOC and production of CoQ10, endothelial nitric oxide synthase (eNOS)-regulated nitric oxide (NO) generation as well as suppressed MDA generation.	Nitric Oxide	206-218	nitric oxide synthase 3	Homo sapiens	190-194
35441585-6	2022	Cabozantinib ameliorated high glucose-induced reduction in the expression of endothelial nitric oxide synthase (eNOS) and the production of nitric oxide (NO) in hGECs.	cabozantinib	0-12	nitric oxide synthase 3	Homo sapiens	77-110
35441585-6	2022	Cabozantinib ameliorated high glucose-induced reduction in the expression of endothelial nitric oxide synthase (eNOS) and the production of nitric oxide (NO) in hGECs.	cabozantinib	0-12	nitric oxide synthase 3	Homo sapiens	112-116
35441585-6	2022	Cabozantinib ameliorated high glucose-induced reduction in the expression of endothelial nitric oxide synthase (eNOS) and the production of nitric oxide (NO) in hGECs.	Glucose	30-37	nitric oxide synthase 3	Homo sapiens	77-110
35380411-6	2022	Relaxation was partially blocked by the addition of the eNOS blocker Nomega-nitro-L-arginine, or the large conductance potassium channel blocker paxilline.	Nitroarginine	69-92	nitric oxide synthase 3	Homo sapiens	56-60
35441585-6	2022	Cabozantinib ameliorated high glucose-induced reduction in the expression of endothelial nitric oxide synthase (eNOS) and the production of nitric oxide (NO) in hGECs.	Glucose	30-37	nitric oxide synthase 3	Homo sapiens	112-116
35107761-4	2022	CR promotes eNOS activity and SIRT1 expression which in turn improves vasodilation resulting in greater regulation of blood pressure and blood flow.	Chromium	0-2	nitric oxide synthase 3	Homo sapiens	12-16
35357665-16	2022	The quantification of NO levels and analysis of mRNA expressions of eNOS was to determine the nitric oxide demand caused due to OxLDL + CRP complex.	Nitric Oxide	94-106	nitric oxide synthase 3	Homo sapiens	68-72
35431954-0	2022	Radix Astragalus Polysaccharide Accelerates Angiogenesis by Activating AKT/eNOS to Promote Nerve Regeneration and Functional Recovery.	Polysaccharides	17-31	nitric oxide synthase 3	Homo sapiens	75-79
35433336-3	2022	Physical exercise-activated adenosine monophosphate (AMP)-activated protein kinase (AMPK) signaling induces endothelial nitric oxide (NO) synthase (eNOS), increases NO bio-availability, and inhibits palmitoylation, leading to specific and immediate SARS-CoV-2 protection.	Adenosine	28-37	nitric oxide synthase 3	Homo sapiens	148-152
35332670-0	2022	Intelligent Nanodelivery System-Generated 1 O2 Mediates Tumor Vessel Normalization by Activating Endothelial TRPV4-eNOS Signaling.	Oxygen	44-46	nitric oxide synthase 3	Homo sapiens	115-119
35433336-3	2022	Physical exercise-activated adenosine monophosphate (AMP)-activated protein kinase (AMPK) signaling induces endothelial nitric oxide (NO) synthase (eNOS), increases NO bio-availability, and inhibits palmitoylation, leading to specific and immediate SARS-CoV-2 protection.	Adenosine Monophosphate	53-56	nitric oxide synthase 3	Homo sapiens	148-152
35433336-3	2022	Physical exercise-activated adenosine monophosphate (AMP)-activated protein kinase (AMPK) signaling induces endothelial nitric oxide (NO) synthase (eNOS), increases NO bio-availability, and inhibits palmitoylation, leading to specific and immediate SARS-CoV-2 protection.	Nitric Oxide	120-132	nitric oxide synthase 3	Homo sapiens	148-152
34999313-7	2022	Hydroxyurea treatment lowered TNF-induced VCAM1 and NOS3 expression but did not affect heme-induced HMOX1 expression.	Hydroxyurea	0-11	nitric oxide synthase 3	Homo sapiens	52-56
35195045-2	2022	In cultured ECs tyrosine phosphorylation of PECAM-1 has been shown to activate eNOS in response to shear stress.	Tyrosine	16-24	nitric oxide synthase 3	Homo sapiens	79-83
35100630-1	2022	OBJECTIVE:  To assess the influence of oxidative stress on the gene expression of nitric oxide synthases (NOS 3 and NOS 2) and, hence, the cardiovascular responses in preeclampsia.	Nitric Oxide	82-94	nitric oxide synthase 3	Homo sapiens	106-111
35112931-1	2022	As a deficiency in tetrahydrobiopterin (BH4), a cofactor for endothelial nitric oxide synthase, has been implicated in the age-related decline in vascular function, this study aimed to determine the impact of acute BH4 supplementation on flow-mediated vasodilation (FMD) in old adults.	sapropterin	19-38	nitric oxide synthase 3	Homo sapiens	61-94
35112931-1	2022	As a deficiency in tetrahydrobiopterin (BH4), a cofactor for endothelial nitric oxide synthase, has been implicated in the age-related decline in vascular function, this study aimed to determine the impact of acute BH4 supplementation on flow-mediated vasodilation (FMD) in old adults.	sapropterin	40-43	nitric oxide synthase 3	Homo sapiens	61-94
35100630-10	2022	Nitric oxide may play a role in this mechanism, but interactions with other vasoactive /biological substances cannot be overlooked, as the gene expression of NOS3 and NOS2 has been reduced.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	158-162
35209223-6	2022	Bioinformatics analysis revealed these proteins are mainly ATP-binding and/or ATPase activity proteins, such as CKB, HSP86, HSP70-1, HSP90, ATPSF1beta and ACTG1, and highly associated with the regulation of the role of PKR in interferon induction and the antiviral response signaling pathway (P = 10-6), PI3K/AKT signaling pathway (P = 10-5) and eNOS signaling pathway (P = 10-4).	Adenosine Triphosphate	59-62	nitric oxide synthase 3	Homo sapiens	346-350
35252440-4	2022	Our data reveals that HAnano  modulates higher expression of genes related with endothelial cell performance and viability, such as VEGF, eNOS, and AKT, and further angiogenesis in vitro by promoting endothelial cell migration.	hanano	22-28	nitric oxide synthase 3	Homo sapiens	138-142
35199130-0	2022	(Normalization of the ratio of nitric oxide and peroxynitrite by promoting eNOS dimer activity is a new direction for diabetic nephropathy treatment).	Nitric Oxide	31-43	nitric oxide synthase 3	Homo sapiens	75-79
35199130-0	2022	(Normalization of the ratio of nitric oxide and peroxynitrite by promoting eNOS dimer activity is a new direction for diabetic nephropathy treatment).	Peroxynitrous Acid	48-61	nitric oxide synthase 3	Homo sapiens	75-79
35199130-7	2022	ONOO- is a hyper-reactive oxidant and nitrating agent in vivo which can cause the uncoupling of eNOS.	onoo	0-4	nitric oxide synthase 3	Homo sapiens	96-100
35199130-8	2022	The uncoupled eNOS does not produce NO but produces superoxide.	Superoxides	52-62	nitric oxide synthase 3	Homo sapiens	14-18
35209223-7	2022	The results show that baicalin exerts multiply pharmacological functions, such as antiviral, anti-inflammatory, antitumor, and antioxidant functions, through regulating the PKR and PI3K/AKT/eNOS signaling pathways by targeting ATP-binding and ATPase activity proteins.	baicalin	22-30	nitric oxide synthase 3	Homo sapiens	190-194
35209223-7	2022	The results show that baicalin exerts multiply pharmacological functions, such as antiviral, anti-inflammatory, antitumor, and antioxidant functions, through regulating the PKR and PI3K/AKT/eNOS signaling pathways by targeting ATP-binding and ATPase activity proteins.	Adenosine Triphosphate	227-230	nitric oxide synthase 3	Homo sapiens	190-194
35170653-8	2022	CONCLUSION: Asymmetrical dimethylarginine is an important marker of endothelial dysfunction and endogenous endothelial nitric oxide synthase inhibitor.	dimethylarginine	25-41	nitric oxide synthase 3	Homo sapiens	107-140
35167029-6	2022	Arsenic has been shown to inactivate endothelial nitric oxide synthase leading to a reduction of the generation and bioavailability of nitric oxide.	Arsenic	0-7	nitric oxide synthase 3	Homo sapiens	37-70
35167029-6	2022	Arsenic has been shown to inactivate endothelial nitric oxide synthase leading to a reduction of the generation and bioavailability of nitric oxide.	Nitric Oxide	135-147	nitric oxide synthase 3	Homo sapiens	37-70
35157107-0	2022	Differential effects of single fatty acids and fatty acid mixtures on the phosphoinositide 3-kinase/Akt/eNOS pathway in endothelial cells.	Fatty Acids	31-42	nitric oxide synthase 3	Homo sapiens	104-108
35157107-0	2022	Differential effects of single fatty acids and fatty acid mixtures on the phosphoinositide 3-kinase/Akt/eNOS pathway in endothelial cells.	Fatty Acids	47-57	nitric oxide synthase 3	Homo sapiens	104-108
35157107-2	2022	Non-esterified fatty acids (NEFA) enriched in saturated fatty acids (SFA) are thought to reduce vascular reactivity by attenuating insulin signalling via vasodilator pathways (phosphoinositide 3-kinase (PI3K)/Akt/endothelial nitric oxide synthase (eNOS)) and enhancing signalling via pro-inflammatory pathways.	Fatty Acids	15-26	nitric oxide synthase 3	Homo sapiens	213-246
35157107-2	2022	Non-esterified fatty acids (NEFA) enriched in saturated fatty acids (SFA) are thought to reduce vascular reactivity by attenuating insulin signalling via vasodilator pathways (phosphoinositide 3-kinase (PI3K)/Akt/endothelial nitric oxide synthase (eNOS)) and enhancing signalling via pro-inflammatory pathways.	Fatty Acids	15-26	nitric oxide synthase 3	Homo sapiens	248-252
35157107-2	2022	Non-esterified fatty acids (NEFA) enriched in saturated fatty acids (SFA) are thought to reduce vascular reactivity by attenuating insulin signalling via vasodilator pathways (phosphoinositide 3-kinase (PI3K)/Akt/endothelial nitric oxide synthase (eNOS)) and enhancing signalling via pro-inflammatory pathways.	Fatty Acids	46-67	nitric oxide synthase 3	Homo sapiens	213-246
35157107-2	2022	Non-esterified fatty acids (NEFA) enriched in saturated fatty acids (SFA) are thought to reduce vascular reactivity by attenuating insulin signalling via vasodilator pathways (phosphoinositide 3-kinase (PI3K)/Akt/endothelial nitric oxide synthase (eNOS)) and enhancing signalling via pro-inflammatory pathways.	Fatty Acids	46-67	nitric oxide synthase 3	Homo sapiens	248-252
35157107-5	2022	RESULTS: Oleic acid (OA, 100 microM) was shown to down regulate expression of the insulin receptor, PTEN and a PI3K catalytic (p110beta) and regulatory (p85alpha) subunit compared to palmitic, linoleic and stearic acids (P < 0.04), and promote greater eNOS phosphorylation at Ser1177.	Oleic Acid	9-19	nitric oxide synthase 3	Homo sapiens	252-256
35206003-6	2022	Additionally, DOPAL significantly increases eNOS phosphorylation, while IPy maintained it.	3,4-dihydroxyphenylacetaldehyde	14-19	nitric oxide synthase 3	Homo sapiens	44-48
35157107-8	2022	CONCLUSION: Our findings provide novel insights into the modulation of the PI3K/Akt/eNOS pathway by single fatty acids and fatty acid mixtures.	Fatty Acids	107-118	nitric oxide synthase 3	Homo sapiens	84-88
35157107-8	2022	CONCLUSION: Our findings provide novel insights into the modulation of the PI3K/Akt/eNOS pathway by single fatty acids and fatty acid mixtures.	Fatty Acids	123-133	nitric oxide synthase 3	Homo sapiens	84-88
35185568-13	2022	The integration analysis of metabolomics and network pharmacology shows that KFXYS may regulate the key targets including ARG1, NOS2, NOS3, etc.	kfxys	77-82	nitric oxide synthase 3	Homo sapiens	134-138
35213910-1	2022	OBJECTIVE:  To investigate the expression of endothelin-1 (ET-1) and endothelial nitric oxide (NO) synthase (eNOS) in normal and preeclamptic (PE) placentae.	Nitric Oxide	81-93	nitric oxide synthase 3	Homo sapiens	109-113
35204748-4	2022	In addition, nitrogen species (nitrotyrosine, iNOS, eNOS) and inflammation markers (IL-6, NFkB, and S100 protein) were increased in granulocytes of CML while anti-inflammatory levels of IL-10 were decreased in plasma.	Nitrogen	13-21	nitric oxide synthase 3	Homo sapiens	52-56
35139776-5	2022	By activating farnesoid X receptor (FXR), metformin increases the expression of vascular endothelial growth factor-A (VEGF-A) and endothelial nitric oxide synthase (eNOS), improves the production of nitric oxide (NO) and decreases the production of ROS.	Metformin	42-51	nitric oxide synthase 3	Homo sapiens	130-163
35139776-5	2022	By activating farnesoid X receptor (FXR), metformin increases the expression of vascular endothelial growth factor-A (VEGF-A) and endothelial nitric oxide synthase (eNOS), improves the production of nitric oxide (NO) and decreases the production of ROS.	Metformin	42-51	nitric oxide synthase 3	Homo sapiens	165-169
35139776-7	2022	Thus, metformin appears to regulate islet microvascular endothelial cell (IMEC) proliferation, apoptosis and oxidative stress by activating the FXR/VEGF-A/eNOS pathway.	Metformin	6-15	nitric oxide synthase 3	Homo sapiens	155-159
34994373-0	2022	A study of lovastatin and L-arginine co-loaded PLGA nanomedicine for enhancing nitric oxide production and eNOS expression.	Lovastatin	11-21	nitric oxide synthase 3	Homo sapiens	107-111
34994373-0	2022	A study of lovastatin and L-arginine co-loaded PLGA nanomedicine for enhancing nitric oxide production and eNOS expression.	Arginine	26-36	nitric oxide synthase 3	Homo sapiens	107-111
35096612-10	2021	In the finasteride arm, stronger associations were observed among men with lower serum lycopene for NOS3-rs1799983, higher serum alpha-carotene, beta-carotene, and beta-cryptoxanthin for LIG3-rs1052536, or lower serum retinol for SOD2-rs1799725.	Finasteride	7-18	nitric oxide synthase 3	Homo sapiens	100-104
35096612-10	2021	In the finasteride arm, stronger associations were observed among men with lower serum lycopene for NOS3-rs1799983, higher serum alpha-carotene, beta-carotene, and beta-cryptoxanthin for LIG3-rs1052536, or lower serum retinol for SOD2-rs1799725.	Lycopene	87-95	nitric oxide synthase 3	Homo sapiens	100-104
35006685-4	2022	Zn-MOFs could enhance the morphogenesis of vascular endothelial cells (ECs) via the PI3K/Akt/eNOS pathway.	zn-mofs	0-7	nitric oxide synthase 3	Homo sapiens	93-97
35083247-3	2021	Thus, we sought to determine if acute administration of tetrahydrobiopterin (BH4), an essential cofactor for endothelial nitric oxide synthase (eNOS), would improve hyperemia and brachial artery vasodilation during progressive handgrip exercise in SSc.	sapropterin	56-75	nitric oxide synthase 3	Homo sapiens	109-142
35083247-3	2021	Thus, we sought to determine if acute administration of tetrahydrobiopterin (BH4), an essential cofactor for endothelial nitric oxide synthase (eNOS), would improve hyperemia and brachial artery vasodilation during progressive handgrip exercise in SSc.	sapropterin	56-75	nitric oxide synthase 3	Homo sapiens	144-148
35083247-3	2021	Thus, we sought to determine if acute administration of tetrahydrobiopterin (BH4), an essential cofactor for endothelial nitric oxide synthase (eNOS), would improve hyperemia and brachial artery vasodilation during progressive handgrip exercise in SSc.	sapropterin	77-80	nitric oxide synthase 3	Homo sapiens	109-142
35083247-3	2021	Thus, we sought to determine if acute administration of tetrahydrobiopterin (BH4), an essential cofactor for endothelial nitric oxide synthase (eNOS), would improve hyperemia and brachial artery vasodilation during progressive handgrip exercise in SSc.	sapropterin	77-80	nitric oxide synthase 3	Homo sapiens	144-148
35083247-9	2021	These results demonstrate the efficacy of acute BH4 administration to improve both resistance and conduit vessel endothelial function in SSc, suggesting that eNOS recoupling may be an effective strategy for improving vasodilatory capacity in this patient group.	sapropterin	48-51	nitric oxide synthase 3	Homo sapiens	158-162
35633333-7	2022	Genes create a paired hierarchy of interaction according to their functional activity; the largest contribution to the probable vascular damage depends on the allelic polymorphism NOS3-786CT (p<0,05), the lowest - on the allelic polymorphism P2RY12-744CC (H2H2).	h2h2	256-260	nitric oxide synthase 3	Homo sapiens	180-184
35072089-6	2022	For example, the effects of endogenous nitric oxide (NO) are shown to be mediated by the eNOS protein and that eNOS-derived endothelial NO is most effective in regulating blood pressure oscillations via modulating the baroreflex mechanisms.	Nitric Oxide	39-51	nitric oxide synthase 3	Homo sapiens	89-93
35072089-6	2022	For example, the effects of endogenous nitric oxide (NO) are shown to be mediated by the eNOS protein and that eNOS-derived endothelial NO is most effective in regulating blood pressure oscillations via modulating the baroreflex mechanisms.	Nitric Oxide	39-51	nitric oxide synthase 3	Homo sapiens	111-115
33933650-3	2021	Specific sphingolipids such as sphingosine-1-phosphate (S1P) have been shown to mediate the vaso-dilatory effects of plasma HDL via interaction with the endothelial nitric oxide synthase pathway.	Sphingolipids	9-22	nitric oxide synthase 3	Homo sapiens	153-186
33933650-3	2021	Specific sphingolipids such as sphingosine-1-phosphate (S1P) have been shown to mediate the vaso-dilatory effects of plasma HDL via interaction with the endothelial nitric oxide synthase pathway.	sphingosine 1-phosphate	31-54	nitric oxide synthase 3	Homo sapiens	153-186
33933650-3	2021	Specific sphingolipids such as sphingosine-1-phosphate (S1P) have been shown to mediate the vaso-dilatory effects of plasma HDL via interaction with the endothelial nitric oxide synthase pathway.	sphingosine 1-phosphate	56-59	nitric oxide synthase 3	Homo sapiens	153-186
34050207-0	2021	Hypertonic stress modulates eNOS function through O-GlcNAc modification at Thr-866.	o-glcnac	50-58	nitric oxide synthase 3	Homo sapiens	28-32
33934624-8	2021	Overexpression of FXYD1 in HEK293 cells revealed a possible mechanism, where FXYD1 protected against redox modification of eNOS cysteines.	Cysteine	128-137	nitric oxide synthase 3	Homo sapiens	123-127
34050207-0	2021	Hypertonic stress modulates eNOS function through O-GlcNAc modification at Thr-866.	Threonine	75-78	nitric oxide synthase 3	Homo sapiens	28-32
34050207-1	2021	O-GlcNAcylation, an energy-sensitive posttranslational modification, can regulate the activity of endothelial nitric oxide synthase (eNOS).	o-glcnacylation	0-15	nitric oxide synthase 3	Homo sapiens	98-131
34050207-1	2021	O-GlcNAcylation, an energy-sensitive posttranslational modification, can regulate the activity of endothelial nitric oxide synthase (eNOS).	o-glcnacylation	0-15	nitric oxide synthase 3	Homo sapiens	133-137
34050207-2	2021	Previous studies found that Thr866 is the key site for low-glucose-mediated regulation of eNOS O-GlcNAc.	Glucose	59-66	nitric oxide synthase 3	Homo sapiens	90-94
34050207-2	2021	Previous studies found that Thr866 is the key site for low-glucose-mediated regulation of eNOS O-GlcNAc.	o-glcnac	95-103	nitric oxide synthase 3	Homo sapiens	90-94
34050207-4	2021	Therefore, we first explored the effects of physical and chemical factors on eNOS O-GlcNAc and its Thr866 site.	o-glcnac	82-90	nitric oxide synthase 3	Homo sapiens	77-81
34050207-5	2021	In this study, hypertonic stress, hyperthermia and hydrogen peroxide all increased the expression levels of eNOS O-GlcNAc, whereas hypoxia and high levels of alcohol had no effect.	Hydrogen Peroxide	51-68	nitric oxide synthase 3	Homo sapiens	108-112
34050207-5	2021	In this study, hypertonic stress, hyperthermia and hydrogen peroxide all increased the expression levels of eNOS O-GlcNAc, whereas hypoxia and high levels of alcohol had no effect.	o-glcnac	113-121	nitric oxide synthase 3	Homo sapiens	108-112
34050207-5	2021	In this study, hypertonic stress, hyperthermia and hydrogen peroxide all increased the expression levels of eNOS O-GlcNAc, whereas hypoxia and high levels of alcohol had no effect.	Alcohols	158-165	nitric oxide synthase 3	Homo sapiens	108-112
34050207-6	2021	on the expression levels of eNOS O-GlcNAc; by contrast, low pH led to a decrease in eNOS O-GlcNAc levels.	o-glcnac	33-41	nitric oxide synthase 3	Homo sapiens	28-32
34050207-6	2021	on the expression levels of eNOS O-GlcNAc; by contrast, low pH led to a decrease in eNOS O-GlcNAc levels.	o-glcnac	89-97	nitric oxide synthase 3	Homo sapiens	84-88
34050207-7	2021	Notably, eNOS O-GlcNAc protein levels were unchanged after Thr866 site mutation only under hypertonic conditions, suggesting that hypertonic stress may act through the Thr866 site.	o-glcnac	14-22	nitric oxide synthase 3	Homo sapiens	9-13
34050207-8	2021	Upon exploring the mechanism of hypertonic stress on eNOS O-GlcNAc activity and function, we found that hypertonic stress can upregulate the expression of O-linked N-acetylglucosamine (GlcNAc) transferase (OGT), which is dependent on AMPK.	o-glcnac	58-66	nitric oxide synthase 3	Homo sapiens	53-57
34016263-8	2021	Exogenous C16:0-ceramide directly increased superoxide via tetrahydrobiopterin-mediated endothelial nitric oxide synthase uncoupling and dysregulated protein phosphatase 2 in human aortic endothelial cells.	c16:0-ceramide	10-24	nitric oxide synthase 3	Homo sapiens	88-121
34059731-6	2021	A cooperation mechanism for the mechanotransduction of fluid shear stress to nitric oxide production was elucidated in which glypican-1 senses flow and phosphorylates PECAM-1 leading to endothelial nitric oxide synthase phosphorylation and nitric oxide production.	Nitric Oxide	77-89	nitric oxide synthase 3	Homo sapiens	186-219
32653904-2	2021	The latter form a signal transduction complex that mediates the endothelial cell response to shear stress, including the activation of the endothelial nitric oxide (NO) synthase (eNOS).	Nitric Oxide	151-163	nitric oxide synthase 3	Homo sapiens	179-183
32653904-8	2021	Two kinases i.e. abelson-tyrosine protein kinase (ABL)1 and Src were identified as eNOS Tyr81 kinases as their inhibition and downregulation significantly reduced the basal and Yoda1-induced tyrosine phosphorylation and activity of eNOS.	Tyrosine	25-33	nitric oxide synthase 3	Homo sapiens	83-87
32653904-8	2021	Two kinases i.e. abelson-tyrosine protein kinase (ABL)1 and Src were identified as eNOS Tyr81 kinases as their inhibition and downregulation significantly reduced the basal and Yoda1-induced tyrosine phosphorylation and activity of eNOS.	Tyrosine	25-33	nitric oxide synthase 3	Homo sapiens	232-236
34051107-1	2021	Up until today, there are still uncertainties regarding the occurrence of isoforms of the nitric oxide synthase (eNOS, nNOS) in the human prostate.	Nitric Oxide	90-102	nitric oxide synthase 3	Homo sapiens	113-117
34016263-8	2021	Exogenous C16:0-ceramide directly increased superoxide via tetrahydrobiopterin-mediated endothelial nitric oxide synthase uncoupling and dysregulated protein phosphatase 2 in human aortic endothelial cells.	Superoxides	44-54	nitric oxide synthase 3	Homo sapiens	88-121
34016263-8	2021	Exogenous C16:0-ceramide directly increased superoxide via tetrahydrobiopterin-mediated endothelial nitric oxide synthase uncoupling and dysregulated protein phosphatase 2 in human aortic endothelial cells.	sapropterin	59-78	nitric oxide synthase 3	Homo sapiens	88-121
33982419-0	2021	Depiction of Haloa by Solomon Enos.	haloa	13-18	nitric oxide synthase 3	Homo sapiens	30-34
34011981-4	2021	Endothelial nitric oxide synthase (eNOS) generates nitric oxide (NO) that maintains endothelial homeostasis.	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	35-39
34020670-7	2021	LY294002 inhibited the biological function of HUVECs through inhibition of the PI3K/AKT/eNOS pathway.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	0-8	nitric oxide synthase 3	Homo sapiens	88-92
33888602-4	2021	We have previously shown that mechanistic/mammalian target of rapamycin (mTOR) drives cerebrovascular dysfunction in models of AD by reducing the activity of endothelial nitric oxide synthase (eNOS), and that attenuation of mTOR activity with rapamycin is sufficient to restore eNOS-dependent cerebrovascular function.	Sirolimus	62-71	nitric oxide synthase 3	Homo sapiens	158-191
33888602-4	2021	We have previously shown that mechanistic/mammalian target of rapamycin (mTOR) drives cerebrovascular dysfunction in models of AD by reducing the activity of endothelial nitric oxide synthase (eNOS), and that attenuation of mTOR activity with rapamycin is sufficient to restore eNOS-dependent cerebrovascular function.	Sirolimus	62-71	nitric oxide synthase 3	Homo sapiens	193-197
33888602-4	2021	We have previously shown that mechanistic/mammalian target of rapamycin (mTOR) drives cerebrovascular dysfunction in models of AD by reducing the activity of endothelial nitric oxide synthase (eNOS), and that attenuation of mTOR activity with rapamycin is sufficient to restore eNOS-dependent cerebrovascular function.	Sirolimus	62-71	nitric oxide synthase 3	Homo sapiens	278-282
34026871-9	2021	In addition, A20 overexpression in HCAEC increased eNOS phosphorylation at Ser-1177, which is key for the function of this enzyme.	Serine	75-78	nitric oxide synthase 3	Homo sapiens	51-55
33964050-2	2021	We investigated the effects of CAV1-T29107A and endothelial nitric oxide synthase (eNOS) G894T polymorphisms on the serum levels of testosterone, NO and prostate-specific antigen (PSA) in patients with PC.	Testosterone	132-144	nitric oxide synthase 3	Homo sapiens	48-81
33372726-5	2021	Western blotting analysis results showed that CdCl2 decreases eNOS and peNOS expression.	Cadmium Chloride	46-51	nitric oxide synthase 3	Homo sapiens	62-66
33946046-11	2021	The downregulated eNOS and reduced production of NO induced by ox-LDL were reversed by the introduction of Azilsartan.	azilsartan	107-117	nitric oxide synthase 3	Homo sapiens	18-22
33621475-7	2021	In both BeWo and explants, the protective effect of NP-Plac1-hIGF1 treatment against H2O2 inducedcell death/lactate dehydrogenase release was prevented by eNOS inhibition (P=0.003 and P<0.0001, respectively).	Hydrogen Peroxide	85-89	nitric oxide synthase 3	Homo sapiens	155-159
33556535-0	2021	Artemisinin protects endothelial function and vasodilation from oxidative damage via activation of PI3K/Akt/eNOS pathway.	artemisinin	0-11	nitric oxide synthase 3	Homo sapiens	108-112
33913201-0	2021	Bufalin inhibits peritoneal dissemination of gastric cancer through endothelial nitric oxide synthase-mitogen-activated protein kinases signaling pathway.	bufalin	0-7	nitric oxide synthase 3	Homo sapiens	68-101
33913201-9	2021	NOS3, which was an independent prognostic factor of GC patients, was predicted to be a potential target of bufalin.	bufalin	107-114	nitric oxide synthase 3	Homo sapiens	0-4
33913201-10	2021	Further experiments proved that bufalin reduced the phosphorylation of NOS3, thereby inhibiting the mitogen-activated protein kinase (MAPK) signaling pathway, and ultimately suppressed GCPD by inhibiting EMT process.	bufalin	32-39	nitric oxide synthase 3	Homo sapiens	71-75
33913201-12	2021	Bufalin could suppress GCPD through NOS3-MAPK signaling pathway, which provided more evidence support for intraperitoneal perfusion of bufalin to treat GCPD.	bufalin	0-7	nitric oxide synthase 3	Homo sapiens	36-40
33913201-12	2021	Bufalin could suppress GCPD through NOS3-MAPK signaling pathway, which provided more evidence support for intraperitoneal perfusion of bufalin to treat GCPD.	bufalin	135-142	nitric oxide synthase 3	Homo sapiens	36-40
33933809-0	2021	Increased secretion of VEGF-C from SiO2-induced pulmonary macrophages promotes lymphangiogenesis through the Src/eNOS pathway in silicosis.	Silicon Dioxide	35-39	nitric oxide synthase 3	Homo sapiens	113-117
33899971-9	2021	Intra-individual changes in FMD following END and RT were associated with the NOS3 SNP, with TT homozygotes significantly favouring only END (P=0.016) and TC/CC tending to favour RT only (P=0.056).	Technetium	155-157	nitric oxide synthase 3	Homo sapiens	78-82
33578126-4	2021	Our previous work has shown that the mitochondrial redistribution of uncoupled eNOS impairs mitochondrial bioenergetics and increases mito-ROS generation.	mito-ros	134-142	nitric oxide synthase 3	Homo sapiens	79-83
33578126-6	2021	Our data show that the increase in mito-ROS involved in LPS-mediated inflammasome activation is associated with the disruption of mitochondrial bioenergetics in human lung microvascular endothelial cells (HLMVEC) and the mitochondrial redistribution of eNOS.	mito-ros	35-43	nitric oxide synthase 3	Homo sapiens	253-257
33578126-7	2021	These effects are dependent on RhoA-ROCK signaling and are mediated via increased phosphorylation of eNOS at Threonine (T)-495.	Threonine	109-118	nitric oxide synthase 3	Homo sapiens	101-105
33578126-11	2021	Thus, our findings show that the mitochondrial redistribution of uncoupled eNOS is intimately involved in the activation of the inflammatory response in ALI and implicate attenuating mito-ROS as a therapeutic strategy in humans.	mito-ros	183-191	nitric oxide synthase 3	Homo sapiens	75-79
33967958-7	2021	Results: High (>16.7 mmol/L) concentration of glucose upregulated the expression of miR-21, leading to the activation and inhibition of the PTEN/AKT/eNOS and MAPK/ET-1 pathways, and upregulation of NO and downregulation of ET-1 secretion, respectively.	Glucose	46-53	nitric oxide synthase 3	Homo sapiens	149-153
33854083-0	2021	Author Correction: Influence of NOS3 rs2070744 genotypes on hepatocellular carcinoma patients treated with lenvatinib.	lenvatinib	107-117	nitric oxide synthase 3	Homo sapiens	32-36
33864889-8	2021	Elevated asymmetric and symmetric dimethylarginine combined with reduced arginine levels compromised endothelial nitric oxide synthase activity and nitric oxide signaling.	dimethylarginine	34-50	nitric oxide synthase 3	Homo sapiens	101-134
33864889-8	2021	Elevated asymmetric and symmetric dimethylarginine combined with reduced arginine levels compromised endothelial nitric oxide synthase activity and nitric oxide signaling.	Arginine	42-50	nitric oxide synthase 3	Homo sapiens	101-134
33895940-8	2021	We found that activation of endothelial nitric oxide synthase (eNOS) under low-dose ethanol conditions with a shift to activation of inducible NOS (iNOS) under chronic high ethanol exposure conditions, which appeared to regulate these contrasting effects.	Ethanol	84-91	nitric oxide synthase 3	Homo sapiens	28-61
33895940-8	2021	We found that activation of endothelial nitric oxide synthase (eNOS) under low-dose ethanol conditions with a shift to activation of inducible NOS (iNOS) under chronic high ethanol exposure conditions, which appeared to regulate these contrasting effects.	Ethanol	84-91	nitric oxide synthase 3	Homo sapiens	63-67
33895940-8	2021	We found that activation of endothelial nitric oxide synthase (eNOS) under low-dose ethanol conditions with a shift to activation of inducible NOS (iNOS) under chronic high ethanol exposure conditions, which appeared to regulate these contrasting effects.	Ethanol	173-180	nitric oxide synthase 3	Homo sapiens	28-61
33895940-8	2021	We found that activation of endothelial nitric oxide synthase (eNOS) under low-dose ethanol conditions with a shift to activation of inducible NOS (iNOS) under chronic high ethanol exposure conditions, which appeared to regulate these contrasting effects.	Ethanol	173-180	nitric oxide synthase 3	Homo sapiens	63-67
33895940-10	2021	We concluded that the effects of low-dose ethanol increased the diffusive movement of waste metabolites via eNOS-derived NO, which increased the arterial endothelial-smooth muscle cell dilative reactivity without affecting BBB integrity, whereas a prolonged induction of iNOS under chronic ethanol exposure conditions caused oxidative damage of the arterial endothelial-smooth muscle layers resulting in cerebral amyloid-like angiopathy.	Ethanol	42-49	nitric oxide synthase 3	Homo sapiens	108-112
33895940-10	2021	We concluded that the effects of low-dose ethanol increased the diffusive movement of waste metabolites via eNOS-derived NO, which increased the arterial endothelial-smooth muscle cell dilative reactivity without affecting BBB integrity, whereas a prolonged induction of iNOS under chronic ethanol exposure conditions caused oxidative damage of the arterial endothelial-smooth muscle layers resulting in cerebral amyloid-like angiopathy.	Ethanol	290-297	nitric oxide synthase 3	Homo sapiens	108-112
33893961-1	2021	We studied association of polymorphic markers Glu298Asp (rs1799983), C774T (rs1549758), and T786C (rs2070744) of the NOS3 gene with the risk of atopic dermatitis.	glu298asp	46-55	nitric oxide synthase 3	Homo sapiens	117-121
33422633-8	2021	Interestingly, inhibition of mTORC1-S6K1 pathway using rapamycin significantly restored the IRS-1/Akt/eNOS activation, suggesting a feedback regulation of IRS-1/Akt signal through S6K1.	Sirolimus	55-64	nitric oxide synthase 3	Homo sapiens	102-106
33128486-1	2021	PURPOSE: Acute ischemic stroke induces deoxyhemoglobin accumulation around the ischemic region while activating endothelial nitric oxide synthase (eNOS) coupling and the subsequent release of nitric oxide (NO).	Nitric Oxide	124-136	nitric oxide synthase 3	Homo sapiens	147-151
33373686-13	2021	Thus, Curcumin-Veliparib combination suppresses angiogenesis through deregulation of the PI3K-AKT-eNOS pathway downstream to the NECTIN-4.	curcumin-veliparib	6-24	nitric oxide synthase 3	Homo sapiens	98-102
33539947-0	2021	Endothelial-Transcytosed Myeloperoxidase Activates Endothelial Nitric Oxide Synthase via a Phospholipase C-Dependent Calcium Signaling Pathway.	Calcium	117-124	nitric oxide synthase 3	Homo sapiens	51-84
33539947-3	2021	Here we examined the short-term implications of HOCl produced by endothelial-transcytosed MPO for eNOS activity.	Hypochlorous Acid	48-52	nitric oxide synthase 3	Homo sapiens	98-102
33539947-5	2021	Exposure of MPO-containing ECs to low micromolar concentrations of H2O2 yielded enhanced rates of H2O2 consumption that correlated with HOCl formation and increased eNOS enzyme activity.	Hydrogen Peroxide	67-71	nitric oxide synthase 3	Homo sapiens	165-169
33539947-6	2021	The MPO-dependent activation of eNOS occurred despite reduced cellular uptake of the eNOS substrate L-arginine, which involved a decrease in the maximal activity (Vmax), but not substrate affinity (Km), of the major endothelial L-arginine transporter, cationic amino acid transporter-1.	Arginine	100-110	nitric oxide synthase 3	Homo sapiens	32-36
33539947-6	2021	The MPO-dependent activation of eNOS occurred despite reduced cellular uptake of the eNOS substrate L-arginine, which involved a decrease in the maximal activity (Vmax), but not substrate affinity (Km), of the major endothelial L-arginine transporter, cationic amino acid transporter-1.	Arginine	100-110	nitric oxide synthase 3	Homo sapiens	85-89
33539947-6	2021	The MPO-dependent activation of eNOS occurred despite reduced cellular uptake of the eNOS substrate L-arginine, which involved a decrease in the maximal activity (Vmax), but not substrate affinity (Km), of the major endothelial L-arginine transporter, cationic amino acid transporter-1.	Arginine	228-238	nitric oxide synthase 3	Homo sapiens	32-36
33539947-6	2021	The MPO-dependent activation of eNOS occurred despite reduced cellular uptake of the eNOS substrate L-arginine, which involved a decrease in the maximal activity (Vmax), but not substrate affinity (Km), of the major endothelial L-arginine transporter, cationic amino acid transporter-1.	Arginine	228-238	nitric oxide synthase 3	Homo sapiens	85-89
33539947-7	2021	Activation of eNOS in MPO-containing ECs exposed to H2O2 involved a rapid elevation in cytosolic calcium and increased eNOS phosphorylation at Ser-1179 and de-phosphorylation at Thr-497.	Hydrogen Peroxide	52-56	nitric oxide synthase 3	Homo sapiens	14-18
33539947-7	2021	Activation of eNOS in MPO-containing ECs exposed to H2O2 involved a rapid elevation in cytosolic calcium and increased eNOS phosphorylation at Ser-1179 and de-phosphorylation at Thr-497.	Hydrogen Peroxide	52-56	nitric oxide synthase 3	Homo sapiens	119-123
33539947-7	2021	Activation of eNOS in MPO-containing ECs exposed to H2O2 involved a rapid elevation in cytosolic calcium and increased eNOS phosphorylation at Ser-1179 and de-phosphorylation at Thr-497.	Calcium	97-104	nitric oxide synthase 3	Homo sapiens	14-18
33539947-7	2021	Activation of eNOS in MPO-containing ECs exposed to H2O2 involved a rapid elevation in cytosolic calcium and increased eNOS phosphorylation at Ser-1179 and de-phosphorylation at Thr-497.	Serine	143-146	nitric oxide synthase 3	Homo sapiens	14-18
33539947-7	2021	Activation of eNOS in MPO-containing ECs exposed to H2O2 involved a rapid elevation in cytosolic calcium and increased eNOS phosphorylation at Ser-1179 and de-phosphorylation at Thr-497.	Threonine	178-181	nitric oxide synthase 3	Homo sapiens	14-18
33539947-8	2021	These signaling events were attenuated by intracellular calcium chelation, removal of extracellular calcium and inhibition of phospholipase C. This study shows that stimulation of endothelial-transcytosed MPO activates eNOS by promoting phospholipase C-dependent calcium signaling and altered eNOS phosphorylation at Ser-1179 and Thr-497.	Calcium	56-63	nitric oxide synthase 3	Homo sapiens	219-223
33539947-8	2021	These signaling events were attenuated by intracellular calcium chelation, removal of extracellular calcium and inhibition of phospholipase C. This study shows that stimulation of endothelial-transcytosed MPO activates eNOS by promoting phospholipase C-dependent calcium signaling and altered eNOS phosphorylation at Ser-1179 and Thr-497.	Calcium	56-63	nitric oxide synthase 3	Homo sapiens	293-297
33539947-8	2021	These signaling events were attenuated by intracellular calcium chelation, removal of extracellular calcium and inhibition of phospholipase C. This study shows that stimulation of endothelial-transcytosed MPO activates eNOS by promoting phospholipase C-dependent calcium signaling and altered eNOS phosphorylation at Ser-1179 and Thr-497.	Calcium	100-107	nitric oxide synthase 3	Homo sapiens	219-223
33539947-8	2021	These signaling events were attenuated by intracellular calcium chelation, removal of extracellular calcium and inhibition of phospholipase C. This study shows that stimulation of endothelial-transcytosed MPO activates eNOS by promoting phospholipase C-dependent calcium signaling and altered eNOS phosphorylation at Ser-1179 and Thr-497.	Calcium	100-107	nitric oxide synthase 3	Homo sapiens	293-297
33539947-8	2021	These signaling events were attenuated by intracellular calcium chelation, removal of extracellular calcium and inhibition of phospholipase C. This study shows that stimulation of endothelial-transcytosed MPO activates eNOS by promoting phospholipase C-dependent calcium signaling and altered eNOS phosphorylation at Ser-1179 and Thr-497.	Calcium	100-107	nitric oxide synthase 3	Homo sapiens	219-223
33539947-8	2021	These signaling events were attenuated by intracellular calcium chelation, removal of extracellular calcium and inhibition of phospholipase C. This study shows that stimulation of endothelial-transcytosed MPO activates eNOS by promoting phospholipase C-dependent calcium signaling and altered eNOS phosphorylation at Ser-1179 and Thr-497.	Calcium	100-107	nitric oxide synthase 3	Homo sapiens	293-297
33539947-8	2021	These signaling events were attenuated by intracellular calcium chelation, removal of extracellular calcium and inhibition of phospholipase C. This study shows that stimulation of endothelial-transcytosed MPO activates eNOS by promoting phospholipase C-dependent calcium signaling and altered eNOS phosphorylation at Ser-1179 and Thr-497.	Serine	317-320	nitric oxide synthase 3	Homo sapiens	219-223
33539947-8	2021	These signaling events were attenuated by intracellular calcium chelation, removal of extracellular calcium and inhibition of phospholipase C. This study shows that stimulation of endothelial-transcytosed MPO activates eNOS by promoting phospholipase C-dependent calcium signaling and altered eNOS phosphorylation at Ser-1179 and Thr-497.	Serine	317-320	nitric oxide synthase 3	Homo sapiens	293-297
33539947-8	2021	These signaling events were attenuated by intracellular calcium chelation, removal of extracellular calcium and inhibition of phospholipase C. This study shows that stimulation of endothelial-transcytosed MPO activates eNOS by promoting phospholipase C-dependent calcium signaling and altered eNOS phosphorylation at Ser-1179 and Thr-497.	Threonine	330-333	nitric oxide synthase 3	Homo sapiens	219-223
33539947-8	2021	These signaling events were attenuated by intracellular calcium chelation, removal of extracellular calcium and inhibition of phospholipase C. This study shows that stimulation of endothelial-transcytosed MPO activates eNOS by promoting phospholipase C-dependent calcium signaling and altered eNOS phosphorylation at Ser-1179 and Thr-497.	Threonine	330-333	nitric oxide synthase 3	Homo sapiens	293-297
33373686-11	2021	Curcumin antagonised the NECTIN-4-induced angiogenesis through inhibition of PI3K-AKT mediated eNOS pathway and Veliparib synergized the effect of Curcumin.	Curcumin	0-8	nitric oxide synthase 3	Homo sapiens	95-99
33529913-8	2021	In vitro, IL-1beta stimulation downregulated eNOS expression levels in human aortic endothelial cells (HAECs) in a concentration- and time-dependent manner, while pretreatment with 1 microM of the proteasome inhibitor MG132 reversed this effect.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	218-223	nitric oxide synthase 3	Homo sapiens	45-49
33529913-9	2021	In addition, treatment with 10 mg/kg MG132 also prevented the proteolysis of eNOS and improved endothelium-dependent vascular relaxation in vivo.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	37-42	nitric oxide synthase 3	Homo sapiens	77-81
33529913-10	2021	Notably, treatment with 30 mg/kg melatonin downregulated NLRP3 expression levels and decreased IL-1beta secretion, subsequently increasing the expression of eNOS and improving endothelium-dependent vascular relaxation.	Melatonin	33-42	nitric oxide synthase 3	Homo sapiens	157-161
33611830-8	2021	The protective effects mediated by MARCH5 overexpression on ECs could be inhibited by eNOS inhibitor L-NAME and Akt inhibitor LY294002.	NG-Nitroarginine Methyl Ester	101-107	nitric oxide synthase 3	Homo sapiens	86-90
32977740-11	2021	The low expression of Cav-1 in GO adipocytes was associated with low expression of Glut-4 but also with an increased expression of NOX-2 and active eNOS phosphorylated on serine 1177.	Serine	171-177	nitric oxide synthase 3	Homo sapiens	148-152
32363908-2	2021	Endothelial nitric oxide synthase (eNOS) produced nitric oxide (NO) signaling in the vasculature plays an important role in maintaining vascular homeostasis.	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	35-39
33775188-6	2021	L-NAME (NOS inhibitor) totally mimics the actions of Ang II on eNOS, NO production and autophagy levels.	NG-Nitroarginine Methyl Ester	0-6	nitric oxide synthase 3	Homo sapiens	63-67
33998893-8	2021	The anti-inflammatory capacity of 25 muM CBD was concurrent with reduction in levels of phosphorylated mammalian target of rapamycin Ser 2448, endothelial nitric oxide synthase, and induction of cyclooxygenase 2 relative to M(LPS).	Cannabidiol	41-44	nitric oxide synthase 3	Homo sapiens	143-176
33548859-6	2021	Another mechanism is the progressive inhibition of the placental endothelial nitric oxide synthase (eNOS) by oxidative stress, which results in eNOS uncoupling via several events such as a depletion of the eNOS substrate L-arginine due to increased arginase activity, an oxidation of the eNOS cofactor tetrahydrobiopterin (BH4), or eNOS post-translational modifications (for instance by S-glutathionylation).	Arginine	221-231	nitric oxide synthase 3	Homo sapiens	65-98
33548859-6	2021	Another mechanism is the progressive inhibition of the placental endothelial nitric oxide synthase (eNOS) by oxidative stress, which results in eNOS uncoupling via several events such as a depletion of the eNOS substrate L-arginine due to increased arginase activity, an oxidation of the eNOS cofactor tetrahydrobiopterin (BH4), or eNOS post-translational modifications (for instance by S-glutathionylation).	Arginine	221-231	nitric oxide synthase 3	Homo sapiens	100-104
33548859-6	2021	Another mechanism is the progressive inhibition of the placental endothelial nitric oxide synthase (eNOS) by oxidative stress, which results in eNOS uncoupling via several events such as a depletion of the eNOS substrate L-arginine due to increased arginase activity, an oxidation of the eNOS cofactor tetrahydrobiopterin (BH4), or eNOS post-translational modifications (for instance by S-glutathionylation).	Arginine	221-231	nitric oxide synthase 3	Homo sapiens	144-148
33548859-6	2021	Another mechanism is the progressive inhibition of the placental endothelial nitric oxide synthase (eNOS) by oxidative stress, which results in eNOS uncoupling via several events such as a depletion of the eNOS substrate L-arginine due to increased arginase activity, an oxidation of the eNOS cofactor tetrahydrobiopterin (BH4), or eNOS post-translational modifications (for instance by S-glutathionylation).	Arginine	221-231	nitric oxide synthase 3	Homo sapiens	144-148
33548859-6	2021	Another mechanism is the progressive inhibition of the placental endothelial nitric oxide synthase (eNOS) by oxidative stress, which results in eNOS uncoupling via several events such as a depletion of the eNOS substrate L-arginine due to increased arginase activity, an oxidation of the eNOS cofactor tetrahydrobiopterin (BH4), or eNOS post-translational modifications (for instance by S-glutathionylation).	Arginine	221-231	nitric oxide synthase 3	Homo sapiens	144-148
33548859-6	2021	Another mechanism is the progressive inhibition of the placental endothelial nitric oxide synthase (eNOS) by oxidative stress, which results in eNOS uncoupling via several events such as a depletion of the eNOS substrate L-arginine due to increased arginase activity, an oxidation of the eNOS cofactor tetrahydrobiopterin (BH4), or eNOS post-translational modifications (for instance by S-glutathionylation).	sapropterin	302-321	nitric oxide synthase 3	Homo sapiens	65-98
33548859-6	2021	Another mechanism is the progressive inhibition of the placental endothelial nitric oxide synthase (eNOS) by oxidative stress, which results in eNOS uncoupling via several events such as a depletion of the eNOS substrate L-arginine due to increased arginase activity, an oxidation of the eNOS cofactor tetrahydrobiopterin (BH4), or eNOS post-translational modifications (for instance by S-glutathionylation).	sapropterin	302-321	nitric oxide synthase 3	Homo sapiens	100-104
33548859-6	2021	Another mechanism is the progressive inhibition of the placental endothelial nitric oxide synthase (eNOS) by oxidative stress, which results in eNOS uncoupling via several events such as a depletion of the eNOS substrate L-arginine due to increased arginase activity, an oxidation of the eNOS cofactor tetrahydrobiopterin (BH4), or eNOS post-translational modifications (for instance by S-glutathionylation).	sapropterin	302-321	nitric oxide synthase 3	Homo sapiens	144-148
33548859-6	2021	Another mechanism is the progressive inhibition of the placental endothelial nitric oxide synthase (eNOS) by oxidative stress, which results in eNOS uncoupling via several events such as a depletion of the eNOS substrate L-arginine due to increased arginase activity, an oxidation of the eNOS cofactor tetrahydrobiopterin (BH4), or eNOS post-translational modifications (for instance by S-glutathionylation).	sapropterin	302-321	nitric oxide synthase 3	Homo sapiens	144-148
33548859-6	2021	Another mechanism is the progressive inhibition of the placental endothelial nitric oxide synthase (eNOS) by oxidative stress, which results in eNOS uncoupling via several events such as a depletion of the eNOS substrate L-arginine due to increased arginase activity, an oxidation of the eNOS cofactor tetrahydrobiopterin (BH4), or eNOS post-translational modifications (for instance by S-glutathionylation).	sapropterin	302-321	nitric oxide synthase 3	Homo sapiens	144-148
33548859-6	2021	Another mechanism is the progressive inhibition of the placental endothelial nitric oxide synthase (eNOS) by oxidative stress, which results in eNOS uncoupling via several events such as a depletion of the eNOS substrate L-arginine due to increased arginase activity, an oxidation of the eNOS cofactor tetrahydrobiopterin (BH4), or eNOS post-translational modifications (for instance by S-glutathionylation).	sapropterin	323-326	nitric oxide synthase 3	Homo sapiens	65-98
33548859-6	2021	Another mechanism is the progressive inhibition of the placental endothelial nitric oxide synthase (eNOS) by oxidative stress, which results in eNOS uncoupling via several events such as a depletion of the eNOS substrate L-arginine due to increased arginase activity, an oxidation of the eNOS cofactor tetrahydrobiopterin (BH4), or eNOS post-translational modifications (for instance by S-glutathionylation).	sapropterin	323-326	nitric oxide synthase 3	Homo sapiens	100-104
33548859-6	2021	Another mechanism is the progressive inhibition of the placental endothelial nitric oxide synthase (eNOS) by oxidative stress, which results in eNOS uncoupling via several events such as a depletion of the eNOS substrate L-arginine due to increased arginase activity, an oxidation of the eNOS cofactor tetrahydrobiopterin (BH4), or eNOS post-translational modifications (for instance by S-glutathionylation).	sapropterin	323-326	nitric oxide synthase 3	Homo sapiens	144-148
33548859-6	2021	Another mechanism is the progressive inhibition of the placental endothelial nitric oxide synthase (eNOS) by oxidative stress, which results in eNOS uncoupling via several events such as a depletion of the eNOS substrate L-arginine due to increased arginase activity, an oxidation of the eNOS cofactor tetrahydrobiopterin (BH4), or eNOS post-translational modifications (for instance by S-glutathionylation).	sapropterin	323-326	nitric oxide synthase 3	Homo sapiens	144-148
33548859-6	2021	Another mechanism is the progressive inhibition of the placental endothelial nitric oxide synthase (eNOS) by oxidative stress, which results in eNOS uncoupling via several events such as a depletion of the eNOS substrate L-arginine due to increased arginase activity, an oxidation of the eNOS cofactor tetrahydrobiopterin (BH4), or eNOS post-translational modifications (for instance by S-glutathionylation).	sapropterin	323-326	nitric oxide synthase 3	Homo sapiens	144-148
33548859-7	2021	The uncoupling of eNOS triggers a switch of its activity from a NO-producing enzyme to a NADPH oxidase-like system generating O2 -, thereby potentiating ROS production and oxidative stress.	Oxygen	126-130	nitric oxide synthase 3	Homo sapiens	18-22
33548859-7	2021	The uncoupling of eNOS triggers a switch of its activity from a NO-producing enzyme to a NADPH oxidase-like system generating O2 -, thereby potentiating ROS production and oxidative stress.	ros	153-156	nitric oxide synthase 3	Homo sapiens	18-22
33548859-8	2021	Moreover, in PE placentas, eNOS could be post-translationally modified by lipid peroxidation-derived aldehydes such as 4-oxononenal (ONE) a highly bioreactive agent, able to inhibit eNOS activity and NO production.	Aldehydes	101-110	nitric oxide synthase 3	Homo sapiens	27-31
33548859-8	2021	Moreover, in PE placentas, eNOS could be post-translationally modified by lipid peroxidation-derived aldehydes such as 4-oxononenal (ONE) a highly bioreactive agent, able to inhibit eNOS activity and NO production.	Aldehydes	101-110	nitric oxide synthase 3	Homo sapiens	182-186
33548859-8	2021	Moreover, in PE placentas, eNOS could be post-translationally modified by lipid peroxidation-derived aldehydes such as 4-oxononenal (ONE) a highly bioreactive agent, able to inhibit eNOS activity and NO production.	ORTHO-ONE	119-131	nitric oxide synthase 3	Homo sapiens	27-31
33548859-8	2021	Moreover, in PE placentas, eNOS could be post-translationally modified by lipid peroxidation-derived aldehydes such as 4-oxononenal (ONE) a highly bioreactive agent, able to inhibit eNOS activity and NO production.	ORTHO-ONE	119-131	nitric oxide synthase 3	Homo sapiens	182-186
32363908-4	2021	CRITICAL ISSUES: Under conditions of tetrahydrobiopterin (BH4) depletion, eNOS generated superoxide trigger pathological events.	sapropterin	37-56	nitric oxide synthase 3	Homo sapiens	74-78
32363908-4	2021	CRITICAL ISSUES: Under conditions of tetrahydrobiopterin (BH4) depletion, eNOS generated superoxide trigger pathological events.	sapropterin	58-61	nitric oxide synthase 3	Homo sapiens	74-78
32363908-4	2021	CRITICAL ISSUES: Under conditions of tetrahydrobiopterin (BH4) depletion, eNOS generated superoxide trigger pathological events.	Superoxides	89-99	nitric oxide synthase 3	Homo sapiens	74-78
32363908-7	2021	Recent Advances: Being NO signaling activators and regulators of eNOS signaling, BH4 treatment is getting widespread attention either as potential therapeutic agents or as preventive agents.	sapropterin	81-84	nitric oxide synthase 3	Homo sapiens	65-69
33790801-0	2021	NOS3 Polymorphisms Can Influence the Effect of Multicomponent Training on Blood Pressure, Nitrite Concentration and Physical Fitness in Prehypertensive and Hypertensive Older Adult Women.	Nitrites	90-97	nitric oxide synthase 3	Homo sapiens	0-4
33790801-3	2021	It analyzed the influence of NOS3 polymorphisms [-786T > C, 894G > T (Glu298Asp), and intron 4b/a] on the response of blood pressure (BP), nitrite concentration, and physical fitness in older adult women.	Nitrites	139-146	nitric oxide synthase 3	Homo sapiens	29-33
33683570-4	2021	in Cardiovasc Res, 2020. https://doi.org/10.1093/cvr/cvaa213 ), showing that VE-PTP regulates eNOS in a direct-manner, dephosphorylating eNOS at Tyr81 and indirect at Ser1177 and the effects of a VE-PTP inhibitor, AKB-9778, in the blood pressure from diabetic patients.	AKB-9778	214-222	nitric oxide synthase 3	Homo sapiens	94-98
33747912-1	2021	Background: NOS3 (endothelial NOS, eNOS) is a member of the nitric oxide synthase (NOS) enzyme family, mainly participating in nitric oxide (NO) generation.	Nitric Oxide	60-72	nitric oxide synthase 3	Homo sapiens	12-16
33747912-1	2021	Background: NOS3 (endothelial NOS, eNOS) is a member of the nitric oxide synthase (NOS) enzyme family, mainly participating in nitric oxide (NO) generation.	Nitric Oxide	60-72	nitric oxide synthase 3	Homo sapiens	18-33
33747912-1	2021	Background: NOS3 (endothelial NOS, eNOS) is a member of the nitric oxide synthase (NOS) enzyme family, mainly participating in nitric oxide (NO) generation.	Nitric Oxide	60-72	nitric oxide synthase 3	Homo sapiens	35-39
33747912-11	2021	The expression of NOS3 was related to the response to QS-11 and brivinib in STAD.	brivinib	64-72	nitric oxide synthase 3	Homo sapiens	18-22
33675874-2	2021	Chronic alcohol consumption decreases endothelial nitric oxide synthase (eNOS)-derived NO production typical of LSEC dysfunction.	Alcohols	8-15	nitric oxide synthase 3	Homo sapiens	38-71
33675874-2	2021	Chronic alcohol consumption decreases endothelial nitric oxide synthase (eNOS)-derived NO production typical of LSEC dysfunction.	Alcohols	8-15	nitric oxide synthase 3	Homo sapiens	73-77
33010104-6	2021	Endothelial nitric oxide synthase (eNOS) dependence was examined by use of L-NAME and eNOS knockout, respectively.	NG-Nitroarginine Methyl Ester	75-81	nitric oxide synthase 3	Homo sapiens	0-33
33010104-6	2021	Endothelial nitric oxide synthase (eNOS) dependence was examined by use of L-NAME and eNOS knockout, respectively.	NG-Nitroarginine Methyl Ester	75-81	nitric oxide synthase 3	Homo sapiens	35-39
33656060-5	2021	The differentially expressed proteins were identified in the signaling pathways of granzyme B, sirtuins, eIF2, actin cytoskeleton, eNOS, acute phase response and calcium and were connected to the upstream regulators MYC, PI3K SMARCA4 and cancer-related chemical drugs.	Calcium	162-169	nitric oxide synthase 3	Homo sapiens	131-135
33497797-5	2021	In this study, we developed an endothelial cell based computational model integrating endothelial cell nitric oxide synthase (eNOS) biochemical pathway with downstream reactions and interactions of oxidative stress, tetrahydrobiopterin (BH4) synthesis and biopterin ratio ([BH4]/[TBP]), Asc and glutathione (GSH).	sapropterin	216-235	nitric oxide synthase 3	Homo sapiens	86-124
33497797-5	2021	In this study, we developed an endothelial cell based computational model integrating endothelial cell nitric oxide synthase (eNOS) biochemical pathway with downstream reactions and interactions of oxidative stress, tetrahydrobiopterin (BH4) synthesis and biopterin ratio ([BH4]/[TBP]), Asc and glutathione (GSH).	sapropterin	216-235	nitric oxide synthase 3	Homo sapiens	126-130
33497797-5	2021	In this study, we developed an endothelial cell based computational model integrating endothelial cell nitric oxide synthase (eNOS) biochemical pathway with downstream reactions and interactions of oxidative stress, tetrahydrobiopterin (BH4) synthesis and biopterin ratio ([BH4]/[TBP]), Asc and glutathione (GSH).	sapropterin	237-240	nitric oxide synthase 3	Homo sapiens	86-124
33497797-5	2021	In this study, we developed an endothelial cell based computational model integrating endothelial cell nitric oxide synthase (eNOS) biochemical pathway with downstream reactions and interactions of oxidative stress, tetrahydrobiopterin (BH4) synthesis and biopterin ratio ([BH4]/[TBP]), Asc and glutathione (GSH).	sapropterin	237-240	nitric oxide synthase 3	Homo sapiens	126-130
33497797-5	2021	In this study, we developed an endothelial cell based computational model integrating endothelial cell nitric oxide synthase (eNOS) biochemical pathway with downstream reactions and interactions of oxidative stress, tetrahydrobiopterin (BH4) synthesis and biopterin ratio ([BH4]/[TBP]), Asc and glutathione (GSH).	Biopterin	226-235	nitric oxide synthase 3	Homo sapiens	86-124
33497797-5	2021	In this study, we developed an endothelial cell based computational model integrating endothelial cell nitric oxide synthase (eNOS) biochemical pathway with downstream reactions and interactions of oxidative stress, tetrahydrobiopterin (BH4) synthesis and biopterin ratio ([BH4]/[TBP]), Asc and glutathione (GSH).	Biopterin	226-235	nitric oxide synthase 3	Homo sapiens	126-130
33497797-5	2021	In this study, we developed an endothelial cell based computational model integrating endothelial cell nitric oxide synthase (eNOS) biochemical pathway with downstream reactions and interactions of oxidative stress, tetrahydrobiopterin (BH4) synthesis and biopterin ratio ([BH4]/[TBP]), Asc and glutathione (GSH).	sapropterin	274-277	nitric oxide synthase 3	Homo sapiens	86-124
33497797-5	2021	In this study, we developed an endothelial cell based computational model integrating endothelial cell nitric oxide synthase (eNOS) biochemical pathway with downstream reactions and interactions of oxidative stress, tetrahydrobiopterin (BH4) synthesis and biopterin ratio ([BH4]/[TBP]), Asc and glutathione (GSH).	sapropterin	274-277	nitric oxide synthase 3	Homo sapiens	126-130
33497797-5	2021	In this study, we developed an endothelial cell based computational model integrating endothelial cell nitric oxide synthase (eNOS) biochemical pathway with downstream reactions and interactions of oxidative stress, tetrahydrobiopterin (BH4) synthesis and biopterin ratio ([BH4]/[TBP]), Asc and glutathione (GSH).	Ascorbic Acid	287-290	nitric oxide synthase 3	Homo sapiens	86-124
33497797-5	2021	In this study, we developed an endothelial cell based computational model integrating endothelial cell nitric oxide synthase (eNOS) biochemical pathway with downstream reactions and interactions of oxidative stress, tetrahydrobiopterin (BH4) synthesis and biopterin ratio ([BH4]/[TBP]), Asc and glutathione (GSH).	Ascorbic Acid	287-290	nitric oxide synthase 3	Homo sapiens	126-130
33497797-5	2021	In this study, we developed an endothelial cell based computational model integrating endothelial cell nitric oxide synthase (eNOS) biochemical pathway with downstream reactions and interactions of oxidative stress, tetrahydrobiopterin (BH4) synthesis and biopterin ratio ([BH4]/[TBP]), Asc and glutathione (GSH).	Glutathione	295-306	nitric oxide synthase 3	Homo sapiens	86-124
33497797-5	2021	In this study, we developed an endothelial cell based computational model integrating endothelial cell nitric oxide synthase (eNOS) biochemical pathway with downstream reactions and interactions of oxidative stress, tetrahydrobiopterin (BH4) synthesis and biopterin ratio ([BH4]/[TBP]), Asc and glutathione (GSH).	Glutathione	295-306	nitric oxide synthase 3	Homo sapiens	126-130
33497797-5	2021	In this study, we developed an endothelial cell based computational model integrating endothelial cell nitric oxide synthase (eNOS) biochemical pathway with downstream reactions and interactions of oxidative stress, tetrahydrobiopterin (BH4) synthesis and biopterin ratio ([BH4]/[TBP]), Asc and glutathione (GSH).	Glutathione	308-311	nitric oxide synthase 3	Homo sapiens	86-124
33497797-5	2021	In this study, we developed an endothelial cell based computational model integrating endothelial cell nitric oxide synthase (eNOS) biochemical pathway with downstream reactions and interactions of oxidative stress, tetrahydrobiopterin (BH4) synthesis and biopterin ratio ([BH4]/[TBP]), Asc and glutathione (GSH).	Glutathione	308-311	nitric oxide synthase 3	Homo sapiens	126-130
33497797-11	2021	We predicted that glutathione peroxidase and peroxiredoxin in combination with GSH and Asc can restore eNOS coupling and NO production under oxidative stress conditions.	Glutathione	18-29	nitric oxide synthase 3	Homo sapiens	103-107
33497797-11	2021	We predicted that glutathione peroxidase and peroxiredoxin in combination with GSH and Asc can restore eNOS coupling and NO production under oxidative stress conditions.	Glutathione	79-82	nitric oxide synthase 3	Homo sapiens	103-107
32325273-2	2021	Recently serum collectrin has emerged as a new member of the renin-angiotensin system that regulates the blood pressure through nitric oxide -endothelial nitric oxide synthase pathway.	Nitric Oxide	128-140	nitric oxide synthase 3	Homo sapiens	142-175
32614624-5	2021	Endothelial cells exposed to ACNs downregulated gene expression of AKT1 and endothelial nitric oxide synthase (eNOS), while PAs upregulated AKT1 and vascular endothelial growth factor (VEGF) gene expression.	Anthocyanins	29-33	nitric oxide synthase 3	Homo sapiens	76-109
32700783-3	2021	Strikingly, we found that increased di-, and tri-methylation of histone H3 lysine 9 (H3K9me2 and H3K9me3) expression were associated with upregulation of methyltransferase G9a and downregulation of endothelial nitric oxide synthase and CuZn-SOD expression in preeclamptic HUVECs.	Lysine	75-81	nitric oxide synthase 3	Homo sapiens	198-231
32614624-6	2021	Combination of ACNs:PAs decreased gene expression of AKT1 and eNOS, while protein levels of AKT1 increased.	Anthocyanins	15-19	nitric oxide synthase 3	Homo sapiens	62-66
33995953-1	2021	Objectives: We investigated whether NOS3-c.894G>T transversion (rs1799983), which causes the substitution of glutamate with aspartate (E298D) in the oxygenase domain of endothelial nitric oxide synthase (eNOS), is associated with susceptibility to metabolic syndrome (MetS) risk in Iranian-Azerbaijanis.	Glutamic Acid	109-118	nitric oxide synthase 3	Homo sapiens	36-40
33995953-1	2021	Objectives: We investigated whether NOS3-c.894G>T transversion (rs1799983), which causes the substitution of glutamate with aspartate (E298D) in the oxygenase domain of endothelial nitric oxide synthase (eNOS), is associated with susceptibility to metabolic syndrome (MetS) risk in Iranian-Azerbaijanis.	Glutamic Acid	109-118	nitric oxide synthase 3	Homo sapiens	169-202
33995953-1	2021	Objectives: We investigated whether NOS3-c.894G>T transversion (rs1799983), which causes the substitution of glutamate with aspartate (E298D) in the oxygenase domain of endothelial nitric oxide synthase (eNOS), is associated with susceptibility to metabolic syndrome (MetS) risk in Iranian-Azerbaijanis.	Glutamic Acid	109-118	nitric oxide synthase 3	Homo sapiens	204-208
33995953-1	2021	Objectives: We investigated whether NOS3-c.894G>T transversion (rs1799983), which causes the substitution of glutamate with aspartate (E298D) in the oxygenase domain of endothelial nitric oxide synthase (eNOS), is associated with susceptibility to metabolic syndrome (MetS) risk in Iranian-Azerbaijanis.	Aspartic Acid	124-133	nitric oxide synthase 3	Homo sapiens	36-40
33995953-1	2021	Objectives: We investigated whether NOS3-c.894G>T transversion (rs1799983), which causes the substitution of glutamate with aspartate (E298D) in the oxygenase domain of endothelial nitric oxide synthase (eNOS), is associated with susceptibility to metabolic syndrome (MetS) risk in Iranian-Azerbaijanis.	Aspartic Acid	124-133	nitric oxide synthase 3	Homo sapiens	169-202
33995953-1	2021	Objectives: We investigated whether NOS3-c.894G>T transversion (rs1799983), which causes the substitution of glutamate with aspartate (E298D) in the oxygenase domain of endothelial nitric oxide synthase (eNOS), is associated with susceptibility to metabolic syndrome (MetS) risk in Iranian-Azerbaijanis.	Aspartic Acid	124-133	nitric oxide synthase 3	Homo sapiens	204-208
33638940-6	2021	eNOS activity was assessed by detecting the phosphorylation (Ser 1179) of eNOS.	Serine	61-64	nitric oxide synthase 3	Homo sapiens	0-4
33638940-6	2021	eNOS activity was assessed by detecting the phosphorylation (Ser 1179) of eNOS.	Serine	61-64	nitric oxide synthase 3	Homo sapiens	74-78
33638940-11	2021	HDL-treatment enhanced the phosphorylation of eNOS at Ser 1179, but pretreatment with AGEs inhibited the phosphorylation of eNOS Ser 1179.	Serine	54-57	nitric oxide synthase 3	Homo sapiens	46-50
33638940-11	2021	HDL-treatment enhanced the phosphorylation of eNOS at Ser 1179, but pretreatment with AGEs inhibited the phosphorylation of eNOS Ser 1179.	Serine	129-132	nitric oxide synthase 3	Homo sapiens	124-128
32614624-5	2021	Endothelial cells exposed to ACNs downregulated gene expression of AKT1 and endothelial nitric oxide synthase (eNOS), while PAs upregulated AKT1 and vascular endothelial growth factor (VEGF) gene expression.	Anthocyanins	29-33	nitric oxide synthase 3	Homo sapiens	111-115
33289873-0	2021	Retraction Note: Fibrauretine reduces ischemia/reperfusion injury via RISK/eNOS activation.	fibrauretine	17-29	nitric oxide synthase 3	Homo sapiens	75-79
33602001-15	2021	Higher levels of E2 and its receptors (ESR1 and ESR2) are positively associated with observed higher levels of eNOS signaling pathway metabolites.	Estradiol	17-19	nitric oxide synthase 3	Homo sapiens	111-115
33557218-11	2021	Quercetin, a component of honey, can improve vasodilation by enhancing nitric oxide production via endothelial nitric oxide synthase and stimulate calcium-activated potassium channels.	Quercetin	0-9	nitric oxide synthase 3	Homo sapiens	99-132
33157202-4	2021	Whereas treatment with TGFbeta1 and TGFbeta2 or Akt1 gene silencing promoted EndMT accompanied by increased ALK5 expression and reduced ALK1 expression accompanied by increased expression of N-cadherin and reduced expression of eNOS in HMECs, treatment with ALK-5 inhibitor (SB431542) blunted these effects.	4-(5-benzo(1,3)dioxol-5-yl-4-pyridin-2-yl-1H-imidazol-2-yl)benzamide	275-283	nitric oxide synthase 3	Homo sapiens	228-232
33658920-12	2020	Furthermore, iodixanol induced the phosphorylation of protein kinase C (PKC) beta II, p47, Rac1, and endothelial nitric oxide synthase (eNOS) at Thr495, which elicited ROS release and ONOO- generation.	iodixanol	13-22	nitric oxide synthase 3	Homo sapiens	101-134
33658920-12	2020	Furthermore, iodixanol induced the phosphorylation of protein kinase C (PKC) beta II, p47, Rac1, and endothelial nitric oxide synthase (eNOS) at Thr495, which elicited ROS release and ONOO- generation.	iodixanol	13-22	nitric oxide synthase 3	Homo sapiens	136-140
33658920-12	2020	Furthermore, iodixanol induced the phosphorylation of protein kinase C (PKC) beta II, p47, Rac1, and endothelial nitric oxide synthase (eNOS) at Thr495, which elicited ROS release and ONOO- generation.	Reactive Oxygen Species	168-171	nitric oxide synthase 3	Homo sapiens	101-134
33658920-12	2020	Furthermore, iodixanol induced the phosphorylation of protein kinase C (PKC) beta II, p47, Rac1, and endothelial nitric oxide synthase (eNOS) at Thr495, which elicited ROS release and ONOO- generation.	Reactive Oxygen Species	168-171	nitric oxide synthase 3	Homo sapiens	136-140
33658920-12	2020	Furthermore, iodixanol induced the phosphorylation of protein kinase C (PKC) beta II, p47, Rac1, and endothelial nitric oxide synthase (eNOS) at Thr495, which elicited ROS release and ONOO- generation.	onoo	184-188	nitric oxide synthase 3	Homo sapiens	101-134
33658920-12	2020	Furthermore, iodixanol induced the phosphorylation of protein kinase C (PKC) beta II, p47, Rac1, and endothelial nitric oxide synthase (eNOS) at Thr495, which elicited ROS release and ONOO- generation.	onoo	184-188	nitric oxide synthase 3	Homo sapiens	136-140
33603465-12	2021	Expression of MAPK1, NR3C1, NOS1, NOS2 and NOS3 genes were significantly regulated by sinomenine in both MCF-7 cells and MDA-MB-231 cells.	sinomenine	86-96	nitric oxide synthase 3	Homo sapiens	43-47
33603465-15	2021	Conclusion: MAPK1, NR3C1, NOS1, NOS2 and NOS3 were identified as the putative targets of sinomenine for treating breast cancer.	sinomenine	89-99	nitric oxide synthase 3	Homo sapiens	41-45
33557218-11	2021	Quercetin, a component of honey, can improve vasodilation by enhancing nitric oxide production via endothelial nitric oxide synthase and stimulate calcium-activated potassium channels.	Nitric Oxide	71-83	nitric oxide synthase 3	Homo sapiens	99-132
33044583-11	2021	However, both the 1.8 cineole treatment and alpha-pinene treatments significantly decreased TNF-alpha, IL-1beta, IL-6, and eNOS mRNA expression induced by LPS.	Eucalyptol	22-29	nitric oxide synthase 3	Homo sapiens	123-127
33044583-11	2021	However, both the 1.8 cineole treatment and alpha-pinene treatments significantly decreased TNF-alpha, IL-1beta, IL-6, and eNOS mRNA expression induced by LPS.	alpha-pinene	44-56	nitric oxide synthase 3	Homo sapiens	123-127
33506378-5	2021	Wortmannin suppressed the angiogenic factors, because VEGF, VEGFR1, and eNOS genes were downregulated in those cells, highlighting the importance of PI3K/AKT signaling on driving angiogenic phenotype and angiogenesis performance within the peri-implant tissue reaction.	Wortmannin	0-10	nitric oxide synthase 3	Homo sapiens	72-76
32959938-8	2021	It can be concluded that berries" bioactive compounds are efficient in mitigation of hypertension through improvement of vascular function, angiotensin-converting enzyme"s (ACE) inhibitory activity, increasing endothelial nitric oxide synthase (eNOS) activity, and nitric oxide (NO) production, besides anti-oxidative and anti-inflammatory activities.	Nitric Oxide	222-234	nitric oxide synthase 3	Homo sapiens	245-249
33300071-11	2021	PA decreased the production of NO, and the levels of phosphorylated-eNOS, whereas knockdown of CCN1 partially abrogated these effects triggered by PA.	Palmitic Acid	0-2	nitric oxide synthase 3	Homo sapiens	68-72
33302164-12	2021	Only low-dose NAC increased NOS3 mRNA abundance and tetrahydrobiopterin reduction (BH4/BH2 ratio).	Acetylcysteine	14-17	nitric oxide synthase 3	Homo sapiens	28-32
33499404-1	2021	Nitric oxide (NO) is formed during the oxidation of L-arginine to L-citrulline by the action of multiple isoenzymes of NO synthase (NOS): neuronal NOS (nNOS), endotelial NOS (eNOS), and inducible NOS (iNOS).	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	175-179
33554972-9	2021	When treated with a cardiotoxic anti-cancer agent, such as doxorubicin (DOX, used to treat leukemia, lymphoma and breast cancer), the viability of DOX-treated CSs is significantly reduced at 10 microM genetic and chemical inhibition of endothelial nitric oxide synthase, a downstream target of DOX in HCFs and HCAECs, reduced its toxicity in CSs.	Doxorubicin	59-70	nitric oxide synthase 3	Homo sapiens	236-269
33554972-9	2021	When treated with a cardiotoxic anti-cancer agent, such as doxorubicin (DOX, used to treat leukemia, lymphoma and breast cancer), the viability of DOX-treated CSs is significantly reduced at 10 microM genetic and chemical inhibition of endothelial nitric oxide synthase, a downstream target of DOX in HCFs and HCAECs, reduced its toxicity in CSs.	Doxorubicin	72-75	nitric oxide synthase 3	Homo sapiens	236-269
33554972-9	2021	When treated with a cardiotoxic anti-cancer agent, such as doxorubicin (DOX, used to treat leukemia, lymphoma and breast cancer), the viability of DOX-treated CSs is significantly reduced at 10 microM genetic and chemical inhibition of endothelial nitric oxide synthase, a downstream target of DOX in HCFs and HCAECs, reduced its toxicity in CSs.	Doxorubicin	147-150	nitric oxide synthase 3	Homo sapiens	236-269
33554972-9	2021	When treated with a cardiotoxic anti-cancer agent, such as doxorubicin (DOX, used to treat leukemia, lymphoma and breast cancer), the viability of DOX-treated CSs is significantly reduced at 10 microM genetic and chemical inhibition of endothelial nitric oxide synthase, a downstream target of DOX in HCFs and HCAECs, reduced its toxicity in CSs.	Doxorubicin	147-150	nitric oxide synthase 3	Homo sapiens	236-269
33499404-1	2021	Nitric oxide (NO) is formed during the oxidation of L-arginine to L-citrulline by the action of multiple isoenzymes of NO synthase (NOS): neuronal NOS (nNOS), endotelial NOS (eNOS), and inducible NOS (iNOS).	Citrulline	66-78	nitric oxide synthase 3	Homo sapiens	175-179
32396609-7	2021	Empagliflozin reduced oxidative stress/eNOS-dependent PKGIalpha oxidation and polymerization resulting in a higher fraction of PKGIalpha monomers, which translocated back to the cytosol.	empagliflozin	0-13	nitric oxide synthase 3	Homo sapiens	39-43
33438233-11	2021	All silica NPs have the smallest effect on the NO-eNOS pathway, but the irregular spherical SBA-15 reduces the eNOS modifier KLF4.	sba-15	92-98	nitric oxide synthase 3	Homo sapiens	111-115
33467058-9	2021	P2Y11R agonist modulated vasoactive factors in human ECs, that is, endothelial nitric oxide synthase (eNOS) and endothelin-1, reduced SMC proliferation and prevented the switch towards a synthetic phenotype.	p2y11r	0-6	nitric oxide synthase 3	Homo sapiens	67-100
33467058-9	2021	P2Y11R agonist modulated vasoactive factors in human ECs, that is, endothelial nitric oxide synthase (eNOS) and endothelin-1, reduced SMC proliferation and prevented the switch towards a synthetic phenotype.	p2y11r	0-6	nitric oxide synthase 3	Homo sapiens	102-106
33413061-3	2021	While the exact mechanisms of endothelial dysfunction in RA remain to be established, there is good evidence that RA patients have relatively high circulating concentrations of the methylated arginine asymmetric dimethylarginine (ADMA), a potent endogenous inhibitor of endothelial NO synthase (eNOS).	Arginine	192-200	nitric oxide synthase 3	Homo sapiens	295-299
33406458-1	2022	Currently, endothelium-dependent vasodilatation involves three main mechanisms: production of nitric oxide (NO) by endothelial nitric oxide synthase (eNOS), synthesis of prostanoids by cyclooxygenase, and/or opening of calcium-sensitive potassium channels.	Nitric Oxide	94-106	nitric oxide synthase 3	Homo sapiens	115-148
33406458-1	2022	Currently, endothelium-dependent vasodilatation involves three main mechanisms: production of nitric oxide (NO) by endothelial nitric oxide synthase (eNOS), synthesis of prostanoids by cyclooxygenase, and/or opening of calcium-sensitive potassium channels.	Nitric Oxide	94-106	nitric oxide synthase 3	Homo sapiens	150-154
33505452-10	2021	Endothelial nitric oxide synthase was also favored in cardiomyocytes treated with fenofibrate.	Fenofibrate	82-93	nitric oxide synthase 3	Homo sapiens	0-33
33414434-3	2021	Using the biotin switch method, subcellular fractionation, immunofluorescence, and luciferase reporter assays, we found that NMDA-stimulated NF-kappaB activity selectively in hippocampal neurons, while endothelial nitric oxide synthase (eNOS), an enzyme expressed in neurons, is involved in the S-nitrosylation of p65 and consequent NF-kappaB inhibition in cerebrocortical, i.e., resistant neurons.	N-Methylaspartate	125-129	nitric oxide synthase 3	Homo sapiens	237-241
33413061-3	2021	While the exact mechanisms of endothelial dysfunction in RA remain to be established, there is good evidence that RA patients have relatively high circulating concentrations of the methylated arginine asymmetric dimethylarginine (ADMA), a potent endogenous inhibitor of endothelial NO synthase (eNOS).	dimethylarginine	212-228	nitric oxide synthase 3	Homo sapiens	295-299
33413061-3	2021	While the exact mechanisms of endothelial dysfunction in RA remain to be established, there is good evidence that RA patients have relatively high circulating concentrations of the methylated arginine asymmetric dimethylarginine (ADMA), a potent endogenous inhibitor of endothelial NO synthase (eNOS).	N,N-dimethylarginine	230-234	nitric oxide synthase 3	Homo sapiens	295-299
33371812-9	2021	The present study shows that EGCG prevents homocysteine-induced endothelial cell apoptosis via enhancing SIRT1/AMPK as well as Akt/eNOS signaling pathways.	Homocysteine	43-55	nitric oxide synthase 3	Homo sapiens	131-135
34019276-4	2021	ROS and calcium signaling also promote endothelial nitric oxide (NO) synthase (eNOS) uncoupling, decreasing NO production and increasing vascular resistance through persistent vasoconstriction and SMC proliferation.	Reactive Oxygen Species	0-3	nitric oxide synthase 3	Homo sapiens	79-83
34019276-4	2021	ROS and calcium signaling also promote endothelial nitric oxide (NO) synthase (eNOS) uncoupling, decreasing NO production and increasing vascular resistance through persistent vasoconstriction and SMC proliferation.	Calcium	8-15	nitric oxide synthase 3	Homo sapiens	79-83
34019276-4	2021	ROS and calcium signaling also promote endothelial nitric oxide (NO) synthase (eNOS) uncoupling, decreasing NO production and increasing vascular resistance through persistent vasoconstriction and SMC proliferation.	Nitric Oxide	51-63	nitric oxide synthase 3	Homo sapiens	79-83
33371812-7	2021	Besides, EGCG also restores homocysteine-mediated dephosphorylation of Akt and decreases endothelial NO synthase (eNOS) expression.	epigallocatechin gallate	9-13	nitric oxide synthase 3	Homo sapiens	114-118
32564765-0	2021	The Influence Of Endothelial Nitric Oxide Synthase (Enos) Genetic Polymorphisms On Cholesterol Blood Levels Among Type 2 Diabetic Patients On Atorvastatin Therapy.	Cholesterol	83-94	nitric oxide synthase 3	Homo sapiens	17-50
33371812-7	2021	Besides, EGCG also restores homocysteine-mediated dephosphorylation of Akt and decreases endothelial NO synthase (eNOS) expression.	Homocysteine	28-40	nitric oxide synthase 3	Homo sapiens	114-118
33371812-9	2021	The present study shows that EGCG prevents homocysteine-induced endothelial cell apoptosis via enhancing SIRT1/AMPK as well as Akt/eNOS signaling pathways.	epigallocatechin gallate	29-33	nitric oxide synthase 3	Homo sapiens	131-135
32447519-7	2021	Additionally, molecular docking simulation confifirmed that scutellarin exhibited a relatively high potential for binding to the active sites of NOS3 and F2.	scutellarin	60-71	nitric oxide synthase 3	Homo sapiens	145-149
33596565-9	2021	The objectives of this study were to evaluate prognostic role of molecular (endothelin-1) and genetic factors (gene polymorphisms of endothelial nitric oxide (NO) synthase (NOS3, rs1799983), endothelin-1 receptor type A (EDNRA, C+70G, rs5335) and NADPH oxidase (C242T, rs4673) in development of endothelial dysfunction and anthracycline-induced cardiotoxicity in women without cardiovascular diseases.	Anthracyclines	323-336	nitric oxide synthase 3	Homo sapiens	173-177
33164880-10	2021	Mechanistically, miR-153-3p regulates the VEGF/VEGFR2/PI3K/Akt/eNOS pathways by targeting ANGPT1.	mir-153-3p	17-27	nitric oxide synthase 3	Homo sapiens	63-67
33164880-12	2021	Collectively, MSCs-derived exosomes with low-expressed miR-153-3p notably promotes the activation of ANGPT1 and the VEGF/VEGFR2 /PI3K/Akt/eNOS pathways, thereby preventing the damages endothelial cells and cardiomyocytes against hypoxia.	mir-153-3p	55-65	nitric oxide synthase 3	Homo sapiens	138-142
32564765-0	2021	The Influence Of Endothelial Nitric Oxide Synthase (Enos) Genetic Polymorphisms On Cholesterol Blood Levels Among Type 2 Diabetic Patients On Atorvastatin Therapy.	Cholesterol	83-94	nitric oxide synthase 3	Homo sapiens	52-56
32564765-0	2021	The Influence Of Endothelial Nitric Oxide Synthase (Enos) Genetic Polymorphisms On Cholesterol Blood Levels Among Type 2 Diabetic Patients On Atorvastatin Therapy.	Atorvastatin	142-154	nitric oxide synthase 3	Homo sapiens	17-50
32564765-0	2021	The Influence Of Endothelial Nitric Oxide Synthase (Enos) Genetic Polymorphisms On Cholesterol Blood Levels Among Type 2 Diabetic Patients On Atorvastatin Therapy.	Atorvastatin	142-154	nitric oxide synthase 3	Homo sapiens	52-56
32564765-10	2021	However, patients with eNOS rs1799983, 4a/4a, and rs61722009 G/G genotypes showed a significantly lower levels of baseline total cholesterol (TC) and low density lipoprotein (LDL) than did patients carrying the rs1799983 4b/4b or rs61722009 T/T genotype (p < 0.05).	Cholesterol	129-140	nitric oxide synthase 3	Homo sapiens	23-27
32564765-10	2021	However, patients with eNOS rs1799983, 4a/4a, and rs61722009 G/G genotypes showed a significantly lower levels of baseline total cholesterol (TC) and low density lipoprotein (LDL) than did patients carrying the rs1799983 4b/4b or rs61722009 T/T genotype (p < 0.05).	Technetium	142-144	nitric oxide synthase 3	Homo sapiens	23-27
33129903-7	2021	To mimic low oxygen environment, an in vitro hypoxic endothelial dysfunction model was developed which showed decreased expressions of phosphorylated eNOS (serine 1177) when compared to the cells cultured in normoxic condition.	Serine	156-162	nitric oxide synthase 3	Homo sapiens	150-154
33140223-1	2021	Generation of nitric oxide (NO) by the nitric oxide synthase (NOS) enzymes plays multiple signalling roles in every organ system, with crucial roles in the cardiovascular system, mediated by endothelial nitric oxide synthase (eNOS, encoded by NOS3) and neuronal nitric oxide synthase (nNOS, encoded by NOS1) in regulation of blood pressure, flow, oxygen delivery and cardiac function.	Nitric Oxide	14-26	nitric oxide synthase 3	Homo sapiens	191-224
33140223-1	2021	Generation of nitric oxide (NO) by the nitric oxide synthase (NOS) enzymes plays multiple signalling roles in every organ system, with crucial roles in the cardiovascular system, mediated by endothelial nitric oxide synthase (eNOS, encoded by NOS3) and neuronal nitric oxide synthase (nNOS, encoded by NOS1) in regulation of blood pressure, flow, oxygen delivery and cardiac function.	Nitric Oxide	14-26	nitric oxide synthase 3	Homo sapiens	226-230
33140223-1	2021	Generation of nitric oxide (NO) by the nitric oxide synthase (NOS) enzymes plays multiple signalling roles in every organ system, with crucial roles in the cardiovascular system, mediated by endothelial nitric oxide synthase (eNOS, encoded by NOS3) and neuronal nitric oxide synthase (nNOS, encoded by NOS1) in regulation of blood pressure, flow, oxygen delivery and cardiac function.	Nitric Oxide	14-26	nitric oxide synthase 3	Homo sapiens	243-247
33140223-1	2021	Generation of nitric oxide (NO) by the nitric oxide synthase (NOS) enzymes plays multiple signalling roles in every organ system, with crucial roles in the cardiovascular system, mediated by endothelial nitric oxide synthase (eNOS, encoded by NOS3) and neuronal nitric oxide synthase (nNOS, encoded by NOS1) in regulation of blood pressure, flow, oxygen delivery and cardiac function.	Oxygen	347-353	nitric oxide synthase 3	Homo sapiens	226-230
33140223-1	2021	Generation of nitric oxide (NO) by the nitric oxide synthase (NOS) enzymes plays multiple signalling roles in every organ system, with crucial roles in the cardiovascular system, mediated by endothelial nitric oxide synthase (eNOS, encoded by NOS3) and neuronal nitric oxide synthase (nNOS, encoded by NOS1) in regulation of blood pressure, flow, oxygen delivery and cardiac function.	Oxygen	347-353	nitric oxide synthase 3	Homo sapiens	243-247
33129903-9	2021	The nC/R hydrogel was found to enhance phosphorylation of eNOS at serine 1177 site in cultured endothelial cells subjected to hypoxia.	Serine	66-72	nitric oxide synthase 3	Homo sapiens	58-62
33221570-7	2021	Mechanistically, this occurs via the mitochondrial redistribution of uncoupled eNOS secondary to a PKC-dependent phosphorylation of eNOS at Threonine 495 (T495).	Threonine	140-149	nitric oxide synthase 3	Homo sapiens	79-83
33780370-9	2021	Tumor necrosis factor inhibition and stimulation of endothelial nitric oxide synthase were proposed to be the primary mechanism of actions which confer elevated bradycardia risk when using donepezil.	Donepezil	189-198	nitric oxide synthase 3	Homo sapiens	52-85
33320446-0	2021	Gastrodin prevents homocysteine-induced human umbilical vein endothelial cells injury via PI3K/Akt/eNOS and Nrf2/ARE pathway.	Homocysteine	19-31	nitric oxide synthase 3	Homo sapiens	99-103
32740409-10	2021	CONCLUSION: Aliskiren restored endothelial function and induced a more prompt peripheral vasodilation in hypertensive and diabetic patients possibly through the increased production of nitric oxide via the enhanced expression and function of the active phosphorylated form of endothelial nitric oxide synthase.	aliskiren	12-21	nitric oxide synthase 3	Homo sapiens	276-309
33221570-7	2021	Mechanistically, this occurs via the mitochondrial redistribution of uncoupled eNOS secondary to a PKC-dependent phosphorylation of eNOS at Threonine 495 (T495).	Threonine	140-149	nitric oxide synthase 3	Homo sapiens	132-136
32122268-7	2021	Stem cell/oxygen-releasing HP system increased cGMP level and nNOS, eNOS, a-SMA and M3 expression, while decreasing fibrosis and apoptosis in the corpus cavernosum.	Oxygen	10-16	nitric oxide synthase 3	Homo sapiens	68-72
32122268-7	2021	Stem cell/oxygen-releasing HP system increased cGMP level and nNOS, eNOS, a-SMA and M3 expression, while decreasing fibrosis and apoptosis in the corpus cavernosum.	Hematoporphyrins	27-29	nitric oxide synthase 3	Homo sapiens	68-72
33371217-7	2020	In turn, nitric oxide production through eNOS was essential for TEM by modulating VE-cadherin on Y731.	Nitric Oxide	9-21	nitric oxide synthase 3	Homo sapiens	41-45
33356884-9	2021	Finally, we showed that Nicaraven improved the functions of endothelial cells, seen as the up-regulation of endothelial nitric oxide synthase and increased nitric oxide levels.	nicaraven	24-33	nitric oxide synthase 3	Homo sapiens	108-141
33157320-0	2020	Does eNOS derived nitric oxide protect the young from severe COVID-19 complications?	Nitric Oxide	18-30	nitric oxide synthase 3	Homo sapiens	5-9
33414716-6	2020	NO is produced by the activity of endothelial NO synthase (eNOS) on its substrate, L-arginine.	Arginine	83-93	nitric oxide synthase 3	Homo sapiens	34-57
33414716-6	2020	NO is produced by the activity of endothelial NO synthase (eNOS) on its substrate, L-arginine.	Arginine	83-93	nitric oxide synthase 3	Homo sapiens	59-63
33414716-7	2020	Reduced availability of L-arginine to eNOS has been implicated in vascular dysfunction in diabetes.	Arginine	24-34	nitric oxide synthase 3	Homo sapiens	38-42
33291075-4	2020	Mammalian target of rapamycin (mTOR) colocalized with PKG in pre-granulosa cells and was essential for eNOS/cGMP/PKG pathway-induced primordial follicle activation.	Cyclic GMP	108-112	nitric oxide synthase 3	Homo sapiens	103-107
33291075-5	2020	The eNOS/cGMP/PKG pathway was found to stabilize mTOR protein.	Cyclic GMP	9-13	nitric oxide synthase 3	Homo sapiens	4-8
33291075-8	2020	However, agonists of the eNOS/cGMP/PKG pathway reduced FBXW7 mRNA levels.	Cyclic GMP	30-34	nitric oxide synthase 3	Homo sapiens	25-29
33291075-9	2020	FBXW7 overexpression suppressed primordial follicle activation and prevented the eNOS/cGMP/PKG pathway from activating primordial follicles and stabilizing mTOR protein.	Cyclic GMP	86-90	nitric oxide synthase 3	Homo sapiens	81-85
33271854-3	2020	We studied single nucleotide polymorphisms (SNPs) in the NOS3, DDAH1, DDAH2, PRMT1, and AGXT2 genes that are part of the L-arginine-ADMA-NO pathway, and their association with DCI.	l-arginine-adma-no	121-139	nitric oxide synthase 3	Homo sapiens	57-61
33208017-0	2020	The impact of NOS3 gene polymorphism on papillary thyroid cancer susceptibility in patients undergoing radioiodine therapy.	Iodine-131	103-114	nitric oxide synthase 3	Homo sapiens	14-18
33208017-2	2020	Noting that the NOS3 gene polymorphism interferes with nitric oxide production, this study aims to identify and analyze the NOS3 gene polymorphism in the intron 4 region in patients with papillary thyroid cancer.	Nitric Oxide	55-67	nitric oxide synthase 3	Homo sapiens	16-20
32483670-14	2020	PGE1 activated eNOS and GTPCH1 and inhibition of eNOS or GTPCH1 led to the attenuation of the protective functions of PGE1 in LPS-induced cells.	Alprostadil	118-122	nitric oxide synthase 3	Homo sapiens	49-53
32483670-15	2020	PGE1 protected HCMEC/D3 cells from injuries induced by LPS by activation of eNOS and GTPCH1, suggesting that PGE1 might be used to help maintain cerebral microcirculation in future.	Alprostadil	0-4	nitric oxide synthase 3	Homo sapiens	76-80
32483670-15	2020	PGE1 protected HCMEC/D3 cells from injuries induced by LPS by activation of eNOS and GTPCH1, suggesting that PGE1 might be used to help maintain cerebral microcirculation in future.	Alprostadil	109-113	nitric oxide synthase 3	Homo sapiens	76-80
33049495-7	2020	RESULTS: Juglanin reduces OSS-induced oxidative stress by reducing the production of ROS through downregulation of NOX-2 and rescuing OSS-induced reduced expression of eNOS.	juglanin	9-17	nitric oxide synthase 3	Homo sapiens	168-172
33049495-7	2020	RESULTS: Juglanin reduces OSS-induced oxidative stress by reducing the production of ROS through downregulation of NOX-2 and rescuing OSS-induced reduced expression of eNOS.	OSS	26-29	nitric oxide synthase 3	Homo sapiens	168-172
33049495-7	2020	RESULTS: Juglanin reduces OSS-induced oxidative stress by reducing the production of ROS through downregulation of NOX-2 and rescuing OSS-induced reduced expression of eNOS.	OSS	134-137	nitric oxide synthase 3	Homo sapiens	168-172
32483670-0	2020	Prostaglandin E1 Improves Cerebral Microcirculation Through Activation of Endothelial NOS and GRPCH1.	Alprostadil	0-16	nitric oxide synthase 3	Homo sapiens	74-89
32483670-9	2020	The modulation of PGE1 in eNOS and GTPCH1 production, viability, inflammation, and apoptosis was investigated.	Alprostadil	18-22	nitric oxide synthase 3	Homo sapiens	26-30
32483670-10	2020	The inhibitor of eNOS or GTPCH1 was introduced to examine impacts of eNOS or GTPCH1 could have on the PGE1 function.	Alprostadil	102-106	nitric oxide synthase 3	Homo sapiens	69-73
32483670-14	2020	PGE1 activated eNOS and GTPCH1 and inhibition of eNOS or GTPCH1 led to the attenuation of the protective functions of PGE1 in LPS-induced cells.	Alprostadil	0-4	nitric oxide synthase 3	Homo sapiens	15-19
33253900-1	2021	Catalyzed by endothelial nitric oxide (NO) synthase (eNOS) activity.	Nitric Oxide	25-37	nitric oxide synthase 3	Homo sapiens	53-57
33242203-10	2021	Meanwhile, endothelial dysfunction caused by IH REVs was reversed by Akt activator SC79 as well as Erk kinase inhibitor PD98059, suggesting that PI3K/Akt/eNOS and Erk1/2/ET-1 pathways were implicated in IH REV-induced impaired EDRs.	Ile-His	45-47	nitric oxide synthase 3	Homo sapiens	154-158
33242203-10	2021	Meanwhile, endothelial dysfunction caused by IH REVs was reversed by Akt activator SC79 as well as Erk kinase inhibitor PD98059, suggesting that PI3K/Akt/eNOS and Erk1/2/ET-1 pathways were implicated in IH REV-induced impaired EDRs.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	120-127	nitric oxide synthase 3	Homo sapiens	154-158
33293942-0	2020	Nitric Oxide Mediates Inflammation in Type II Diabetes Mellitus through the PPARgamma/eNOS Signaling Pathway.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	86-90
33180478-6	2020	VPP and IPP treatment reduced the level of reactive oxygen species and EV-induced expression of adhesion molecules and restored the ability of tube formation by upregulating endothelial nitric oxide synthase expression.	valyl-prolyl-proline	0-3	nitric oxide synthase 3	Homo sapiens	174-207
33180478-6	2020	VPP and IPP treatment reduced the level of reactive oxygen species and EV-induced expression of adhesion molecules and restored the ability of tube formation by upregulating endothelial nitric oxide synthase expression.	isoleucyl-prolyl-proline	8-11	nitric oxide synthase 3	Homo sapiens	174-207
32811745-12	2020	A484954 promoted the dimerization of eNOS in human endothelial cells.	a484954	0-7	nitric oxide synthase 3	Homo sapiens	37-41
33030168-3	2020	Previous studies indicate that UVB radiation induces the activation and uncoupling of constitutive nitric oxide synthases (cNOS), which produce nitric oxide and peroxynitrite; both have been shown to regulate autophagy responses.	Nitric Oxide	99-111	nitric oxide synthase 3	Homo sapiens	123-127
33030168-3	2020	Previous studies indicate that UVB radiation induces the activation and uncoupling of constitutive nitric oxide synthases (cNOS), which produce nitric oxide and peroxynitrite; both have been shown to regulate autophagy responses.	Peroxynitrous Acid	161-174	nitric oxide synthase 3	Homo sapiens	86-121
33030168-3	2020	Previous studies indicate that UVB radiation induces the activation and uncoupling of constitutive nitric oxide synthases (cNOS), which produce nitric oxide and peroxynitrite; both have been shown to regulate autophagy responses.	Peroxynitrous Acid	161-174	nitric oxide synthase 3	Homo sapiens	123-127
32879145-3	2020	Several lines of evidence indicate that CSE impairs endothelium-derived nitric oxide (NO)-dependent vasodilation by reducing the activity and protein expression of endothelial NO synthase (eNOS), whereas ACR elicits endothelium-dependent vasorelaxation by increasing the production of NO and expression of eNOS.	Nitric Oxide	72-84	nitric oxide synthase 3	Homo sapiens	164-187
32879145-6	2020	The CSE- and ACR-induced decrease in the phosphorylation and expression of eNOS was counteracted by glutathione (reduced form), an antioxidant.	Acrolein	13-16	nitric oxide synthase 3	Homo sapiens	75-79
32879145-6	2020	The CSE- and ACR-induced decrease in the phosphorylation and expression of eNOS was counteracted by glutathione (reduced form), an antioxidant.	Glutathione	100-111	nitric oxide synthase 3	Homo sapiens	75-79
33182831-8	2020	In addition, Securiniga suffruticosa increased the protein expression of GTPCH (Guanosine triphosphate cyclohydrolase I) and the production of BH4 in HUVEC which are related with eNOS coupling pathway.	sapropterin	143-146	nitric oxide synthase 3	Homo sapiens	179-183
32002792-0	2020	Nobiletin Regulates ROS/ADMA/DDAHII/eNOS/NO Pathway and Alleviates Vascular Endothelium Injury by Iron Overload.	nobiletin	0-9	nitric oxide synthase 3	Homo sapiens	36-40
32002792-4	2020	In this study, we have identified the protective effects of Nob, and its underlying molecular mechanism in human umbilical vein endothelial cells (HUVECs) suffered from iron overload via ROS/ADMA/DDAHII/eNOS/NO pathway.	nobiletin	60-63	nitric oxide synthase 3	Homo sapiens	203-207
32002792-6	2020	Besides, Nob could upregulate DDAHII expression and activity, promote eNOS phosphorylation to produce more NO, reduce ADMA content, and therefore increase superoxide dismutase, catalase, and glutathione peroxidase activities, and decrease malondialdehyde level and ROS generation.	nobiletin	9-12	nitric oxide synthase 3	Homo sapiens	70-74
32002792-10	2020	These data suggested that the protective mechanism of Nob was to inhibit ROS burst, upregulate DDAHII expression and activity, promote eNOS phosphorylation, produce NO, reduce ADMA content, and ultimately alleviate iron overload damage in vascular endothelium.	nobiletin	54-57	nitric oxide synthase 3	Homo sapiens	135-139
32827633-8	2020	Opiate coupling to cNOS and subsequent production and release of mitochondrial nitric oxide (NO) suggests an evolutionary linkage to similar physiological events in prokaryotic cells.	Nitric Oxide	79-91	nitric oxide synthase 3	Homo sapiens	19-23
32568451-4	2020	Endothelial NO, synthesized from L-arginine by endothelial NO synthase (eNOS), inhibits apoptosis and promotes angiogenesis and tumor cell proliferation.	Arginine	33-43	nitric oxide synthase 3	Homo sapiens	72-76
33051476-0	2020	Influence of NOS3 rs2070744 genotypes on hepatocellular carcinoma patients treated with lenvatinib.	lenvatinib	88-98	nitric oxide synthase 3	Homo sapiens	13-17
33051476-7	2020	However, the SNP combination pattern of the NOS3 rs2070744 and FGFR4 rs351855 genotypes may be helpful as treatment effect predictors and prognostic factors for HCC patients treated with lenvatinib.	lenvatinib	187-197	nitric oxide synthase 3	Homo sapiens	44-48
33050870-4	2021	Gene variants of the endothelial nitric oxide (eNOS) affect the plasma levels of NO.	Nitric Oxide	33-45	nitric oxide synthase 3	Homo sapiens	47-51
32994087-0	2020	Corrigendum to "Ac2-26 ameliorates lung ischemia-reperfusion injury via the eNOS pathway" [Biomed.	annexin A1 peptide (2-26)	16-22	nitric oxide synthase 3	Homo sapiens	76-80
32371540-0	2020	Association of NOS3 and ANGPT2 gene polymorphisms with survival in patients with hepatocellular carcinoma receiving sorafenib: results of the multicenter prospective INNOVATE study.	Sorafenib	116-125	nitric oxide synthase 3	Homo sapiens	15-19
32559890-6	2020	Using Western blotting and specific pharmacological inhibitors in the acute study, we have shown that direct BPA"s action in EA.hy926 cells involves activation of estrogen receptor (ER), phosphorylation of protein kinase B (PKB/Akt) and endothelial nitric oxide synthase (eNOS)-mediated production of NO.	bisphenol A	109-112	nitric oxide synthase 3	Homo sapiens	237-270
32559890-6	2020	Using Western blotting and specific pharmacological inhibitors in the acute study, we have shown that direct BPA"s action in EA.hy926 cells involves activation of estrogen receptor (ER), phosphorylation of protein kinase B (PKB/Akt) and endothelial nitric oxide synthase (eNOS)-mediated production of NO.	bisphenol A	109-112	nitric oxide synthase 3	Homo sapiens	272-276
32559890-7	2020	Collectively, these data indicate that BPA induces functional and molecular changes in EA.hy926 cells associated with the promotion of endothelial integrity through activation of the ER/Akt/eNOS pathway.	bisphenol A	39-42	nitric oxide synthase 3	Homo sapiens	190-194
33042519-4	2020	These discussions primarily focus on endothelial nitric oxide synthase (eNOS) as the source of nitric oxide.	Nitric Oxide	49-61	nitric oxide synthase 3	Homo sapiens	72-76
33133730-4	2020	Herein, facilitated by a selective and sensitive fluorescence probe, we observed that some NO modulators displayed unexpected behaviors with both NO scavenger carboxy-PTIO and endothelial nitric oxide synthase (eNOS) inhibitor N(omega)-nitro-l-arginine methyl ester (l-NAME) failing to decrease intracellular free NO level in EA.	NG-Nitroarginine Methyl Ester	227-265	nitric oxide synthase 3	Homo sapiens	176-209
33133730-4	2020	Herein, facilitated by a selective and sensitive fluorescence probe, we observed that some NO modulators displayed unexpected behaviors with both NO scavenger carboxy-PTIO and endothelial nitric oxide synthase (eNOS) inhibitor N(omega)-nitro-l-arginine methyl ester (l-NAME) failing to decrease intracellular free NO level in EA.	NG-Nitroarginine Methyl Ester	227-265	nitric oxide synthase 3	Homo sapiens	211-215
33133730-4	2020	Herein, facilitated by a selective and sensitive fluorescence probe, we observed that some NO modulators displayed unexpected behaviors with both NO scavenger carboxy-PTIO and endothelial nitric oxide synthase (eNOS) inhibitor N(omega)-nitro-l-arginine methyl ester (l-NAME) failing to decrease intracellular free NO level in EA.	NG-Nitroarginine Methyl Ester	267-273	nitric oxide synthase 3	Homo sapiens	176-209
33133730-4	2020	Herein, facilitated by a selective and sensitive fluorescence probe, we observed that some NO modulators displayed unexpected behaviors with both NO scavenger carboxy-PTIO and endothelial nitric oxide synthase (eNOS) inhibitor N(omega)-nitro-l-arginine methyl ester (l-NAME) failing to decrease intracellular free NO level in EA.	NG-Nitroarginine Methyl Ester	267-273	nitric oxide synthase 3	Homo sapiens	211-215
32600711-10	2020	Molecular studies demonstrated the reduced expression of tumor suppressor (p53) and elevated anti-apoptotic protein (Bcl-xL) levels along with enhanced NO production through endothelial nitric oxide synthase (eNOS) activation as the plausible mechanisms underlying protective role of EHN against Cd-induced vascular toxicity.	ehn	284-287	nitric oxide synthase 3	Homo sapiens	174-207
33052245-8	2020	TritonX-100 at a dose of 0.125% was utilized to inactivate the eNOS activity in endothelium to investigate the role of CMEC-derived eNOS in TXL-induced cardioprotection.	Octoxynol	0-11	nitric oxide synthase 3	Homo sapiens	63-67
32713709-6	2020	Interestingly, MPsHED significantly decreased eNOS expression up to ~25% and increased ROS production up to ~75% on in vitro treated HUVECs.	mpshed	15-21	nitric oxide synthase 3	Homo sapiens	46-50
32759013-4	2020	Our work has shown that, in the systemic circulation, folic acid in high dose rapidly improves nitric oxide mediated vasodilation, by activating endothelial nitric oxide synthase (eNOS).	Folic Acid	54-64	nitric oxide synthase 3	Homo sapiens	145-178
32759013-4	2020	Our work has shown that, in the systemic circulation, folic acid in high dose rapidly improves nitric oxide mediated vasodilation, by activating endothelial nitric oxide synthase (eNOS).	Folic Acid	54-64	nitric oxide synthase 3	Homo sapiens	180-184
32759013-4	2020	Our work has shown that, in the systemic circulation, folic acid in high dose rapidly improves nitric oxide mediated vasodilation, by activating endothelial nitric oxide synthase (eNOS).	Nitric Oxide	95-107	nitric oxide synthase 3	Homo sapiens	145-178
32759013-4	2020	Our work has shown that, in the systemic circulation, folic acid in high dose rapidly improves nitric oxide mediated vasodilation, by activating endothelial nitric oxide synthase (eNOS).	Nitric Oxide	95-107	nitric oxide synthase 3	Homo sapiens	180-184
33162896-0	2020	Angiotensin II Decreases Endothelial Nitric Oxide Synthase Phosphorylation via AT1R Nox/ROS/PP2A Pathway.	Reactive Oxygen Species	88-91	nitric oxide synthase 3	Homo sapiens	25-58
33162896-3	2020	In this study, we reported that AngII/AT1R-mediated activated protein phosphatase 2A (PP2A) downregulated endothelial nitric oxide synthase (eNOS) phosphorylation via Nox/ROS pathway.	Reactive Oxygen Species	171-174	nitric oxide synthase 3	Homo sapiens	106-139
33162896-3	2020	In this study, we reported that AngII/AT1R-mediated activated protein phosphatase 2A (PP2A) downregulated endothelial nitric oxide synthase (eNOS) phosphorylation via Nox/ROS pathway.	Reactive Oxygen Species	171-174	nitric oxide synthase 3	Homo sapiens	141-145
33162896-4	2020	AngII treatment reduced the levels of phosphorylation of eNOS Ser1177 and nitric oxide (NO) content along with phosphorylation of PP2Ac (PP2A catalytic subunit) Tyr307, meanwhile increased the PP2A activity and ROS production in human umbilical vein endothelial cells (HUVECs).	Reactive Oxygen Species	211-214	nitric oxide synthase 3	Homo sapiens	57-61
33162896-6	2020	The pretreatment of 10-8 M PP2A inhibitor okadaic acid (OA) reversed the levels of eNOS Ser1177 and NO content.	Okadaic Acid	42-54	nitric oxide synthase 3	Homo sapiens	83-87
33162896-6	2020	The pretreatment of 10-8 M PP2A inhibitor okadaic acid (OA) reversed the levels of eNOS Ser1177 and NO content.	Okadaic Acid	56-58	nitric oxide synthase 3	Homo sapiens	83-87
33052245-12	2020	Upon uptake into CMECs, linc-ROR downregulates its target miR-145-5p leading to activation of the eNOS pathway by facilitating the expression of p70s6k1 in these cells.	linc-ror	24-32	nitric oxide synthase 3	Homo sapiens	98-102
32957896-2	2021	Nitric oxide (NO), produced by the enzyme endothelial nitric oxide synthase (eNOS) in endothelial cells, has considerable effects on bone cell function.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	42-75
32957896-2	2021	Nitric oxide (NO), produced by the enzyme endothelial nitric oxide synthase (eNOS) in endothelial cells, has considerable effects on bone cell function.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	77-81
32908983-9	2020	Key Point: PI3K/eNOS pathway-mediated, inflammation-triggered vWF secretion is the target of the pharmacological manipulation of the cAMP-EPAC system.	Cyclic AMP	133-137	nitric oxide synthase 3	Homo sapiens	16-20
32463112-5	2020	The presence of the nitric oxide-scavenging protein, hemoglobin alpha, limits TRPV4EC -eNOS signalling in mesenteric arteries.	Nitric Oxide	20-32	nitric oxide synthase 3	Homo sapiens	87-91
32407761-5	2020	Furthermore, the increase of NOS and extracellular signal regulated kinases1/2 (ERK1/2) phosphorylation mediated by APJ/B2R dimer can be inhibited by U0126 and U73122, respectively, suggesting that the heterodimer might activate the PLC/ERK1/2/eNOS signaling pathway, and finally leading to a significant increase in cell proliferation.	U 0126	150-155	nitric oxide synthase 3	Homo sapiens	244-248
32407761-5	2020	Furthermore, the increase of NOS and extracellular signal regulated kinases1/2 (ERK1/2) phosphorylation mediated by APJ/B2R dimer can be inhibited by U0126 and U73122, respectively, suggesting that the heterodimer might activate the PLC/ERK1/2/eNOS signaling pathway, and finally leading to a significant increase in cell proliferation.	1-(6-((3-methoxyestra-1,3,5(10)-trien-17-yl)amino)hexyl)-1H-pyrrole-2,5-dione	160-166	nitric oxide synthase 3	Homo sapiens	244-248
32888132-7	2020	Both chronic morphine and methadone treatment increased NO level and eNOS expression in HUVECs.	Morphine	13-21	nitric oxide synthase 3	Homo sapiens	69-73
32888132-7	2020	Both chronic morphine and methadone treatment increased NO level and eNOS expression in HUVECs.	Methadone	26-35	nitric oxide synthase 3	Homo sapiens	69-73
32888132-9	2020	Lithium pretreatment (10 mM) in both morphine and methadone received groups significantly reduced nitrite and cAMP levels as well as eNOS expression as compared to the control.	Lithium	0-7	nitric oxide synthase 3	Homo sapiens	133-137
32888132-9	2020	Lithium pretreatment (10 mM) in both morphine and methadone received groups significantly reduced nitrite and cAMP levels as well as eNOS expression as compared to the control.	Methadone	50-59	nitric oxide synthase 3	Homo sapiens	133-137
32888132-0	2020	Lithium reverses the effect of opioids on eNOS/nitric oxide pathway in human umbilical vein endothelial cells.	Lithium	0-7	nitric oxide synthase 3	Homo sapiens	42-46
32888132-0	2020	Lithium reverses the effect of opioids on eNOS/nitric oxide pathway in human umbilical vein endothelial cells.	Nitric Oxide	47-59	nitric oxide synthase 3	Homo sapiens	42-46
32463112-12	2020	However, the TRPV4 channel agonist GSK1016790A (10 nM) selectively activated IK/SK channels in MAs and eNOS in PAs, revealing preferential TRPV4EC -IK/SK channel coupling in MAs and TRPV4EC -eNOS coupling in PAs.	N-(1-((4-(2-(((2,4-dichlorophenyl)sulfonyl)amino)-3-hydroxypropanoyl)-1-piperazinyl)carbonyl)-3-methylbutyl)-1-benzothiophene-2-carboxamide	35-46	nitric oxide synthase 3	Homo sapiens	103-107
32463112-12	2020	However, the TRPV4 channel agonist GSK1016790A (10 nM) selectively activated IK/SK channels in MAs and eNOS in PAs, revealing preferential TRPV4EC -IK/SK channel coupling in MAs and TRPV4EC -eNOS coupling in PAs.	N-(1-((4-(2-(((2,4-dichlorophenyl)sulfonyl)amino)-3-hydroxypropanoyl)-1-piperazinyl)carbonyl)-3-methylbutyl)-1-benzothiophene-2-carboxamide	35-46	nitric oxide synthase 3	Homo sapiens	191-195
32922141-12	2020	Collectively, these findings led to the assumption that the downregulation of IL-6/JAK2/STAT3 signaling by cinnamaldehyde, tadalafil, and aliskiren could alleviate joint destruction by MMP-3 and RANKL, reduce iNOS, and enhance eNOS expressions.	cinnamaldehyde	107-121	nitric oxide synthase 3	Homo sapiens	227-231
32544536-9	2020	These findings suggest a causative role of E2 and its receptors ESR1 and ESR2 in augmenting eNOS activity and NO availability during healthy high altitude ascent.	Estradiol	43-45	nitric oxide synthase 3	Homo sapiens	92-96
32863226-0	2020	Specific O-GlcNAc modification at Ser-615 modulates eNOS function.	Serine	34-37	nitric oxide synthase 3	Homo sapiens	52-56
32863226-3	2020	Nitric Oxide (NO) deficiency is considered a hallmark of IPAH and altered function of endothelial nitric oxide synthase (eNOS), decreases NO production.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	86-119
32863226-3	2020	Nitric Oxide (NO) deficiency is considered a hallmark of IPAH and altered function of endothelial nitric oxide synthase (eNOS), decreases NO production.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	121-125
32863226-5	2020	In diabetes, dysregulated glucose metabolism has been shown to regulate eNOS function through inhibition of Ser-1177 phosphorylation.	Serine	108-111	nitric oxide synthase 3	Homo sapiens	72-76
32863226-7	2020	Here we show that increased protein O-GlcNAc occurs on eNOS in PAH and Ser-615 appears to be a novel site of O-GlcNAc modification resulting in reduced eNOS dimerization.	p-Aminohippuric Acid	63-66	nitric oxide synthase 3	Homo sapiens	55-59
32863226-7	2020	Here we show that increased protein O-GlcNAc occurs on eNOS in PAH and Ser-615 appears to be a novel site of O-GlcNAc modification resulting in reduced eNOS dimerization.	Serine	71-74	nitric oxide synthase 3	Homo sapiens	152-156
32863226-8	2020	Functional characterization of Ser-615 demonstrated the importance of this residue on the regulation of eNOS activity through control of Ser-1177 phosphorylation.	Serine	31-34	nitric oxide synthase 3	Homo sapiens	104-108
32863226-8	2020	Functional characterization of Ser-615 demonstrated the importance of this residue on the regulation of eNOS activity through control of Ser-1177 phosphorylation.	Serine	137-140	nitric oxide synthase 3	Homo sapiens	104-108
32863226-9	2020	Here we demonstrate a previously unidentified regulatory mechanism of eNOS whereby the O-GlcNAc modification of Ser-615 results in reduced eNOS activity and endothelial dysfunction under conditions of glucose dysregulation.	Serine	112-115	nitric oxide synthase 3	Homo sapiens	70-74
32863226-9	2020	Here we demonstrate a previously unidentified regulatory mechanism of eNOS whereby the O-GlcNAc modification of Ser-615 results in reduced eNOS activity and endothelial dysfunction under conditions of glucose dysregulation.	Serine	112-115	nitric oxide synthase 3	Homo sapiens	139-143
32590330-1	2020	Hydrogen peroxide (H2O2) modulates critical phosphorylation pathways in vascular endothelial cells, many of which affect endothelial nitric oxide synthase (eNOS) signal transduction.	Hydrogen Peroxide	0-17	nitric oxide synthase 3	Homo sapiens	121-154
32590330-1	2020	Hydrogen peroxide (H2O2) modulates critical phosphorylation pathways in vascular endothelial cells, many of which affect endothelial nitric oxide synthase (eNOS) signal transduction.	Hydrogen Peroxide	0-17	nitric oxide synthase 3	Homo sapiens	156-160
32590330-1	2020	Hydrogen peroxide (H2O2) modulates critical phosphorylation pathways in vascular endothelial cells, many of which affect endothelial nitric oxide synthase (eNOS) signal transduction.	Hydrogen Peroxide	19-23	nitric oxide synthase 3	Homo sapiens	121-154
32590330-1	2020	Hydrogen peroxide (H2O2) modulates critical phosphorylation pathways in vascular endothelial cells, many of which affect endothelial nitric oxide synthase (eNOS) signal transduction.	Hydrogen Peroxide	19-23	nitric oxide synthase 3	Homo sapiens	156-160
32590330-2	2020	Both intracellular and extracellular sources of H2O2 have been implicated in eNOS regulation, yet the specific endothelial pathways remain incompletely understood.	Hydrogen Peroxide	48-52	nitric oxide synthase 3	Homo sapiens	77-81
32590330-10	2020	Addition of extracellular H2O2 had only a nominal effect on phosphorylation of eNOS, kinase Akt or AMP-activated protein kinase (AMPK).	Hydrogen Peroxide	26-30	nitric oxide synthase 3	Homo sapiens	79-83
32590330-12	2020	We also found that the AMPK inhibitor Compound C completely blocked nuclear H2O2-promoted eNOS phosphorylation.	Hydrogen Peroxide	76-80	nitric oxide synthase 3	Homo sapiens	90-94
32590330-14	2020	We conclude that H2O2 generated in the cell nucleus activates AMPK, leading to eNOS phosphorylation; in contrast, AMPK activation by cytosol- or caveolae-derived H2O2 does not promote eNOS phosphorylation via AMPK.	Hydrogen Peroxide	17-21	nitric oxide synthase 3	Homo sapiens	79-83
32922141-12	2020	Collectively, these findings led to the assumption that the downregulation of IL-6/JAK2/STAT3 signaling by cinnamaldehyde, tadalafil, and aliskiren could alleviate joint destruction by MMP-3 and RANKL, reduce iNOS, and enhance eNOS expressions.	Tadalafil	123-132	nitric oxide synthase 3	Homo sapiens	227-231
32922141-12	2020	Collectively, these findings led to the assumption that the downregulation of IL-6/JAK2/STAT3 signaling by cinnamaldehyde, tadalafil, and aliskiren could alleviate joint destruction by MMP-3 and RANKL, reduce iNOS, and enhance eNOS expressions.	aliskiren	138-147	nitric oxide synthase 3	Homo sapiens	227-231
32908689-13	2020	Conclusion: The results are congruent with the following proposed sequence of events leading to a protective response of the organism during the pathogenesis of primary pterygium: a decreased level of eNOS provokes a decline in the level of NO in pterygium tissue, which then leads to reduced S-nitrosylation of GSH or other thiols and possibly to the modulation of the intracellular level of GSH through synthesis and/or mobilization from other tissues.	Glutathione	312-315	nitric oxide synthase 3	Homo sapiens	201-205
32908689-13	2020	Conclusion: The results are congruent with the following proposed sequence of events leading to a protective response of the organism during the pathogenesis of primary pterygium: a decreased level of eNOS provokes a decline in the level of NO in pterygium tissue, which then leads to reduced S-nitrosylation of GSH or other thiols and possibly to the modulation of the intracellular level of GSH through synthesis and/or mobilization from other tissues.	Sulfhydryl Compounds	325-331	nitric oxide synthase 3	Homo sapiens	201-205
32908689-13	2020	Conclusion: The results are congruent with the following proposed sequence of events leading to a protective response of the organism during the pathogenesis of primary pterygium: a decreased level of eNOS provokes a decline in the level of NO in pterygium tissue, which then leads to reduced S-nitrosylation of GSH or other thiols and possibly to the modulation of the intracellular level of GSH through synthesis and/or mobilization from other tissues.	Glutathione	393-396	nitric oxide synthase 3	Homo sapiens	201-205
32784365-2	2020	Of the three NOS isoforms, NOS3 is significantly increased at both the RNA and protein levels by exposure to the very potent and selective ligand of the AHR, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).	Polychlorinated Dibenzodioxins	158-193	nitric oxide synthase 3	Homo sapiens	27-31
32824997-8	2020	Piceatannol was proposed to bind with VEGF, thus attenuating VEGF in activating VEGF receptor and blocking VEGF-mediated downstream signaling, including expressions of phosphorylated eNOS, Erk and Akt.	3,3',4,5'-tetrahydroxystilbene	0-11	nitric oxide synthase 3	Homo sapiens	183-187
32739909-3	2020	There are three forms of NOS, which are neuronal (nNOS), inducible (iNOS), and endothelial (eNOS) nitric oxide synthase.	Nitric Oxide	98-110	nitric oxide synthase 3	Homo sapiens	92-96
33520822-1	2020	seed extract</compound-id> may protect against acute palmitate-induced impairment in cultured human umbilical vein endothelial cells by adjusting the Akt/eNOS pathway, ROS: NO ratio and ET-1 concentration.	Palmitates	53-62	nitric oxide synthase 3	Homo sapiens	154-158
32784365-2	2020	Of the three NOS isoforms, NOS3 is significantly increased at both the RNA and protein levels by exposure to the very potent and selective ligand of the AHR, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).	Polychlorinated Dibenzodioxins	195-199	nitric oxide synthase 3	Homo sapiens	27-31
32848435-0	2020	Erratum: (-)-Epigallocatechin-3-Gallate Inhibits eNOS Uncoupling and Alleviates High Glucose-Induced Dysfunction and Apoptosis of Human Umbilical Vein Endothelial Cells by PI3K/AKT/eNOS Pathway [Corrigendum].	epigallocatechin gallate	9-39	nitric oxide synthase 3	Homo sapiens	49-53
32848435-0	2020	Erratum: (-)-Epigallocatechin-3-Gallate Inhibits eNOS Uncoupling and Alleviates High Glucose-Induced Dysfunction and Apoptosis of Human Umbilical Vein Endothelial Cells by PI3K/AKT/eNOS Pathway [Corrigendum].	epigallocatechin gallate	9-39	nitric oxide synthase 3	Homo sapiens	181-185
32253901-1	2020	Aim To assess endothelial nitric oxide synthase (eNOS) gene (G894T) polymorphism and nitric oxide (NO) level in hypertensive diabetic Bataknese patients.	Nitric Oxide	26-38	nitric oxide synthase 3	Homo sapiens	49-53
31310708-2	2020	Over the years, this phenomenon was extended to a number of arterial preparations of different species and revisited, from a mechanistic point of view, with the successive demonstration that it depends on calcium handling in the vascular smooth muscle cells, is endothelium-dependent and requires the production of nitric oxide (NO) by endothelial nitric oxide synthase (eNOS) and the activation of soluble guanylyl cyclase (sGC).	Calcium	205-212	nitric oxide synthase 3	Homo sapiens	336-369
32519277-1	2020	Endothelial Nitric Oxide Synthase (eNOS) is an indispensable regulator of blood pressure through producing Nitric Oxide (NO).	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	35-39
32848891-9	2020	Conclusion: The association between OPN and impaired arginine/NO pathway could play a role in the inhibition of endothelial NO synthase (eNOS) and/or in the arginase activation in the context of CAD patients.	Arginine	53-61	nitric oxide synthase 3	Homo sapiens	112-135
32848891-9	2020	Conclusion: The association between OPN and impaired arginine/NO pathway could play a role in the inhibition of endothelial NO synthase (eNOS) and/or in the arginase activation in the context of CAD patients.	Arginine	53-61	nitric oxide synthase 3	Homo sapiens	137-141
32277314-1	2020	The impaired bioavailability of endogenous nitric oxide (NO) in sickle cell anemia (SCA) may be influenced by polymorphisms in the endothelial nitric oxide synthase gene (eNOS).	Nitric Oxide	43-55	nitric oxide synthase 3	Homo sapiens	131-164
32277314-1	2020	The impaired bioavailability of endogenous nitric oxide (NO) in sickle cell anemia (SCA) may be influenced by polymorphisms in the endothelial nitric oxide synthase gene (eNOS).	Nitric Oxide	43-55	nitric oxide synthase 3	Homo sapiens	171-175
32753341-9	2021	CONCLUSION: Variants of the NOS3 gene could influence the response to iPDE5.	ipde5	70-75	nitric oxide synthase 3	Homo sapiens	28-32
32691498-5	2020	Exposure to low doses of BPA leads to decreased levels and activities of several antioxidant enzymes, increased activity of endothelial nitric oxide synthase (eNOS), and increased production of nitric oxide (NO) via the upregulation of ER and PR.	bisphenol A	25-28	nitric oxide synthase 3	Homo sapiens	124-157
32691498-5	2020	Exposure to low doses of BPA leads to decreased levels and activities of several antioxidant enzymes, increased activity of endothelial nitric oxide synthase (eNOS), and increased production of nitric oxide (NO) via the upregulation of ER and PR.	bisphenol A	25-28	nitric oxide synthase 3	Homo sapiens	159-163
32691498-5	2020	Exposure to low doses of BPA leads to decreased levels and activities of several antioxidant enzymes, increased activity of endothelial nitric oxide synthase (eNOS), and increased production of nitric oxide (NO) via the upregulation of ER and PR.	Nitric Oxide	136-148	nitric oxide synthase 3	Homo sapiens	159-163
32559798-1	2020	OBJECTIVE:  We examined the interaction of polymorphisms in the genes heme oxygenase-1 (HMOX1) and nitric oxide synthase (NOS3) in patients with preeclampsia (PE) as well as the responsiveness to methyldopa and to total antihypertensive therapy.	Methyldopa	196-206	nitric oxide synthase 3	Homo sapiens	122-126
32559798-3	2020	RESULTS:  We found interactions between genotypes of the HMOX-1 and NOS3 genes and responsiveness to methyldopa and that PE genotyped as AT presents lower levels of protein HO-1 compared with AA.	Methyldopa	101-111	nitric oxide synthase 3	Homo sapiens	68-72
32505644-0	2020	Extracellular Ca2+ promotes nitric oxide production via Ca2+-sensing receptor-Gq/11 protein-endothelial nitric oxide synthase signaling in human vascular endothelial cells.	Nitric Oxide	28-40	nitric oxide synthase 3	Homo sapiens	92-125
32559798-4	2020	CONCLUSION:  We found interactions between the HMOX-1 and NOS3 genes and responsiveness to methyldopa and that the HMOX1 polymorphism affects the levels of enzyme HO-1 in responsiveness to methyldopa and to total antihypertensive therapy.	Methyldopa	91-101	nitric oxide synthase 3	Homo sapiens	58-62
32559798-4	2020	CONCLUSION:  We found interactions between the HMOX-1 and NOS3 genes and responsiveness to methyldopa and that the HMOX1 polymorphism affects the levels of enzyme HO-1 in responsiveness to methyldopa and to total antihypertensive therapy.	Methyldopa	189-199	nitric oxide synthase 3	Homo sapiens	58-62
32750030-9	2020	Results showed that aspirin increased eNOS level and reduced injury to the endothelial cells (ECs) caused by ox-LDL, Ang-II, and HG treatment in a dose-dependent manner.	Aspirin	20-27	nitric oxide synthase 3	Homo sapiens	38-42
32935809-6	2020	Nevertheless, there was a highly negative correlation between ADMA and NO-eNOS(p<0.001, p<0.001).	N,N-dimethylarginine	62-66	nitric oxide synthase 3	Homo sapiens	74-78
32750030-11	2020	p-NF-kappaB and p-p38 mitogen-activated protein kinase inhibition, sVCAM-1 and sICAM-1 secretion, and eNOS activity promotion by aspirin treatment were found to be dependent on Beclin-1.	Aspirin	129-136	nitric oxide synthase 3	Homo sapiens	102-106
32633262-1	2020	OBJECTIVE: The aim of the present study was to examine the association between 2 polymorphisms of the endothelial nitric oxide (eNOS) gene (-786T>C and +894G>T) and the no-reflow/slow-flow phenomenon in post-primary percutaneous coronary intervention (PPCI) patients.	Nitric Oxide	114-126	nitric oxide synthase 3	Homo sapiens	128-132
32579479-0	2020	Novel Concept for the Regulation of eNOS (Endothelial Nitric Oxide Synthase) Activity: Inhibitory Effects of the Enigma Homolog Protein and the PHLPP (Pleckstrin Homology Domain and Leucine-Rich Repeat Protein Phosphatase)-2 on Akt (Protein Kinase B)-Dependent Nitric Oxide Synthase Activation.	Leucine	182-189	nitric oxide synthase 3	Homo sapiens	36-40
32579479-0	2020	Novel Concept for the Regulation of eNOS (Endothelial Nitric Oxide Synthase) Activity: Inhibitory Effects of the Enigma Homolog Protein and the PHLPP (Pleckstrin Homology Domain and Leucine-Rich Repeat Protein Phosphatase)-2 on Akt (Protein Kinase B)-Dependent Nitric Oxide Synthase Activation.	Leucine	182-189	nitric oxide synthase 3	Homo sapiens	42-75
32371009-7	2020	Part of the review emphasizes noise-triggered uncoupling/dysregulation of endothelial and neuronal nitric oxide synthase (eNOS and nNOS) and its central role for vascular dysfunction.	Nitric Oxide	99-111	nitric oxide synthase 3	Homo sapiens	122-126
32707934-3	2020	Moreover, different polyphenolic compounds have the ability to increase the activity/expression of endothelial nitric oxide synthase (eNOS) with a subsequent enhancement of NO generation.	polyphenolic compounds	20-42	nitric oxide synthase 3	Homo sapiens	99-132
32707934-3	2020	Moreover, different polyphenolic compounds have the ability to increase the activity/expression of endothelial nitric oxide synthase (eNOS) with a subsequent enhancement of NO generation.	polyphenolic compounds	20-42	nitric oxide synthase 3	Homo sapiens	134-138
32765028-0	2020	(-)-Epigallocatechin-3-Gallate Inhibits eNOS Uncoupling and Alleviates High Glucose-Induced Dysfunction and Apoptosis of Human Umbilical Vein Endothelial Cells by PI3K/AKT/eNOS Pathway.	epigallocatechin gallate	0-30	nitric oxide synthase 3	Homo sapiens	40-44
32765028-0	2020	(-)-Epigallocatechin-3-Gallate Inhibits eNOS Uncoupling and Alleviates High Glucose-Induced Dysfunction and Apoptosis of Human Umbilical Vein Endothelial Cells by PI3K/AKT/eNOS Pathway.	epigallocatechin gallate	0-30	nitric oxide synthase 3	Homo sapiens	172-176
32765028-13	2020	Conclusion: EGCG could inhibit eNOS uncoupling and alleviate endothelial dysfunction and apoptosis of HG-treated HUVECs by activating the PI3K/AKT/eNOS pathway.	epigallocatechin gallate	12-16	nitric oxide synthase 3	Homo sapiens	31-35
32765028-13	2020	Conclusion: EGCG could inhibit eNOS uncoupling and alleviate endothelial dysfunction and apoptosis of HG-treated HUVECs by activating the PI3K/AKT/eNOS pathway.	epigallocatechin gallate	12-16	nitric oxide synthase 3	Homo sapiens	147-151
32407984-0	2020	Nicorandil reversed homocysteine-induced coronary microvascular dysfunction via regulating PI3K/Akt/eNOS pathway.	Nicorandil	0-10	nitric oxide synthase 3	Homo sapiens	100-104
32407984-0	2020	Nicorandil reversed homocysteine-induced coronary microvascular dysfunction via regulating PI3K/Akt/eNOS pathway.	Homocysteine	20-32	nitric oxide synthase 3	Homo sapiens	100-104
32407984-7	2020	RESULTS: The results showed that nicorandil improved cell viability and p-PI3K/PI3K, p-Akt/Akt, and p-eNOS/eNOS expression in the vitro HHcy and hypoxia models.	Nicorandil	33-43	nitric oxide synthase 3	Homo sapiens	102-106
32407984-7	2020	RESULTS: The results showed that nicorandil improved cell viability and p-PI3K/PI3K, p-Akt/Akt, and p-eNOS/eNOS expression in the vitro HHcy and hypoxia models.	Nicorandil	33-43	nitric oxide synthase 3	Homo sapiens	107-111
32407984-11	2020	CONCLUSION: The results suggest that nicorandil improves Hcy-induced coronary microvascular dysfunction through the PI3K/Akt/eNOS signalling pathway.	Nicorandil	37-47	nitric oxide synthase 3	Homo sapiens	125-129
32407984-11	2020	CONCLUSION: The results suggest that nicorandil improves Hcy-induced coronary microvascular dysfunction through the PI3K/Akt/eNOS signalling pathway.	Homocysteine	57-60	nitric oxide synthase 3	Homo sapiens	125-129
32388267-8	2020	In conclusion, the induction of apoptosis and antiproliferative properties by Sorafenib were related to Trx1 downregulation that appeared to play a relevant role on SNO of NOS3 and CD95 in HepG2 cells.	Sorafenib	78-87	nitric oxide synthase 3	Homo sapiens	172-176
32606304-5	2020	We found that beta-catenin depleted human umbilical vein ECs (HUVEC) stimulated with pharmacological activators of endothelial NO synthase (eNOS) showed a reduction in eNOS phosphorylation (Ser1177) as well as reduced intracellular cyclic guanosine monophosphate levels compared to control cells in static cultures.	Cyclic GMP	232-262	nitric oxide synthase 3	Homo sapiens	115-138
32606304-5	2020	We found that beta-catenin depleted human umbilical vein ECs (HUVEC) stimulated with pharmacological activators of endothelial NO synthase (eNOS) showed a reduction in eNOS phosphorylation (Ser1177) as well as reduced intracellular cyclic guanosine monophosphate levels compared to control cells in static cultures.	Cyclic GMP	232-262	nitric oxide synthase 3	Homo sapiens	140-144
32630586-0	2020	Zearalenone-Induced Interaction between PXR and Sp1 Increases Binding of Sp1 to a Promoter Site of the eNOS, Decreasing Its Transcription and NO Production in BAECs.	Zearalenone	0-11	nitric oxide synthase 3	Homo sapiens	103-107
32630586-3	2020	A promoter analysis using 5"-serially deleted human eNOS promoter revealed that the proximal region (-135 to +22) was responsible for ZEN-mediated reduction of the human eNOS promoter activity.	Zearalenone	134-137	nitric oxide synthase 3	Homo sapiens	52-56
32630586-3	2020	A promoter analysis using 5"-serially deleted human eNOS promoter revealed that the proximal region (-135 to +22) was responsible for ZEN-mediated reduction of the human eNOS promoter activity.	Zearalenone	134-137	nitric oxide synthase 3	Homo sapiens	170-174
32008955-1	2020	INTRODUCTION: Nitric oxide (NO) is a free radical involved in carcinogenesis and is synthesized by endothelial nitric oxide synthase (eNOS).	Nitric Oxide	14-26	nitric oxide synthase 3	Homo sapiens	134-138
32508185-6	2020	In endothelial cells from patients with T2DM, normal glucose conditions (24 hours at 5 mmol/L) lowered O-GlcNAc levels and restored insulin-mediated activation of endothelial nitric oxide synthase, whereas high glucose conditions (30 mmol/L) maintained both O-GlcNAc levels and impaired insulin action.	Glucose	53-60	nitric oxide synthase 3	Homo sapiens	163-196
32508185-7	2020	Treatment of endothelial cells with Thiamet G, an O-GlcNAcase inhibitor, increased O-GlcNAc levels and blunted the improvement of insulin-mediated endothelial nitric oxide synthase phosphorylation by glucose normalization.	thiamet G	36-45	nitric oxide synthase 3	Homo sapiens	147-180
32508185-7	2020	Treatment of endothelial cells with Thiamet G, an O-GlcNAcase inhibitor, increased O-GlcNAc levels and blunted the improvement of insulin-mediated endothelial nitric oxide synthase phosphorylation by glucose normalization.	Glucose	200-207	nitric oxide synthase 3	Homo sapiens	147-180
32508185-8	2020	Conclusions Taken together, our findings indicate a role for O-GlcNAc modification in the dynamic, glucose-induced impairment of endothelial nitric oxide synthase activation in endothelial cells from patients with T2DM.	o-glcnac	61-69	nitric oxide synthase 3	Homo sapiens	129-162
32508185-8	2020	Conclusions Taken together, our findings indicate a role for O-GlcNAc modification in the dynamic, glucose-induced impairment of endothelial nitric oxide synthase activation in endothelial cells from patients with T2DM.	Glucose	99-106	nitric oxide synthase 3	Homo sapiens	129-162
32402583-7	2020	H2O2 downregulated the expression of eNOS and upregulated iNOS, which in turn contribute to an elevated NO generation and protein nitrosylation.	Hydrogen Peroxide	0-4	nitric oxide synthase 3	Homo sapiens	37-41
32587663-3	2020	Diabetes-mediated generation of excess reactive oxygen species (ROS) may contribute to vascular dysfunction via damage to mitochondria and regulation of endothelial nitric oxide synthase (eNOS).	Reactive Oxygen Species	39-62	nitric oxide synthase 3	Homo sapiens	153-186
32587663-3	2020	Diabetes-mediated generation of excess reactive oxygen species (ROS) may contribute to vascular dysfunction via damage to mitochondria and regulation of endothelial nitric oxide synthase (eNOS).	Reactive Oxygen Species	39-62	nitric oxide synthase 3	Homo sapiens	188-192
32587663-3	2020	Diabetes-mediated generation of excess reactive oxygen species (ROS) may contribute to vascular dysfunction via damage to mitochondria and regulation of endothelial nitric oxide synthase (eNOS).	Reactive Oxygen Species	64-67	nitric oxide synthase 3	Homo sapiens	153-186
32587663-3	2020	Diabetes-mediated generation of excess reactive oxygen species (ROS) may contribute to vascular dysfunction via damage to mitochondria and regulation of endothelial nitric oxide synthase (eNOS).	Reactive Oxygen Species	64-67	nitric oxide synthase 3	Homo sapiens	188-192
32008955-1	2020	INTRODUCTION: Nitric oxide (NO) is a free radical involved in carcinogenesis and is synthesized by endothelial nitric oxide synthase (eNOS).	Nitric Oxide	14-26	nitric oxide synthase 3	Homo sapiens	99-132
32008955-2	2020	Genetic changes in the eNOS enzyme affect its activity, and the nitric oxide produced by inhibiting apoptosis can lead to cancer cell proliferation and metastasis.	Nitric Oxide	64-76	nitric oxide synthase 3	Homo sapiens	23-27
32612429-8	2020	The patients and control groups with CC polymorphisms and TT polymorphisms on eNOS T-786C and G894T gene regions had higher plasma ADMA levels.	N,N-dimethylarginine	131-135	nitric oxide synthase 3	Homo sapiens	78-82
32152543-1	2020	Nitric oxide synthase 3 (NOS3) produces the gasotransmitter nitric oxide (NO), which drives critical cellular signaling pathways by S-nitrosylating target proteins.	Nitric Oxide	60-72	nitric oxide synthase 3	Homo sapiens	0-23
32333783-0	2020	Treatment with 2-methoxyestradiol increases endothelial nitric oxide synthase activity via scavenger receptor class BI in human umbilical vein endothelial cells.	2-Methoxyestradiol	15-33	nitric oxide synthase 3	Homo sapiens	44-77
32333783-2	2020	Nitric oxide (NO) released by endothelial nitric oxide synthase (eNOS) plays an important role in regulating cardiovascular homeostasis.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	30-63
32333783-2	2020	Nitric oxide (NO) released by endothelial nitric oxide synthase (eNOS) plays an important role in regulating cardiovascular homeostasis.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	65-69
32333783-8	2020	The effect of 2ME2 treatment on the promoter activity of hSR-BI/CLA-1 was abrogated by treatment with LY294002, a specific inhibitor of phosphatidylinositol 3-kinase, as was the increase in HDL-induced eNOS activation.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	102-110	nitric oxide synthase 3	Homo sapiens	202-206
32333783-12	2020	These results indicate that 2ME2 treatment increases HDL-dependent eNOS phosphorylation by upregulating endothelial hSR-BI/CLA-1 expression, suggesting that 2ME2 has a potential therapeutic value in the treatment of preeclampsia.	2-Methoxyestradiol	28-32	nitric oxide synthase 3	Homo sapiens	67-71
32333783-12	2020	These results indicate that 2ME2 treatment increases HDL-dependent eNOS phosphorylation by upregulating endothelial hSR-BI/CLA-1 expression, suggesting that 2ME2 has a potential therapeutic value in the treatment of preeclampsia.	2-Methoxyestradiol	157-161	nitric oxide synthase 3	Homo sapiens	67-71
32152543-1	2020	Nitric oxide synthase 3 (NOS3) produces the gasotransmitter nitric oxide (NO), which drives critical cellular signaling pathways by S-nitrosylating target proteins.	Nitric Oxide	60-72	nitric oxide synthase 3	Homo sapiens	25-29
32173528-4	2020	Green tea polyphenol (-)-epigallocatechin-3-O-gallate (EGCG) directly binds to cell-surface 67LR and induces apoptosis through the protein kinase B (Akt)/endothelial nitric oxide synthase/nitric oxide/cyclic GMP (cGMP) axis.	Polyphenols	10-20	nitric oxide synthase 3	Homo sapiens	154-187
31792366-1	2020	Because nitric oxide could play an important role in the pathogenesis of migraine (suggested by experimental, neuropathological, biochemical, and pharmacological data), and a recent meta-analysis showed an association between the single-nucleotide polymorphism (SNP) rs2070744 in the endothelial nitric oxide synthase (eNOS or NOS3) gene (chromosome 7q36.1) and the risk for migraine in Caucasians, we attempted to replicate the possible association between this SNP and the and the risk for migraine in the Caucasian Spanish population.	Nitric Oxide	8-20	nitric oxide synthase 3	Homo sapiens	284-317
31792366-1	2020	Because nitric oxide could play an important role in the pathogenesis of migraine (suggested by experimental, neuropathological, biochemical, and pharmacological data), and a recent meta-analysis showed an association between the single-nucleotide polymorphism (SNP) rs2070744 in the endothelial nitric oxide synthase (eNOS or NOS3) gene (chromosome 7q36.1) and the risk for migraine in Caucasians, we attempted to replicate the possible association between this SNP and the and the risk for migraine in the Caucasian Spanish population.	Nitric Oxide	8-20	nitric oxide synthase 3	Homo sapiens	327-331
32696742-0	2020	[Palmitic acid decreases phosphorylation of eNOS Ser1177 by activating protein phosphatase 2C (PP2C) of human umbilical vein endothelial cells].	Palmitic Acid	1-14	nitric oxide synthase 3	Homo sapiens	44-48
32696742-1	2020	Objective To investigate the roles of protein phosphatase 2C (PP2C) activated by palmitic acid (PA) in the phosphorylation modulation of endothelial nitric oxide (eNOS) at the site of serine 1177 (eNOS Ser1177) in human umbilical vein endothelial cells (HUVECs).	Palmitic Acid	81-94	nitric oxide synthase 3	Homo sapiens	163-167
32696742-1	2020	Objective To investigate the roles of protein phosphatase 2C (PP2C) activated by palmitic acid (PA) in the phosphorylation modulation of endothelial nitric oxide (eNOS) at the site of serine 1177 (eNOS Ser1177) in human umbilical vein endothelial cells (HUVECs).	Palmitic Acid	96-98	nitric oxide synthase 3	Homo sapiens	163-167
32696742-1	2020	Objective To investigate the roles of protein phosphatase 2C (PP2C) activated by palmitic acid (PA) in the phosphorylation modulation of endothelial nitric oxide (eNOS) at the site of serine 1177 (eNOS Ser1177) in human umbilical vein endothelial cells (HUVECs).	Palmitic Acid	96-98	nitric oxide synthase 3	Homo sapiens	197-201
32696742-1	2020	Objective To investigate the roles of protein phosphatase 2C (PP2C) activated by palmitic acid (PA) in the phosphorylation modulation of endothelial nitric oxide (eNOS) at the site of serine 1177 (eNOS Ser1177) in human umbilical vein endothelial cells (HUVECs).	Nitric Oxide	149-161	nitric oxide synthase 3	Homo sapiens	163-167
32696742-1	2020	Objective To investigate the roles of protein phosphatase 2C (PP2C) activated by palmitic acid (PA) in the phosphorylation modulation of endothelial nitric oxide (eNOS) at the site of serine 1177 (eNOS Ser1177) in human umbilical vein endothelial cells (HUVECs).	Serine	184-190	nitric oxide synthase 3	Homo sapiens	163-167
32696742-6	2020	Results Compared with the control group, the phosphorylation levels of eNOS Ser1177 and NO content decreased significantly in the PA group.	Palmitic Acid	130-132	nitric oxide synthase 3	Homo sapiens	71-75
32696742-7	2020	The PP2C inhibitor sanguinarine reversed PA-induced decrease of eNOS Ser1177 phosphorylation level and NO content.	sanguinarine	19-31	nitric oxide synthase 3	Homo sapiens	64-68
32696742-7	2020	The PP2C inhibitor sanguinarine reversed PA-induced decrease of eNOS Ser1177 phosphorylation level and NO content.	Palmitic Acid	41-43	nitric oxide synthase 3	Homo sapiens	64-68
32696742-10	2020	Conclusion PA reduces the phosphorylation level of endothelial eNOS Ser1177 in HUVECs by activating PP2C.	Palmitic Acid	11-13	nitric oxide synthase 3	Homo sapiens	63-67
32566272-0	2020	Aliskiren Improved the Endothelial Repair Capacity of Endothelial Progenitor Cells from Patients with Hypertension via the Tie2/PI3k/Akt/eNOS Signalling Pathway.	aliskiren	0-9	nitric oxide synthase 3	Homo sapiens	137-141
32566272-6	2020	Furthermore, aliskiren increased the phosphorylation of Tie2, Akt, and eNOS.	aliskiren	13-22	nitric oxide synthase 3	Homo sapiens	71-75
32173528-4	2020	Green tea polyphenol (-)-epigallocatechin-3-O-gallate (EGCG) directly binds to cell-surface 67LR and induces apoptosis through the protein kinase B (Akt)/endothelial nitric oxide synthase/nitric oxide/cyclic GMP (cGMP) axis.	epigallocatechin gallate	21-53	nitric oxide synthase 3	Homo sapiens	154-187
32173528-4	2020	Green tea polyphenol (-)-epigallocatechin-3-O-gallate (EGCG) directly binds to cell-surface 67LR and induces apoptosis through the protein kinase B (Akt)/endothelial nitric oxide synthase/nitric oxide/cyclic GMP (cGMP) axis.	epigallocatechin gallate	55-59	nitric oxide synthase 3	Homo sapiens	154-187
32486343-1	2020	: Reactive nitrogen species (RNS) are formed when there is an abnormal increase in the level of nitric oxide (NO) produced by the inducible nitric oxide synthase (iNOS) and/or by the uncoupled endothelial nitric oxide synthase (eNOS).	Nitrogen	11-19	nitric oxide synthase 3	Homo sapiens	193-226
32486343-1	2020	: Reactive nitrogen species (RNS) are formed when there is an abnormal increase in the level of nitric oxide (NO) produced by the inducible nitric oxide synthase (iNOS) and/or by the uncoupled endothelial nitric oxide synthase (eNOS).	Nitrogen	11-19	nitric oxide synthase 3	Homo sapiens	228-232
32486343-1	2020	: Reactive nitrogen species (RNS) are formed when there is an abnormal increase in the level of nitric oxide (NO) produced by the inducible nitric oxide synthase (iNOS) and/or by the uncoupled endothelial nitric oxide synthase (eNOS).	Reactive Nitrogen Species	29-32	nitric oxide synthase 3	Homo sapiens	193-226
32486343-1	2020	: Reactive nitrogen species (RNS) are formed when there is an abnormal increase in the level of nitric oxide (NO) produced by the inducible nitric oxide synthase (iNOS) and/or by the uncoupled endothelial nitric oxide synthase (eNOS).	Reactive Nitrogen Species	29-32	nitric oxide synthase 3	Homo sapiens	228-232
32486343-1	2020	: Reactive nitrogen species (RNS) are formed when there is an abnormal increase in the level of nitric oxide (NO) produced by the inducible nitric oxide synthase (iNOS) and/or by the uncoupled endothelial nitric oxide synthase (eNOS).	Nitric Oxide	96-108	nitric oxide synthase 3	Homo sapiens	228-232
32455928-6	2020	H2O2 treatment significantly increased senescence in endothelial cells and mural cells, human neonatal dermal fibroblasts (hNDFs), as measured by increased p21 levels and reduced NOS3 expression.	Hydrogen Peroxide	0-4	nitric oxide synthase 3	Homo sapiens	179-183
32382091-9	2020	Pharmacological inhibitors of the mevalonate pathway prevented fractionated-radiation-induced suppression of KLF2, TM, and eNOS expression.	Mevalonic Acid	34-44	nitric oxide synthase 3	Homo sapiens	123-127
32302123-4	2020	Compounds with a meta-relationship between the aminoquinoline and a positively charged tail moiety were potent and had up to nearly 900-fold selectivity for human nNOS over human eNOS.	Aminoquinolines	47-61	nitric oxide synthase 3	Homo sapiens	179-183
32302123-5	2020	X-ray crystallography indicates that the amino groups of some compounds occupy a water-filled pocket surrounding an nNOS-specific aspartate residue (absent in eNOS).	Aspartic Acid	130-139	nitric oxide synthase 3	Homo sapiens	159-163
32251485-8	2020	Compared with healthy neutrophils, X-CGD neutrophils under A23187 stimulation exhibited significantly increased NO and decreased H2O2, and promoted downregulated NOS3 and EDN1 expression in HUVECs.	Calcimycin	59-65	nitric oxide synthase 3	Homo sapiens	162-166
32370169-8	2020	Additionally, transfection with inhibitors (anti-miR) of miR-92a-3p significantly rescued the eNOS suppression induced by lipopolysaccharide.	mir-92a-3p	57-67	nitric oxide synthase 3	Homo sapiens	94-98
32525818-4	2020	Myricetin increased nitric oxide production in HUVEC through decreased ROS levels and increased nitric oxide production and eNOS activation.	myricetin	0-9	nitric oxide synthase 3	Homo sapiens	124-128
32525818-4	2020	Myricetin increased nitric oxide production in HUVEC through decreased ROS levels and increased nitric oxide production and eNOS activation.	Nitric Oxide	20-32	nitric oxide synthase 3	Homo sapiens	124-128
32525818-5	2020	Activation of eNOS enzyme was achieved by an increase of cellular calcium concentration.	Calcium	66-73	nitric oxide synthase 3	Homo sapiens	14-18
32351667-7	2020	Converted to a superoxide-producing enzyme, uncoupled eNOS not only leads to reduction of the nitric oxide (NO) generation but also potentiates the preexisting oxidative stress, which contributes significantly to atherogenesis.	Superoxides	15-25	nitric oxide synthase 3	Homo sapiens	54-58
32351667-7	2020	Converted to a superoxide-producing enzyme, uncoupled eNOS not only leads to reduction of the nitric oxide (NO) generation but also potentiates the preexisting oxidative stress, which contributes significantly to atherogenesis.	Nitric Oxide	94-106	nitric oxide synthase 3	Homo sapiens	54-58
32300005-1	2020	Nitric oxide (NO) produced by endothelial nitric oxide synthase (eNOS) is a critical mediator of vascular function.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	30-63
32300005-1	2020	Nitric oxide (NO) produced by endothelial nitric oxide synthase (eNOS) is a critical mediator of vascular function.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	65-69
32251485-11	2020	In conclusions, eNOS and ET-1 significantly down-regulated in co-culture with stimulated X-CGD neutrophils through their excessive NO and the lack of ROS production.	ros	150-153	nitric oxide synthase 3	Homo sapiens	16-20
32251485-12	2020	These findings suggest that ROS generated from neutrophils may mediate arterial tone affecting eNOS and ET-1 expression via their NO and ROS production.	ros	28-31	nitric oxide synthase 3	Homo sapiens	95-99
32251485-12	2020	These findings suggest that ROS generated from neutrophils may mediate arterial tone affecting eNOS and ET-1 expression via their NO and ROS production.	ros	137-140	nitric oxide synthase 3	Homo sapiens	95-99
32022285-0	2020	Relation of nitric oxide synthase gene (NOS3) polymorphisms to varicocele risk and post-varicocelectomy seminal oxidative stress reduction.	Oxides	19-24	nitric oxide synthase 3	Homo sapiens	40-44
32124475-4	2020	We observed nitric oxide (NO) production in human primary ECs stimulated with exogenous CCL28, which also induced direct binding of CCR10 and eNOS resulting in inhibition of eNOS activity.	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	142-146
32124475-4	2020	We observed nitric oxide (NO) production in human primary ECs stimulated with exogenous CCL28, which also induced direct binding of CCR10 and eNOS resulting in inhibition of eNOS activity.	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	174-178
32179814-7	2020	Besides, melatonin prevented the positive actions that docetaxel exerts on the expression of other factors related to angiogenesis like JAG1, ANPEP, IGF-1, CXCL6, AKT1, ERK1, ERK2, MMP14 and NOS3 and neutralized the stimulating actions of vinorelbine on the expression of FIGF, FGFR3, CXCL6, CCL2, ERK1, ERK2, AKT1, NOS3 and MMP14.	Docetaxel	55-64	nitric oxide synthase 3	Homo sapiens	191-195
32174438-1	2020	In the current study, poly 4-hydroxyphenyl methacrylate-carbon nano-onions (PHPMA-CNOs = f-CNOs) are synthesized and reinforced with natural protein gelatin (GL) to engineer GL/f-CNOs composite hydrogels under the sonochemical method.	poly 4-hydroxyphenyl methacrylate	22-55	nitric oxide synthase 3	Homo sapiens	82-86
32174438-1	2020	In the current study, poly 4-hydroxyphenyl methacrylate-carbon nano-onions (PHPMA-CNOs = f-CNOs) are synthesized and reinforced with natural protein gelatin (GL) to engineer GL/f-CNOs composite hydrogels under the sonochemical method.	poly 4-hydroxyphenyl methacrylate	22-55	nitric oxide synthase 3	Homo sapiens	91-95
32174438-1	2020	In the current study, poly 4-hydroxyphenyl methacrylate-carbon nano-onions (PHPMA-CNOs = f-CNOs) are synthesized and reinforced with natural protein gelatin (GL) to engineer GL/f-CNOs composite hydrogels under the sonochemical method.	poly 4-hydroxyphenyl methacrylate	22-55	nitric oxide synthase 3	Homo sapiens	91-95
32174438-1	2020	In the current study, poly 4-hydroxyphenyl methacrylate-carbon nano-onions (PHPMA-CNOs = f-CNOs) are synthesized and reinforced with natural protein gelatin (GL) to engineer GL/f-CNOs composite hydrogels under the sonochemical method.	Carbon	56-62	nitric oxide synthase 3	Homo sapiens	82-86
32174438-1	2020	In the current study, poly 4-hydroxyphenyl methacrylate-carbon nano-onions (PHPMA-CNOs = f-CNOs) are synthesized and reinforced with natural protein gelatin (GL) to engineer GL/f-CNOs composite hydrogels under the sonochemical method.	Carbon	56-62	nitric oxide synthase 3	Homo sapiens	91-95
32174438-1	2020	In the current study, poly 4-hydroxyphenyl methacrylate-carbon nano-onions (PHPMA-CNOs = f-CNOs) are synthesized and reinforced with natural protein gelatin (GL) to engineer GL/f-CNOs composite hydrogels under the sonochemical method.	Carbon	56-62	nitric oxide synthase 3	Homo sapiens	91-95
32174438-7	2020	Furthermore, GL/f-CNOs hydrogels efficiently load the 5-fluorouracil (5-FU) and show a pH-responsive sustained drug release over 15 days.	Fluorouracil	54-68	nitric oxide synthase 3	Homo sapiens	18-22
32174438-7	2020	Furthermore, GL/f-CNOs hydrogels efficiently load the 5-fluorouracil (5-FU) and show a pH-responsive sustained drug release over 15 days.	Fluorouracil	70-74	nitric oxide synthase 3	Homo sapiens	18-22
32228174-8	2021	Interestingly, we found that the changes mentioned were linked with reduced levels of nitrites both at 24 h (< 171 pmol/mug protein; P < 0.001), and 48 h (< 250 pmol/mug protein; P < 0.05), which was associated with a reduced expression of mRNA of eNOS in endothelial cells incubated with TPP and high glucose.	Nitrites	86-94	nitric oxide synthase 3	Homo sapiens	248-252
32179814-7	2020	Besides, melatonin prevented the positive actions that docetaxel exerts on the expression of other factors related to angiogenesis like JAG1, ANPEP, IGF-1, CXCL6, AKT1, ERK1, ERK2, MMP14 and NOS3 and neutralized the stimulating actions of vinorelbine on the expression of FIGF, FGFR3, CXCL6, CCL2, ERK1, ERK2, AKT1, NOS3 and MMP14.	Melatonin	9-18	nitric oxide synthase 3	Homo sapiens	191-195
32179814-7	2020	Besides, melatonin prevented the positive actions that docetaxel exerts on the expression of other factors related to angiogenesis like JAG1, ANPEP, IGF-1, CXCL6, AKT1, ERK1, ERK2, MMP14 and NOS3 and neutralized the stimulating actions of vinorelbine on the expression of FIGF, FGFR3, CXCL6, CCL2, ERK1, ERK2, AKT1, NOS3 and MMP14.	Melatonin	9-18	nitric oxide synthase 3	Homo sapiens	316-320
32179814-7	2020	Besides, melatonin prevented the positive actions that docetaxel exerts on the expression of other factors related to angiogenesis like JAG1, ANPEP, IGF-1, CXCL6, AKT1, ERK1, ERK2, MMP14 and NOS3 and neutralized the stimulating actions of vinorelbine on the expression of FIGF, FGFR3, CXCL6, CCL2, ERK1, ERK2, AKT1, NOS3 and MMP14.	Docetaxel	55-64	nitric oxide synthase 3	Homo sapiens	316-320
32161546-12	2020	Furthermore, it promoted the expression of total eNOS and the phosphorylation of eNOS at serine (Ser) 1177 but inhibited the phosphorylation at threonine (Thr) 495, which was significantly reversed by PI3K-specific inhibitor LY294002.	Serine	89-95	nitric oxide synthase 3	Homo sapiens	81-85
32022550-0	2020	The Inhibited Nitric Oxide Production of Human Endothelial Nitric Oxide Synthase by Nitrated and Oxygenated Polycyclic Aromatic Hydrocarbons.	Nitric Oxide	14-26	nitric oxide synthase 3	Homo sapiens	47-80
32022550-0	2020	The Inhibited Nitric Oxide Production of Human Endothelial Nitric Oxide Synthase by Nitrated and Oxygenated Polycyclic Aromatic Hydrocarbons.	Polycyclic Aromatic Hydrocarbons	108-140	nitric oxide synthase 3	Homo sapiens	47-80
32022550-3	2020	The eNOS enzymatic activity and NO production were promoted by NAP, ANT and FLU, however, eNOS activity was dropped by 52.8%, 52.1%, 52.5% and 44.5% and NO production was decreased by 31.1%, 50.3%, 65.0% and 35.0% after 24 h exposure to 0.01 microM 1-NNAP, 9-NANT, 9,10-AQ and 9-FLU, respectively.	N-(2-naphthalenesulfonyl)aspartyl-(2-phenethyl)amide	63-66	nitric oxide synthase 3	Homo sapiens	4-8
32022550-4	2020	The mRNA expression of eNOS and protein expression of phosphorylated eNOS (Ser1177) were increased by three PAHs but decreased by four NPAHs/OPAHs.	seryl-seryl-seryl-arginine	75-82	nitric oxide synthase 3	Homo sapiens	69-73
32022550-4	2020	The mRNA expression of eNOS and protein expression of phosphorylated eNOS (Ser1177) were increased by three PAHs but decreased by four NPAHs/OPAHs.	alpha-conotoxin ImI	108-112	nitric oxide synthase 3	Homo sapiens	23-27
32022550-4	2020	The mRNA expression of eNOS and protein expression of phosphorylated eNOS (Ser1177) were increased by three PAHs but decreased by four NPAHs/OPAHs.	alpha-conotoxin ImI	108-112	nitric oxide synthase 3	Homo sapiens	69-73
32440316-9	2020	In the nitrate tolerance group, the level of activated eNOS decreased and the level of deactivated eNOS increased.	Nitrates	7-14	nitric oxide synthase 3	Homo sapiens	55-59
32440316-9	2020	In the nitrate tolerance group, the level of activated eNOS decreased and the level of deactivated eNOS increased.	Nitrates	7-14	nitric oxide synthase 3	Homo sapiens	99-103
31925643-0	2020	Fenretinide reduces angiogenesis by downregulating CDH5, FOXM1 and eNOS genes and suppressing microRNA-10b.	Fenretinide	0-11	nitric oxide synthase 3	Homo sapiens	67-71
31925643-6	2020	In this study, we aimed to investigate the effects of the fenretinide on some miRNAs involving in angiogenesis process and on the expression of CDH5, FOXM1 and eNOS genes upregulated in angiogenesis.	Fenretinide	58-69	nitric oxide synthase 3	Homo sapiens	160-164
31925643-13	2020	Our results have shown that fenretinide exhibited anti-angiogenic activity through the down-regulation of CDH5, FOXM1 and eNOS genes, and suppression of miR-10b.	Fenretinide	28-39	nitric oxide synthase 3	Homo sapiens	122-126
32161546-12	2020	Furthermore, it promoted the expression of total eNOS and the phosphorylation of eNOS at serine (Ser) 1177 but inhibited the phosphorylation at threonine (Thr) 495, which was significantly reversed by PI3K-specific inhibitor LY294002.	Serine	97-100	nitric oxide synthase 3	Homo sapiens	81-85
32103904-0	2020	Hydrogen Sulfide Protects Against High Glucose-Induced Human Umbilical Vein Endothelial Cell Injury Through Activating PI3K/Akt/eNOS Pathway.	Hydrogen Sulfide	0-16	nitric oxide synthase 3	Homo sapiens	128-132
31981723-7	2020	Additionally, our results suggest that these effects of BPAF mediate cardiomyocyte hypertrophy apparently due to an increase in the production of reactive nitrogen species (RNS) via an increase in endothelial NO synthase (eNOS).	4,4'-hexafluorisopropylidene diphenol	56-60	nitric oxide synthase 3	Homo sapiens	222-226
31914408-1	2020	Production of reactive oxygen species due to dysregulated endothelial nitric oxide synthase (eNOS) activity is linked to vascular dysfunction.	Oxygen	23-29	nitric oxide synthase 3	Homo sapiens	58-91
32103904-0	2020	Hydrogen Sulfide Protects Against High Glucose-Induced Human Umbilical Vein Endothelial Cell Injury Through Activating PI3K/Akt/eNOS Pathway.	Glucose	39-46	nitric oxide synthase 3	Homo sapiens	128-132
32103904-5	2020	Moreover, H2S activates PI3K/Akt/eNOS pathway in endothelial cells.	Hydrogen Sulfide	10-13	nitric oxide synthase 3	Homo sapiens	33-37
32103904-6	2020	Thus, the present study aimed to determine if H2S exerts protective effects against HG-induced injuries of human umbilical vein endothelial cells (HUVECs) via activating PI3K/Akt/eNOS signaling.	Hydrogen Sulfide	46-49	nitric oxide synthase 3	Homo sapiens	179-183
32103904-9	2020	Results: HG treatment significantly inhibited PI3K/Akt/eNOS signaling in HUVECs, which was partially reversed by the H2S treatment.	Hydrogen Sulfide	117-120	nitric oxide synthase 3	Homo sapiens	55-59
32103904-13	2020	Importantly, the cytoprotective effect of H2S against HG-induced injury was inhibited by LY294002 (an inhibitor of PI3K/Akt/eNOS signaling pathway).	Hydrogen Sulfide	42-45	nitric oxide synthase 3	Homo sapiens	124-128
32103904-13	2020	Importantly, the cytoprotective effect of H2S against HG-induced injury was inhibited by LY294002 (an inhibitor of PI3K/Akt/eNOS signaling pathway).	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	89-97	nitric oxide synthase 3	Homo sapiens	124-128
32103904-14	2020	Conclusion: The present study demonstrated that exogenous H2S protects endothelial cells against HG-induced injuries by activating PI3K/Akt/eNOS pathway.	Hydrogen Sulfide	58-61	nitric oxide synthase 3	Homo sapiens	140-144
32103904-15	2020	Based on the above findings, we proposed that reduced endogenous H2S levels and the subsequent PI3K/Akt/eNOS signaling impairment may be the important pathophysiological mechanism underlying hyperglycemia-induced vascular injuries.	Hydrogen Sulfide	65-68	nitric oxide synthase 3	Homo sapiens	104-108
31782159-4	2020	In addition, we examined whether the application of the endothelial nitric oxide synthase cofactor, tetrahydrobiopterin, would restore microvascular function in response to flow and high intraluminal pressure in young adult binge drinkers.	sapropterin	100-119	nitric oxide synthase 3	Homo sapiens	56-89
31782159-11	2020	These binge-induced dysfunctions may be reversed by tetrahydrobiopterin, which suggests a role of oxidative stress and/or uncoupled endothelial nitric oxide synthase in binge drinking.	sapropterin	52-71	nitric oxide synthase 3	Homo sapiens	132-165
32242853-18	2020	In RA patients the disturbances of circadian rhythms of endothelial nitric oxide synthase or toll-like receptors 2 expression are associated with an increase of resistance to disease-modifying therapy with methotrexate.	Methotrexate	206-218	nitric oxide synthase 3	Homo sapiens	56-89
31904280-3	2020	ADMA, an endogenous endothelial nitric oxide synthase (NOS3) inhibitor, is selectively metabolized by dimethylarginine dimethylaminohydrolase (DDAH).	N,N-dimethylarginine	0-4	nitric oxide synthase 3	Homo sapiens	55-59
31230218-0	2020	Role of ATP-Sensitive Potassium Channel (KATP) and eNOS in Mediating the Protective Effect of Nicorandil in Cyclophosphamide-Induced Cardiotoxicity.	Nicorandil	94-104	nitric oxide synthase 3	Homo sapiens	51-55
31230218-6	2020	Moreover, the role of endothelial nitric oxide synthase (eNOS) was confirmed by coadministration of nitro-omega-L-arginine (L-NNA) (25 mg/kg/day) for 5 days.	nitro-omega-l-arginine	100-122	nitric oxide synthase 3	Homo sapiens	22-55
31230218-6	2020	Moreover, the role of endothelial nitric oxide synthase (eNOS) was confirmed by coadministration of nitro-omega-L-arginine (L-NNA) (25 mg/kg/day) for 5 days.	nitro-omega-l-arginine	100-122	nitric oxide synthase 3	Homo sapiens	57-61
31230218-6	2020	Moreover, the role of endothelial nitric oxide synthase (eNOS) was confirmed by coadministration of nitro-omega-L-arginine (L-NNA) (25 mg/kg/day) for 5 days.	Nitroarginine	124-129	nitric oxide synthase 3	Homo sapiens	57-61
31964986-0	2020	CR6-interacting factor 1 deficiency reduces endothelial nitric oxide synthase activity by inhibiting biosynthesis of tetrahydrobiopterin.	sapropterin	117-136	nitric oxide synthase 3	Homo sapiens	44-77
31972975-2	2020	We previously developed novel tools called nanotriggers (NT), which recognized constitutive NO-synthase, eNOS or neuronal NOS (nNOS), mainly via their 2" phosphate group which is also present in NADPH in its binding site.	Phosphates	154-163	nitric oxide synthase 3	Homo sapiens	105-109
31973180-7	2020	Our results demonstrate that the 5 mixture prevents the DOX-dependent mitochondrial damage and oxidative stress better than the previous BCAAem, implying a KLF15/eNOS/mTORC1 signaling axis.	Doxorubicin	56-59	nitric oxide synthase 3	Homo sapiens	162-166
32411442-5	2020	The key proteins (Tie2, Akt, eNOS, and GTPCH I) in the guanosine triphosphate cyclohydrolase/tetrahydrobiopterin (GTPCH/BH4) pathway and Tie2/Akt/eNOS signaling pathway were evaluated in these women.	Guanosine Triphosphate	55-77	nitric oxide synthase 3	Homo sapiens	29-33
32411442-5	2020	The key proteins (Tie2, Akt, eNOS, and GTPCH I) in the guanosine triphosphate cyclohydrolase/tetrahydrobiopterin (GTPCH/BH4) pathway and Tie2/Akt/eNOS signaling pathway were evaluated in these women.	Guanosine Triphosphate	55-77	nitric oxide synthase 3	Homo sapiens	146-150
32411442-5	2020	The key proteins (Tie2, Akt, eNOS, and GTPCH I) in the guanosine triphosphate cyclohydrolase/tetrahydrobiopterin (GTPCH/BH4) pathway and Tie2/Akt/eNOS signaling pathway were evaluated in these women.	sapropterin	93-112	nitric oxide synthase 3	Homo sapiens	29-33
32411442-5	2020	The key proteins (Tie2, Akt, eNOS, and GTPCH I) in the guanosine triphosphate cyclohydrolase/tetrahydrobiopterin (GTPCH/BH4) pathway and Tie2/Akt/eNOS signaling pathway were evaluated in these women.	sapropterin	120-123	nitric oxide synthase 3	Homo sapiens	29-33
32411442-5	2020	The key proteins (Tie2, Akt, eNOS, and GTPCH I) in the guanosine triphosphate cyclohydrolase/tetrahydrobiopterin (GTPCH/BH4) pathway and Tie2/Akt/eNOS signaling pathway were evaluated in these women.	sapropterin	120-123	nitric oxide synthase 3	Homo sapiens	146-150
31996864-2	2020	Endothelial nitric oxide synthase (eNOS) is necessary to produce nitric oxide that causes pulmonary endothelial vasodilation.	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	35-39
31996864-2	2020	Endothelial nitric oxide synthase (eNOS) is necessary to produce nitric oxide that causes pulmonary endothelial vasodilation.	Nitric Oxide	65-77	nitric oxide synthase 3	Homo sapiens	35-39
32804118-2	2020	Emerging evidences suggest important regulatory roles of red blood cells (RBCs) on nitric oxide (NO) bioavailability, mainly by modulating their endothelial nitric oxide synthase (eNOS) enzyme activity.	Nitric Oxide	83-95	nitric oxide synthase 3	Homo sapiens	145-178
32804118-2	2020	Emerging evidences suggest important regulatory roles of red blood cells (RBCs) on nitric oxide (NO) bioavailability, mainly by modulating their endothelial nitric oxide synthase (eNOS) enzyme activity.	Nitric Oxide	83-95	nitric oxide synthase 3	Homo sapiens	180-184
32819257-11	2020	CONCLUSION: These results suggest that the PIM-1/eNOS/NO pathway plays a vital role, in which Propofol protects against TNF-alpha-induced blood-brain barrier disruption.	Propofol	94-102	nitric oxide synthase 3	Homo sapiens	49-53
31567371-9	2020	We found that current smokers with rs1799983-GT or TT within eNOS gene have the highest CHD risk, compared to never smokers with rs1799983-GG genotype, OR (95% CI) = 2.74 (1.78-3.85), after covariates adjustment for age, gender, BMI, and alcohol drinking.	Ethanol	238-245	nitric oxide synthase 3	Homo sapiens	61-65
32490931-7	2020	It is known that estradiol exerts a protective effect on endothelial function, activating the generation of nitric oxide (NO) via endothelial nitric oxide synthase.	Estradiol	17-26	nitric oxide synthase 3	Homo sapiens	130-163
32490931-7	2020	It is known that estradiol exerts a protective effect on endothelial function, activating the generation of nitric oxide (NO) via endothelial nitric oxide synthase.	Nitric Oxide	108-120	nitric oxide synthase 3	Homo sapiens	130-163
32427079-6	2020	Nitric oxide (NO) bioavailability can decrease due to deficient NO production by eNOS and/or NO release to vascular smooth muscle cells, which impairs endothelial function.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	81-85
32242776-9	2020	DHA and EPA also increased eNOS activity and induced nitric oxide production.	Docosahexaenoic Acids	0-3	nitric oxide synthase 3	Homo sapiens	27-31
32242776-9	2020	DHA and EPA also increased eNOS activity and induced nitric oxide production.	Eicosapentaenoic Acid	8-11	nitric oxide synthase 3	Homo sapiens	27-31
32819257-0	2020	Propofol protects against TNF-alpha-induced blood-brain barrier disruption via the PIM-1/eNOS/NO pathway.	Propofol	0-8	nitric oxide synthase 3	Homo sapiens	89-93
31442681-1	2020	INTRODUCTION: Nitric oxide is a gaseous radical produced by the nitric oxide endothelial synthase (eNOS) whose most studied physiological action is the vasodilation.	Nitric Oxide	14-26	nitric oxide synthase 3	Homo sapiens	77-97
31442681-1	2020	INTRODUCTION: Nitric oxide is a gaseous radical produced by the nitric oxide endothelial synthase (eNOS) whose most studied physiological action is the vasodilation.	Nitric Oxide	14-26	nitric oxide synthase 3	Homo sapiens	99-103
32427079-7	2020	Considering the NO cellular mechanisms, tackling the issue of eNOS uncoupling could avoid endothelial dysfunction: provision of the enzyme cofactor tetrahydrobiopterin (BH4) should elicit NO release from NO donors, to activate soluble guanylyl cyclase.	sapropterin	148-167	nitric oxide synthase 3	Homo sapiens	62-66
32427079-7	2020	Considering the NO cellular mechanisms, tackling the issue of eNOS uncoupling could avoid endothelial dysfunction: provision of the enzyme cofactor tetrahydrobiopterin (BH4) should elicit NO release from NO donors, to activate soluble guanylyl cyclase.	sapropterin	169-172	nitric oxide synthase 3	Homo sapiens	62-66
31356401-14	2020	With ICI118,551 (a beta2AR inhibitor) treatment, shear stress-induced Akt and eNOS phosphorylation as well as VEGF secretion were suppressed.	ici118	5-11	nitric oxide synthase 3	Homo sapiens	78-82
32375152-3	2020	Nitric oxide (NO) derived from endothelial nitric oxide synthase (eNOS) is an important regulator of angiogenesis.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	31-64
32375152-3	2020	Nitric oxide (NO) derived from endothelial nitric oxide synthase (eNOS) is an important regulator of angiogenesis.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	66-70
32375152-7	2020	L-NAME, a specific inhibitor of eNOS, abolished EF-induced HUVEC angiogenesis.	NG-Nitroarginine Methyl Ester	0-6	nitric oxide synthase 3	Homo sapiens	32-36
31672462-2	2020	NO is synthesized from l-arginine through the action of the nitric oxide synthase (NOS) family of enzymes, which includes three isoforms: endothelial NOS (eNOS), neuronal NOS (nNOS) and inducible NOS (iNOS).	Arginine	23-33	nitric oxide synthase 3	Homo sapiens	138-153
32814314-3	2020	It is produced in endothelial cells by endothelial NO synthase (eNOS) that mediates the conversion of the amino acid arginine into NO and citrulline.	Arginine	117-125	nitric oxide synthase 3	Homo sapiens	39-62
32814314-3	2020	It is produced in endothelial cells by endothelial NO synthase (eNOS) that mediates the conversion of the amino acid arginine into NO and citrulline.	Arginine	117-125	nitric oxide synthase 3	Homo sapiens	64-68
32814314-3	2020	It is produced in endothelial cells by endothelial NO synthase (eNOS) that mediates the conversion of the amino acid arginine into NO and citrulline.	Citrulline	138-148	nitric oxide synthase 3	Homo sapiens	39-62
32814314-3	2020	It is produced in endothelial cells by endothelial NO synthase (eNOS) that mediates the conversion of the amino acid arginine into NO and citrulline.	Citrulline	138-148	nitric oxide synthase 3	Homo sapiens	64-68
31106593-7	2019	On the other hand, salicin recovers IL-1beta-induced reduction of endothelial nitric oxide synthase (eNOS) and nitric oxide (NO) release.	salicin	19-26	nitric oxide synthase 3	Homo sapiens	66-99
32814314-4	2020	Asymmetric dimethylarginine (ADMA) acts as an inhibitor of eNOS.	dimethylarginine	11-27	nitric oxide synthase 3	Homo sapiens	59-63
32814314-4	2020	Asymmetric dimethylarginine (ADMA) acts as an inhibitor of eNOS.	N,N-dimethylarginine	29-33	nitric oxide synthase 3	Homo sapiens	59-63
32550950-11	2020	Immunohistochemical studies showed that the I/R-induced elevation in eNOS expression was reduced by AST treatment.	astaxanthine	100-103	nitric oxide synthase 3	Homo sapiens	69-73
32675856-8	2020	HAEC NO production was increased with sepiapterin to couple eNOS.	sepiapterin	38-49	nitric oxide synthase 3	Homo sapiens	60-64
33148831-4	2020	RESULTS: Results: During the study of nitric oxide system (NO-NOS) in patients with SJS, it was observed that NO2  level was increased by 1.53 times, NO3  level - by 3.33 times, activity of total NOS - by 5.78 times, constitutive (cNOS) - by 1.81 times and inducible (iNOS) - by 13.36 times.	Nitric Oxide	38-50	nitric oxide synthase 3	Homo sapiens	231-235
31920721-9	2019	In particular, higher production of reactive oxygen species deriving from a variety of enzymatic sources, including uncoupled endothelial nitric oxide synthase and the electron transport chain, causes DNA damage and activates the NAD+-consuming enzymes polyADP-ribose polymerase 1 (PARP1).	Oxygen	45-51	nitric oxide synthase 3	Homo sapiens	126-159
31920721-9	2019	In particular, higher production of reactive oxygen species deriving from a variety of enzymatic sources, including uncoupled endothelial nitric oxide synthase and the electron transport chain, causes DNA damage and activates the NAD+-consuming enzymes polyADP-ribose polymerase 1 (PARP1).	NAD	230-233	nitric oxide synthase 3	Homo sapiens	126-159
31747921-7	2019	Pravastatin and Geldanamycin (Hsp90 inhibitor) cotreatment increased microsomal eNOS activity.	Pravastatin	0-11	nitric oxide synthase 3	Homo sapiens	80-84
31299139-4	2019	eNOS activity was assessed using L-NAME.	NG-Nitroarginine Methyl Ester	33-39	nitric oxide synthase 3	Homo sapiens	0-4
31299139-10	2019	Inhibition of eNOS with L-NAME had a significant effect in normal but not overweight/obese vessels.	NG-Nitroarginine Methyl Ester	24-30	nitric oxide synthase 3	Homo sapiens	14-18
31677355-15	2019	A stimulus (e.g. shear stress) results in a release of endothelial endogenous calcium, which binds to calmodulin, and activates endothelial nitric oxide synthase (eNOS).	Calcium	78-85	nitric oxide synthase 3	Homo sapiens	128-161
31152363-5	2019	Interestingly, L-NIO, which is a NOS3 inhibitor, confers post-ischemic protection to axon function by attenuating mitochondrial fission and preserving mitochondrial motility via conserving levels of the microtubular adaptor protein Miro-2.	N(G)-iminoethylornithine	15-20	nitric oxide synthase 3	Homo sapiens	33-37
31264341-3	2019	Oestradiol upregulates endothelial nitric oxide synthase gene expression and increases the production of nitric oxide, an important vasodilator.	Estradiol	0-10	nitric oxide synthase 3	Homo sapiens	23-56
31871538-2	2019	Recent publications on adult red blood cells (RBCs) provide evidence that RBCs carry an active nitric oxide synthase (NOS3) enzyme and contribute to vascular functioning and integrity via their active nitric oxide synthesis.	Nitric Oxide	95-107	nitric oxide synthase 3	Homo sapiens	118-122
31871538-2	2019	Recent publications on adult red blood cells (RBCs) provide evidence that RBCs carry an active nitric oxide synthase (NOS3) enzyme and contribute to vascular functioning and integrity via their active nitric oxide synthesis.	Nitric Oxide	201-213	nitric oxide synthase 3	Homo sapiens	118-122
31747921-1	2019	BACKGROUND: Pravastatin, a known inducer of endothelial nitric-oxide synthase (eNOS) was demonstrated in human placenta, however the exact mechanism of it"s action is not fully understood.	Pravastatin	12-23	nitric oxide synthase 3	Homo sapiens	44-77
31747921-1	2019	BACKGROUND: Pravastatin, a known inducer of endothelial nitric-oxide synthase (eNOS) was demonstrated in human placenta, however the exact mechanism of it"s action is not fully understood.	Pravastatin	12-23	nitric oxide synthase 3	Homo sapiens	79-83
31873938-6	2019	These pharmacotherapy aids to withdrawal and tapering opioid dosagadrenoceptor agonists that act through eNOS to inhibit norepinephrine.	Norepinephrine	121-135	nitric oxide synthase 3	Homo sapiens	105-109
31747921-3	2019	METHODS: The eNOS activity of human placental microsomes was determined by the conversion rate of C14 L-arginine into C14 L-citrulline with or without pravastatin and Geldanamycin.	c14 l-arginine	98-112	nitric oxide synthase 3	Homo sapiens	13-17
31747921-3	2019	METHODS: The eNOS activity of human placental microsomes was determined by the conversion rate of C14 L-arginine into C14 L-citrulline with or without pravastatin and Geldanamycin.	c14 l-citrulline	118-134	nitric oxide synthase 3	Homo sapiens	13-17
31747921-3	2019	METHODS: The eNOS activity of human placental microsomes was determined by the conversion rate of C14 L-arginine into C14 L-citrulline with or without pravastatin and Geldanamycin.	Pravastatin	151-162	nitric oxide synthase 3	Homo sapiens	13-17
31747921-3	2019	METHODS: The eNOS activity of human placental microsomes was determined by the conversion rate of C14 L-arginine into C14 L-citrulline with or without pravastatin and Geldanamycin.	geldanamycin	167-179	nitric oxide synthase 3	Homo sapiens	13-17
31747921-6	2019	RESULTS: Pravastatin significantly increased total eNOS activity in healthy (28%, p<0.05) and preeclamptic placentas (32%, p<0.05) using 1 mM Ca2+ promoting the dissociation of a eNOS from it"s inhibitor caveolin.	Pravastatin	9-20	nitric oxide synthase 3	Homo sapiens	51-55
31747921-6	2019	RESULTS: Pravastatin significantly increased total eNOS activity in healthy (28%, p<0.05) and preeclamptic placentas (32%, p<0.05) using 1 mM Ca2+ promoting the dissociation of a eNOS from it"s inhibitor caveolin.	Pravastatin	9-20	nitric oxide synthase 3	Homo sapiens	179-183
31747921-7	2019	Pravastatin and Geldanamycin (Hsp90 inhibitor) cotreatment increased microsomal eNOS activity.	geldanamycin	16-28	nitric oxide synthase 3	Homo sapiens	80-84
31747921-11	2019	Pravastatin induces the placental microsomal arginine uptake leading to the rapid activation of eNOS independently of Ser1177 phosphorylation.	Pravastatin	0-11	nitric oxide synthase 3	Homo sapiens	96-100
31747921-11	2019	Pravastatin induces the placental microsomal arginine uptake leading to the rapid activation of eNOS independently of Ser1177 phosphorylation.	Arginine	45-53	nitric oxide synthase 3	Homo sapiens	96-100
31606200-0	2019	TSH inhibits eNOS expression in HMEC-1 cells through the TSHR/PI3K/AKT signaling pathway.	Thyrotropin	0-3	nitric oxide synthase 3	Homo sapiens	13-17
31606200-7	2019	Mechanism studies demonstrated that TSH promoted AKT phosphorylation (P<0.05), and that LY294002 inhibited the reduction of eNOS expression by TSH.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	88-96	nitric oxide synthase 3	Homo sapiens	124-128
31606200-7	2019	Mechanism studies demonstrated that TSH promoted AKT phosphorylation (P<0.05), and that LY294002 inhibited the reduction of eNOS expression by TSH.	Thyrotropin	143-146	nitric oxide synthase 3	Homo sapiens	124-128
30367728-10	2019	The generation of NO and cGMP by diazoxide was blocked by an endothelial NOS (eNOS)-selective inhibitor, NIO, but not by a neuronal (n)NOS-selective inhibitor, Nomega -propyl-L-arginine (NPA).	Cyclic GMP	25-29	nitric oxide synthase 3	Homo sapiens	61-76
30367728-10	2019	The generation of NO and cGMP by diazoxide was blocked by an endothelial NOS (eNOS)-selective inhibitor, NIO, but not by a neuronal (n)NOS-selective inhibitor, Nomega -propyl-L-arginine (NPA).	Diazoxide	33-42	nitric oxide synthase 3	Homo sapiens	61-76
30367728-10	2019	The generation of NO and cGMP by diazoxide was blocked by an endothelial NOS (eNOS)-selective inhibitor, NIO, but not by a neuronal (n)NOS-selective inhibitor, Nomega -propyl-L-arginine (NPA).	nio	105-108	nitric oxide synthase 3	Homo sapiens	61-76
31525342-1	2019	Decrease in the bioavailability of vasoactive nitric oxide (NO), derived from the endothelial nitric oxide synthase (NOS3), underlines vascular endothelial damage.	Nitric Oxide	46-58	nitric oxide synthase 3	Homo sapiens	82-115
31525342-1	2019	Decrease in the bioavailability of vasoactive nitric oxide (NO), derived from the endothelial nitric oxide synthase (NOS3), underlines vascular endothelial damage.	Nitric Oxide	46-58	nitric oxide synthase 3	Homo sapiens	117-121
31547684-0	2019	Botulinum toxin type A suppresses arterial vasoconstriction by regulating calcium sensitization and the endothelium-dependent endothelial nitric oxide synthase/soluble guanylyl cyclase/cyclic guanosine monophosphate pathway: An in vitro study.	Cyclic GMP	185-215	nitric oxide synthase 3	Homo sapiens	126-159
31479717-11	2019	Combining Tyr capsule(s) with WW abolished the increase in iNOS, eNOS, VEGFA, and CHF expressions promoted by WW (p < 0.05).	Tyrosine	10-13	nitric oxide synthase 3	Homo sapiens	65-69
31421231-0	2019	Sensitive and quantitative method to evaluate DNA methylation of the positive regulatory domains (PRDI, PRDII) and cAMP response element (CRE) in human endothelial nitric oxide synthase promoter.	Cyclic AMP	115-119	nitric oxide synthase 3	Homo sapiens	152-185
30968427-7	2019	sONE acts as a posttranscriptional regulator to endothelial nitric oxide synthase (eNOS) and thus affecting eNOS-induced nitric oxide (NO) production from TNBC cells measured by Greiss reagent.	Nitric Oxide	60-72	nitric oxide synthase 3	Homo sapiens	83-87
31421231-1	2019	Nitric oxide plays a prominent role in the cardiovascular system and much attention has been devoted in the last years on deciphering the regulation of human endothelial nitric oxide synthase (eNOS) expression.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	158-191
31421231-1	2019	Nitric oxide plays a prominent role in the cardiovascular system and much attention has been devoted in the last years on deciphering the regulation of human endothelial nitric oxide synthase (eNOS) expression.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	193-197
31454653-0	2019	Garcimultiflorone K inhibits angiogenesis through Akt/eNOS- and mTOR-dependent pathways in human endothelial progenitor cells.	garcimultiflorone k	0-19	nitric oxide synthase 3	Homo sapiens	54-59
31762720-0	2019	Crocetin promotes angiogenesis in human endothelial cells through PI3K-Akt-eNOS signaling pathway.	crocetin	0-8	nitric oxide synthase 3	Homo sapiens	75-79
31781259-1	2019	Far-infrared ray (FIR) therapy has been reported to exert beneficial effects on cardiovascular function by elevating endothelial nitric oxide synthesis (eNOS) activity and nitric oxide (NO) production.	Nitric Oxide	129-141	nitric oxide synthase 3	Homo sapiens	153-157
31781259-2	2019	Tetrahydrobiopterin (BH4) is a key determinant of eNOS-dependent NO synthesis in vascular endothelial cells.	sapropterin	0-19	nitric oxide synthase 3	Homo sapiens	50-54
31652041-0	2019	Mid-dose losartan mitigates diabetes-induced hepatic damage by regulating iNOS, eNOS, VEGF, and NF-kappaB expressions Background/aim: Losartan,  an  antihypertensive  drug,  is  highly  preferred  in  patients  with  diabetes  mellitus  (DM)  and  hypertension  because of its retarding effect on diabetic nephropathy.	Losartan	9-17	nitric oxide synthase 3	Homo sapiens	80-84
31652041-0	2019	Mid-dose losartan mitigates diabetes-induced hepatic damage by regulating iNOS, eNOS, VEGF, and NF-kappaB expressions Background/aim: Losartan,  an  antihypertensive  drug,  is  highly  preferred  in  patients  with  diabetes  mellitus  (DM)  and  hypertension  because of its retarding effect on diabetic nephropathy.	Losartan	134-142	nitric oxide synthase 3	Homo sapiens	80-84
31652041-6	2019	Conclusion: This  study  indicated  that  mid-dose  losartan  administration  may  have  a  therapeutic  effect  by  inhibiting  apoptosis  and  regulating iNOS, eNOS, VEGF, and NF-kappaB protein expressions in DM-induced hepatic damage.	Losartan	52-60	nitric oxide synthase 3	Homo sapiens	162-166
31824825-7	2019	Western blot analyses revealed that EGM preconditioning with gelatin coating induced the expression of endothelial nitric oxide synthase (eNOS), a mature EC-specific marker, as well as phosphorylated Akt at serine 473, a signaling molecule related to eNOS activation.	4-ETHYLBENZOIC ACID	36-39	nitric oxide synthase 3	Homo sapiens	103-136
31824825-7	2019	Western blot analyses revealed that EGM preconditioning with gelatin coating induced the expression of endothelial nitric oxide synthase (eNOS), a mature EC-specific marker, as well as phosphorylated Akt at serine 473, a signaling molecule related to eNOS activation.	4-ETHYLBENZOIC ACID	36-39	nitric oxide synthase 3	Homo sapiens	138-142
31824825-7	2019	Western blot analyses revealed that EGM preconditioning with gelatin coating induced the expression of endothelial nitric oxide synthase (eNOS), a mature EC-specific marker, as well as phosphorylated Akt at serine 473, a signaling molecule related to eNOS activation.	4-ETHYLBENZOIC ACID	36-39	nitric oxide synthase 3	Homo sapiens	251-255
31762720-3	2019	The current experiment was designed to find the activity of PI3K-Akt-eNOS axis after the treatment of endothelial cells with Crocetin in vitro.	crocetin	125-133	nitric oxide synthase 3	Homo sapiens	69-73
31762720-8	2019	Based on the data from the current experiment, protein level of VEGFR-1, -2 and p-Akt/Akt, p-eNOS/eNOS ratios were increased 72 h after the treatment of HUVECs with Crocetin (p&lt;0.05).	crocetin	165-173	nitric oxide synthase 3	Homo sapiens	93-97
31762720-8	2019	Based on the data from the current experiment, protein level of VEGFR-1, -2 and p-Akt/Akt, p-eNOS/eNOS ratios were increased 72 h after the treatment of HUVECs with Crocetin (p&lt;0.05).	crocetin	165-173	nitric oxide synthase 3	Homo sapiens	98-102
31762720-11	2019	The PI3K/Akt/eNOS axis is required for a Crocetin-associated activity in endothelial cells.	crocetin	41-49	nitric oxide synthase 3	Homo sapiens	13-17
31692706-10	2019	The protective role of Ipt is attributed to an increased production of nitric oxide (NO), as well as an enhanced activation of angiogenic transduction pathways, containing Akt and endothelial nitric oxide synthase.	N-(1-methylethyl)-1,1,2-trimethylpropylamine	23-26	nitric oxide synthase 3	Homo sapiens	180-213
31637188-12	2019	CONCLUSION: Obtusifolin can inhibit cell growth under hypoxic conditions and down-regulate HIF-1/VEGF/eNOS secretions in ARPE-19 cells.	obtusifolin	12-23	nitric oxide synthase 3	Homo sapiens	102-106
31600286-2	2019	Here, we investigated the role of caveolar plasma membrane stabilization by the dynamin-related ATPase EHD2 on eNOS-nitric oxide (NO)-dependent vessel relaxation.	Nitric Oxide	116-128	nitric oxide synthase 3	Homo sapiens	111-115
31595849-5	2019	Finally, the effect of Curcumin on the transcriptional efficiencies of miR-146a, nNOS, eNOS and iNOS was studied using luciferase assay.	Curcumin	23-31	nitric oxide synthase 3	Homo sapiens	87-91
31547608-8	2019	Phenolic extracts derived from RB down-regulated the expression of four genes, ICAM1, CD39, CD73 and NOX4 and up-regulated the expression of another four genes, Nrf2, NQO1, HO1 and eNOS, indicating an antioxidant/ anti-inflammatory effect for RB against endothelial dysfunction.	phenolic acid	0-8	nitric oxide synthase 3	Homo sapiens	181-185
31345420-9	2019	Cells from PGMO also showed lower nitric oxide level and reduced activator serine1177 but increased inhibitor threonine495 phosphorylation of endothelial nitric oxide synthase (eNOS) and saturable transport of l-arginine.	threonine495	110-122	nitric oxide synthase 3	Homo sapiens	142-175
32774841-5	2019	alpha-LA pretreatment remarkably diminished the damage to cell migration ability, recovered the declined levels of the vasodilator factor nitric oxide (NO), elevated the expression level of endothelial nitric oxide synthases (eNOS), and inhibited the upregulated expression of vasoconstrictor factor endothelin-1 (ET-1).	Thioctic Acid	0-8	nitric oxide synthase 3	Homo sapiens	190-224
32774841-5	2019	alpha-LA pretreatment remarkably diminished the damage to cell migration ability, recovered the declined levels of the vasodilator factor nitric oxide (NO), elevated the expression level of endothelial nitric oxide synthases (eNOS), and inhibited the upregulated expression of vasoconstrictor factor endothelin-1 (ET-1).	Thioctic Acid	0-8	nitric oxide synthase 3	Homo sapiens	226-230
31533227-6	2019	Furthermore, in cultured human microvascular endothelial cell-1 (HMEC-1) cells, we showed that pretreatment with VAC dose-dependently increased nitric oxide (NO) generation and the phosphorylation of eNOS under HG conditions.	vinyl acetate	113-116	nitric oxide synthase 3	Homo sapiens	200-204
31533227-9	2019	In addition, both reactive oxygen species (ROS) scavenger N-acetyl-L-cysteine (NAC) and VAC abolished HG-evoked dephosphorylation of AMPK and eNOS, increased miRNA-34a expression, and decreased NO production.	Reactive Oxygen Species	18-41	nitric oxide synthase 3	Homo sapiens	142-146
31533227-9	2019	In addition, both reactive oxygen species (ROS) scavenger N-acetyl-L-cysteine (NAC) and VAC abolished HG-evoked dephosphorylation of AMPK and eNOS, increased miRNA-34a expression, and decreased NO production.	Reactive Oxygen Species	43-46	nitric oxide synthase 3	Homo sapiens	142-146
31533227-9	2019	In addition, both reactive oxygen species (ROS) scavenger N-acetyl-L-cysteine (NAC) and VAC abolished HG-evoked dephosphorylation of AMPK and eNOS, increased miRNA-34a expression, and decreased NO production.	Acetylcysteine	58-77	nitric oxide synthase 3	Homo sapiens	142-146
31533227-9	2019	In addition, both reactive oxygen species (ROS) scavenger N-acetyl-L-cysteine (NAC) and VAC abolished HG-evoked dephosphorylation of AMPK and eNOS, increased miRNA-34a expression, and decreased NO production.	Acetylcysteine	79-82	nitric oxide synthase 3	Homo sapiens	142-146
31533227-10	2019	These results suggest that VAC impedes HG-induced endothelial dysfunction via inhibition of the ROS/AMPK/miRNA-34a/eNOS signaling cascade.	Reactive Oxygen Species	96-99	nitric oxide synthase 3	Homo sapiens	115-119
31203378-16	2019	Liraglutide and exenatide increased nitrate production and endothelial nitric oxide synthase (eNOS) phosphorylation (p <= 0.020).	Exenatide	16-25	nitric oxide synthase 3	Homo sapiens	59-92
31203378-16	2019	Liraglutide and exenatide increased nitrate production and endothelial nitric oxide synthase (eNOS) phosphorylation (p <= 0.020).	Exenatide	16-25	nitric oxide synthase 3	Homo sapiens	94-98
31146011-9	2019	However, NaHS administration increased endothelial nitric oxide synthase (eNOS) expression in brain regions of Hcy treated animals.	sodium bisulfide	9-13	nitric oxide synthase 3	Homo sapiens	39-72
31496872-0	2019	Docosahexaenoic acid reduces adenosine triphosphate-induced calcium influx via inhibition of store-operated calcium channels and enhances baseline endothelial nitric oxide synthase phosphorylation in human endothelial cells.	Docosahexaenoic Acids	0-20	nitric oxide synthase 3	Homo sapiens	147-180
31158660-7	2019	NAC and LOS also suppressed FD-induced SA-beta-gal activity, increased EC proliferation and eNOS expression, and improved endothelial function.	Acetylcysteine	0-3	nitric oxide synthase 3	Homo sapiens	92-96
31146011-9	2019	However, NaHS administration increased endothelial nitric oxide synthase (eNOS) expression in brain regions of Hcy treated animals.	Homocysteine	111-114	nitric oxide synthase 3	Homo sapiens	39-72
31750822-0	2019	[Tanshinone IIA attenuates hydrogen peroxide-induced senescence of human umbilical vein endothelial cells through activating SIRT1/eNOS pathway].	tanshinone	1-15	nitric oxide synthase 3	Homo sapiens	131-135
31750822-0	2019	[Tanshinone IIA attenuates hydrogen peroxide-induced senescence of human umbilical vein endothelial cells through activating SIRT1/eNOS pathway].	Hydrogen Peroxide	27-44	nitric oxide synthase 3	Homo sapiens	131-135
31750822-13	2019	Conversely, the expression of P21 and P16 proteins in the TSA group were lower than those in the model group, and SIRT1 and p-eNOS/eNOS were higher in the TSA group than those in the model group.	tanshinone	155-158	nitric oxide synthase 3	Homo sapiens	126-130
31750822-13	2019	Conversely, the expression of P21 and P16 proteins in the TSA group were lower than those in the model group, and SIRT1 and p-eNOS/eNOS were higher in the TSA group than those in the model group.	tanshinone	155-158	nitric oxide synthase 3	Homo sapiens	131-135
31750822-15	2019	Conclusion TSA attenuates H2O2-induced endothelial cell senescence by activating SIRT1/eNOS signaling pathway.	tanshinone	11-14	nitric oxide synthase 3	Homo sapiens	87-91
31750822-15	2019	Conclusion TSA attenuates H2O2-induced endothelial cell senescence by activating SIRT1/eNOS signaling pathway.	Water	26-30	nitric oxide synthase 3	Homo sapiens	87-91
31582948-8	2019	CONCLUSIONS: Cigarette smoking, alcohol drinking and the Glu298Asp polymorphism of the eNOS gene generate combined effects that increase the susceptibility of the mutant genotype to BP in Chinese male hypertensive subjects.	Ethanol	32-39	nitric oxide synthase 3	Homo sapiens	87-91
32000958-9	2019	Conclusions: In acute period of polytrauma, significant increasing of iNOS and eNOS occurs with percentage prevalence of iNOS over eNOS on the background of H2S decreasing.	Deuterium	157-160	nitric oxide synthase 3	Homo sapiens	79-83
31235251-5	2019	Moreover, nitric oxide (NO) production was significantly reduced by SETD3 over-expression through repressing the expression of inducible NO synthase (iNOS) and endothelial NO synthase (eNOS) in cervical cancer cells.	Nitric Oxide	10-22	nitric oxide synthase 3	Homo sapiens	160-183
31235251-5	2019	Moreover, nitric oxide (NO) production was significantly reduced by SETD3 over-expression through repressing the expression of inducible NO synthase (iNOS) and endothelial NO synthase (eNOS) in cervical cancer cells.	Nitric Oxide	10-22	nitric oxide synthase 3	Homo sapiens	185-189
31239152-2	2019	The Ang II/type 1 receptor (AT1R) signaling pathway can cause endothelial nitric oxide synthase (eNOS)/nitric oxide (NO) dysfunction through various mechanisms leading to ED.	ed	171-173	nitric oxide synthase 3	Homo sapiens	62-95
30900130-2	2019	NOS1, NOS2 and NOS3 genes are implicated in the production of nitric oxide.	Nitric Oxide	62-74	nitric oxide synthase 3	Homo sapiens	15-19
30776841-3	2019	Caveolin-1 is treated to be protein in the cytomembrane entrapped with caveolae in endothelial cells and vascular smooth muscle cells which diminish nitric oxide (NO) by fill up the calcium/calmodulin (Ca2+/CaM) confining point of endothelial nitric oxide synthase (eNOS), decrease NO generation produce endothelial dysfunction and atherosclerotic injury development.	cytomembrane	43-55	nitric oxide synthase 3	Homo sapiens	231-264
30776841-3	2019	Caveolin-1 is treated to be protein in the cytomembrane entrapped with caveolae in endothelial cells and vascular smooth muscle cells which diminish nitric oxide (NO) by fill up the calcium/calmodulin (Ca2+/CaM) confining point of endothelial nitric oxide synthase (eNOS), decrease NO generation produce endothelial dysfunction and atherosclerotic injury development.	cytomembrane	43-55	nitric oxide synthase 3	Homo sapiens	266-270
30244056-4	2019	While expression of both inducible (iNOS) and constitutive NOS (eNOS) isoforms varies considerably in the ovary at various stages of follicular growth and development, selective binding of NO with proteins containing heme moieties have significant influence on ovarian steroidogenesis.	Heme	217-221	nitric oxide synthase 3	Homo sapiens	64-68
31189131-6	2019	Mechanistically, ADK inhibition or knockdown in human umbilical vein endothelial cells (HUVECs) elevated intracellular adenosine level and increased endothelial nitric oxide synthase (NOS3) activity, resulting in an increase in nitric oxide (NO) production.	Nitric Oxide	161-173	nitric oxide synthase 3	Homo sapiens	184-188
31316621-13	2019	This study, to the best of our knowledge, is the first to assess the effects of higenamine on cold-induced vasoconstriction in vivo and its molecular mechanisms on the PI3K/Akt, AMPK/eNOS/nitric oxide, ROS/alpha2C-AR and PTK9 signaling pathways under hypothermia conditions.	higenamine	80-90	nitric oxide synthase 3	Homo sapiens	183-187
31155983-0	2019	Hydrogen sulfide-mediated endothelial function and the interaction with eNOS and PDE5A activity in human internal mammary arteries.	Hydrogen Sulfide	0-16	nitric oxide synthase 3	Homo sapiens	72-76
31189131-8	2019	Additionally, increased phosphorylation of NOS3 in ADK-knockdown HUVECs was regulated by an adenosine receptor-independent mechanism.	Adenosine	92-101	nitric oxide synthase 3	Homo sapiens	43-47
31035054-14	2019	DHI promoted EPCs mobilization via upregulating the expression of Akt, eNOS and MMP-9 in BM.	dehydrosoyasaponin I	0-3	nitric oxide synthase 3	Homo sapiens	71-75
31330833-0	2019	ANGPT2 and NOS3 Polymorphisms and Clinical Outcome in Advanced Hepatocellular Carcinoma Patients Receiving Sorafenib.	Sorafenib	107-116	nitric oxide synthase 3	Homo sapiens	11-15
31336573-1	2019	Nitric oxide (NO) is a well-known vasodilator produced by the vascular endothelium via the enzyme endothelial nitric oxide synthase (eNOS).	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	98-131
31330833-2	2019	The aim of the present study was to evaluate the prognostic value of single-nucleotide polymorphisms on angiopoietin-2 (ANGPT2) and endothelial-derived nitric oxide synthase (NOS3) genes in 135 patients with advanced HCC receiving sorafenib.	Sorafenib	231-240	nitric oxide synthase 3	Homo sapiens	175-179
31330833-8	2019	Our results suggest that ANGPT2rs55633437 and NOS3 rs2070744 polymorphisms could identify a subset of HCC patients more resistant to sorafenib.	Sorafenib	133-142	nitric oxide synthase 3	Homo sapiens	46-50
31354524-11	2019	Melatonin also counteracted the stimulatory effect of radiation on CXCL6, CCL2, ERK1, ERK2, and AKT1 mRNA expression and increased the inhibitory effect of radiation on NOS3 expression.	Melatonin	0-9	nitric oxide synthase 3	Homo sapiens	169-173
31063772-9	2019	Moreover, treatment of Ea.hy926 cells with palmitic acid or TNFalpha also caused a significant decrease in eNOS activity, which was reversed in iNOS silenced Ea.hy926 cells suggesting the role of iNOS in the reduction of eNOS activity.	Palmitic Acid	43-56	nitric oxide synthase 3	Homo sapiens	107-111
31063772-9	2019	Moreover, treatment of Ea.hy926 cells with palmitic acid or TNFalpha also caused a significant decrease in eNOS activity, which was reversed in iNOS silenced Ea.hy926 cells suggesting the role of iNOS in the reduction of eNOS activity.	Palmitic Acid	43-56	nitric oxide synthase 3	Homo sapiens	221-225
31269778-5	2019	High glucose concentrations lead to a loss of mitochondrial networks, increased reactive oxygen species (ROS), endothelial nitric oxide synthase (eNOS) activation and a reduction in cGMP production related to protein kinase G (PKG) activity.	Glucose	5-12	nitric oxide synthase 3	Homo sapiens	146-150
30947567-5	2019	At the same time, high dose silibinin increased NO levels in A431 cells and the endothelial nitric oxide synthase (eNOS) inhibitor NG-nitro-L-arginine methylester (L-NAME) attenuated silibinin-induced cell growth inhibition.	NG-Nitroarginine Methyl Ester	164-170	nitric oxide synthase 3	Homo sapiens	80-113
29471036-8	2019	The specific iNOS inhibitor 1400 W decreases eNOS S-nitrosylation and the association of eNOS and beta-catenin, thereby blocking the beta-catenin signal pathway to alleviate OxLDL-induced endothelial dysfunction.	N-((3-(aminomethyl)phenyl)methyl)ethanimidamide	28-34	nitric oxide synthase 3	Homo sapiens	45-49
29471036-8	2019	The specific iNOS inhibitor 1400 W decreases eNOS S-nitrosylation and the association of eNOS and beta-catenin, thereby blocking the beta-catenin signal pathway to alleviate OxLDL-induced endothelial dysfunction.	N-((3-(aminomethyl)phenyl)methyl)ethanimidamide	28-34	nitric oxide synthase 3	Homo sapiens	89-93
30947567-5	2019	At the same time, high dose silibinin increased NO levels in A431 cells and the endothelial nitric oxide synthase (eNOS) inhibitor NG-nitro-L-arginine methylester (L-NAME) attenuated silibinin-induced cell growth inhibition.	Nitroarginine	131-150	nitric oxide synthase 3	Homo sapiens	80-113
31269778-5	2019	High glucose concentrations lead to a loss of mitochondrial networks, increased reactive oxygen species (ROS), endothelial nitric oxide synthase (eNOS) activation and a reduction in cGMP production related to protein kinase G (PKG) activity.	Glucose	5-12	nitric oxide synthase 3	Homo sapiens	111-144
30947567-5	2019	At the same time, high dose silibinin increased NO levels in A431 cells and the endothelial nitric oxide synthase (eNOS) inhibitor NG-nitro-L-arginine methylester (L-NAME) attenuated silibinin-induced cell growth inhibition.	Silybin	183-192	nitric oxide synthase 3	Homo sapiens	80-113
31280192-1	2019	Endothelial nitric oxide synthase (NOS3 or eNOS) is the enzyme responsible for the highest production of nitric oxide, with the greatest impact on the cardiovascular system, encoded by the eNOS gene, which presents various polymorphisms.	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	43-47
31280192-1	2019	Endothelial nitric oxide synthase (NOS3 or eNOS) is the enzyme responsible for the highest production of nitric oxide, with the greatest impact on the cardiovascular system, encoded by the eNOS gene, which presents various polymorphisms.	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	189-193
31280192-1	2019	Endothelial nitric oxide synthase (NOS3 or eNOS) is the enzyme responsible for the highest production of nitric oxide, with the greatest impact on the cardiovascular system, encoded by the eNOS gene, which presents various polymorphisms.	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	35-39
31280192-2	2019	ENOS gene polymorphisms play an important role in the response to drugs affecting nitric oxide (NO) signaling.	Nitric Oxide	82-94	nitric oxide synthase 3	Homo sapiens	0-4
31280192-3	2019	This review discusses the pharmacogenetic impact of eNOS polymorphisms on the response to drugs affecting NO activity: angiotensin converting enzyme inhibitors, angiotensin II receptor antagonists, calcium blockers, beta-blockers, diuretics, phosphodiesterase inhibitors, and statins.	Calcium	198-205	nitric oxide synthase 3	Homo sapiens	52-56
31316302-9	2019	Conclusion: TLR4 modulates OSS-induced oxidative stress by activating NOX2 and suppressing eNOS.	OSS	27-30	nitric oxide synthase 3	Homo sapiens	91-95
31138610-0	2019	Associations of the NOS3 rs1799983 polymorphism with circulating nitric oxide and lipid levels: a systematic review and meta-analysis.	Nitric Oxide	65-77	nitric oxide synthase 3	Homo sapiens	20-24
31195721-0	2019	Cannabidiol Overcomes Oxaliplatin Resistance by Enhancing NOS3- and SOD2-Induced Autophagy in Human Colorectal Cancer Cells.	Cannabidiol	0-11	nitric oxide synthase 3	Homo sapiens	58-62
30880179-0	2019	Bupivacaine-induced contraction is attenuated by endothelial nitric oxide release modulated by activation of both stimulatory and inhibitory phosphorylation (Ser1177 and Thr495) of endothelial nitric oxide synthase.	Bupivacaine	0-11	nitric oxide synthase 3	Homo sapiens	181-214
30880179-0	2019	Bupivacaine-induced contraction is attenuated by endothelial nitric oxide release modulated by activation of both stimulatory and inhibitory phosphorylation (Ser1177 and Thr495) of endothelial nitric oxide synthase.	Nitric Oxide	61-73	nitric oxide synthase 3	Homo sapiens	181-214
31195721-6	2019	Additionally, phosphorylation of nitric oxide synthase 3 (NOS3) was increased in oxaliplatin-resistant cells compared to that in parent cells.	Oxaliplatin	81-92	nitric oxide synthase 3	Homo sapiens	33-56
31195721-6	2019	Additionally, phosphorylation of nitric oxide synthase 3 (NOS3) was increased in oxaliplatin-resistant cells compared to that in parent cells.	Oxaliplatin	81-92	nitric oxide synthase 3	Homo sapiens	58-62
31195721-7	2019	Combined treatment with oxaliplatin and CBD reduced phospho-NOS3 levels and nitric oxide (NO) production and resulted in the production of reactive oxygen species (ROS) by reducing the levels of superoxide dismutase 2, an antioxidant present in the mitochondria, causing mitochondrial dysfunction.	Oxaliplatin	24-35	nitric oxide synthase 3	Homo sapiens	60-64
31195721-7	2019	Combined treatment with oxaliplatin and CBD reduced phospho-NOS3 levels and nitric oxide (NO) production and resulted in the production of reactive oxygen species (ROS) by reducing the levels of superoxide dismutase 2, an antioxidant present in the mitochondria, causing mitochondrial dysfunction.	Cannabidiol	40-43	nitric oxide synthase 3	Homo sapiens	60-64
31195721-8	2019	Taken together, these results suggest that elevated phosphorylation of NOS3 is essential for oxaliplatin resistance.	Oxaliplatin	93-104	nitric oxide synthase 3	Homo sapiens	71-75
31195721-9	2019	The combination of oxaliplatin and CBD decreased NOS3 phosphorylation, which resulted in autophagy, by inducing the overproduction of ROS through mitochondrial dysfunction, thus overcoming oxaliplatin resistance.	Oxaliplatin	19-30	nitric oxide synthase 3	Homo sapiens	49-53
31195721-9	2019	The combination of oxaliplatin and CBD decreased NOS3 phosphorylation, which resulted in autophagy, by inducing the overproduction of ROS through mitochondrial dysfunction, thus overcoming oxaliplatin resistance.	Cannabidiol	35-38	nitric oxide synthase 3	Homo sapiens	49-53
31195721-9	2019	The combination of oxaliplatin and CBD decreased NOS3 phosphorylation, which resulted in autophagy, by inducing the overproduction of ROS through mitochondrial dysfunction, thus overcoming oxaliplatin resistance.	Reactive Oxygen Species	134-137	nitric oxide synthase 3	Homo sapiens	49-53
31195721-9	2019	The combination of oxaliplatin and CBD decreased NOS3 phosphorylation, which resulted in autophagy, by inducing the overproduction of ROS through mitochondrial dysfunction, thus overcoming oxaliplatin resistance.	Oxaliplatin	189-200	nitric oxide synthase 3	Homo sapiens	49-53
31281371-13	2019	These effects were associated with the increase in p-Akt/Akt and p-eNOS, which could be abolished by LY294002.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	101-109	nitric oxide synthase 3	Homo sapiens	67-71
31281593-4	2019	The reduction in NOS3 was accompanied by decreased migratory capacity, which depends on intact mitochondria and ATP formation.	Adenosine Triphosphate	112-115	nitric oxide synthase 3	Homo sapiens	17-21
31029788-2	2019	The effects of flavonoids shown to improve endothelial performance include regulating blood pressure by modulating endothelial nitric oxide synthase and NADPH oxidases, but their impact on glucose uptake and metabolism has not been explored.	Flavonoids	15-25	nitric oxide synthase 3	Homo sapiens	115-148
30962068-2	2019	We were interested in the endothelial nitric oxide gene (eNOS), given the involvement of this enzyme in functional alterations in the retinal microvasculature in diabetes.	Nitric Oxide	38-50	nitric oxide synthase 3	Homo sapiens	57-61
31006328-10	2019	Suggesting that the impairment was downstream of eNOS (endothelial NO synthase), HA attenuated the vasodilation elicited by the NO donor sodium nitroprusside.	Nitroprusside	137-157	nitric oxide synthase 3	Homo sapiens	49-53
31006328-10	2019	Suggesting that the impairment was downstream of eNOS (endothelial NO synthase), HA attenuated the vasodilation elicited by the NO donor sodium nitroprusside.	Nitroprusside	137-157	nitric oxide synthase 3	Homo sapiens	55-78
30489453-10	2019	CONCLUSION: H2S enhances eNOS-dependent mobilization of bone marrow-derived EPCs and facilitates re-endothelialization following vascular injury.	Deuterium	12-15	nitric oxide synthase 3	Homo sapiens	25-29
31141240-5	2019	We observed that 17beta-estradiol abolished the stimulatory effect of corticotropin-releasing hormone on intracellular reactive oxygen species levels and counteracted its inhibitory effect on endothelial nitric oxide synthase activity and nitric oxide release.	Estradiol	17-33	nitric oxide synthase 3	Homo sapiens	192-225
30160565-5	2019	In vitro observations have shown anthocyanin- and metabolite-induced activation of endothelial nitric oxide synthase and human vascular cell migration.	Anthocyanins	33-44	nitric oxide synthase 3	Homo sapiens	83-116
30937466-3	2019	As an important endothelium-derived relaxation factor, nitric oxide (NO) plays a role in cardiovascular protection and anti-AS function; but in the pathological state, endothelial nitric oxide synthase (eNOS) disorder causes an abnormal production of NO, which may damage endothelial function and trigger AS.	Nitric Oxide	55-67	nitric oxide synthase 3	Homo sapiens	203-207
30937466-10	2019	The former one is mainly related to inflammatory inhibition and protection of the PKB-eNOS signaling pathway; whereas the latter one is associated with the addition of the L-arginine substrate of eNOS, arginase inhibition, and the supplement of tetrahydrobiopterin, which can elevate no level.	Arginine	172-182	nitric oxide synthase 3	Homo sapiens	196-200
29948497-1	2019	To discuss the association of the T786C and G894T polymorphisms of endothelial nitric oxide synthase (eNOS) with the occurrence and prognosis of aneurismal subarachnoid hemorrhage (aSAH).	asah	181-185	nitric oxide synthase 3	Homo sapiens	67-100
29948497-1	2019	To discuss the association of the T786C and G894T polymorphisms of endothelial nitric oxide synthase (eNOS) with the occurrence and prognosis of aneurismal subarachnoid hemorrhage (aSAH).	asah	181-185	nitric oxide synthase 3	Homo sapiens	102-106
29948497-9	2019	The results of the logistic regression analysis indicated that T786C and G894T polymorphisms of eNOS were independent influencing factors on the occurrence of aSAH and the G894T polymorphism was also closely related to the prognosis.	asah	159-163	nitric oxide synthase 3	Homo sapiens	96-100
29948497-10	2019	T786C and G894T polymorphisms of eNOS gene were correlated with the occurrence and prognosis of aSAH, and the G894T polymorphism might be an independent influencing factor.	asah	96-100	nitric oxide synthase 3	Homo sapiens	33-37
30489453-9	2019	Treatment with an eNOS inhibitor (L-NAME) blocked the effects of NaHS on EPCs functions.	NG-Nitroarginine Methyl Ester	34-40	nitric oxide synthase 3	Homo sapiens	18-22
30489453-9	2019	Treatment with an eNOS inhibitor (L-NAME) blocked the effects of NaHS on EPCs functions.	sodium bisulfide	65-69	nitric oxide synthase 3	Homo sapiens	18-22
31052183-10	2019	CONCLUSIONS: Resveratrol increased NO in glaucomatous TM cells, possibly by increasing eNOS expression.	Resveratrol	13-24	nitric oxide synthase 3	Homo sapiens	87-91
30856465-4	2019	Human aortic endothelial cells (HAECs) were treated with RSV to evaluate the gene expression of the endothelial nitric oxide synthase (eNOS).	Resveratrol	57-60	nitric oxide synthase 3	Homo sapiens	100-133
30851383-1	2019	(-)-Epicatechin (Epi) has been demonstrated to activate pathways involved in GPER-stimulated nitric oxide (NO) production via endothelial NO synthase, known as the eNOS/NO pathway.	Catechin	0-15	nitric oxide synthase 3	Homo sapiens	164-168
30851383-1	2019	(-)-Epicatechin (Epi) has been demonstrated to activate pathways involved in GPER-stimulated nitric oxide (NO) production via endothelial NO synthase, known as the eNOS/NO pathway.	Catechin	4-7	nitric oxide synthase 3	Homo sapiens	164-168
30851383-1	2019	(-)-Epicatechin (Epi) has been demonstrated to activate pathways involved in GPER-stimulated nitric oxide (NO) production via endothelial NO synthase, known as the eNOS/NO pathway.	Nitric Oxide	93-105	nitric oxide synthase 3	Homo sapiens	164-168
30856465-7	2019	In addition, RSV increased the promoter activity of the human eNOS gene, as determined by luciferase assays of the eNOS promoter gene.	Resveratrol	13-16	nitric oxide synthase 3	Homo sapiens	62-66
30856465-7	2019	In addition, RSV increased the promoter activity of the human eNOS gene, as determined by luciferase assays of the eNOS promoter gene.	Resveratrol	13-16	nitric oxide synthase 3	Homo sapiens	115-119
30856465-8	2019	The cAMP-response element binding protein (CREB) was identified as the target transcription factor involved in the RSV mediated upregulation of eNOS expression.	Resveratrol	115-118	nitric oxide synthase 3	Homo sapiens	144-148
30856465-9	2019	RSV increased phosphorylation of CREB through protein kinase A (PKA) activation, which induced a CREB-mediated upregulation of eNOS transcription.	Resveratrol	0-3	nitric oxide synthase 3	Homo sapiens	127-131
31052341-1	2019	Resveratrol increases the production of nitric oxide (NO) in endothelial cells by upregulating the expression of endothelial NO synthase (eNOS), stimulating eNOS enzymatic activity, and preventing eNOS uncoupling.	Resveratrol	0-11	nitric oxide synthase 3	Homo sapiens	113-136
31052341-1	2019	Resveratrol increases the production of nitric oxide (NO) in endothelial cells by upregulating the expression of endothelial NO synthase (eNOS), stimulating eNOS enzymatic activity, and preventing eNOS uncoupling.	Resveratrol	0-11	nitric oxide synthase 3	Homo sapiens	138-142
31052341-1	2019	Resveratrol increases the production of nitric oxide (NO) in endothelial cells by upregulating the expression of endothelial NO synthase (eNOS), stimulating eNOS enzymatic activity, and preventing eNOS uncoupling.	Resveratrol	0-11	nitric oxide synthase 3	Homo sapiens	157-161
31211272-2	2019	The reduction in the concentration of nitric oxide (NO) produced by the catalysis of endothelial nitric oxide synthase (eNOS) is associated with higher blood pressure (BP) levels.	Nitric Oxide	38-50	nitric oxide synthase 3	Homo sapiens	85-118
31052341-1	2019	Resveratrol increases the production of nitric oxide (NO) in endothelial cells by upregulating the expression of endothelial NO synthase (eNOS), stimulating eNOS enzymatic activity, and preventing eNOS uncoupling.	Resveratrol	0-11	nitric oxide synthase 3	Homo sapiens	157-161
31052341-1	2019	Resveratrol increases the production of nitric oxide (NO) in endothelial cells by upregulating the expression of endothelial NO synthase (eNOS), stimulating eNOS enzymatic activity, and preventing eNOS uncoupling.	Nitric Oxide	40-52	nitric oxide synthase 3	Homo sapiens	113-136
31052341-1	2019	Resveratrol increases the production of nitric oxide (NO) in endothelial cells by upregulating the expression of endothelial NO synthase (eNOS), stimulating eNOS enzymatic activity, and preventing eNOS uncoupling.	Nitric Oxide	40-52	nitric oxide synthase 3	Homo sapiens	138-142
31052341-1	2019	Resveratrol increases the production of nitric oxide (NO) in endothelial cells by upregulating the expression of endothelial NO synthase (eNOS), stimulating eNOS enzymatic activity, and preventing eNOS uncoupling.	Nitric Oxide	40-52	nitric oxide synthase 3	Homo sapiens	157-161
31052341-1	2019	Resveratrol increases the production of nitric oxide (NO) in endothelial cells by upregulating the expression of endothelial NO synthase (eNOS), stimulating eNOS enzymatic activity, and preventing eNOS uncoupling.	Nitric Oxide	40-52	nitric oxide synthase 3	Homo sapiens	157-161
31040342-13	2019	Human umbilical vein endothelial cells (HUVECs) treated with dextrin confirmed eNOS uncoupling, as verified by the reduced eNOS dimer/monomer ratio.	Dextrins	61-68	nitric oxide synthase 3	Homo sapiens	79-83
31040342-13	2019	Human umbilical vein endothelial cells (HUVECs) treated with dextrin confirmed eNOS uncoupling, as verified by the reduced eNOS dimer/monomer ratio.	Dextrins	61-68	nitric oxide synthase 3	Homo sapiens	123-127
31040342-14	2019	BH4, L-arginine, or BH4 plus L-arginine inhibited eNOS monomerization.	sapropterin	0-3	nitric oxide synthase 3	Homo sapiens	50-54
31040342-14	2019	BH4, L-arginine, or BH4 plus L-arginine inhibited eNOS monomerization.	Arginine	5-15	nitric oxide synthase 3	Homo sapiens	50-54
31040342-14	2019	BH4, L-arginine, or BH4 plus L-arginine inhibited eNOS monomerization.	sapropterin	20-23	nitric oxide synthase 3	Homo sapiens	50-54
31040342-14	2019	BH4, L-arginine, or BH4 plus L-arginine inhibited eNOS monomerization.	Arginine	29-39	nitric oxide synthase 3	Homo sapiens	50-54
31035633-1	2019	Fluid shear stress stimulates endothelial nitric oxide synthase (eNOS) activation and nitric oxide (NO) production through multiple kinases, including protein kinase A (PKA), AMP-activated protein kinase (AMPK), AKT and Ca2+/calmodulin-dependent protein kinase II (CaMKII).	Nitric Oxide	42-54	nitric oxide synthase 3	Homo sapiens	65-69
31211272-2	2019	The reduction in the concentration of nitric oxide (NO) produced by the catalysis of endothelial nitric oxide synthase (eNOS) is associated with higher blood pressure (BP) levels.	Nitric Oxide	38-50	nitric oxide synthase 3	Homo sapiens	120-124
30987646-6	2019	RESULTS: HMVECs that had reduced eNOS expression had a significantly elevated increase in IL-6, IL-8 and IP-10 production after Poly I:C.	Poly I-C	128-136	nitric oxide synthase 3	Homo sapiens	33-37
30987646-7	2019	In addition, the knockdown of eNOS enhanced the change in TEER after Poly I:C stimulation.	Poly I-C	69-77	nitric oxide synthase 3	Homo sapiens	30-34
30987646-10	2019	The addition of the p38 inhibitor, SB203580, in eNOS knockdown cells reduced both cytokine production after Poly I:C, and as well as mitigated the reduction in TEER, suggesting a direct link between eNOS and p38 in TLR3 signaling.	SB 203580	35-43	nitric oxide synthase 3	Homo sapiens	48-52
30987646-10	2019	The addition of the p38 inhibitor, SB203580, in eNOS knockdown cells reduced both cytokine production after Poly I:C, and as well as mitigated the reduction in TEER, suggesting a direct link between eNOS and p38 in TLR3 signaling.	SB 203580	35-43	nitric oxide synthase 3	Homo sapiens	199-203
30987646-10	2019	The addition of the p38 inhibitor, SB203580, in eNOS knockdown cells reduced both cytokine production after Poly I:C, and as well as mitigated the reduction in TEER, suggesting a direct link between eNOS and p38 in TLR3 signaling.	Poly I-C	108-116	nitric oxide synthase 3	Homo sapiens	48-52
30892883-4	2019	The present work, therefore, aims to evaluate the potential effect of stilbenes on inhibiting VEGF and their subsequent effect on the downstream signaling pathway (PLCgamma1, Akt, and eNOS).	Stilbenes	70-79	nitric oxide synthase 3	Homo sapiens	184-188
30892883-9	2019	However, epsilon-viniferin and pallidol simultaneously enhanced eNOS activation, proving to be via Akt activation in the case of epsilon-viniferin.	epsilon-viniferin	9-26	nitric oxide synthase 3	Homo sapiens	64-68
30892883-9	2019	However, epsilon-viniferin and pallidol simultaneously enhanced eNOS activation, proving to be via Akt activation in the case of epsilon-viniferin.	pallidol	31-39	nitric oxide synthase 3	Homo sapiens	64-68
30892883-11	2019	In addition, epsilon-viniferin and pallidol significantly allowed eNOS activation and could likely prevent the side effects caused by anti-VEGF hypertension drugs.	epsilon-viniferin	13-30	nitric oxide synthase 3	Homo sapiens	66-70
30892883-11	2019	In addition, epsilon-viniferin and pallidol significantly allowed eNOS activation and could likely prevent the side effects caused by anti-VEGF hypertension drugs.	pallidol	35-43	nitric oxide synthase 3	Homo sapiens	66-70
30959907-7	2019	Mechanistic investigations revealed that phomaketide A reduced LECs-induced lymphangiogenesis via vascular endothelial growth factor receptor-3 (VEGFR-3), protein kinase Cdelta (PKCdelta), and endothelial nitric oxide synthase (eNOS) signalings.	Phomaketide A	41-54	nitric oxide synthase 3	Homo sapiens	193-226
30866404-1	2019	Nitric oxide (NO) produced by endothelial nitric oxide synthase (eNOS) plays crucial roles in cardiac homeostasis.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	30-63
30690728-4	2019	Adropin incubation restored age-related endothelial-dependent vasodilatory dysfunction and increased the phosphorylated endothelial nitric oxide synthase (eNOS)/eNOS ratio in an age-dependent manner in the SMFAs.	smfas	206-211	nitric oxide synthase 3	Homo sapiens	120-153
30690728-4	2019	Adropin incubation restored age-related endothelial-dependent vasodilatory dysfunction and increased the phosphorylated endothelial nitric oxide synthase (eNOS)/eNOS ratio in an age-dependent manner in the SMFAs.	smfas	206-211	nitric oxide synthase 3	Homo sapiens	155-159
30738311-2	2019	Recent evidence indicates that S-glutathionylation may occur on the endothelial nitric oxide synthase (eNOS), leading to eNOS uncoupling, characterized by a decreased NO production and an increased generation of superoxide anion (O2 -).	Superoxides	212-228	nitric oxide synthase 3	Homo sapiens	68-101
30738311-2	2019	Recent evidence indicates that S-glutathionylation may occur on the endothelial nitric oxide synthase (eNOS), leading to eNOS uncoupling, characterized by a decreased NO production and an increased generation of superoxide anion (O2 -).	Superoxides	212-228	nitric oxide synthase 3	Homo sapiens	103-107
30738311-2	2019	Recent evidence indicates that S-glutathionylation may occur on the endothelial nitric oxide synthase (eNOS), leading to eNOS uncoupling, characterized by a decreased NO production and an increased generation of superoxide anion (O2 -).	Superoxides	212-228	nitric oxide synthase 3	Homo sapiens	121-125
30738311-2	2019	Recent evidence indicates that S-glutathionylation may occur on the endothelial nitric oxide synthase (eNOS), leading to eNOS uncoupling, characterized by a decreased NO production and an increased generation of superoxide anion (O2 -).	Superoxides	230-232	nitric oxide synthase 3	Homo sapiens	68-101
30738311-2	2019	Recent evidence indicates that S-glutathionylation may occur on the endothelial nitric oxide synthase (eNOS), leading to eNOS uncoupling, characterized by a decreased NO production and an increased generation of superoxide anion (O2 -).	Superoxides	230-232	nitric oxide synthase 3	Homo sapiens	103-107
30738311-2	2019	Recent evidence indicates that S-glutathionylation may occur on the endothelial nitric oxide synthase (eNOS), leading to eNOS uncoupling, characterized by a decreased NO production and an increased generation of superoxide anion (O2 -).	Superoxides	230-232	nitric oxide synthase 3	Homo sapiens	121-125
30738311-5	2019	Immunofluorescence, confocal microscopy and western-blot experiments carried out on eNOS immunoprecipitates, revealed a high level of eNOS glutathionylation in PE placentas, mostly reversed by dithiotreitol (DTT), thus indicative of S-glutathionylation.	Dithiothreitol	193-206	nitric oxide synthase 3	Homo sapiens	134-138
30738311-5	2019	Immunofluorescence, confocal microscopy and western-blot experiments carried out on eNOS immunoprecipitates, revealed a high level of eNOS glutathionylation in PE placentas, mostly reversed by dithiotreitol (DTT), thus indicative of S-glutathionylation.	Dithiothreitol	208-211	nitric oxide synthase 3	Homo sapiens	134-138
30738311-8	2019	In contrast, trophoblasts submitted to low/high pO2 changes, exhibited oxidative stress and a (DTT reversible) S-glutathionylation of eNOS, associated with reduced NO production and migration.	PO-2	48-51	nitric oxide synthase 3	Homo sapiens	134-138
30738311-8	2019	In contrast, trophoblasts submitted to low/high pO2 changes, exhibited oxidative stress and a (DTT reversible) S-glutathionylation of eNOS, associated with reduced NO production and migration.	Dithiothreitol	95-98	nitric oxide synthase 3	Homo sapiens	134-138
30738311-9	2019	The autonomous production of NO seemed necessary for the migratory potential of HTR8, as suggested by the inhibitory effect of eNOS silencing by small interfering RNAs, and the eNOS inhibitor L-NAME, in low pO2 conditions.	NG-Nitroarginine Methyl Ester	192-198	nitric oxide synthase 3	Homo sapiens	177-181
30738311-9	2019	The autonomous production of NO seemed necessary for the migratory potential of HTR8, as suggested by the inhibitory effect of eNOS silencing by small interfering RNAs, and the eNOS inhibitor L-NAME, in low pO2 conditions.	PO-2	207-210	nitric oxide synthase 3	Homo sapiens	127-131
30935162-0	2019	Phytoestrogenic Effects of Blackcurrant Anthocyanins Increased Endothelial Nitric Oxide Synthase (eNOS) Expression in Human Endothelial Cells and Ovariectomized Rats.	Anthocyanins	40-52	nitric oxide synthase 3	Homo sapiens	63-96
30935162-0	2019	Phytoestrogenic Effects of Blackcurrant Anthocyanins Increased Endothelial Nitric Oxide Synthase (eNOS) Expression in Human Endothelial Cells and Ovariectomized Rats.	Anthocyanins	40-52	nitric oxide synthase 3	Homo sapiens	98-102
30935162-5	2019	The results showed that eNOS mRNA levels were significantly upregulated in BCE- or anthocyanin-treated human vascular endothelial cells but decreased in cells treated with fulvestrant, an ER antagonist.	Anthocyanins	83-94	nitric oxide synthase 3	Homo sapiens	24-28
30935162-5	2019	The results showed that eNOS mRNA levels were significantly upregulated in BCE- or anthocyanin-treated human vascular endothelial cells but decreased in cells treated with fulvestrant, an ER antagonist.	Fulvestrant	172-183	nitric oxide synthase 3	Homo sapiens	24-28
30935162-6	2019	These results corresponded with NO levels, suggesting that BCE and anthocyanin may regulate NO synthesis via eNOS expression.	bce	59-62	nitric oxide synthase 3	Homo sapiens	109-113
30935162-6	2019	These results corresponded with NO levels, suggesting that BCE and anthocyanin may regulate NO synthesis via eNOS expression.	Anthocyanins	67-78	nitric oxide synthase 3	Homo sapiens	109-113
30319041-9	2019	Phosphate-buffered saline endothelial nitric oxide synthase staining decreased dramatically throughout the study period.	Phosphate-Buffered Saline	0-25	nitric oxide synthase 3	Homo sapiens	26-59
30272818-10	2019	These effects were associated by an increase in p-Akt/Akt and p-eNOS, and a decrease in cleaved caspase-3 could be abolished by LY294002.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	128-136	nitric oxide synthase 3	Homo sapiens	64-68
30639474-5	2019	Increased phosphorylated eNOS was significantly inhibited by a PI3K inhibitor LY294002 and elevated ICAM-1expression was partially blocked by the inhibitors of both PI3K and eNOS (L-NAME).	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	78-86	nitric oxide synthase 3	Homo sapiens	25-29
30639474-5	2019	Increased phosphorylated eNOS was significantly inhibited by a PI3K inhibitor LY294002 and elevated ICAM-1expression was partially blocked by the inhibitors of both PI3K and eNOS (L-NAME).	NG-Nitroarginine Methyl Ester	180-186	nitric oxide synthase 3	Homo sapiens	25-29
30639474-5	2019	Increased phosphorylated eNOS was significantly inhibited by a PI3K inhibitor LY294002 and elevated ICAM-1expression was partially blocked by the inhibitors of both PI3K and eNOS (L-NAME).	NG-Nitroarginine Methyl Ester	180-186	nitric oxide synthase 3	Homo sapiens	174-178
30641122-17	2019	The presence of a minor allele in G894T polymorphism of the NOS3 gene contributes to formation of oxygen transport function of blood.	Oxygen	98-104	nitric oxide synthase 3	Homo sapiens	60-64
30319041-11	2019	Custodiol and glutaraldehyde better preserved vein morphology compared to ISHA and PBS at day 5 and later (p &lt; 0.001), but compared to stronger isotonic saline with heparin and antibiotic their endothelial nitric oxide synthase staining was weaker.	Custodiol	0-9	nitric oxide synthase 3	Homo sapiens	197-230
30949393-6	2019	Hydrangenol also significantly inhibited VEGFR-2-mediated signaling pathways including ERK1/2, AKT, and endothelial nitric oxide synthase.	hydrangenol	0-11	nitric oxide synthase 3	Homo sapiens	104-137
30764838-5	2019	Phosphorylation of Akt and eNOS, as well as NO production were attenuated and accompanied by an increased expression of caspase 3 when HUVECs were subjected to sodium palmitate, and all these changes were restored by pretreatment with U50,488H, the effects of U50,488H were abolished by nor-BNI, and specific inhibitors to PI3K, Akt, eNOS, respectively.	Palmitic Acid	160-176	nitric oxide synthase 3	Homo sapiens	334-338
30764838-0	2019	kappa-Opioid receptor stimulation reduces palmitate-induced apoptosis via Akt/eNOS signaling pathway.	Palmitates	42-51	nitric oxide synthase 3	Homo sapiens	78-82
30764838-5	2019	Phosphorylation of Akt and eNOS, as well as NO production were attenuated and accompanied by an increased expression of caspase 3 when HUVECs were subjected to sodium palmitate, and all these changes were restored by pretreatment with U50,488H, the effects of U50,488H were abolished by nor-BNI, and specific inhibitors to PI3K, Akt, eNOS, respectively.	488h	239-243	nitric oxide synthase 3	Homo sapiens	334-338
30764838-5	2019	Phosphorylation of Akt and eNOS, as well as NO production were attenuated and accompanied by an increased expression of caspase 3 when HUVECs were subjected to sodium palmitate, and all these changes were restored by pretreatment with U50,488H, the effects of U50,488H were abolished by nor-BNI, and specific inhibitors to PI3K, Akt, eNOS, respectively.	Palmitic Acid	160-176	nitric oxide synthase 3	Homo sapiens	27-31
30764838-8	2019	CONCLUSION: This study provides the evidence for the first time that kappa-OR stimulation possesses anti-palmitate-induced apoptosis effect, which is mediated by PI3K/Akt/eNOS signaling pathway.	Palmitates	105-114	nitric oxide synthase 3	Homo sapiens	171-175
30124781-8	2019	MPShh+ treatment significantly increased the expression of Shh signalling pathway genes (PTCH1, SMO, and GLI1) and masters of pro-angiogenic genes (NOS3, VEGFA, KDR, and KLF2) in EPC.	mpshh+	0-6	nitric oxide synthase 3	Homo sapiens	148-152
30496724-11	2019	CONCLUSIONS: Excessive sENG release with decreased eNOS/NO may be involved in PE pathogenesis.	seng	23-27	nitric oxide synthase 3	Homo sapiens	51-55
30741027-1	2019	OBJECTIVES: Nitric oxide (NO) represents the most powerful endogenous molecule with vasodilator action mainly produced by endothelial nitric oxide synthase (eNOS) enzyme.	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	122-155
32550542-7	2019	Conclusion: T786C polymorphism at eNOS locus appeared to be a major contributor in the variable erectile function iPDE5/testosterone response in Spaniards.	ipde5	114-119	nitric oxide synthase 3	Homo sapiens	34-38
32550542-7	2019	Conclusion: T786C polymorphism at eNOS locus appeared to be a major contributor in the variable erectile function iPDE5/testosterone response in Spaniards.	Testosterone	120-132	nitric oxide synthase 3	Homo sapiens	34-38
30132872-4	2019	NE treatment decreased phospho-Ser633-eNOS and beta2 -adrenergic receptor (beta2 -AR) levels in the membrane of human pulmonary artery endothelial cells (HPAECs) analysed by western blot analysis.	phospho	23-30	nitric oxide synthase 3	Homo sapiens	38-42
30741027-1	2019	OBJECTIVES: Nitric oxide (NO) represents the most powerful endogenous molecule with vasodilator action mainly produced by endothelial nitric oxide synthase (eNOS) enzyme.	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	157-161
30621010-9	2019	We highlight the redox-regulatory mechanisms in eNOS function and up- and down-stream signaling pathways (e.g., tetrahydrobiopterin metabolism and soluble guanylyl cyclase/cGMP pathway) and their potential pharmacological exploitation.	sapropterin	112-131	nitric oxide synthase 3	Homo sapiens	48-52
30525561-7	2019	Moreover, the VEGF-mediated phosphorylations of endothelial nitric oxide synthase, protein kinase B, and extracellular signal-regulated kinase were obviously decreased by (3 +- 0.37)-, (2 +- 0.27)- and (6 +- 0.23)-fold, respectively, in the presence of resveratrol at high concentration.	Resveratrol	253-264	nitric oxide synthase 3	Homo sapiens	48-81
32422021-5	2019	The uncoupling of endothelial NO synthase (eNOS) and increased generation of free radicals in hyperglycemic conditions can also lead to the formation of highly reactive nitrogen species such as peroxynitrite, which can lead to DNA damage, carcinogenic mutations, and activation of critical pathways involved in cell proliferation and apoptosis.	Nitrogen	169-177	nitric oxide synthase 3	Homo sapiens	18-41
30621047-5	2019	The resulting vascular subnetwork demonstrates that ellagic acid, caffeic acid, protocatechuic acid, cryptotanshinone, tanshinone I, and tanshinone IIA are linked to NOS3, ARG2, and EDN1 for vascular dilation, implicated with arginine/proline metabolism.	Ellagic Acid	52-64	nitric oxide synthase 3	Homo sapiens	166-170
30621047-5	2019	The resulting vascular subnetwork demonstrates that ellagic acid, caffeic acid, protocatechuic acid, cryptotanshinone, tanshinone I, and tanshinone IIA are linked to NOS3, ARG2, and EDN1 for vascular dilation, implicated with arginine/proline metabolism.	caffeic acid	66-78	nitric oxide synthase 3	Homo sapiens	166-170
30621047-5	2019	The resulting vascular subnetwork demonstrates that ellagic acid, caffeic acid, protocatechuic acid, cryptotanshinone, tanshinone I, and tanshinone IIA are linked to NOS3, ARG2, and EDN1 for vascular dilation, implicated with arginine/proline metabolism.	protocatechuic acid	80-99	nitric oxide synthase 3	Homo sapiens	166-170
30621047-5	2019	The resulting vascular subnetwork demonstrates that ellagic acid, caffeic acid, protocatechuic acid, cryptotanshinone, tanshinone I, and tanshinone IIA are linked to NOS3, ARG2, and EDN1 for vascular dilation, implicated with arginine/proline metabolism.	cryptotanshinone	101-117	nitric oxide synthase 3	Homo sapiens	166-170
30621047-5	2019	The resulting vascular subnetwork demonstrates that ellagic acid, caffeic acid, protocatechuic acid, cryptotanshinone, tanshinone I, and tanshinone IIA are linked to NOS3, ARG2, and EDN1 for vascular dilation, implicated with arginine/proline metabolism.	tanshinone	107-117	nitric oxide synthase 3	Homo sapiens	166-170
30621047-5	2019	The resulting vascular subnetwork demonstrates that ellagic acid, caffeic acid, protocatechuic acid, cryptotanshinone, tanshinone I, and tanshinone IIA are linked to NOS3, ARG2, and EDN1 for vascular dilation, implicated with arginine/proline metabolism.	tanshinone	119-129	nitric oxide synthase 3	Homo sapiens	166-170
30621047-5	2019	The resulting vascular subnetwork demonstrates that ellagic acid, caffeic acid, protocatechuic acid, cryptotanshinone, tanshinone I, and tanshinone IIA are linked to NOS3, ARG2, and EDN1 for vascular dilation, implicated with arginine/proline metabolism.	Arginine	226-234	nitric oxide synthase 3	Homo sapiens	166-170
30621047-5	2019	The resulting vascular subnetwork demonstrates that ellagic acid, caffeic acid, protocatechuic acid, cryptotanshinone, tanshinone I, and tanshinone IIA are linked to NOS3, ARG2, and EDN1 for vascular dilation, implicated with arginine/proline metabolism.	Proline	235-242	nitric oxide synthase 3	Homo sapiens	166-170
30800248-1	2019	Background: Nitric Oxide (NO) which is synthesized by endothelial Nitric Oxide Synthase (eNOS) in both vascular tissues and platelets plays an important role as a protective mediator in the cardiovascular system.	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	54-87
29999409-5	2019	Zn ions are required for the dimerization of endothelial nitric oxide synthase and subsequent generation of NO while generation of NO leads to a rapid mobilization of endothelial Zn stores.	Zinc	0-2	nitric oxide synthase 3	Homo sapiens	45-78
30289292-3	2019	However, low-temperature SDS-PAGE of healthy arteries has revealed considerable variation between studies in the relative expression of eNOS dimers and monomers.	Sodium Dodecyl Sulfate	25-28	nitric oxide synthase 3	Homo sapiens	136-140
30289292-13	2019	NEW &amp; NOTEWORTHY Structural uncoupling of endothelial nitric oxide synthase (eNOS) is considered central to endothelial dysfunction.	Adenosine Monophosphate	5-8	nitric oxide synthase 3	Homo sapiens	46-79
30289292-13	2019	NEW &amp; NOTEWORTHY Structural uncoupling of endothelial nitric oxide synthase (eNOS) is considered central to endothelial dysfunction.	Adenosine Monophosphate	5-8	nitric oxide synthase 3	Homo sapiens	81-85
30627907-4	2019	In human choriocarcinoma cells BeWo b30 (trophoblast model), oxyquinoline increased the expression of a core hypoxia response genes along with up-regulation of NOS3, PDK1, and BNIP3 genes and down-regulation of the PPARGC1B gene.	Oxyquinoline	61-73	nitric oxide synthase 3	Homo sapiens	160-164
32422021-5	2019	The uncoupling of endothelial NO synthase (eNOS) and increased generation of free radicals in hyperglycemic conditions can also lead to the formation of highly reactive nitrogen species such as peroxynitrite, which can lead to DNA damage, carcinogenic mutations, and activation of critical pathways involved in cell proliferation and apoptosis.	Nitrogen	169-177	nitric oxide synthase 3	Homo sapiens	43-47
32422021-5	2019	The uncoupling of endothelial NO synthase (eNOS) and increased generation of free radicals in hyperglycemic conditions can also lead to the formation of highly reactive nitrogen species such as peroxynitrite, which can lead to DNA damage, carcinogenic mutations, and activation of critical pathways involved in cell proliferation and apoptosis.	Peroxynitrous Acid	194-207	nitric oxide synthase 3	Homo sapiens	18-41
32422021-5	2019	The uncoupling of endothelial NO synthase (eNOS) and increased generation of free radicals in hyperglycemic conditions can also lead to the formation of highly reactive nitrogen species such as peroxynitrite, which can lead to DNA damage, carcinogenic mutations, and activation of critical pathways involved in cell proliferation and apoptosis.	Peroxynitrous Acid	194-207	nitric oxide synthase 3	Homo sapiens	43-47
30256050-1	2018	Competitive inhibition of endothelial nitric oxide synthase (eNOS) is the main biological effect of asymmetric dimethylarginine (ADMA), i.e. the methylated derivative of L-arginine.	dimethylarginine	111-127	nitric oxide synthase 3	Homo sapiens	26-59
30380512-7	2018	Osthole increased nitric oxide (NO) production and endothelial nitric oxide synthase (eNOS) phosphorylation in ox-LDL-treated HUVECs.	osthol	0-7	nitric oxide synthase 3	Homo sapiens	51-84
30256050-1	2018	Competitive inhibition of endothelial nitric oxide synthase (eNOS) is the main biological effect of asymmetric dimethylarginine (ADMA), i.e. the methylated derivative of L-arginine.	N,N-dimethylarginine	129-133	nitric oxide synthase 3	Homo sapiens	26-59
30256050-1	2018	Competitive inhibition of endothelial nitric oxide synthase (eNOS) is the main biological effect of asymmetric dimethylarginine (ADMA), i.e. the methylated derivative of L-arginine.	Arginine	170-180	nitric oxide synthase 3	Homo sapiens	26-59
30300735-10	2018	The study for the first time revealed that in the human blood vessels (IMA) the clinically-relevant high concentration of Hcy directly causes endothelial dysfunction by downregulating eNOS protein that may be reversed by AVE3085.	Homocysteine	122-125	nitric oxide synthase 3	Homo sapiens	184-188
30300735-0	2018	Endothelial nitric oxide synthase enhancer AVE3085 reverses endothelial dysfunction induced by homocysteine in human internal mammary arteries.	Homocysteine	95-107	nitric oxide synthase 3	Homo sapiens	0-33
30398085-1	2018	Endothelial nitric oxide synthase (NOS3) is a key enzyme responsible for nitric oxide (NO) generation in the vascular endothelium.	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	35-39
30300735-8	2018	Exposure to Hcy for 24 h downregulated eNOS protein expression (P &lt; 0.05) whereas it upregulated the expression of eNOS at mRNA levels (P &lt; 0.05).	Homocysteine	12-15	nitric oxide synthase 3	Homo sapiens	39-43
30300735-8	2018	Exposure to Hcy for 24 h downregulated eNOS protein expression (P &lt; 0.05) whereas it upregulated the expression of eNOS at mRNA levels (P &lt; 0.05).	Homocysteine	12-15	nitric oxide synthase 3	Homo sapiens	118-122
30582863-1	2018	OBJECTIVE: To determine the features of the nitrogen oxide metabolism and risk of developing endothelial dysfunc-tion in children with e-NOS 4a/4b gene polymorphism, who live under prolonged enter 137Cs to the body.	Nitrogen Oxides	44-58	nitric oxide synthase 3	Homo sapiens	135-140
29739298-11	2018	CONCLUSIONS: Overall, our data may suggest that polymorphism analysis of the VEGF, VEGFR-2, HIF and eNOS genes can identify HCC patients who are more likely to benefit from sorafenib.	Sorafenib	173-182	nitric oxide synthase 3	Homo sapiens	100-104
30342074-5	2018	Diabetes or hypertension-mediated endothelial dysfunction show characteristics such as reduced nitric oxide synthesis through suppression of endothelial nitric oxide synthase activity in endothelial cells, reduced sensitivity of nitric oxide in smooth muscle cells, and inflammation - all of which have been either shown to be directly caused by gene regulatory mechanisms of non-coding RNAs or shown to be having a correlation with them.	Nitric Oxide	95-107	nitric oxide synthase 3	Homo sapiens	141-174
29969842-12	2018	The eNOS activity was 52.0 +- 20.6 pmol l-citrulline/min/106 ECs in nonsmokers and 48.7 +- 19.8 pmol l-citrulline/min/106 ECs in environmental smokers.	Citrulline	40-52	nitric oxide synthase 3	Homo sapiens	4-8
30335983-6	2018	As with many of the aminopyridine inhibitors, a critical active site Asp residue in nNOS versus Asn in eNOS is largely responsible for controlling selectivity.	Aminopyridines	20-33	nitric oxide synthase 3	Homo sapiens	103-107
30335983-6	2018	As with many of the aminopyridine inhibitors, a critical active site Asp residue in nNOS versus Asn in eNOS is largely responsible for controlling selectivity.	Aspartic Acid	69-72	nitric oxide synthase 3	Homo sapiens	103-107
30335983-6	2018	As with many of the aminopyridine inhibitors, a critical active site Asp residue in nNOS versus Asn in eNOS is largely responsible for controlling selectivity.	Asparagine	96-99	nitric oxide synthase 3	Homo sapiens	103-107
30398206-3	2018	The bond lengths in the central CNOS unit are 1.3444 (19), 1.3556 (18) and 1.6567 (15) A for C-N, C-O and C-S, respectively, and the CNOS and C3N moieties are flat and nearly coplanar with each other, consistent with the C-N bond possessing partial double-bond character.	Carbon	32-33	nitric oxide synthase 3	Homo sapiens	133-137
30398206-3	2018	The bond lengths in the central CNOS unit are 1.3444 (19), 1.3556 (18) and 1.6567 (15) A for C-N, C-O and C-S, respectively, and the CNOS and C3N moieties are flat and nearly coplanar with each other, consistent with the C-N bond possessing partial double-bond character.	Nitrogen	33-34	nitric oxide synthase 3	Homo sapiens	133-137
30398206-3	2018	The bond lengths in the central CNOS unit are 1.3444 (19), 1.3556 (18) and 1.6567 (15) A for C-N, C-O and C-S, respectively, and the CNOS and C3N moieties are flat and nearly coplanar with each other, consistent with the C-N bond possessing partial double-bond character.	Carbon	93-94	nitric oxide synthase 3	Homo sapiens	32-36
29969842-12	2018	The eNOS activity was 52.0 +- 20.6 pmol l-citrulline/min/106 ECs in nonsmokers and 48.7 +- 19.8 pmol l-citrulline/min/106 ECs in environmental smokers.	Citrulline	101-113	nitric oxide synthase 3	Homo sapiens	4-8
30398206-3	2018	The bond lengths in the central CNOS unit are 1.3444 (19), 1.3556 (18) and 1.6567 (15) A for C-N, C-O and C-S, respectively, and the CNOS and C3N moieties are flat and nearly coplanar with each other, consistent with the C-N bond possessing partial double-bond character.	Carbon	93-94	nitric oxide synthase 3	Homo sapiens	32-36
30398206-3	2018	The bond lengths in the central CNOS unit are 1.3444 (19), 1.3556 (18) and 1.6567 (15) A for C-N, C-O and C-S, respectively, and the CNOS and C3N moieties are flat and nearly coplanar with each other, consistent with the C-N bond possessing partial double-bond character.	Sulfur	35-36	nitric oxide synthase 3	Homo sapiens	133-137
30168731-11	2018	These data suggest that 4 wk of sildenafil treatment can improve vascular endothelial function in patients with CF, likely through an increase in NOS3 phosphorylation.	Sildenafil Citrate	32-42	nitric oxide synthase 3	Homo sapiens	146-150
30398206-3	2018	The bond lengths in the central CNOS unit are 1.3444 (19), 1.3556 (18) and 1.6567 (15) A for C-N, C-O and C-S, respectively, and the CNOS and C3N moieties are flat and nearly coplanar with each other, consistent with the C-N bond possessing partial double-bond character.	c3n	142-145	nitric oxide synthase 3	Homo sapiens	32-36
30398206-3	2018	The bond lengths in the central CNOS unit are 1.3444 (19), 1.3556 (18) and 1.6567 (15) A for C-N, C-O and C-S, respectively, and the CNOS and C3N moieties are flat and nearly coplanar with each other, consistent with the C-N bond possessing partial double-bond character.	Carbon	93-94	nitric oxide synthase 3	Homo sapiens	32-36
30398206-3	2018	The bond lengths in the central CNOS unit are 1.3444 (19), 1.3556 (18) and 1.6567 (15) A for C-N, C-O and C-S, respectively, and the CNOS and C3N moieties are flat and nearly coplanar with each other, consistent with the C-N bond possessing partial double-bond character.	Nitrogen	95-96	nitric oxide synthase 3	Homo sapiens	32-36
30168731-12	2018	NEW &amp; NOTEWORTHY Findings from the present study demonstrate, for the first time, significant improvement of endothelial function in patients with cystic fibrosis treated with sildenafil that is associated with greater phosphorylation of endothelial nitric oxide synthase.	Sildenafil Citrate	180-190	nitric oxide synthase 3	Homo sapiens	242-275
29737439-10	2018	Taken together, the data establish miR-200b-eNOS regulation as a first hypoxamiR-based mechanism that limits NO bioavailability during hypoxia in endothelial cells, and show that hypoxamiRs could become useful therapeutic targets for cardiovascular diseases and other hypoxic-related diseases including various types of cancer.	hypoxamir	71-80	nitric oxide synthase 3	Homo sapiens	44-48
30217444-2	2018	As we have previously reported, ALDH2 mediates acute ethanol-induced eNOS activation in vitro.	Ethanol	53-60	nitric oxide synthase 3	Homo sapiens	69-73
29737439-10	2018	Taken together, the data establish miR-200b-eNOS regulation as a first hypoxamiR-based mechanism that limits NO bioavailability during hypoxia in endothelial cells, and show that hypoxamiRs could become useful therapeutic targets for cardiovascular diseases and other hypoxic-related diseases including various types of cancer.	hypoxamirs	179-189	nitric oxide synthase 3	Homo sapiens	44-48
30335638-6	2018	BCA-5 decreased the phosphorylation of Akt and endothelial nitric oxide synthase; it also reduced the expression of hypoxia-inducible factor-1alpha and vascular endothelial cell growth factor in a dose-dependent manner.	bca-5	0-5	nitric oxide synthase 3	Homo sapiens	47-80
30185927-8	2018	Using Western blot analysis, we observed that uric acid reduced endothelial nitric oxide synthase phosphorylation during hypoxic conditions.	Uric Acid	46-55	nitric oxide synthase 3	Homo sapiens	64-97
30081213-0	2018	A novel role of sONE/NOS3/NO signaling cascade in mediating hydrogen sulphide bilateral effects on triple negative breast cancer progression.	Hydrogen Sulfide	60-77	nitric oxide synthase 3	Homo sapiens	21-25
30081213-9	2018	Such intricate cross-talk was found to be orchestrated by the novel lncRNA, sONE and its down-stream target NOS3 building up a novel axis, sONE/NOS3/NO, that was shown to play a pivotal role in plotting the bilateral effect of H2S on TNBC progression.	Hydrogen Sulfide	227-230	nitric oxide synthase 3	Homo sapiens	108-112
30081213-9	2018	Such intricate cross-talk was found to be orchestrated by the novel lncRNA, sONE and its down-stream target NOS3 building up a novel axis, sONE/NOS3/NO, that was shown to play a pivotal role in plotting the bilateral effect of H2S on TNBC progression.	Hydrogen Sulfide	227-230	nitric oxide synthase 3	Homo sapiens	144-148
30081213-12	2018	In conclusion, this study provides an insight about the role of exogenous H2S in TNBC cell lines highlighting a novel crosstalk between H2S and NO orchestrated by sONE/NOS3 axis.	Hydrogen Sulfide	74-77	nitric oxide synthase 3	Homo sapiens	168-172
30081213-12	2018	In conclusion, this study provides an insight about the role of exogenous H2S in TNBC cell lines highlighting a novel crosstalk between H2S and NO orchestrated by sONE/NOS3 axis.	Hydrogen Sulfide	136-139	nitric oxide synthase 3	Homo sapiens	168-172
30335864-0	2018	Association of endothelial nitric oxide synthase (eNOS) gene polymorphisms and physical fitness levels with plasma nitrite concentrations and arterial blood pressure values in older adults.	Nitrites	115-122	nitric oxide synthase 3	Homo sapiens	15-48
30335864-1	2018	Endothelial nitric oxide synthase (eNOS) gene polymorphisms are associated with reduced eNOS activity and nitric oxide (NO) production leading to an increase in blood pressure (BP).	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	35-39
30335864-1	2018	Endothelial nitric oxide synthase (eNOS) gene polymorphisms are associated with reduced eNOS activity and nitric oxide (NO) production leading to an increase in blood pressure (BP).	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	88-92
30335864-5	2018	Thus, this study aimed to investigate the association of eNOS gene haplotypes and different levels of TS on nitrite concentrations (NO2-) and BP values in older adult.	Nitrites	108-115	nitric oxide synthase 3	Homo sapiens	57-61
30217444-4	2018	Here, we show that appropriate dose of ethanol preserved the expression and activity of ALDH2 and eNOS, and alleviated senescence-associated phenotypes in human aortic endothelial cells.	Ethanol	39-46	nitric oxide synthase 3	Homo sapiens	98-102
30119249-0	2018	The protective effects of a novel synthetic beta-elemene derivative on human umbilical vein endothelial cells against oxidative stress-induced injury: Involvement of antioxidation and PI3k/Akt/eNOS/NO signaling pathways.	beta-elemene	44-56	nitric oxide synthase 3	Homo sapiens	193-197
30119249-8	2018	Moreover, we found that H2O2 decreased Akt and eNOS phosphorylation, which perhaps, indirectly reduced nitric oxide (NO) production.	Hydrogen Peroxide	24-28	nitric oxide synthase 3	Homo sapiens	47-51
30119249-8	2018	Moreover, we found that H2O2 decreased Akt and eNOS phosphorylation, which perhaps, indirectly reduced nitric oxide (NO) production.	Nitric Oxide	103-115	nitric oxide synthase 3	Homo sapiens	47-51
30119249-10	2018	BEG effects were inhibited by a PI3K inhibitor (wortmannin) and eNOS inhibitor (L-NAME).	NG-Nitroarginine Methyl Ester	80-86	nitric oxide synthase 3	Homo sapiens	64-68
30119249-12	2018	Furthermore, BEG reduced H2O2-induced endothelial cells injury by the involvement of antioxidation and PI3K/Akt/eNOS/NO signaling pathways.	Hydrogen Peroxide	25-29	nitric oxide synthase 3	Homo sapiens	112-116
29705218-9	2018	BH4 increased (P = .013) the ratio of phospho-NOS3 to total NOS3 protein.	sapropterin	0-3	nitric oxide synthase 3	Homo sapiens	46-50
29435831-5	2018	The p-eNOS/eNOS ratios dropped clearly in NaF and NaF + HIS groups, while that in the NaF + HIS group was distinctly higher than that in the NaF group.	Histamine	56-59	nitric oxide synthase 3	Homo sapiens	6-10
29435831-5	2018	The p-eNOS/eNOS ratios dropped clearly in NaF and NaF + HIS groups, while that in the NaF + HIS group was distinctly higher than that in the NaF group.	Histamine	56-59	nitric oxide synthase 3	Homo sapiens	11-15
29435831-8	2018	The PI3K/AKT/eNOS pathway played a crucial role in the reduced expression of NO caused by excessive fluoride exposure.	Fluorides	100-108	nitric oxide synthase 3	Homo sapiens	13-17
29948755-0	2018	microRNAs regulate nitric oxide release from endothelial cells by targeting NOS3.	Nitric Oxide	19-31	nitric oxide synthase 3	Homo sapiens	76-80
29948755-1	2018	Endothelial nitric oxide synthase (eNOS) encoded by nitric oxide synthase 3 (NOS3), can generate nitric oxide (NO) which serves as an important deterrent to the pathogenesis of thrombosis by modulating the activation, adhesion and aggregate formation of platelets.	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	52-75
29948755-1	2018	Endothelial nitric oxide synthase (eNOS) encoded by nitric oxide synthase 3 (NOS3), can generate nitric oxide (NO) which serves as an important deterrent to the pathogenesis of thrombosis by modulating the activation, adhesion and aggregate formation of platelets.	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	77-81
29705218-9	2018	BH4 increased (P = .013) the ratio of phospho-NOS3 to total NOS3 protein.	sapropterin	0-3	nitric oxide synthase 3	Homo sapiens	60-64
29992759-5	2018	Kallistatin reversed H2 O2 -mediated inhibition of endothelial nitric oxide synthase (eNOS), SIRT1, catalase and superoxide dismutase (SOD)-2 expression, and kallistatin alone stimulated the synthesis of these antioxidant enzymes.	Hydrogen Peroxide	21-26	nitric oxide synthase 3	Homo sapiens	86-90
29702252-8	2018	The mechanism of inhibition of SGLT-1 was secondary to diminished affinity of the co-transporter for glucose in NOS3 silenced cells.	Glucose	101-108	nitric oxide synthase 3	Homo sapiens	112-116
29932969-2	2018	Endothelial nitric oxide synthase (eNOS) was reported to modulate carcinogenesis and progression through nitric oxide (NO) production.	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	35-39
30135282-9	2018	The data obtained suggest that if the oxygen supply of the organism is impaired, the endothelial nitric oxide synthase G894T polymorphism may be important for the oxidative stress development.	Oxygen	38-44	nitric oxide synthase 3	Homo sapiens	85-118
30053839-6	2018	RESULTS: Our results showed a positive correlation between G894 T eNOS distribution and Alcohol and Obesity rik factors (P = 0.009 and 0.02 respectively).	Alcohols	88-95	nitric oxide synthase 3	Homo sapiens	66-70
30048241-5	2018	Mechanistically, overexpression of HO-1 enhanced the interaction between HO-1 and endothelial nitric oxide synthase (eNOS), and promoted the interaction between eNOS and its upstream kinase Akt, thus resulting in an enhancement of eNOS phosphorylation at Ser1177 and a subsequent increase of nitric oxide (NO) production.	Nitric Oxide	94-106	nitric oxide synthase 3	Homo sapiens	117-121
30048241-5	2018	Mechanistically, overexpression of HO-1 enhanced the interaction between HO-1 and endothelial nitric oxide synthase (eNOS), and promoted the interaction between eNOS and its upstream kinase Akt, thus resulting in an enhancement of eNOS phosphorylation at Ser1177 and a subsequent increase of nitric oxide (NO) production.	Nitric Oxide	94-106	nitric oxide synthase 3	Homo sapiens	161-165
30048241-5	2018	Mechanistically, overexpression of HO-1 enhanced the interaction between HO-1 and endothelial nitric oxide synthase (eNOS), and promoted the interaction between eNOS and its upstream kinase Akt, thus resulting in an enhancement of eNOS phosphorylation at Ser1177 and a subsequent increase of nitric oxide (NO) production.	Nitric Oxide	94-106	nitric oxide synthase 3	Homo sapiens	161-165
30048241-6	2018	Moreover, HO-1 induction prevented the decrease of eNOS dimer/monomer ratio stimulated by H2O2 via its antioxidant properties.	Hydrogen Peroxide	90-94	nitric oxide synthase 3	Homo sapiens	51-55
29967172-3	2018	The unique expression and activation of the endothelial nitric oxide (eNOS) signaling pathway in these cells and their intimate connections with blood vessels indicate that these neurons exert direct neurovascular coupling.	Nitric Oxide	56-68	nitric oxide synthase 3	Homo sapiens	70-74
29967172-4	2018	Production of nitric oxide (NO) within eNOS-positive NGC neurons increases after environmental perturbations, indicating a role for eNOS/NO in modulating environmentally appropriate levels of GA. Inhibition of NO production causes dysregulated behavioral arousal after exposure to environmental perturbation.	Nitric Oxide	14-26	nitric oxide synthase 3	Homo sapiens	39-43
29985945-1	2018	Ferrochelatase (FECH) is an enzyme necessary for heme synthesis, which is essential for maintaining normal functions of endothelial nitric oxide synthase (eNOS) and soluble guanylyl cyclase (sGC).	Heme	49-53	nitric oxide synthase 3	Homo sapiens	120-153
29995907-0	2018	Propofol prevents human umbilical vein endothelial cell injury from Ang II-induced apoptosis by activating the ACE2-(1-7)-Mas axis and eNOS phosphorylation.	Propofol	0-8	nitric oxide synthase 3	Homo sapiens	135-139
29995907-7	2018	In conclusion, our study revealed that propofol can inhibit endothelial cell apoptosis induced by Ang II by activating the ACE2-Ang (1-7)-Mas axis and further up-regulating the expression and phosphorylation of eNOS.	Propofol	39-47	nitric oxide synthase 3	Homo sapiens	211-215
29985945-8	2018	Moreover, ACh-induced relaxation and ACh-stimulated release of NO were significant reduced, associated with suppression of eNOS protein expression in NMPP-treated groups.	Acetylcholine	10-13	nitric oxide synthase 3	Homo sapiens	123-127
29985945-8	2018	Moreover, ACh-induced relaxation and ACh-stimulated release of NO were significant reduced, associated with suppression of eNOS protein expression in NMPP-treated groups.	Acetylcholine	37-40	nitric oxide synthase 3	Homo sapiens	123-127
29985945-1	2018	Ferrochelatase (FECH) is an enzyme necessary for heme synthesis, which is essential for maintaining normal functions of endothelial nitric oxide synthase (eNOS) and soluble guanylyl cyclase (sGC).	Heme	49-53	nitric oxide synthase 3	Homo sapiens	155-159
29985945-8	2018	Moreover, ACh-induced relaxation and ACh-stimulated release of NO were significant reduced, associated with suppression of eNOS protein expression in NMPP-treated groups.	N-methylprotoporphyrin IX	150-154	nitric oxide synthase 3	Homo sapiens	123-127
29985945-11	2018	In conclusion, deletion of vascular heme production via inhibiting FECH elicits downregulation of eNOS and sGC expression, leading to an impaired NO-mediated relaxation in an oxidative stress-independent manner.	Heme	36-40	nitric oxide synthase 3	Homo sapiens	98-102
29985945-2	2018	We tested the hypothesis that inhibition of vascular FECH to attenuate heme synthesis downregulates eNOS and sGC expression, resulting in impaired NO/cGMP-dependent relaxation.	Heme	71-75	nitric oxide synthase 3	Homo sapiens	100-104
29735634-8	2018	PDE5 and endothelial nitric oxide synthase activity were altered with sildenafil but not tadalafil.	Sildenafil Citrate	70-80	nitric oxide synthase 3	Homo sapiens	9-42
29566307-14	2018	Bilobalide concentration-dependently enhanced the eNOS Ser-1177 phosphorylation and Thr-495 dephosphorylation in activated OECs.	bilobalide	0-10	nitric oxide synthase 3	Homo sapiens	50-54
29566307-14	2018	Bilobalide concentration-dependently enhanced the eNOS Ser-1177 phosphorylation and Thr-495 dephosphorylation in activated OECs.	Serine	55-58	nitric oxide synthase 3	Homo sapiens	50-54
29845232-4	2018	A luciferase reporter assay performed to investigate the regulatory association between miR-24 and NOS3 revealed that miR-24 bound to the NOS3 3" untranslated region and inhibited NOS3 expression.	mir-24	88-94	nitric oxide synthase 3	Homo sapiens	99-103
29845232-4	2018	A luciferase reporter assay performed to investigate the regulatory association between miR-24 and NOS3 revealed that miR-24 bound to the NOS3 3" untranslated region and inhibited NOS3 expression.	mir-24	88-94	nitric oxide synthase 3	Homo sapiens	138-142
29845232-4	2018	A luciferase reporter assay performed to investigate the regulatory association between miR-24 and NOS3 revealed that miR-24 bound to the NOS3 3" untranslated region and inhibited NOS3 expression.	mir-24	88-94	nitric oxide synthase 3	Homo sapiens	138-142
29845232-4	2018	A luciferase reporter assay performed to investigate the regulatory association between miR-24 and NOS3 revealed that miR-24 bound to the NOS3 3" untranslated region and inhibited NOS3 expression.	mir-24	118-124	nitric oxide synthase 3	Homo sapiens	99-103
29845232-4	2018	A luciferase reporter assay performed to investigate the regulatory association between miR-24 and NOS3 revealed that miR-24 bound to the NOS3 3" untranslated region and inhibited NOS3 expression.	mir-24	118-124	nitric oxide synthase 3	Homo sapiens	138-142
29845232-4	2018	A luciferase reporter assay performed to investigate the regulatory association between miR-24 and NOS3 revealed that miR-24 bound to the NOS3 3" untranslated region and inhibited NOS3 expression.	mir-24	118-124	nitric oxide synthase 3	Homo sapiens	138-142
29845232-7	2018	Vascular smooth muscle cells (VSMCs) transfected with an miR-24 inhibitor exhibited increased expression levels of NOS3, whereas those transfected with an miR-24 mimic or NOS3 small interfering RNA exhibited reduced expression levels of NOS3, compared with the control.	mir-24	57-63	nitric oxide synthase 3	Homo sapiens	115-119
29845232-8	2018	These results indicated a negative regulatory association between miR-24 and NOS3.	mir-24	66-72	nitric oxide synthase 3	Homo sapiens	77-81
29845232-9	2018	Downregulation of NOS3 may induce vasospasm following SAH, which may be due to the upregualtion of miR-24 in VSMCs.	mir-24	99-105	nitric oxide synthase 3	Homo sapiens	18-22
29845232-9	2018	Downregulation of NOS3 may induce vasospasm following SAH, which may be due to the upregualtion of miR-24 in VSMCs.	vsmcs	109-114	nitric oxide synthase 3	Homo sapiens	18-22
29804448-6	2018	Among the NCG-associated amino acids, arginine and glutamine, markedly increased PGRMC1 and eNOS expression in porcine trophectoderm cells ( P &lt; 0.05), whereas glutamate could stimulate the expression of vimentin and lamin A/C in porcine trophectoderm (pTr) cells ( P &lt; 0.05) and proline stimulated lamin A/C expression ( P &lt; 0.05).	Arginine	38-46	nitric oxide synthase 3	Homo sapiens	92-96
29804448-6	2018	Among the NCG-associated amino acids, arginine and glutamine, markedly increased PGRMC1 and eNOS expression in porcine trophectoderm cells ( P &lt; 0.05), whereas glutamate could stimulate the expression of vimentin and lamin A/C in porcine trophectoderm (pTr) cells ( P &lt; 0.05) and proline stimulated lamin A/C expression ( P &lt; 0.05).	Glutamine	51-60	nitric oxide synthase 3	Homo sapiens	92-96
29618412-2	2018	Nitric oxide, which is synthesized in the intestine by endothelial nitric oxide synthase (eNOS), acts as a potent vasodilator and antioxidant within the mesentery and may play a role in prevention of NEC.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	55-88
29603822-0	2018	Manganese-Based Nanozymes: Multienzyme Redox Activity and Effect on the Nitric Oxide Produced by Endothelial Nitric Oxide Synthase.	Manganese	0-9	nitric oxide synthase 3	Homo sapiens	97-130
29603822-0	2018	Manganese-Based Nanozymes: Multienzyme Redox Activity and Effect on the Nitric Oxide Produced by Endothelial Nitric Oxide Synthase.	Nitric Oxide	72-84	nitric oxide synthase 3	Homo sapiens	97-130
29524646-0	2018	Cigarette smoke constituents cause endothelial nitric oxide synthase dysfunction and uncoupling due to depletion of tetrahydrobiopterin with degradation of GTP cyclohydrolase.	sapropterin	116-135	nitric oxide synthase 3	Homo sapiens	35-68
29566572-1	2018	OBJECTIVE: Tetrahydrobiopterin (BH4) is the essential cofactor of endothelial nitric oxide synthase (eNOS) and intracellular levels of BH4 is regulated by oxidative stress.	sapropterin	11-30	nitric oxide synthase 3	Homo sapiens	66-99
29573704-5	2018	Treatment of human aortic endothelial cells with hippurate reduced the expression of endothelial nitric oxide synthase (eNOS) and increased the expression of intercellular cell adhesion molecule-1 (ICAM-1) and von Willebrand factor (vWF).	hippuric acid	49-58	nitric oxide synthase 3	Homo sapiens	85-118
29566572-1	2018	OBJECTIVE: Tetrahydrobiopterin (BH4) is the essential cofactor of endothelial nitric oxide synthase (eNOS) and intracellular levels of BH4 is regulated by oxidative stress.	sapropterin	32-35	nitric oxide synthase 3	Homo sapiens	66-99
29514045-4	2018	In this study, DNA methyltransferase inhibitor, 5-aza-2"-deoxycytidine (5-aza-dC) significantly elevated the endothelial markers expression (CD31/PECAM1, CD105/ENG, eNOS and VE-cadherin), as well as promoted the capacity of angiogenesis on Matrigel.	Decitabine	48-70	nitric oxide synthase 3	Homo sapiens	165-169
29514045-4	2018	In this study, DNA methyltransferase inhibitor, 5-aza-2"-deoxycytidine (5-aza-dC) significantly elevated the endothelial markers expression (CD31/PECAM1, CD105/ENG, eNOS and VE-cadherin), as well as promoted the capacity of angiogenesis on Matrigel.	Decitabine	72-80	nitric oxide synthase 3	Homo sapiens	165-169
29766980-0	2018	Ripasudil Attenuates Lipopolysaccharide (LPS)-Mediated Apoptosis and Inflammation in Pulmonary Microvascular Endothelial Cells via ROCK2/eNOS Signaling.	K-115	0-9	nitric oxide synthase 3	Homo sapiens	137-141
29766980-6	2018	Several cells were also co-administrated with the endothelial nitric oxide synthase (eNOS) inhibitor Nomega-Nitro-L-arginine methyl ester hydrochloride (L-NAME).	L-NAME hydrochloride	101-151	nitric oxide synthase 3	Homo sapiens	50-83
29766980-6	2018	Several cells were also co-administrated with the endothelial nitric oxide synthase (eNOS) inhibitor Nomega-Nitro-L-arginine methyl ester hydrochloride (L-NAME).	L-NAME hydrochloride	101-151	nitric oxide synthase 3	Homo sapiens	85-89
29766980-6	2018	Several cells were also co-administrated with the endothelial nitric oxide synthase (eNOS) inhibitor Nomega-Nitro-L-arginine methyl ester hydrochloride (L-NAME).	NG-Nitroarginine Methyl Ester	153-159	nitric oxide synthase 3	Homo sapiens	50-83
29766980-6	2018	Several cells were also co-administrated with the endothelial nitric oxide synthase (eNOS) inhibitor Nomega-Nitro-L-arginine methyl ester hydrochloride (L-NAME).	NG-Nitroarginine Methyl Ester	153-159	nitric oxide synthase 3	Homo sapiens	85-89
29766980-12	2018	Ripasudil suppressed ROCK2 activity and further increased the eNOS activity.	K-115	0-9	nitric oxide synthase 3	Homo sapiens	62-66
29766980-13	2018	Ripasudil treatment increased the phosphorylation of eNOS, increased the expression level of Bcl2, and decreased the expression level of active caspase3 in LPS-treated PMVECs.	K-115	0-9	nitric oxide synthase 3	Homo sapiens	53-57
29766980-16	2018	CONCLUSIONS The novel ROCK2 inhibitor ripasudil suppressed LPS-induced apoptosis and inflammation in PMVECs by regulating the ROCK2/eNOS signaling pathway.	K-115	38-47	nitric oxide synthase 3	Homo sapiens	132-136
29466710-1	2018	Uncoupled endothelial nitric oxide synthase (eNOS) produces O2- instead of nitric oxide (NO).	Nitric Oxide	22-34	nitric oxide synthase 3	Homo sapiens	45-49
29563255-5	2018	Upon addition of the Ca2+ ionophore A23187 to activate eNOS, we observed eNOS Ser1177 phosphorylation, its translocation to beta-catenin-positive cell-cell junctions, and increased colocalization of eNOS and Cav-1 within 5 min.	Calcimycin	36-42	nitric oxide synthase 3	Homo sapiens	55-59
29563255-5	2018	Upon addition of the Ca2+ ionophore A23187 to activate eNOS, we observed eNOS Ser1177 phosphorylation, its translocation to beta-catenin-positive cell-cell junctions, and increased colocalization of eNOS and Cav-1 within 5 min.	Calcimycin	36-42	nitric oxide synthase 3	Homo sapiens	73-77
29563255-5	2018	Upon addition of the Ca2+ ionophore A23187 to activate eNOS, we observed eNOS Ser1177 phosphorylation, its translocation to beta-catenin-positive cell-cell junctions, and increased colocalization of eNOS and Cav-1 within 5 min.	Calcimycin	36-42	nitric oxide synthase 3	Homo sapiens	73-77
29563255-6	2018	We also observed Cav-1 S-nitrosylation and destabilization of Cav-1 oligomers in cells treated with A23187 as well as insulin or albumin, and this could be blocked by L-NAME, PP2, or eNOS siRNA.	Calcimycin	100-106	nitric oxide synthase 3	Homo sapiens	183-187
29466710-1	2018	Uncoupled endothelial nitric oxide synthase (eNOS) produces O2- instead of nitric oxide (NO).	Oxygen	60-62	nitric oxide synthase 3	Homo sapiens	10-43
29466710-1	2018	Uncoupled endothelial nitric oxide synthase (eNOS) produces O2- instead of nitric oxide (NO).	Oxygen	60-62	nitric oxide synthase 3	Homo sapiens	45-49
29466710-6	2018	Furthermore, inhibition of eNOS by L-NAME conspicuously attenuated low SS-induced O2- releasing, indicating eNOS uncoupling.	NG-Nitroarginine Methyl Ester	35-41	nitric oxide synthase 3	Homo sapiens	27-31
29466710-11	2018	Notably, although low SS had no influence on eNOS Ser1177 phosphorylation, whereas boosted eNOS Ser1177 phosphorylation by rapamycin were in favor of the eNOS recoupling through restoration of autophagic flux.	Sirolimus	123-132	nitric oxide synthase 3	Homo sapiens	91-95
29466710-11	2018	Notably, although low SS had no influence on eNOS Ser1177 phosphorylation, whereas boosted eNOS Ser1177 phosphorylation by rapamycin were in favor of the eNOS recoupling through restoration of autophagic flux.	Sirolimus	123-132	nitric oxide synthase 3	Homo sapiens	91-95
29372262-6	2018	Hyperhomocysteinemia has been reported to increase the endogenous competitive inhibitors of eNOS viz L-N-monomethyl arginine (L-NMMA) and asymmetric dimethyl arginine (ADMA) that may contribute to vascular endothelial dysfunction.	l-n-monomethyl arginine	101-124	nitric oxide synthase 3	Homo sapiens	92-96
29372262-6	2018	Hyperhomocysteinemia has been reported to increase the endogenous competitive inhibitors of eNOS viz L-N-monomethyl arginine (L-NMMA) and asymmetric dimethyl arginine (ADMA) that may contribute to vascular endothelial dysfunction.	N(G)-monomethylarginine acetate	126-132	nitric oxide synthase 3	Homo sapiens	92-96
29372262-6	2018	Hyperhomocysteinemia has been reported to increase the endogenous competitive inhibitors of eNOS viz L-N-monomethyl arginine (L-NMMA) and asymmetric dimethyl arginine (ADMA) that may contribute to vascular endothelial dysfunction.	dimethylarginine	149-166	nitric oxide synthase 3	Homo sapiens	92-96
29372262-6	2018	Hyperhomocysteinemia has been reported to increase the endogenous competitive inhibitors of eNOS viz L-N-monomethyl arginine (L-NMMA) and asymmetric dimethyl arginine (ADMA) that may contribute to vascular endothelial dysfunction.	N,N-dimethylarginine	168-172	nitric oxide synthase 3	Homo sapiens	92-96
29372262-8	2018	The increased cholesterol and triglyceride level and decreased protective HDL level, decreases the activity and expression of eNOS and disrupts the integrity of vascular endothelium, due to oxidative stress.	Cholesterol	14-25	nitric oxide synthase 3	Homo sapiens	126-130
29496565-0	2018	Endothelial nitric oxide synthase polymorphisms affect the changes in blood pressure and nitric oxide bioavailability induced by propofol.	Propofol	129-137	nitric oxide synthase 3	Homo sapiens	0-33
29496565-1	2018	Propofol anesthesia is usually accompanied by hypotension, which is at least in part related to enhanced endothelial nitric oxide synthase (NOS3)-derived NO bioavailability.	Propofol	0-8	nitric oxide synthase 3	Homo sapiens	105-138
29496565-1	2018	Propofol anesthesia is usually accompanied by hypotension, which is at least in part related to enhanced endothelial nitric oxide synthase (NOS3)-derived NO bioavailability.	Propofol	0-8	nitric oxide synthase 3	Homo sapiens	140-144
29496565-8	2018	Our results suggest that NOS3 polymorphisms and haplotypes influence the hypotensive responses to propofol, possibly by affecting NO bioavailability.	Propofol	98-106	nitric oxide synthase 3	Homo sapiens	25-29
29444470-11	2018	In addition, the hepatic phosphorylated mammalian target of rapamycin (mTOR) and P70S6K protein expressions were significantly downregulated and endothelial nitric oxide synthase (eNOS) expression upregulated by sirolimus.	Sirolimus	212-221	nitric oxide synthase 3	Homo sapiens	145-178
29512753-11	2018	Additionally, a Cell Counting Kit-8 assay demonstrated that specific inhibitors of NOS3 and BDNF/neurotrophic receptor tyrosine kinase, type 2 signaling reduced the IC50 of MCF-7/MDR cells in response to various anticancer drugs, including adriamycin, cisplatin and 5-fluorouracil.	Doxorubicin	240-250	nitric oxide synthase 3	Homo sapiens	83-87
29512753-11	2018	Additionally, a Cell Counting Kit-8 assay demonstrated that specific inhibitors of NOS3 and BDNF/neurotrophic receptor tyrosine kinase, type 2 signaling reduced the IC50 of MCF-7/MDR cells in response to various anticancer drugs, including adriamycin, cisplatin and 5-fluorouracil.	Cisplatin	252-261	nitric oxide synthase 3	Homo sapiens	83-87
29512753-11	2018	Additionally, a Cell Counting Kit-8 assay demonstrated that specific inhibitors of NOS3 and BDNF/neurotrophic receptor tyrosine kinase, type 2 signaling reduced the IC50 of MCF-7/MDR cells in response to various anticancer drugs, including adriamycin, cisplatin and 5-fluorouracil.	Fluorouracil	266-280	nitric oxide synthase 3	Homo sapiens	83-87
29351417-9	2018	Zn2+ also regulated inflammation-related key molecules such as heme oxygenase-1, selectin L, IL-10, and platelet endothelial cell adhesion molecule 1, as well as vascular tone-related prostaglandin I2 synthase and nitric oxide synthase-3.	Zinc	0-4	nitric oxide synthase 3	Homo sapiens	214-237
29410170-2	2018	l-Arginine is the substrate for endothelial NO synthase (eNOS) which is activated by intracellular alkalization, but nothing is known regarding modulation of system y+/CATs and system y+L activity, and eNOS activity by the pHi in HUVECs.	Arginine	0-10	nitric oxide synthase 3	Homo sapiens	32-55
29410170-2	2018	l-Arginine is the substrate for endothelial NO synthase (eNOS) which is activated by intracellular alkalization, but nothing is known regarding modulation of system y+/CATs and system y+L activity, and eNOS activity by the pHi in HUVECs.	Arginine	0-10	nitric oxide synthase 3	Homo sapiens	57-61
29410170-8	2018	Acidic pHi reduced NO synthesis and eNOS serine1177 phosphorylation.	serine1177	41-51	nitric oxide synthase 3	Homo sapiens	36-40
29632805-7	2018	A combination treatment with recombinant human vascular endothelial growth factor C and eNOS inhibitor (Nomega-nitro-l-arginine methyl ester hydrochloride) resulted in the down-regulation of p-VASP, as well as a decreased migration and invasion ability of the CCA cell line.	L-NAME hydrochloride	104-154	nitric oxide synthase 3	Homo sapiens	88-92
29412499-8	2018	By contrast, pretreatment of SP attenuated TNF-alpha-induced cellular apoptosis, accompanied by an increase in the phosphorylation of Akt, eNOS expression, and NO production.	TFF2 protein, human	29-31	nitric oxide synthase 3	Homo sapiens	139-143
29412499-9	2018	Blockage of NK-1R, phosphorylated Akt or eNOS by CP-96345, A6730, or L-NAME entirely eliminated the effect of SP.	CP 96345	49-57	nitric oxide synthase 3	Homo sapiens	41-45
29412499-9	2018	Blockage of NK-1R, phosphorylated Akt or eNOS by CP-96345, A6730, or L-NAME entirely eliminated the effect of SP.	TFF2 protein, human	110-112	nitric oxide synthase 3	Homo sapiens	41-45
29412499-10	2018	CONCLUSIONS: SP can protect the vascular endothelium against inflammation-induced damage through modulation of the Akt/eNOS/NO signaling pathway.	TFF2 protein, human	13-15	nitric oxide synthase 3	Homo sapiens	119-123
29046298-3	2018	Using LY344864 , a selective 5-HT1F receptor agonist, we determined that the 5-HT1F receptor is coupled to Galphai/o and induces MB through Gbetagamma-dependent activation of Akt, endothelial nitric oxide synthase (eNOS), cyclic guanosine-monophosphate (cGMP), protein kinase G (PKG), and peroxisome proliferator-activated receptor-gamma coactivator-1alpha (PGC-1alpha).	LY 344864	6-14	nitric oxide synthase 3	Homo sapiens	180-213
29084084-0	2018	Hydrogen sulfide improves endothelial dysfunction in hypertension by activating peroxisome proliferator-activated receptor delta/endothelial nitric oxide synthase signaling.	Hydrogen Sulfide	0-16	nitric oxide synthase 3	Homo sapiens	129-162
29084084-1	2018	OBJECTIVE: We aimed to elucidate the ameliorative effect of hydrogen sulfide (H2S) on endothelium-dependent relaxation disturbances via peroxisome proliferator-activated receptor delta/endothelial nitric oxide synthase (PPARdelta/eNOS) pathway activation in hypertensive patients and rats.	Hydrogen Sulfide	60-76	nitric oxide synthase 3	Homo sapiens	185-218
29084084-1	2018	OBJECTIVE: We aimed to elucidate the ameliorative effect of hydrogen sulfide (H2S) on endothelium-dependent relaxation disturbances via peroxisome proliferator-activated receptor delta/endothelial nitric oxide synthase (PPARdelta/eNOS) pathway activation in hypertensive patients and rats.	Hydrogen Sulfide	60-76	nitric oxide synthase 3	Homo sapiens	230-234
29084084-1	2018	OBJECTIVE: We aimed to elucidate the ameliorative effect of hydrogen sulfide (H2S) on endothelium-dependent relaxation disturbances via peroxisome proliferator-activated receptor delta/endothelial nitric oxide synthase (PPARdelta/eNOS) pathway activation in hypertensive patients and rats.	Hydrogen Sulfide	78-81	nitric oxide synthase 3	Homo sapiens	185-218
29084084-1	2018	OBJECTIVE: We aimed to elucidate the ameliorative effect of hydrogen sulfide (H2S) on endothelium-dependent relaxation disturbances via peroxisome proliferator-activated receptor delta/endothelial nitric oxide synthase (PPARdelta/eNOS) pathway activation in hypertensive patients and rats.	Hydrogen Sulfide	78-81	nitric oxide synthase 3	Homo sapiens	230-234
29084084-13	2018	NaHS upregulated PPARdelta expression, increased protein kinase B (Akt) or adenosine monophosphate kinase-activated protein kinase (AMPK) phosphorylation, and enhanced eNOS phosphorylation.	sodium bisulfide	0-4	nitric oxide synthase 3	Homo sapiens	168-172
29084084-15	2018	CONCLUSION: H2S plays a protective function in renal arterial endothelium in hypertension by activating the PPARdelta/PI3K/Akt/eNOS or PPARdelta/AMPK/eNOS pathway.	Hydrogen Sulfide	12-15	nitric oxide synthase 3	Homo sapiens	127-131
29084084-15	2018	CONCLUSION: H2S plays a protective function in renal arterial endothelium in hypertension by activating the PPARdelta/PI3K/Akt/eNOS or PPARdelta/AMPK/eNOS pathway.	Hydrogen Sulfide	12-15	nitric oxide synthase 3	Homo sapiens	150-154
29359785-10	2018	The potential mechanism is that the G894T polymorphism leads to altered protein structure, which affects the function of eNOS in generating nitric oxide and cardiovascular diastole.	Nitric Oxide	140-152	nitric oxide synthase 3	Homo sapiens	121-125
28466478-2	2018	Produced by nitric oxide synthase 3 (NOS3), nitric oxide is considered to be one of the important mediators of oxidative stress in testis tissue.	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	37-41
29046298-3	2018	Using LY344864 , a selective 5-HT1F receptor agonist, we determined that the 5-HT1F receptor is coupled to Galphai/o and induces MB through Gbetagamma-dependent activation of Akt, endothelial nitric oxide synthase (eNOS), cyclic guanosine-monophosphate (cGMP), protein kinase G (PKG), and peroxisome proliferator-activated receptor-gamma coactivator-1alpha (PGC-1alpha).	LY 344864	6-14	nitric oxide synthase 3	Homo sapiens	215-219
28499789-8	2018	RESULTS: There were significant differences in genotype frequencies of eNOS Glu298Asp polymorphism between case and control groups (GG+TG vs. TT; p=0.002; OR=0.22, 95% CI 0.83 to 0.62).	Thioguanine	135-137	nitric oxide synthase 3	Homo sapiens	71-75
29210030-11	2018	Simvastatin and atorvastatin improve endothelial dysfunction mainly by enhancing endothelial nitric oxide synthase (eNOS) expression and phosphorylation and NO production.	Simvastatin	0-11	nitric oxide synthase 3	Homo sapiens	81-114
29269309-2	2018	NADPH oxidases (Noxs) and endothelial nitric oxide synthase (eNOS) are important enzymatic sources of reactive oxygen species (ROS) in diabetic vasculature.	Reactive Oxygen Species	102-125	nitric oxide synthase 3	Homo sapiens	26-59
29269309-2	2018	NADPH oxidases (Noxs) and endothelial nitric oxide synthase (eNOS) are important enzymatic sources of reactive oxygen species (ROS) in diabetic vasculature.	Reactive Oxygen Species	127-130	nitric oxide synthase 3	Homo sapiens	26-59
29210030-11	2018	Simvastatin and atorvastatin improve endothelial dysfunction mainly by enhancing endothelial nitric oxide synthase (eNOS) expression and phosphorylation and NO production.	Atorvastatin	16-28	nitric oxide synthase 3	Homo sapiens	81-114
29386501-11	2018	Emodin treatment recovered PPAR-gamma activity and phosphorylation, eNOS phosphorylation, and HSP90/eNOS coupling in HAECS in a concentration-dependent manner, which was reversed by the PPAR-gamma inhibitor GW9662, and the eNOS inhibitor, L-NAME.	2-chloro-5-nitrobenzanilide	207-213	nitric oxide synthase 3	Homo sapiens	68-72
29386501-11	2018	Emodin treatment recovered PPAR-gamma activity and phosphorylation, eNOS phosphorylation, and HSP90/eNOS coupling in HAECS in a concentration-dependent manner, which was reversed by the PPAR-gamma inhibitor GW9662, and the eNOS inhibitor, L-NAME.	2-chloro-5-nitrobenzanilide	207-213	nitric oxide synthase 3	Homo sapiens	100-104
29386501-11	2018	Emodin treatment recovered PPAR-gamma activity and phosphorylation, eNOS phosphorylation, and HSP90/eNOS coupling in HAECS in a concentration-dependent manner, which was reversed by the PPAR-gamma inhibitor GW9662, and the eNOS inhibitor, L-NAME.	2-chloro-5-nitrobenzanilide	207-213	nitric oxide synthase 3	Homo sapiens	100-104
29386501-12	2018	The recovery of HSP90/eNOS coupling by emodin was impaired by GW9662 treatment.	2-chloro-5-nitrobenzanilide	62-68	nitric oxide synthase 3	Homo sapiens	22-26
29549671-0	2018	Lower levels of Caveolin-1 and higher levels of endothelial nitric oxide synthase are observed in abdominal aortic aneurysm patients treated with simvastatin.	Simvastatin	146-157	nitric oxide synthase 3	Homo sapiens	48-81
29416330-6	2018	Uncoupled eNOS and overexpression of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase contributed to high production of ONOO-.	oxido nitrite	131-136	nitric oxide synthase 3	Homo sapiens	10-14
29416330-8	2018	Vitamin D3 restored uncoupled eNOS and endothelial function by increasing cytoprotective NO and decreasing the cytotoxic ONOO-.	Cholecalciferol	0-10	nitric oxide synthase 3	Homo sapiens	30-34
29416330-9	2018	The beneficial effect of vitamin D3 is associated with a favorable rate of NO and ONOO- release, restoration of the [NO]/[ONOO-] and the overall decrease in the overexpression of eNOS, inducible nitric oxide synthase and NADPH oxidase.	Cholecalciferol	25-35	nitric oxide synthase 3	Homo sapiens	179-183
28982690-3	2018	METHODS: We analyzed the association of common and rare genetic variants in 2 genes that mediate nitric oxide signaling (Nitric Oxide Synthase 3 [NOS3] and Guanylate Cyclase 1, Soluble, Alpha 3 [GUCY1A3]) with a range of human phenotypes.	Nitric Oxide	97-109	nitric oxide synthase 3	Homo sapiens	121-144
28982690-3	2018	METHODS: We analyzed the association of common and rare genetic variants in 2 genes that mediate nitric oxide signaling (Nitric Oxide Synthase 3 [NOS3] and Guanylate Cyclase 1, Soluble, Alpha 3 [GUCY1A3]) with a range of human phenotypes.	Nitric Oxide	97-109	nitric oxide synthase 3	Homo sapiens	146-150
29549671-1	2018	This study was undertaken to verify whether simvastatin modulates Cav-1/eNOS expression, and if this modulation is associated with changes in pro- and anti-inflammatory cytokine and Toll-like receptor 4 (TLR4) level in abdominal aortic aneurysm (AAA).	Simvastatin	44-55	nitric oxide synthase 3	Homo sapiens	72-76
29549671-3	2018	Simvastatin treatment decreased Cav-1 (p&lt;0.05) and increased eNOS expression (p&lt;0.01) in the AAA wall.	Simvastatin	0-11	nitric oxide synthase 3	Homo sapiens	64-68
29549671-5	2018	The changes in Cav-1 and eNOS were associated with a trend towards decreased IL-6 and IL-17 concentration (p&gt;0.05) and increased IL-10 concentration (p=0.055); however, TLR4 expression was unaffected, suggesting that simvastatin influences Cav-1 and eNOS in the AAA wall by other mechanisms.	Simvastatin	220-231	nitric oxide synthase 3	Homo sapiens	25-29
29549671-6	2018	Simvastatin may modulate Cav-1 and eNOS expression in the aneurysmal wall, indicating a potentially beneficial role for statins in AAA patients.	Simvastatin	0-11	nitric oxide synthase 3	Homo sapiens	35-39
30125887-0	2018	NOS3 895G&amp;gt;T and CBR3 730G&amp;gt;A Are Associated with Recurrence Risk in Non-Muscle-Invasive Bladder Cancer with Intravesical Instillations of THP.	Adenosine Monophosphate	10-13	nitric oxide synthase 3	Homo sapiens	0-4
30178377-9	2018	Cytokine stimulation was found to differentially affect gene expression of major ROS synthesizing enzymes: eNOS was decreased whereas COX-2 and NOX-4 were increased.	ros	81-84	nitric oxide synthase 3	Homo sapiens	107-111
29162452-6	2018	Western blotting results indicated that DT-13 could down-regulate phosphorylation of endothelial nitric oxide synthase (eNOS) significantly in TNF-alpha-induced human umbilical vein endothelial cells (HUVECs).	DT-13	40-45	nitric oxide synthase 3	Homo sapiens	85-118
30125887-0	2018	NOS3 895G&amp;gt;T and CBR3 730G&amp;gt;A Are Associated with Recurrence Risk in Non-Muscle-Invasive Bladder Cancer with Intravesical Instillations of THP.	pirarubicin	151-154	nitric oxide synthase 3	Homo sapiens	0-4
30125887-10	2018	CONCLUSIONS: Our results suggest that NOS3 895G&gt;T and CBR3 730G&gt;A are genetic markers that can be used to predict tumor recurrence in NMIBC patients receiving intravesical instillations of THP.	pirarubicin	195-198	nitric oxide synthase 3	Homo sapiens	38-42
30360781-2	2018	Maintenance of normal endothelial cell function is a critical role of endothelial nitric oxide synthase (eNOS) activity and physiologic nitric oxide (NO) signaling in the vascular wall.	Nitric Oxide	82-94	nitric oxide synthase 3	Homo sapiens	105-109
28925872-3	2018	Several sources of ROS have been identified in aortic tissues using experimental models: inflammation, increased activity of NAD(P)H or NOX, over-expression of inducible nitric oxide synthase (iNOS), uncoupled endothelial nitric oxide synthase (eNOS), platelets activation and iron release from hemoglobin.	Reactive Oxygen Species	19-22	nitric oxide synthase 3	Homo sapiens	210-243
28925872-3	2018	Several sources of ROS have been identified in aortic tissues using experimental models: inflammation, increased activity of NAD(P)H or NOX, over-expression of inducible nitric oxide synthase (iNOS), uncoupled endothelial nitric oxide synthase (eNOS), platelets activation and iron release from hemoglobin.	Reactive Oxygen Species	19-22	nitric oxide synthase 3	Homo sapiens	245-249
29090664-5	2018	RESULTS: Polymorphisms in the main enzymes of anthracyclines metabolism (CBR, AKR, NQO1, NOS3) have been related to lower enzymatic activity and higher cardiotoxicity.	Anthracyclines	46-60	nitric oxide synthase 3	Homo sapiens	89-93
29602923-9	2018	Among children who died, a combination of genotypes ID &amp; DD of the gene ACE +4ab &amp; 4AA of the eNOS gene was found significantly more often than in children who survived, and at the border of statistical significance - the isolated genotype 4ab &amp; 4 aa of the eNOS gene.	Adenosine Monophosphate	56-59	nitric oxide synthase 3	Homo sapiens	102-106
29602923-9	2018	Among children who died, a combination of genotypes ID &amp; DD of the gene ACE +4ab &amp; 4AA of the eNOS gene was found significantly more often than in children who survived, and at the border of statistical significance - the isolated genotype 4ab &amp; 4 aa of the eNOS gene.	Adenosine Monophosphate	56-59	nitric oxide synthase 3	Homo sapiens	270-274
29602923-9	2018	Among children who died, a combination of genotypes ID &amp; DD of the gene ACE +4ab &amp; 4AA of the eNOS gene was found significantly more often than in children who survived, and at the border of statistical significance - the isolated genotype 4ab &amp; 4 aa of the eNOS gene.	Adenosine Monophosphate	86-89	nitric oxide synthase 3	Homo sapiens	102-106
29602923-9	2018	Among children who died, a combination of genotypes ID &amp; DD of the gene ACE +4ab &amp; 4AA of the eNOS gene was found significantly more often than in children who survived, and at the border of statistical significance - the isolated genotype 4ab &amp; 4 aa of the eNOS gene.	Adenosine Monophosphate	86-89	nitric oxide synthase 3	Homo sapiens	270-274
29602923-9	2018	Among children who died, a combination of genotypes ID &amp; DD of the gene ACE +4ab &amp; 4AA of the eNOS gene was found significantly more often than in children who survived, and at the border of statistical significance - the isolated genotype 4ab &amp; 4 aa of the eNOS gene.	Adenosine Monophosphate	86-89	nitric oxide synthase 3	Homo sapiens	102-106
29602923-9	2018	Among children who died, a combination of genotypes ID &amp; DD of the gene ACE +4ab &amp; 4AA of the eNOS gene was found significantly more often than in children who survived, and at the border of statistical significance - the isolated genotype 4ab &amp; 4 aa of the eNOS gene.	Adenosine Monophosphate	86-89	nitric oxide synthase 3	Homo sapiens	270-274
28912066-9	2017	Our results suggest that Epac and PKA activate eNOS via Ser 1177 phosphorylation by activating the PI3K/Akt pathway, and independently of AMPK or CaMKII activation or [Ca2+]c increase.	Serine	56-59	nitric oxide synthase 3	Homo sapiens	47-51
29037842-0	2017	Puerarin inhibits expression of tissue factor induced by oxidative low-density lipoprotein through activating the PI3K/Akt/eNOS pathway and inhibiting activation of ERK1/2 and NF-kappaB.	puerarin	0-8	nitric oxide synthase 3	Homo sapiens	123-127
29037842-8	2017	SIGNIFICANCE: These results suggested that puerarin suppressed TF expression in HUVECs through activating the PI3K/Akt/endothelial nitric oxide synthase signaling pathway and inhibiting the activation of ERK1/2 and NF-kappaB.	puerarin	43-51	nitric oxide synthase 3	Homo sapiens	119-152
28958937-2	2017	To highlight the potential role and effect of membrane phospholipids on the structure and activity of eNOS, we have incorporated the recombinant oxygenase subunit of eNOS into lipid nanodiscs.	Phospholipids	55-68	nitric oxide synthase 3	Homo sapiens	102-106
28912066-0	2017	The cAMP effectors PKA and Epac activate endothelial NO synthase through PI3K/Akt pathway in human endothelial cells.	Cyclic AMP	4-8	nitric oxide synthase 3	Homo sapiens	41-64
30647683-2	2017	Endothelial nitric oxide synthase (eNOS) gene is responsible for the bioavailability of nitric oxide and endothelial function.	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	35-39
28912066-1	2017	3",5"-Cyclic adenosine monophosphate (cAMP) exerts an endothelium-dependent vasorelaxant action by stimulating endothelial NO synthase (eNOS) activity, and the subsequent NO release, through cAMP protein kinase (PKA) and exchange protein directly activated by cAMP (Epac) activation in endothelial cells.	3",5"-cyclic adenosine monophosphate	0-36	nitric oxide synthase 3	Homo sapiens	111-134
28912066-1	2017	3",5"-Cyclic adenosine monophosphate (cAMP) exerts an endothelium-dependent vasorelaxant action by stimulating endothelial NO synthase (eNOS) activity, and the subsequent NO release, through cAMP protein kinase (PKA) and exchange protein directly activated by cAMP (Epac) activation in endothelial cells.	3",5"-cyclic adenosine monophosphate	0-36	nitric oxide synthase 3	Homo sapiens	136-140
28912066-1	2017	3",5"-Cyclic adenosine monophosphate (cAMP) exerts an endothelium-dependent vasorelaxant action by stimulating endothelial NO synthase (eNOS) activity, and the subsequent NO release, through cAMP protein kinase (PKA) and exchange protein directly activated by cAMP (Epac) activation in endothelial cells.	Cyclic AMP	38-42	nitric oxide synthase 3	Homo sapiens	111-134
28912066-1	2017	3",5"-Cyclic adenosine monophosphate (cAMP) exerts an endothelium-dependent vasorelaxant action by stimulating endothelial NO synthase (eNOS) activity, and the subsequent NO release, through cAMP protein kinase (PKA) and exchange protein directly activated by cAMP (Epac) activation in endothelial cells.	Cyclic AMP	38-42	nitric oxide synthase 3	Homo sapiens	136-140
28912066-2	2017	Here, we have investigated the mechanism by which the cAMP-Epac/PKA pathway activates eNOS.	Cyclic AMP	54-58	nitric oxide synthase 3	Homo sapiens	86-90
28912066-5	2017	In DAF-2-loaded HUVEC monolayers, forskolin, PKA and Epac activators significantly increased NO release, and the forskolin effect was reduced by inhibition of PKA (Rp-cAMPs), Epac (ESI-09), eNOS (L-NAME) or phosphoinositide 3-kinase (PI3K; LY-294,002).	4,5-diaminofluorescein	3-8	nitric oxide synthase 3	Homo sapiens	190-194
28912066-5	2017	In DAF-2-loaded HUVEC monolayers, forskolin, PKA and Epac activators significantly increased NO release, and the forskolin effect was reduced by inhibition of PKA (Rp-cAMPs), Epac (ESI-09), eNOS (L-NAME) or phosphoinositide 3-kinase (PI3K; LY-294,002).	Colforsin	34-43	nitric oxide synthase 3	Homo sapiens	190-194
28912066-5	2017	In DAF-2-loaded HUVEC monolayers, forskolin, PKA and Epac activators significantly increased NO release, and the forskolin effect was reduced by inhibition of PKA (Rp-cAMPs), Epac (ESI-09), eNOS (L-NAME) or phosphoinositide 3-kinase (PI3K; LY-294,002).	Colforsin	113-122	nitric oxide synthase 3	Homo sapiens	190-194
28912066-7	2017	In Western blot experiments, Serine 1177 phosphorylated-eNOS was significantly increased in HUVEC by cAMP-elevating agents and PKA or Epac activators.	Serine	29-35	nitric oxide synthase 3	Homo sapiens	56-60
28912066-7	2017	In Western blot experiments, Serine 1177 phosphorylated-eNOS was significantly increased in HUVEC by cAMP-elevating agents and PKA or Epac activators.	Cyclic AMP	101-105	nitric oxide synthase 3	Homo sapiens	56-60
28409476-8	2017	Phosphorylation of eNOS at the serine 1177 (S1177) residue and ET-1 mRNA levels were also not significantly affected.	Serine	31-37	nitric oxide synthase 3	Homo sapiens	19-23
28899725-0	2017	Nitric oxide donor [Ru(terpy)(bdq)NO]3+ induces uncoupling and phosphorylation of endothelial nitric oxide synthase promoting oxidant production.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	82-115
29079038-3	2017	Genetic polymorphisms of the endothelial nitric oxide synthase (eNOS) gene have been linked to decreased nitric oxide (NO) levels, coronary artery spasm, and myocardial infarction.	Nitric Oxide	41-53	nitric oxide synthase 3	Homo sapiens	64-68
29132319-2	2017	Nitric oxide is important for the functional integrity of the vascular endothelium and is produced in endothelial cells by the enzyme endothelial nitric oxide synthase (eNOS).	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	134-167
29132319-2	2017	Nitric oxide is important for the functional integrity of the vascular endothelium and is produced in endothelial cells by the enzyme endothelial nitric oxide synthase (eNOS).	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	169-173
28919424-7	2017	Use of the AMPK inhibitor (Compound C) or Akt inhibitor (MK-2206) reduced eNOS phosphorylation and attenuated adiponectin-induced endothelial progenitor cell proliferation, migration and tube formation compared to the controls (p &lt; 0.05).	MK 2206	57-64	nitric oxide synthase 3	Homo sapiens	74-78
28899725-0	2017	Nitric oxide donor [Ru(terpy)(bdq)NO]3+ induces uncoupling and phosphorylation of endothelial nitric oxide synthase promoting oxidant production.	[ru(terpy)(bdq)no]3+	19-39	nitric oxide synthase 3	Homo sapiens	82-115
28849094-0	2017	Hydrogen sulfide facilities production of nitric oxide via the Akt/endothelial nitric oxide synthases signaling pathway to protect human umbilical vein endothelial cells from injury by angiotensin II.	Hydrogen Sulfide	0-16	nitric oxide synthase 3	Homo sapiens	67-101
28870504-0	2017	The oxidized phospholipid POVPC impairs endothelial function and vasodilation via uncoupling endothelial nitric oxide synthase.	Phospholipids	13-25	nitric oxide synthase 3	Homo sapiens	93-126
28870504-2	2017	We recently have shown that 25-hydroxycholesterol found in atherosclerotic lesions could impair endothelial function and vasodilation by uncoupling and inhibiting endothelial nitric oxide synthase (eNOS).	25-hydroxycholesterol	28-49	nitric oxide synthase 3	Homo sapiens	163-196
28870504-2	2017	We recently have shown that 25-hydroxycholesterol found in atherosclerotic lesions could impair endothelial function and vasodilation by uncoupling and inhibiting endothelial nitric oxide synthase (eNOS).	25-hydroxycholesterol	28-49	nitric oxide synthase 3	Homo sapiens	198-202
28729163-0	2017	Computational analysis of interactions of oxidative stress and tetrahydrobiopterin reveals instability in eNOS coupling.	sapropterin	63-82	nitric oxide synthase 3	Homo sapiens	106-110
28729163-2	2017	There is a reduction in tetrahydrobiopterin (BH4), which is a cofactor for the endothelial nitric oxide synthase (eNOS), resulting in eNOS uncoupling.	sapropterin	24-43	nitric oxide synthase 3	Homo sapiens	79-112
28729163-2	2017	There is a reduction in tetrahydrobiopterin (BH4), which is a cofactor for the endothelial nitric oxide synthase (eNOS), resulting in eNOS uncoupling.	sapropterin	24-43	nitric oxide synthase 3	Homo sapiens	114-118
28729163-2	2017	There is a reduction in tetrahydrobiopterin (BH4), which is a cofactor for the endothelial nitric oxide synthase (eNOS), resulting in eNOS uncoupling.	sapropterin	24-43	nitric oxide synthase 3	Homo sapiens	134-138
28729163-2	2017	There is a reduction in tetrahydrobiopterin (BH4), which is a cofactor for the endothelial nitric oxide synthase (eNOS), resulting in eNOS uncoupling.	sapropterin	45-48	nitric oxide synthase 3	Homo sapiens	79-112
28729163-2	2017	There is a reduction in tetrahydrobiopterin (BH4), which is a cofactor for the endothelial nitric oxide synthase (eNOS), resulting in eNOS uncoupling.	sapropterin	45-48	nitric oxide synthase 3	Homo sapiens	114-118
28729163-2	2017	There is a reduction in tetrahydrobiopterin (BH4), which is a cofactor for the endothelial nitric oxide synthase (eNOS), resulting in eNOS uncoupling.	sapropterin	45-48	nitric oxide synthase 3	Homo sapiens	134-138
28729163-4	2017	Our understanding of the complex interactions of eNOS uncoupling, oxidative stress and BH4 availability is not complete and a quantitative understanding of these interactions is required.	sapropterin	87-90	nitric oxide synthase 3	Homo sapiens	49-53
28729163-5	2017	In the present study, we developed a computational model for eNOS uncoupling that considers the temporal changes in biopterin ratio in the oxidative stress conditions.	Biopterin	116-125	nitric oxide synthase 3	Homo sapiens	61-65
28849094-0	2017	Hydrogen sulfide facilities production of nitric oxide via the Akt/endothelial nitric oxide synthases signaling pathway to protect human umbilical vein endothelial cells from injury by angiotensin II.	Nitric Oxide	42-54	nitric oxide synthase 3	Homo sapiens	67-101
28849094-9	2017	Thus, H2S stimulates the production of NO and protects HUVECs via inducing the Akt/eNOS signaling pathway.	Hydrogen Sulfide	6-9	nitric oxide synthase 3	Homo sapiens	83-87
29190920-6	2017	Furthermore, we showed that 3-ANE blocked VEGF-mediated endothelial nitric oxide synthase (eNOS) phosphorylation, vascular permeability and NO production in HUVECs, via disrupting the VEGF-induced association of eNOS and heat-shock protein 90 (HSP90).	3-ane	28-33	nitric oxide synthase 3	Homo sapiens	56-89
28797660-0	2017	Evaluation of genetic effect of NOS3 and GxE interaction on the variability of serum bilirubin in a Han Chinese population.	Bilirubin	85-94	nitric oxide synthase 3	Homo sapiens	32-36
28797660-1	2017	Bilirubin was shown to be related to the generation and functional exertion of endothelial nitric oxide synthase (eNOS) whilst the genetic effect of NOS3 on bilirubin variability was rarely reported.	Bilirubin	0-9	nitric oxide synthase 3	Homo sapiens	79-112
28797660-1	2017	Bilirubin was shown to be related to the generation and functional exertion of endothelial nitric oxide synthase (eNOS) whilst the genetic effect of NOS3 on bilirubin variability was rarely reported.	Bilirubin	157-166	nitric oxide synthase 3	Homo sapiens	149-153
28797660-2	2017	Herein we assessed the associations of three single nucleotide polymorphisms (SNPs) of NOS3 (rs4496877, rs1808593, and rs3918186) with bilirubin elevation in 2077 adults.	Bilirubin	135-144	nitric oxide synthase 3	Homo sapiens	87-91
28797660-9	2017	Our findings supported that NOS3 harbors the genetic susceptibility to the bilirubin elevation.	Bilirubin	75-84	nitric oxide synthase 3	Homo sapiens	28-32
28797660-10	2017	Age, gender, smoking, and drinking could be involved in the genetic modification of NOS3 on the bilirubin variability.	Bilirubin	96-105	nitric oxide synthase 3	Homo sapiens	84-88
28803324-2	2017	NO is a gas synthesized from Larginine (a conditionally essential amino acid) and oxygen by endothelial nitric oxide synthase (eNOS).	Arginine	29-38	nitric oxide synthase 3	Homo sapiens	92-125
28803324-2	2017	NO is a gas synthesized from Larginine (a conditionally essential amino acid) and oxygen by endothelial nitric oxide synthase (eNOS).	Oxygen	82-88	nitric oxide synthase 3	Homo sapiens	92-125
29059213-8	2017	In cultured endothelial cells, bradykinin treatment produced the anticipated rapid influx of Ca2+ and transient CaMKII and eNOS activation, whereas CaMKII inhibition blocked eNOS phosphorylation on Ser-1179 and dephosphorylation at Thr-497.	Serine	198-201	nitric oxide synthase 3	Homo sapiens	174-178
29059213-9	2017	Ca2+/CaM binding to eNOS and resultant NO production in vitro were decreased under CaMKII inhibition.	cafestol palmitate	5-8	nitric oxide synthase 3	Homo sapiens	20-24
29262615-6	2017	Moreover, cavin-1 knockdown increased the activity of endothelial nitric oxide synthase (eNOS) and the production of nitric oxide (NO).	Nitric Oxide	66-78	nitric oxide synthase 3	Homo sapiens	89-93
29262615-7	2017	Consequently, an eNOS inhibitor, N-Nitro-L-Arginine Methyl Ester (L-NAME), not only suppressed the activity of specificity protein (Sp1) and nuclear factor kappa B (NF-kappaB), but also inhibited both activities via activating adenosine 5"-monophosphate- activated protein kinase (AMPK).	n-nitro-l-arginine methyl ester	33-64	nitric oxide synthase 3	Homo sapiens	17-21
29262615-7	2017	Consequently, an eNOS inhibitor, N-Nitro-L-Arginine Methyl Ester (L-NAME), not only suppressed the activity of specificity protein (Sp1) and nuclear factor kappa B (NF-kappaB), but also inhibited both activities via activating adenosine 5"-monophosphate- activated protein kinase (AMPK).	NG-Nitroarginine Methyl Ester	66-72	nitric oxide synthase 3	Homo sapiens	17-21
28727928-3	2017	In ECs, the major producer of nitric oxide is the endothelial nitric oxide synthase (eNOS) enzyme that is encoded by the NOS3 gene.	Nitric Oxide	30-42	nitric oxide synthase 3	Homo sapiens	50-83
28727928-3	2017	In ECs, the major producer of nitric oxide is the endothelial nitric oxide synthase (eNOS) enzyme that is encoded by the NOS3 gene.	Nitric Oxide	30-42	nitric oxide synthase 3	Homo sapiens	85-89
28727928-3	2017	In ECs, the major producer of nitric oxide is the endothelial nitric oxide synthase (eNOS) enzyme that is encoded by the NOS3 gene.	Nitric Oxide	30-42	nitric oxide synthase 3	Homo sapiens	121-125
28664667-0	2017	Pitavastatin up-regulates eNOS production by suppressing miR-155 expression in lipopolysaccharide-stimulated human umbilical vein endothelial cells.	pitavastatin	0-12	nitric oxide synthase 3	Homo sapiens	26-30
28664667-9	2017	Pitavastatin ameliorated LPS-induced endothelial dysfunction through upregulation of eNOS expression and downregulation of miR-155 expression.	pitavastatin	0-12	nitric oxide synthase 3	Homo sapiens	85-89
28664667-10	2017	CONCLUSION: Pitavastatin increases eNOS expression and inhibits of LPS-induced miR-155 expression.	pitavastatin	12-24	nitric oxide synthase 3	Homo sapiens	35-39
28559108-8	2017	Only GTN elicited phosphorylation of eNOS at Ser1177 and Thr495.	Nitroglycerin	5-8	nitric oxide synthase 3	Homo sapiens	37-41
29024947-9	2017	H2S donor-induced NOS3 activation was blocked by AKT1 but not MAPK3/1 inhibition.	Hydrogen Sulfide	0-3	nitric oxide synthase 3	Homo sapiens	18-22
28950822-7	2017	Statins also enhance the expression, enzymatic activity and coupling of endothelial nitric oxide synthase (eNOS), through mevalonate-dependent effects.	Mevalonic Acid	122-132	nitric oxide synthase 3	Homo sapiens	72-105
29104511-8	2017	In addition to BAPTA-AM and W7, L-NAME, an eNOS antagonist, abolished insulin-induced Akt phosphorylation at Ser473 in both si-Neg and si-ATP2B1-transfected endothelial cells.	NG-Nitroarginine Methyl Ester	32-38	nitric oxide synthase 3	Homo sapiens	43-47
29024947-10	2017	In keeping with our previous studies showing a crucial role of AKT1, MAPK3/1, and NOS3/NO in placental angiogenesis, these data show that trophoblast-derived endogenous H2S stimulates placental angiogenesis, involving activation of AKT1, NOS3/NO, and MAPK3/1.	Hydrogen Sulfide	169-172	nitric oxide synthase 3	Homo sapiens	82-86
29024947-10	2017	In keeping with our previous studies showing a crucial role of AKT1, MAPK3/1, and NOS3/NO in placental angiogenesis, these data show that trophoblast-derived endogenous H2S stimulates placental angiogenesis, involving activation of AKT1, NOS3/NO, and MAPK3/1.	Hydrogen Sulfide	169-172	nitric oxide synthase 3	Homo sapiens	238-242
28904082-2	2017	We tested the hypothesis that reduced availability of the endothelial nitric oxide synthase [eNOS] substrate L-arginine is an underlying mechanism to vascular endothelial dysfunction across menopause stages.	Arginine	109-119	nitric oxide synthase 3	Homo sapiens	58-91
28980911-2	2017	We sought to determine if acute oral administration of tetrahydrobiopterin (BH4), an essential cofactor for endothelial nitric oxide synthase, would augment endothelial function in patients with SSc.	sapropterin	55-74	nitric oxide synthase 3	Homo sapiens	108-141
28980911-2	2017	We sought to determine if acute oral administration of tetrahydrobiopterin (BH4), an essential cofactor for endothelial nitric oxide synthase, would augment endothelial function in patients with SSc.	sapropterin	76-79	nitric oxide synthase 3	Homo sapiens	108-141
28877324-8	2017	Normalization of nitric oxide levels with l-arginine 9 g/d or l-citrulline 800 mg/d, both of which relieve vasospastic angina in Prinzmetal"s angina, which has the same eNOS genotype as primary osteonecrosis, may slow or stop the progression of osteonecrosis.	Citrulline	62-74	nitric oxide synthase 3	Homo sapiens	169-173
28904082-10	2017	The relative L-arginine deficiency may be related to elevated levels of the methylarginine L-NMMA, which would compete with L-arginine for eNOS and for intracellular transport, reducing NO biosynthesis.	methylarginine l-nmma	76-97	nitric oxide synthase 3	Homo sapiens	139-143
28904082-2	2017	We tested the hypothesis that reduced availability of the endothelial nitric oxide synthase [eNOS] substrate L-arginine is an underlying mechanism to vascular endothelial dysfunction across menopause stages.	Arginine	109-119	nitric oxide synthase 3	Homo sapiens	93-97
28904082-10	2017	The relative L-arginine deficiency may be related to elevated levels of the methylarginine L-NMMA, which would compete with L-arginine for eNOS and for intracellular transport, reducing NO biosynthesis.	Arginine	13-23	nitric oxide synthase 3	Homo sapiens	139-143
28904082-6	2017	The methylarginine and eNOS inhibitor L-NMMA was higher in early and late postmenopausal women compared to premenopausal and early and late perimenopausal women (all P &lt; 0.001), and was inversely correlated with FMD (r = -0.30, P = 0.001).	omega-N-Methylarginine	38-44	nitric oxide synthase 3	Homo sapiens	23-27
28624453-5	2017	Folic acid also decreased cyclooxygenase-2 (COX-2) and hypoxia-inducible factor 1-alpha (HIF-1alpha) expression and altered endothelial nitric oxide synthase (eNOS) signaling by increasing p-eNOS(Ser1177) and decreasing p-eNOS(Thr495) in a dose-dependent manner.	Folic Acid	0-10	nitric oxide synthase 3	Homo sapiens	124-157
28852041-5	2017	The increased eNOS expression was associated to higher enzymatic activity and nitric oxide production.	Nitric Oxide	78-90	nitric oxide synthase 3	Homo sapiens	14-18
28831159-3	2017	Instead, expression of endothelial nitric oxide synthase (eNOS), which generates the potent vasodilator nitric oxide (NO), is decreased.	Nitric Oxide	35-47	nitric oxide synthase 3	Homo sapiens	58-62
28831159-6	2017	HMG Co-A reductase negatively regulates eNOS, and the PLD2-deficiency phenotype of decreased eNOS expression and activity could be rescued by cholesterol supplementation and HMG Co-A reductase inhibition.	Cholesterol	142-153	nitric oxide synthase 3	Homo sapiens	93-97
28371087-7	2017	Influence of clopidogrel was further evaluated in NOS3 downregulated HUVEC by RNAi.	Clopidogrel	13-24	nitric oxide synthase 3	Homo sapiens	50-54
28371087-12	2017	NOS3 downregulated HUVEC model revealed that ICAM-1 modification by clopidogrel is dependent of this via, whereas MCP-1 is modulated in an NO-independent form.	Clopidogrel	68-79	nitric oxide synthase 3	Homo sapiens	0-4
28371277-6	2017	Compared to the blank group, PI3K, Akt and eNOS were down-regulated in the miR-138 mimic and LY294002 groups but were up-regulated in the miR-138 inhibitor group.	mir-138	75-82	nitric oxide synthase 3	Homo sapiens	43-47
28605668-1	2017	OBJECTIVE(S): Many lines of evidence suggest that reduced production of nitric oxide (NO) due to single nucleotide polymorphisms in endothelial nitric oxide synthase (eNOS) gene may affect the implantation and maintenance of pregnancy.	Nitric Oxide	72-84	nitric oxide synthase 3	Homo sapiens	132-165
28605668-1	2017	OBJECTIVE(S): Many lines of evidence suggest that reduced production of nitric oxide (NO) due to single nucleotide polymorphisms in endothelial nitric oxide synthase (eNOS) gene may affect the implantation and maintenance of pregnancy.	Nitric Oxide	72-84	nitric oxide synthase 3	Homo sapiens	167-171
28188926-6	2017	An increasing proportion of these are being recognized as redox regulated-proteins, that reside in the immediate vicinity of the two major cellular sources of ROS, nicotinamide adenine dinucleotide phosphate oxidase (Nox) and uncoupled endothelial nitric oxide synthase (eNOS).	Reactive Oxygen Species	159-162	nitric oxide synthase 3	Homo sapiens	236-269
28371277-6	2017	Compared to the blank group, PI3K, Akt and eNOS were down-regulated in the miR-138 mimic and LY294002 groups but were up-regulated in the miR-138 inhibitor group.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	93-101	nitric oxide synthase 3	Homo sapiens	43-47
28371277-7	2017	The miR-138 mimic and LY294002 groups showed decreased concentrations of TNF-alpha, IL-6, IL-8 and NO and reduced activities of LDH and eNOS, while opposite trends were observed in the miR-138 inhibitor group.	mir-138	4-11	nitric oxide synthase 3	Homo sapiens	136-140
28371277-7	2017	The miR-138 mimic and LY294002 groups showed decreased concentrations of TNF-alpha, IL-6, IL-8 and NO and reduced activities of LDH and eNOS, while opposite trends were observed in the miR-138 inhibitor group.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	22-30	nitric oxide synthase 3	Homo sapiens	136-140
28371277-10	2017	These findings indicate that up-regulation of miR-138 alleviates HCAEC injury and inflammatory response by inhibiting the PI3K/Akt/eNOS signalling pathway.	mir-138	46-53	nitric oxide synthase 3	Homo sapiens	131-135
28978108-8	2017	Overall, our data demonstrate that tunicamycin induced ER stress promotes prostate cancer cell death by activating mTORC1 through eNOS-RagC pathway.	Tunicamycin	35-46	nitric oxide synthase 3	Homo sapiens	130-134
28627664-0	2017	Sodium tanshinone IIA sulfonate suppresses heat stress-induced endothelial cell apoptosis by promoting NO production through upregulating the PI3K/AKT/eNOS pathway.	tanshinone II A sodium sulfonate	0-31	nitric oxide synthase 3	Homo sapiens	151-155
28627664-5	2017	The results presented in the present study demonstrated that the PI3K/AKT pathway was stimulated by STS treatment and that eNOS phosphorylation at Ser-1177 was also upregulated, resulting in increased nitric oxide production in HUVECs under heat stress.	Serine	147-150	nitric oxide synthase 3	Homo sapiens	123-127
28627664-5	2017	The results presented in the present study demonstrated that the PI3K/AKT pathway was stimulated by STS treatment and that eNOS phosphorylation at Ser-1177 was also upregulated, resulting in increased nitric oxide production in HUVECs under heat stress.	Nitric Oxide	201-213	nitric oxide synthase 3	Homo sapiens	123-127
28627664-6	2017	Using specific inhibitors, the authors confirmed that STS-induced endothelial nitric oxide synthase (eNOS) phosphorylation at Ser-1177 was activated by protein kinase B phosphorylation at Ser-473, involving activation of phosphatidylinositol-3 kinase (PI3K).	tanshinone II A sodium sulfonate	54-57	nitric oxide synthase 3	Homo sapiens	66-99
28627664-6	2017	Using specific inhibitors, the authors confirmed that STS-induced endothelial nitric oxide synthase (eNOS) phosphorylation at Ser-1177 was activated by protein kinase B phosphorylation at Ser-473, involving activation of phosphatidylinositol-3 kinase (PI3K).	tanshinone II A sodium sulfonate	54-57	nitric oxide synthase 3	Homo sapiens	101-105
28627664-6	2017	Using specific inhibitors, the authors confirmed that STS-induced endothelial nitric oxide synthase (eNOS) phosphorylation at Ser-1177 was activated by protein kinase B phosphorylation at Ser-473, involving activation of phosphatidylinositol-3 kinase (PI3K).	Serine	126-129	nitric oxide synthase 3	Homo sapiens	66-99
28627664-6	2017	Using specific inhibitors, the authors confirmed that STS-induced endothelial nitric oxide synthase (eNOS) phosphorylation at Ser-1177 was activated by protein kinase B phosphorylation at Ser-473, involving activation of phosphatidylinositol-3 kinase (PI3K).	Serine	126-129	nitric oxide synthase 3	Homo sapiens	101-105
28627664-6	2017	Using specific inhibitors, the authors confirmed that STS-induced endothelial nitric oxide synthase (eNOS) phosphorylation at Ser-1177 was activated by protein kinase B phosphorylation at Ser-473, involving activation of phosphatidylinositol-3 kinase (PI3K).	Serine	188-191	nitric oxide synthase 3	Homo sapiens	66-99
28627664-6	2017	Using specific inhibitors, the authors confirmed that STS-induced endothelial nitric oxide synthase (eNOS) phosphorylation at Ser-1177 was activated by protein kinase B phosphorylation at Ser-473, involving activation of phosphatidylinositol-3 kinase (PI3K).	Serine	188-191	nitric oxide synthase 3	Homo sapiens	101-105
28214453-0	2017	Reciprocal regulation of eNOS, H2S and CO-synthesizing enzymes in human atheroma: Correlation with plaque stability and effects of simvastatin.	Simvastatin	131-142	nitric oxide synthase 3	Homo sapiens	25-29
28214453-8	2017	NT levels were decreased in stable plaques with a concomitant increase of eNOS phosphorylation and expression and Akt activation compared to unstable lesions.	3-nitrotyrosine	0-2	nitric oxide synthase 3	Homo sapiens	74-78
28214453-11	2017	Simvastatin decreased iNOS, HO-1, HIF-1alpha and CSE whilst it increased eNOS phosphorylation.	Simvastatin	0-11	nitric oxide synthase 3	Homo sapiens	73-77
28214453-13	2017	Simvastatin, besides its known effect on eNOS upregulation, reduced the HIF-1alpha and its downstream targets.	Simvastatin	0-11	nitric oxide synthase 3	Homo sapiens	41-45
28708111-5	2017	A review of all current studies would suggest that IPC/RIPC relies on creating a small tissue injury resulting in the release of adenosine and l-arginine which act through the Adenosine receptors and the haem-oxygenase and endothelial nitric oxide synthase systems to reduce hepatocyte necrosis and improve the hepatic microcirculation post reperfusion.	Adenosine	129-138	nitric oxide synthase 3	Homo sapiens	223-256
28708111-5	2017	A review of all current studies would suggest that IPC/RIPC relies on creating a small tissue injury resulting in the release of adenosine and l-arginine which act through the Adenosine receptors and the haem-oxygenase and endothelial nitric oxide synthase systems to reduce hepatocyte necrosis and improve the hepatic microcirculation post reperfusion.	Arginine	143-153	nitric oxide synthase 3	Homo sapiens	223-256
28639572-12	2017	CONCLUSIONS: Increased ox-LDL, hs-CRP, and e-NOS are likely to be a result of oxidative stress, a condition in which an imbalance occurs between the production and inactivation of reactive nitrogen and oxygen species.	reactive nitrogen	180-197	nitric oxide synthase 3	Homo sapiens	43-48
28620990-2	2017	The main determinant of nitric oxide levels is enzyme nitric oxide synthase encoded by the NOS3 gene, the common variants in this gene may be responsible for variations in plasma enzyme levels.	Nitric Oxide	24-36	nitric oxide synthase 3	Homo sapiens	91-95
28725180-7	2017	Moreover, eNOS inhibition in cortical cells has a negative impact on cell survival after excitotoxic stimulation with N-methyl-D-aspartate (NMDA).	N-Methylaspartate	118-138	nitric oxide synthase 3	Homo sapiens	10-14
28725180-7	2017	Moreover, eNOS inhibition in cortical cells has a negative impact on cell survival after excitotoxic stimulation with N-methyl-D-aspartate (NMDA).	N-Methylaspartate	140-144	nitric oxide synthase 3	Homo sapiens	10-14
28725180-9	2017	Taken together, our results show that eNOS is located at excitatory synapses where it could represent a source for NO production and thus, the contribution of eNOS-derived nitric oxide to the regulation of neuronal survival and function deserves further investigations.	Nitric Oxide	172-184	nitric oxide synthase 3	Homo sapiens	38-42
28725180-9	2017	Taken together, our results show that eNOS is located at excitatory synapses where it could represent a source for NO production and thus, the contribution of eNOS-derived nitric oxide to the regulation of neuronal survival and function deserves further investigations.	Nitric Oxide	172-184	nitric oxide synthase 3	Homo sapiens	159-163
28383821-0	2017	H2 S-induced gastric fundus smooth muscle tension potentiation is mediated by the phosphoinositide 3-kinase/Akt/endothelial nitric oxide synthase pathway.	Hydrogen Sulfide	0-4	nitric oxide synthase 3	Homo sapiens	112-145
28383821-14	2017	Endothelial nitric oxide synthase (eNOS) phosphorylation at serine 1177 and Akt phosphorylation at serine 308 and threonine 473 were significantly inhibited by NaHS.	Serine	60-66	nitric oxide synthase 3	Homo sapiens	0-33
28412252-3	2017	Serial passaging from passage (P)1 to P4 (replicative senescence) of porcine coronary artery ECs, or treatment of P1 ECs with the endothelial nitric oxide synthase (eNOS) inhibitor L-NAME (premature senescence) induced acquisition of markers of senescence including increased senescence-associated-beta-galactosidase (SA-beta-gal) activity and p53, p21, p16 expression.	NG-Nitroarginine Methyl Ester	181-187	nitric oxide synthase 3	Homo sapiens	130-163
28383821-14	2017	Endothelial nitric oxide synthase (eNOS) phosphorylation at serine 1177 and Akt phosphorylation at serine 308 and threonine 473 were significantly inhibited by NaHS.	Serine	60-66	nitric oxide synthase 3	Homo sapiens	35-39
28383821-14	2017	Endothelial nitric oxide synthase (eNOS) phosphorylation at serine 1177 and Akt phosphorylation at serine 308 and threonine 473 were significantly inhibited by NaHS.	sodium bisulfide	160-164	nitric oxide synthase 3	Homo sapiens	0-33
28383821-14	2017	Endothelial nitric oxide synthase (eNOS) phosphorylation at serine 1177 and Akt phosphorylation at serine 308 and threonine 473 were significantly inhibited by NaHS.	sodium bisulfide	160-164	nitric oxide synthase 3	Homo sapiens	35-39
28383821-16	2017	However, eNOS phosphorylation at serine 1177 and Akt phosphorylation at serine 308 and threonine 473 were significantly potentiated by AOAA.	Serine	33-39	nitric oxide synthase 3	Homo sapiens	9-13
28383821-17	2017	Cystathionine beta-synthase siRNA interference significantly increased eNOS phosphorylation at serine 1177 and Akt phosphorylation at serine 308 and threonine 473.	Serine	95-101	nitric oxide synthase 3	Homo sapiens	71-75
28581447-8	2017	Under basal conditions, adenosine stimulated NO production, eNOS phosphorylation at serine 1177 from 5 minutes to 4 hours and inhibited eNOS phosphorylation at threonine 495 from 5 minutes to 6 hours, but increased phosphorylation of ERK1/2, p38MAPK, and p70S6K only after exposure for 5 minutes.	Adenosine	24-33	nitric oxide synthase 3	Homo sapiens	60-64
28161429-8	2017	Results of western blot showed SIM post-treatment increased significantly phosphor-eNOS (Ser1177) expression but no total eNOS expression.	Simvastatin	31-34	nitric oxide synthase 3	Homo sapiens	83-87
28654706-2	2017	Previous studies showed that bovine eNOS serine 1179 (Serine 1177 for human eNOS) phosphorylation enhanced NO synthesis.	Serine	41-47	nitric oxide synthase 3	Homo sapiens	76-80
28654706-2	2017	Previous studies showed that bovine eNOS serine 1179 (Serine 1177 for human eNOS) phosphorylation enhanced NO synthesis.	Serine	54-60	nitric oxide synthase 3	Homo sapiens	76-80
28366876-4	2017	VEGF/VEGFR2 induces calpain 2 dependent activation of PI3K/AMPK/Akt/eNOS pathway, and consequent nitric oxide production and physiological angiogenesis.	Nitric Oxide	97-109	nitric oxide synthase 3	Homo sapiens	68-72
26660451-4	2017	Thus, the consequences of the interaction (redox crosstalk) of superoxide/hydrogen peroxide produced by mitochondria with other ROS producing enzymes such as NADPH oxidases (Nox) are of outstanding importance and will be discussed including the consequences for endothelial nitric oxide synthase (eNOS) uncoupling as well as the redox regulation of the vascular function/tone in general (soluble guanylyl cyclase, endothelin-1, prostanoid synthesis).	Superoxides	63-73	nitric oxide synthase 3	Homo sapiens	262-295
26660451-4	2017	Thus, the consequences of the interaction (redox crosstalk) of superoxide/hydrogen peroxide produced by mitochondria with other ROS producing enzymes such as NADPH oxidases (Nox) are of outstanding importance and will be discussed including the consequences for endothelial nitric oxide synthase (eNOS) uncoupling as well as the redox regulation of the vascular function/tone in general (soluble guanylyl cyclase, endothelin-1, prostanoid synthesis).	Hydrogen Peroxide	74-91	nitric oxide synthase 3	Homo sapiens	262-295
26660451-4	2017	Thus, the consequences of the interaction (redox crosstalk) of superoxide/hydrogen peroxide produced by mitochondria with other ROS producing enzymes such as NADPH oxidases (Nox) are of outstanding importance and will be discussed including the consequences for endothelial nitric oxide synthase (eNOS) uncoupling as well as the redox regulation of the vascular function/tone in general (soluble guanylyl cyclase, endothelin-1, prostanoid synthesis).	ros	128-131	nitric oxide synthase 3	Homo sapiens	262-295
26660451-4	2017	Thus, the consequences of the interaction (redox crosstalk) of superoxide/hydrogen peroxide produced by mitochondria with other ROS producing enzymes such as NADPH oxidases (Nox) are of outstanding importance and will be discussed including the consequences for endothelial nitric oxide synthase (eNOS) uncoupling as well as the redox regulation of the vascular function/tone in general (soluble guanylyl cyclase, endothelin-1, prostanoid synthesis).	Prostaglandins	428-438	nitric oxide synthase 3	Homo sapiens	262-295
28218444-8	2017	The 8 mg/mL PEG-Scl2-2 hydrogels also appeared to support similar or improved levels of EOC homeostatic marker expression relative to PEG-collagen hydrogels based on von Willebrand factor, collagen IV, NOS3, thrombomodulin, and E-selectin assessment.	Polyethylene Glycols	12-15	nitric oxide synthase 3	Homo sapiens	202-206
28581447-8	2017	Under basal conditions, adenosine stimulated NO production, eNOS phosphorylation at serine 1177 from 5 minutes to 4 hours and inhibited eNOS phosphorylation at threonine 495 from 5 minutes to 6 hours, but increased phosphorylation of ERK1/2, p38MAPK, and p70S6K only after exposure for 5 minutes.	Threonine	160-169	nitric oxide synthase 3	Homo sapiens	136-140
28581447-11	2017	Our data demonstrated that adenosine prevents hypothermic injury to the endothelium by activating ERK1/2, eNOS, p70S6K, and p38MAPK signaling pathways at early time points.	Adenosine	27-36	nitric oxide synthase 3	Homo sapiens	106-110
28581447-8	2017	Under basal conditions, adenosine stimulated NO production, eNOS phosphorylation at serine 1177 from 5 minutes to 4 hours and inhibited eNOS phosphorylation at threonine 495 from 5 minutes to 6 hours, but increased phosphorylation of ERK1/2, p38MAPK, and p70S6K only after exposure for 5 minutes.	Adenosine	24-33	nitric oxide synthase 3	Homo sapiens	136-140
28581447-8	2017	Under basal conditions, adenosine stimulated NO production, eNOS phosphorylation at serine 1177 from 5 minutes to 4 hours and inhibited eNOS phosphorylation at threonine 495 from 5 minutes to 6 hours, but increased phosphorylation of ERK1/2, p38MAPK, and p70S6K only after exposure for 5 minutes.	Serine	84-90	nitric oxide synthase 3	Homo sapiens	60-64
28368445-9	2017	CoCl2-induced increase in MP release was associated with upregulation of caveolin-1 and downregulation of eNOS expression in trophoblasts (P &lt; 0.05), which could be attenuated by 1,25(OH)2D3.	cobaltous chloride	0-5	nitric oxide synthase 3	Homo sapiens	106-110
28368445-14	2017	Inhibition of caspase-3 cleavage and ROCK1 activation, together with upregulation of eNOS expression, could be the potential cellular/molecular mechanism(s) of vitamin D protective effects on placental trophoblasts.	Vitamin D	160-169	nitric oxide synthase 3	Homo sapiens	85-89
28178430-0	2017	Nitric oxide synthesis-promoting effects of valsartan in human umbilical vein endothelial cells via the Akt/adenosine monophosphate-activated protein kinase/endothelial nitric oxide synthase pathway.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	157-190
28562663-2	2017	Although the role of ADMA as an inhibitor of endothelial nitric oxide synthase (eNOS) is well-recognized, cellular interactions between ARG and ADMA are not well-characterized.	N,N-dimethylarginine	21-25	nitric oxide synthase 3	Homo sapiens	45-78
28178430-0	2017	Nitric oxide synthesis-promoting effects of valsartan in human umbilical vein endothelial cells via the Akt/adenosine monophosphate-activated protein kinase/endothelial nitric oxide synthase pathway.	Valsartan	44-53	nitric oxide synthase 3	Homo sapiens	157-190
32264405-5	2017	In the present study, we report that ZONF induce angiogenesis through MAPK/Akt/eNOS mediated nitric oxide formation, which further acts in a cGMP dependent manner.	Nitric Oxide	93-105	nitric oxide synthase 3	Homo sapiens	79-83
28422712-2	2017	We hypothesized that polymorphisms in NOS3, ABCB1 and IL23R were related to individual differences in alcohol sensitivity and the development of alcohol-induced ONFH.	Alcohols	102-109	nitric oxide synthase 3	Homo sapiens	38-42
28422712-2	2017	We hypothesized that polymorphisms in NOS3, ABCB1 and IL23R were related to individual differences in alcohol sensitivity and the development of alcohol-induced ONFH.	Alcohols	145-152	nitric oxide synthase 3	Homo sapiens	38-42
28422712-8	2017	CONCLUSIONS: This study provides evidence for three alcohol-induced ONFH susceptibility genes (NOS3, ABCB1 and IL23R) in Chinese males and polymorphisms of them may be associated with alcohol-induced ONFH risk.	Alcohols	52-59	nitric oxide synthase 3	Homo sapiens	95-99
28422712-8	2017	CONCLUSIONS: This study provides evidence for three alcohol-induced ONFH susceptibility genes (NOS3, ABCB1 and IL23R) in Chinese males and polymorphisms of them may be associated with alcohol-induced ONFH risk.	Alcohols	184-191	nitric oxide synthase 3	Homo sapiens	95-99
32264405-5	2017	In the present study, we report that ZONF induce angiogenesis through MAPK/Akt/eNOS mediated nitric oxide formation, which further acts in a cGMP dependent manner.	Cyclic GMP	141-145	nitric oxide synthase 3	Homo sapiens	79-83
28317089-0	2017	EGCG protects against homocysteine-induced human umbilical vein endothelial cells apoptosis by modulating mitochondrial-dependent apoptotic signaling and PI3K/Akt/eNOS signaling pathways.	epigallocatechin gallate	0-4	nitric oxide synthase 3	Homo sapiens	163-167
28500309-9	2017	In contrast, resveratrol significantly reduced TNFalpha-induced Endothelin-1 (a vasoconstrictor) and significantly increased the phosphorylation of endothelial nitric oxide synthase (eNOS).	Resveratrol	13-24	nitric oxide synthase 3	Homo sapiens	148-181
28481400-5	2017	Among the genes involved, eNOS (endothelial nitric oxide synthase gene), which is responsible for the production of endothelial nitric oxide (an important arterial vasodilator), when presented in polymorphic variation can determine production, malfunction, and predisposition to atherosclerosis.	Nitric Oxide	44-56	nitric oxide synthase 3	Homo sapiens	26-30
28317089-0	2017	EGCG protects against homocysteine-induced human umbilical vein endothelial cells apoptosis by modulating mitochondrial-dependent apoptotic signaling and PI3K/Akt/eNOS signaling pathways.	Homocysteine	22-34	nitric oxide synthase 3	Homo sapiens	163-167
28317089-8	2017	In addition, EGCG enhanced the protein ratio of p-Akt/Akt, endothelial nitric oxide synthase (eNOS) activation and nitric oxide (NO) formation in injured cells.	epigallocatechin gallate	13-17	nitric oxide synthase 3	Homo sapiens	59-92
28526204-0	2017	The -786 T/C polymorphism of NOS3 gene is a susceptibility marker of COPD among Tunisians that correlates with nitric oxide levels and airflow obstruction.	Nitric Oxide	111-123	nitric oxide synthase 3	Homo sapiens	29-33
28317089-8	2017	In addition, EGCG enhanced the protein ratio of p-Akt/Akt, endothelial nitric oxide synthase (eNOS) activation and nitric oxide (NO) formation in injured cells.	epigallocatechin gallate	13-17	nitric oxide synthase 3	Homo sapiens	94-98
28317089-9	2017	In conclusion, the present study shows that EGCG prevents Hcy-induced HUVECs apoptosis via modulating mitochondrial apoptotic and PI3K/Akt/eNOS signaling pathways.	epigallocatechin gallate	44-48	nitric oxide synthase 3	Homo sapiens	139-143
28317089-9	2017	In conclusion, the present study shows that EGCG prevents Hcy-induced HUVECs apoptosis via modulating mitochondrial apoptotic and PI3K/Akt/eNOS signaling pathways.	Homocysteine	58-61	nitric oxide synthase 3	Homo sapiens	139-143
27380043-8	2017	In addition, TMP could notably down-regulate the characteristic proteins in Rho/ROCK signaling pathway such as RhoA and Rac1, which triggered abnormal changes of eNOS and ROS, respectively.	tetramethylpyrazine	13-16	nitric oxide synthase 3	Homo sapiens	162-166
28235804-1	2017	Endothelial nitric-oxide synthase (eNOS) and its bioactive product, nitric oxide (NO), mediate many endothelial cell functions, including angiogenesis and vascular permeability.	Nitric Oxide	68-80	nitric oxide synthase 3	Homo sapiens	0-33
28565879-6	2017	Exposure of human umbilical vein endothelial cells (HUVEC) to a high glucose concentration decreased NO and endothelial nitric oxide synthase (eNOS) levels but increased inducible NOS (iNOS) levels.	Glucose	69-76	nitric oxide synthase 3	Homo sapiens	108-141
28484701-9	2017	More importantly, DUSP4 overexpression upregulates eNOS protein expression (1.62 +- 0.33 versus 0.65 +- 0.16) during H/R-induced stress.	r	119-120	nitric oxide synthase 3	Homo sapiens	51-55
28235804-1	2017	Endothelial nitric-oxide synthase (eNOS) and its bioactive product, nitric oxide (NO), mediate many endothelial cell functions, including angiogenesis and vascular permeability.	Nitric Oxide	68-80	nitric oxide synthase 3	Homo sapiens	35-39
28284350-0	2017	Ketamine upregulates eNOS expression in human astroglial A172 cells: Possible role in its antidepressive properties.	Ketamine	0-8	nitric oxide synthase 3	Homo sapiens	21-25
28284350-3	2017	We investigated the effect of ketamine on eNOS expression in human A172 astroglial cells.	Ketamine	30-38	nitric oxide synthase 3	Homo sapiens	42-46
28284350-4	2017	Ketamine (50-500muM) increased eNOS expression at 4-24h in a concentration-dependent manner.	Ketamine	0-8	nitric oxide synthase 3	Homo sapiens	31-35
28108596-2	2017	This NADP(H) depletion was shown to limit the production of nitric oxide by endothelial nitric oxide synthase (eNOS), which requires NADPH for nitric oxide production, resulting in greatly altered endothelial function.	NADP	5-12	nitric oxide synthase 3	Homo sapiens	76-109
28394935-2	2017	We show here that nitric oxide (NO) generated by endothelial nitric oxide synthase (eNOS) controls the coalescence of protein kinase C-theta (PKC-theta) at the central supramolecular activation cluster (c-SMAC) of the IS.	Nitric Oxide	18-30	nitric oxide synthase 3	Homo sapiens	49-82
28268155-2	2017	AIM: To investigate the effect of these variations of NOS3 on ED phenotypes and the response to sildenafil in a Han Chinese population.	Sildenafil Citrate	96-106	nitric oxide synthase 3	Homo sapiens	54-58
28268155-14	2017	STRENGTHS &amp; LIMITATIONS: This study provides strong evidence that NOS3 functional variation is an independent risk factor for ED in the Han Chinese population, which should be confirmed in larger cohorts considering the limited number of subjects in this study.	Adenosine Monophosphate	11-14	nitric oxide synthase 3	Homo sapiens	70-74
28108596-2	2017	This NADP(H) depletion was shown to limit the production of nitric oxide by endothelial nitric oxide synthase (eNOS), which requires NADPH for nitric oxide production, resulting in greatly altered endothelial function.	Nitric Oxide	60-72	nitric oxide synthase 3	Homo sapiens	76-109
28108596-2	2017	This NADP(H) depletion was shown to limit the production of nitric oxide by endothelial nitric oxide synthase (eNOS), which requires NADPH for nitric oxide production, resulting in greatly altered endothelial function.	NADP	133-138	nitric oxide synthase 3	Homo sapiens	76-109
27590258-0	2017	Phosphocreatine protects endothelial cells from Methylglyoxal induced oxidative stress and apoptosis via the regulation of PI3K/Akt/eNOS and NF-kappaB pathway.	Phosphocreatine	0-15	nitric oxide synthase 3	Homo sapiens	132-136
28071686-11	2017	ARG1 and NOS3 in cluster 4 were enriched in biological process of arginine catabolic process.	Arginine	66-74	nitric oxide synthase 3	Homo sapiens	9-13
27590258-10	2017	In addition, the antiapoptotic effect of PCr enhanced p-Akt/Akt protein ratio, NO synthase (eNOS) activation, NO production and cGMP levels and also was partially suppressed by a PI3K inhibitor (LY294002).	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	195-203	nitric oxide synthase 3	Homo sapiens	92-96
28346478-9	2017	A synergistic effect between eNOS and Cav-1 polymorphisms on IS risk elevation was significantly influenced by alcohol drinking, heavy cigarette smoking (P-trend&lt;0.01), and hypercholesterolemia (P-trend &lt; 0.001).	Alcohols	111-118	nitric oxide synthase 3	Homo sapiens	29-33
28252100-3	2017	Pretreatment of XMJ (25, 50, 100 mug/ml) for 30 minutes concentration-dependently activated eNOS, improved cell viabilities, increased NO generations, and reduced ROS productions in human umbilical vein endothelial cells incubated with H2O2 for 2 hours, accompanied with restoration of BH4.	4-[[(1E)-2-(4-CHLOROPHENYL)ETHENYL]SULFONYL]-1-[[1-(4-PYRIDINYL)-4-PIPERIDINYL]METHYL]PIPERAZINONE	16-19	nitric oxide synthase 3	Homo sapiens	92-96
28345531-6	2017	Catechins cause an increase in the activity of endothelial nitric oxide synthase (eNOS) and increased production of nitric oxide (NO) and decrease in blood pressure.	Catechin	0-9	nitric oxide synthase 3	Homo sapiens	47-80
28322298-0	2017	H2S regulates endothelial nitric oxide synthase protein stability by promoting microRNA-455-3p expression.	Hydrogen Sulfide	0-3	nitric oxide synthase 3	Homo sapiens	14-47
28322298-1	2017	The aims of the present study are to determine whether hydrogen sulfide (H2S) is involved in the expression of endothelial nitric oxide synthase (eNOS) and nitric oxide (NO) production, and to identify the role of microRNA-455-3p (miR-455-3p) during those processes.	Hydrogen Sulfide	55-71	nitric oxide synthase 3	Homo sapiens	111-144
28322298-1	2017	The aims of the present study are to determine whether hydrogen sulfide (H2S) is involved in the expression of endothelial nitric oxide synthase (eNOS) and nitric oxide (NO) production, and to identify the role of microRNA-455-3p (miR-455-3p) during those processes.	Hydrogen Sulfide	55-71	nitric oxide synthase 3	Homo sapiens	146-150
28322298-1	2017	The aims of the present study are to determine whether hydrogen sulfide (H2S) is involved in the expression of endothelial nitric oxide synthase (eNOS) and nitric oxide (NO) production, and to identify the role of microRNA-455-3p (miR-455-3p) during those processes.	Hydrogen Sulfide	73-76	nitric oxide synthase 3	Homo sapiens	111-144
28322298-1	2017	The aims of the present study are to determine whether hydrogen sulfide (H2S) is involved in the expression of endothelial nitric oxide synthase (eNOS) and nitric oxide (NO) production, and to identify the role of microRNA-455-3p (miR-455-3p) during those processes.	Hydrogen Sulfide	73-76	nitric oxide synthase 3	Homo sapiens	146-150
28322298-1	2017	The aims of the present study are to determine whether hydrogen sulfide (H2S) is involved in the expression of endothelial nitric oxide synthase (eNOS) and nitric oxide (NO) production, and to identify the role of microRNA-455-3p (miR-455-3p) during those processes.	Nitric Oxide	123-135	nitric oxide synthase 3	Homo sapiens	146-150
28322298-2	2017	In cultured human umbilical vein endothelial cells (HUVECs), the expression of miR-455-3p, eNOS protein and the NO production was detected after administration with 50 muM NaHS.	sodium bisulfide	172-176	nitric oxide synthase 3	Homo sapiens	91-95
28322298-3	2017	The results indicated that H2S could augment the expression of miR-455-3p and eNOS protein, leading to the increase of NO level.	Hydrogen Sulfide	27-30	nitric oxide synthase 3	Homo sapiens	78-82
28322298-5	2017	Moreover, H2S and miR-455-3p could no longer increase the protein level of eNOS in the presence of proteasome inhibitor, MG-132.	Hydrogen Sulfide	10-13	nitric oxide synthase 3	Homo sapiens	75-79
28322298-5	2017	Moreover, H2S and miR-455-3p could no longer increase the protein level of eNOS in the presence of proteasome inhibitor, MG-132.	mir-455-3p	18-28	nitric oxide synthase 3	Homo sapiens	75-79
28322298-5	2017	Moreover, H2S and miR-455-3p could no longer increase the protein level of eNOS in the presence of proteasome inhibitor, MG-132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	121-127	nitric oxide synthase 3	Homo sapiens	75-79
28322298-8	2017	Our data suggest that the stability of eNOS protein and the NO production could be regulated by H2S through miR-455-3p.	Hydrogen Sulfide	96-99	nitric oxide synthase 3	Homo sapiens	39-43
28034894-5	2017	Herein, we hypothesized that hypo-osmotic stress following water ingestion modulates the eNOS/NO pathway, thereby alternating vascular resistance.	Water	59-64	nitric oxide synthase 3	Homo sapiens	89-93
28034894-12	2017	RBCs in vitro were stimulated with angiopoietin-1, Tie-2, or 0.8% saline and showed significant increase in Tie-2, Akt, and eNOS phosphorylation upon angiopoietin-1 treatment and enhanced activation upon cotreatment of angiopoietin-1 and 0.8% saline.	Sodium Chloride	66-72	nitric oxide synthase 3	Homo sapiens	124-128
28034894-13	2017	CONCLUSIONS: The hypo-osmotic stimulus of water ingestion increases angiopoietin-1 secretion and subsequently activates the Tie-2/Akt/eNOS signaling pathway in RBCs, thereby revealing a novel biological mechanism simultaneously occurring with the osmopressor response.	Water	42-47	nitric oxide synthase 3	Homo sapiens	134-138
27569446-1	2017	Nitric oxide (NO) is a vasoactive substance synthesized from l-arginine by neuronal (NOS1), endothelial (NOS3), and inducible (NOS2) nitric oxide synthases.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	105-109
27696692-0	2017	Gene-Gene Interactions Among PRKCA, NOS3 and BDKRB2 Polymorphisms Affect the Antihypertensive Effects of Enalapril.	Enalapril	105-114	nitric oxide synthase 3	Homo sapiens	36-40
28395021-6	2017	Protective effects of tipifarnib were associated with inhibition of Ras and RhoB, actin depolymerization and increased eNOS expression in vitro and in vivo.	tipifarnib	22-32	nitric oxide synthase 3	Homo sapiens	119-123
27998008-0	2017	Antihypertensive methyldopa, labetalol, hydralazine, and clonidine reversed tumour necrosis factor-alpha inhibited endothelial nitric oxide synthase expression in endothelial-trophoblast cellular networks.	Methyldopa	17-27	nitric oxide synthase 3	Homo sapiens	115-148
27998008-0	2017	Antihypertensive methyldopa, labetalol, hydralazine, and clonidine reversed tumour necrosis factor-alpha inhibited endothelial nitric oxide synthase expression in endothelial-trophoblast cellular networks.	Labetalol	29-38	nitric oxide synthase 3	Homo sapiens	115-148
27998008-0	2017	Antihypertensive methyldopa, labetalol, hydralazine, and clonidine reversed tumour necrosis factor-alpha inhibited endothelial nitric oxide synthase expression in endothelial-trophoblast cellular networks.	Hydralazine	40-51	nitric oxide synthase 3	Homo sapiens	115-148
27998008-0	2017	Antihypertensive methyldopa, labetalol, hydralazine, and clonidine reversed tumour necrosis factor-alpha inhibited endothelial nitric oxide synthase expression in endothelial-trophoblast cellular networks.	Clonidine	57-66	nitric oxide synthase 3	Homo sapiens	115-148
27998008-8	2017	Methyldopa, labetalol, hydralazine and clonidine reversed the inhibitory effect of TNF-alpha on eNOS mRNA expression.	Methyldopa	0-10	nitric oxide synthase 3	Homo sapiens	96-100
27998008-8	2017	Methyldopa, labetalol, hydralazine and clonidine reversed the inhibitory effect of TNF-alpha on eNOS mRNA expression.	Labetalol	12-21	nitric oxide synthase 3	Homo sapiens	96-100
27998008-8	2017	Methyldopa, labetalol, hydralazine and clonidine reversed the inhibitory effect of TNF-alpha on eNOS mRNA expression.	Hydralazine	23-34	nitric oxide synthase 3	Homo sapiens	96-100
27998008-8	2017	Methyldopa, labetalol, hydralazine and clonidine reversed the inhibitory effect of TNF-alpha on eNOS mRNA expression.	Clonidine	39-48	nitric oxide synthase 3	Homo sapiens	96-100
27998008-9	2017	After pre-incubating endothelial cells with TNF-alpha and sFlt-1, all the medications except methyldopa lost their effect on eNOS mRNA expression.	Methyldopa	93-103	nitric oxide synthase 3	Homo sapiens	125-129
28260990-7	2017	The effect of rauwolscine on the dexmedetomidine-mediated change in phenylephrine-induced endothelial nitric oxide synthase (eNOS) phosphorylation in human umbilical vein endothelial cells was examined using western blotting.	Yohimbine	14-25	nitric oxide synthase 3	Homo sapiens	90-123
28260990-7	2017	The effect of rauwolscine on the dexmedetomidine-mediated change in phenylephrine-induced endothelial nitric oxide synthase (eNOS) phosphorylation in human umbilical vein endothelial cells was examined using western blotting.	Dexmedetomidine	33-48	nitric oxide synthase 3	Homo sapiens	90-123
28260990-7	2017	The effect of rauwolscine on the dexmedetomidine-mediated change in phenylephrine-induced endothelial nitric oxide synthase (eNOS) phosphorylation in human umbilical vein endothelial cells was examined using western blotting.	Phenylephrine	68-81	nitric oxide synthase 3	Homo sapiens	90-123
28138348-0	2017	Cholesterol Enrichment Impairs Capacitative Calcium Entry, eNOS Phosphorylation &amp; Shear Stress-Induced NO Production.	Cholesterol	0-11	nitric oxide synthase 3	Homo sapiens	59-63
27913896-3	2017	RESULTS: Adenoviral delivery of human eNOS gene into mouse bone marrow-derived MSCs (BM-MSCs) conferred resistance to oxygen glucose deprivation (OGD)-induced cell death in vitro, and elevated the bioavailability of nitric oxide when injected into the myocardium in vivo.	Nitric Oxide	216-228	nitric oxide synthase 3	Homo sapiens	38-42
28138348-5	2017	Although calcium signaling is complex, we have previously shown that NO production by endothelial nitric oxide synthase (eNOS) is preferentially activated by calcium influx via store-operated channels.	Calcium	9-16	nitric oxide synthase 3	Homo sapiens	86-119
29927218-3	2017	Similar to other gaseous signaling molecules,H2S playeda pivotal role in the pathophysiological processes of cardiovascular disease due to its various biological activities, including anti-oxidative, antiapoptotic, proangiogenic, vasodilating capacities, modulating endothelial nitric oxide synthase activity, and so on.	Hydrogen Sulfide	45-48	nitric oxide synthase 3	Homo sapiens	266-299
28138348-5	2017	Although calcium signaling is complex, we have previously shown that NO production by endothelial nitric oxide synthase (eNOS) is preferentially activated by calcium influx via store-operated channels.	Calcium	9-16	nitric oxide synthase 3	Homo sapiens	121-125
28138348-5	2017	Although calcium signaling is complex, we have previously shown that NO production by endothelial nitric oxide synthase (eNOS) is preferentially activated by calcium influx via store-operated channels.	Calcium	158-165	nitric oxide synthase 3	Homo sapiens	86-119
28138348-5	2017	Although calcium signaling is complex, we have previously shown that NO production by endothelial nitric oxide synthase (eNOS) is preferentially activated by calcium influx via store-operated channels.	Calcium	158-165	nitric oxide synthase 3	Homo sapiens	121-125
28138348-7	2017	Our results show that cholesterol enrichment abolished ATP-induced eNOS phosphorylation and attenuated the calcium response by the preferential inhibition of CCE.	Cholesterol	22-33	nitric oxide synthase 3	Homo sapiens	67-71
28138348-7	2017	Our results show that cholesterol enrichment abolished ATP-induced eNOS phosphorylation and attenuated the calcium response by the preferential inhibition of CCE.	Adenosine Triphosphate	55-58	nitric oxide synthase 3	Homo sapiens	67-71
28138348-8	2017	Furthermore, cholesterol enrichment also inhibited shear stress-induced NO production and eNOS phosporylation, consistent with our previous results showing a significant role for ATP autocrine stimulation and subsequent activation of CCE in the endothelial flow response.	Cholesterol	13-24	nitric oxide synthase 3	Homo sapiens	90-94
28000882-0	2017	Modulation of low shear stress-induced eNOS multi-site phosphorylation and nitric oxide production via protein kinase and ERK1/2 signaling.	Nitric Oxide	75-87	nitric oxide synthase 3	Homo sapiens	39-43
28000882-8	2017	LSS-stimulated phosphorylation of eNOS-Ser1177 and -Thr495 were suppressed by the Akt inhibitor, perifosine, and extracellular signal regulated kinases1/2 (ERK1/2) inhibitor, PD98059, respectively.	perifosine	97-107	nitric oxide synthase 3	Homo sapiens	34-38
28000882-8	2017	LSS-stimulated phosphorylation of eNOS-Ser1177 and -Thr495 were suppressed by the Akt inhibitor, perifosine, and extracellular signal regulated kinases1/2 (ERK1/2) inhibitor, PD98059, respectively.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	175-182	nitric oxide synthase 3	Homo sapiens	34-38
28000882-9	2017	Additionally, the phosphorylation of eNOS-Ser633 inhibited by LSS was restored by the protein kinase A activator, 8-Bromo-cAMP.	8-Bromo Cyclic Adenosine Monophosphate	114-126	nitric oxide synthase 3	Homo sapiens	37-41
28395329-12	2017	These results suggest that upregulation of eNOSSer1177 and AktSer473 phosphorylation and inhibition of ROCK1 cleavage in EC and modulation of eNOS and caveolin-1 expression in MP could be plausible mechanisms of vitamin D protective effects on ECs.	Vitamin D	212-221	nitric oxide synthase 3	Homo sapiens	43-47
28062183-5	2017	Our data indicate that beta-arrestins and Akt/eNOS downstream signaling are required for early SS-induced NO production in SVECs, which is consistent with the idea that beta-arrestins and caveolin-1 are part of a pre-assembled complex associated with the cellular mechanotransduction machinery.	H-SER-SER-OH	95-97	nitric oxide synthase 3	Homo sapiens	46-50
27554845-6	2017	Palmitate-induced impairment of NO production was restored by the glycomimetics, through activation of Akt/eNOS signaling.	Palmitates	0-9	nitric oxide synthase 3	Homo sapiens	107-111
28395329-9	2017	We found that under lowered oxygen condition, 1,25(OH)2D3 could upregulate EC eNOS, p-eNOSSer1177, and p-AktSer473 expression, but inhibit cleaved ROCK1 expression.	Oxygen	28-34	nitric oxide synthase 3	Homo sapiens	78-82
30765915-1	2018	Endothelial nitric oxide synthase (NOS3) generates nitric oxide in blood vessels and is involved in the regulation of vascular function, metabolism and muscle fibre type transformations.	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	35-39
27765751-6	2017	GPBAR1 is expressed in endothelial cells and liver sinusoidal cells (LSECs) and responds to LCA by regulating the expression of both endothelial nitric oxide synthase (eNOS) and cystathionine-gamma-lyase (CSE), an enzyme involved in generation of hydrogen sulfide (H2S).	Lithocholic Acid	92-95	nitric oxide synthase 3	Homo sapiens	133-166
28395329-9	2017	We found that under lowered oxygen condition, 1,25(OH)2D3 could upregulate EC eNOS, p-eNOSSer1177, and p-AktSer473 expression, but inhibit cleaved ROCK1 expression.	Calcitriol	46-57	nitric oxide synthase 3	Homo sapiens	78-82
28116308-5	2017	UA inhibited endothelial nitric oxide synthase (eNOS) expression and nitric oxide (NO) production in HUVECs, increased intracellular HMGB1 expression and extracellular HMGB1 secretion, and upregulated RAGE expression.	Uric Acid	0-2	nitric oxide synthase 3	Homo sapiens	13-46
28395329-11	2017	Strikingly, we also found that oxidative stress-induced decrease in ratio of eNOS and caveolin-1 expression in MP could be attenuated when 1,25(OH)2D3 was present in culture.	(oh)2d3	143-150	nitric oxide synthase 3	Homo sapiens	77-81
29050484-0	2017	eNOS and XRCC4 VNTR variants contribute to formation of nicotine dependence and/or schizophrenia.	Nicotine	56-64	nitric oxide synthase 3	Homo sapiens	0-4
29050484-1	2017	BACKGROUND: This study aimed to evaluate whether VNTR variants in the Endothelial Nitric Oxide Synthase (eNOS) and the XRCC4 gene play any role in nicotine dependence (ND) and/or Schizophrenia+ND (Sch+ND) ethiopathogenesis.	Nicotine	147-155	nitric oxide synthase 3	Homo sapiens	70-103
29050484-1	2017	BACKGROUND: This study aimed to evaluate whether VNTR variants in the Endothelial Nitric Oxide Synthase (eNOS) and the XRCC4 gene play any role in nicotine dependence (ND) and/or Schizophrenia+ND (Sch+ND) ethiopathogenesis.	Nicotine	147-155	nitric oxide synthase 3	Homo sapiens	105-109
28337882-1	2017	This study aimed to investigate the correlation between blood asymmetric dimethylarginine (ADMA) and the complications of patients with cardiovascular diseases through studying the level changes of ADMA, endothelial nitric oxide synthase (eNOS) and NO.	N,N-dimethylarginine	91-95	nitric oxide synthase 3	Homo sapiens	204-237
26792585-8	2017	Additionally, MHBFC caused a significant increase in PI3K, phosphorylation of Akt, mammalian target of rapamycin, and endothelial nitric oxide synthase, and a decrease in the expression of cleaved caspase-3, Beclin1, and conversion of microtubule-associated protein 1 light chain 3.	17-methoxyl-7-hydroxy-benzene-furanchalcone	14-19	nitric oxide synthase 3	Homo sapiens	118-151
28946141-1	2017	BACKGROUND/AIMS: Endothelial nitric oxide synthase (eNOS) is one of the most important enzymes for producting nitric oxide (NO), which regulate the function of many organs and cells.	Nitric Oxide	29-41	nitric oxide synthase 3	Homo sapiens	52-56
28115138-6	2017	In addition, endogenous 2-AG prevented cerebral vasculature dysfunction following SO2 inhalation by inhibiting endothelin 1 (ET-1), vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule 1 (ICAM-1) expression, elevating endothelial nitric oxide synthase (eNOS) level, and restoring the imbalance between thromboxane A2 (TXA2) and prostaglandin I2 (PGI2).	glyceryl 2-arachidonate	24-28	nitric oxide synthase 3	Homo sapiens	244-277
29104725-1	2017	The purpose of this study was to verify the influence of the genotype or haplotype (interaction) of the NOS3 polymorphisms [-786T&gt;C, 894G&gt;T (Glu298Asp), and intron 4b/a] on the response to multicomponent training (various capacities and motor skills) on blood pressure (BP), nitrite concentration, redox status, and physical fitness in older adult women.	Nitrites	281-288	nitric oxide synthase 3	Homo sapiens	104-108
28478454-3	2017	Delivery of arginine to membrane bound eNOS by the cationic amino acid transporter-1 (CAT-1) has been shown to modulate eNOS activity.	Arginine	12-20	nitric oxide synthase 3	Homo sapiens	39-43
28478454-3	2017	Delivery of arginine to membrane bound eNOS by the cationic amino acid transporter-1 (CAT-1) has been shown to modulate eNOS activity.	Arginine	12-20	nitric oxide synthase 3	Homo sapiens	120-124
27958382-0	2017	Polymorphisms of ABCC5 and NOS3 genes influence doxorubicin cardiotoxicity in survivors of childhood acute lymphoblastic leukemia.	Doxorubicin	48-59	nitric oxide synthase 3	Homo sapiens	27-31
28025449-2	2017	Recent studies have shown that metformin can enhance bone formation through induction of endothelial nitric oxide synthase (eNOS).	Metformin	31-40	nitric oxide synthase 3	Homo sapiens	89-122
27773804-0	2016	Aliskiren attenuates the effects of interleukin-6 on endothelial nitric oxide synthase and caveolin-1 in human aortic endothelial cells.	aliskiren	0-9	nitric oxide synthase 3	Homo sapiens	53-86
27773804-3	2016	In this study, we examined the effects of pretreatment with aliskiren on the changes of IL-6-induced expression and activation of eNOS and caveolin-1 in cultured HAECs.	aliskiren	60-69	nitric oxide synthase 3	Homo sapiens	130-134
27773804-4	2016	IL-6 inhibited and aliskiren increased the phosphorylation of eNOS at Ser1177; however, eNOS protein and mRNA expression were not changed.	aliskiren	19-28	nitric oxide synthase 3	Homo sapiens	62-66
27773804-5	2016	Pretreatment with aliskiren attenuated the inhibitory effects of IL-6 on eNOS phosphorylation and nitric oxide production.	aliskiren	18-27	nitric oxide synthase 3	Homo sapiens	73-77
27773804-8	2016	The binding of eNOS and caveolin-1, as determined by a co-immunoprecipitation assay, was increased by IL-6 treatment and decreased by aliskiren pretreatment.	aliskiren	134-143	nitric oxide synthase 3	Homo sapiens	15-19
27773804-10	2016	In conclusion, aliskiren attenuates the inhibitory effects of IL-6 on eNOS phosphorylation and nitric oxide production and IL-6 induced caveolin-1 phosphorylation.	aliskiren	15-24	nitric oxide synthase 3	Homo sapiens	70-74
27773804-11	2016	In addition, aliskiren reverses the effects of IL-6 on the eNOS-caveolin-1 interaction.	aliskiren	13-22	nitric oxide synthase 3	Homo sapiens	59-63
27401251-9	2016	NOSTRIN inhibited production of nitric oxide (NO) by suppressing the activation of endothelial nitric oxide synthase (eNOS).	Nitric Oxide	32-44	nitric oxide synthase 3	Homo sapiens	83-116
27798230-1	2016	Hyaluronan (HA) in the endothelial glycocalyx serves as a mechanotransducer for high-shear-stress-stimulated endothelial nitric oxide synthase (eNOS) phosphorylation and nitric oxide (NO) production.	Hyaluronic Acid	0-10	nitric oxide synthase 3	Homo sapiens	109-142
27798230-1	2016	Hyaluronan (HA) in the endothelial glycocalyx serves as a mechanotransducer for high-shear-stress-stimulated endothelial nitric oxide synthase (eNOS) phosphorylation and nitric oxide (NO) production.	Hyaluronic Acid	12-14	nitric oxide synthase 3	Homo sapiens	109-142
27927230-0	2016	Molecular control of nitric oxide synthesis through eNOS and caveolin-1 interaction regulates osteogenic differentiation of adipose-derived stem cells by modulation of Wnt/beta-catenin signaling.	Nitric Oxide	21-33	nitric oxide synthase 3	Homo sapiens	52-56
27927230-6	2016	Cells were also exposed to a NO donor (NONOate) and the eNOS inhibitor, L-NAME.	NG-Nitroarginine Methyl Ester	72-78	nitric oxide synthase 3	Homo sapiens	56-60
27927230-7	2016	RESULTS: NO production as measured by nitrite was significantly increased in eNOS and CAV-1F92A transduced eASCs +(5.59 +- 0.22 muM) compared to eNOS alone (4.81 +- 0.59 muM) and un-transduced control cells (0.91 +- 0.23 muM) (p &lt; 0.05).	Nitrites	38-45	nitric oxide synthase 3	Homo sapiens	77-81
27927230-10	2016	Canonical Wnt signaling pathway-associated Wnt3a and Wnt8a gene expressions were increased in eNOS-CAV-1F92A cells undergoing osteogenesis whilst non-canonical Wnt5a was decreased and similar results were seen with NONOate treatment.	pelargonic acid	215-222	nitric oxide synthase 3	Homo sapiens	94-98
27927230-11	2016	Treatment of osteogenic cultures with 2 mM L-NAME resulted in reduced Runx2, ALP, and Wnt3a expressions, whilst Wnt5a expression was increased in eNOS-delivered cells.	NG-Nitroarginine Methyl Ester	43-49	nitric oxide synthase 3	Homo sapiens	146-150
27927230-12	2016	Co-transduction of eASCs with a Wnt pathway responsive lenti-TCF/LEF-dGFP reporter only showed activity in osteogenic cultures co-transduced with a doxycycline inducible eNOS.	Doxycycline	148-159	nitric oxide synthase 3	Homo sapiens	170-174
27833015-6	2016	Our data showed that TMAO significantly triggered oxidative stress and activated TXNIP-NLRP3 inflammasome whereat inflammatory cytokines interleukin (IL)-1beta and IL-18 were released in a dose- and time-dependent manner, but endothelial nitric oxide synthase (eNOS) and production of nitric oxide (NO) were inhibited.	trimethyloxamine	21-25	nitric oxide synthase 3	Homo sapiens	226-259
27665476-0	2016	Ghrelin protects against palmitic acid or lipopolysaccharide-induced hepatocyte apoptosis through inhibition of MAPKs/iNOS and restoration of Akt/eNOS pathways.	Ghrelin	0-7	nitric oxide synthase 3	Homo sapiens	146-150
27665476-10	2016	Results of western blotting and immunofluorescence showed that protein levels of iNOS in ghrelin- pretreated group were significantly reduced compared with LPS- or PA- treated group, while protein levels of eNOS were restored by ghrelin pretreatment.	Ghrelin	89-96	nitric oxide synthase 3	Homo sapiens	207-211
27665476-10	2016	Results of western blotting and immunofluorescence showed that protein levels of iNOS in ghrelin- pretreated group were significantly reduced compared with LPS- or PA- treated group, while protein levels of eNOS were restored by ghrelin pretreatment.	Ghrelin	229-236	nitric oxide synthase 3	Homo sapiens	207-211
27665476-14	2016	CONCLUSIONS: Ghrelin pretreatment attenuated LPS- or PA-induced hepatocyte apoptosis, which may least partly via inhibition of mitogen-activated protein kinases (MAPKs)/iNOS and restoration of Akt/eNOS pathways.	Ghrelin	13-20	nitric oxide synthase 3	Homo sapiens	197-201
27665476-14	2016	CONCLUSIONS: Ghrelin pretreatment attenuated LPS- or PA-induced hepatocyte apoptosis, which may least partly via inhibition of mitogen-activated protein kinases (MAPKs)/iNOS and restoration of Akt/eNOS pathways.	Palmitic Acid	53-55	nitric oxide synthase 3	Homo sapiens	197-201
26672612-3	2016	Serial passaging from P1 to P4 (replicative senescence) and treatment of P1 endothelial cells with the eNOS inhibitor L-NAME (premature senescence) promoted acquisition of markers of senescence, enhanced ROS formation, decreased eNOS expression, and upregulation of angiotensin-converting enzyme (ACE) and AT1 receptors.	NG-Nitroarginine Methyl Ester	118-124	nitric oxide synthase 3	Homo sapiens	103-107
26672612-3	2016	Serial passaging from P1 to P4 (replicative senescence) and treatment of P1 endothelial cells with the eNOS inhibitor L-NAME (premature senescence) promoted acquisition of markers of senescence, enhanced ROS formation, decreased eNOS expression, and upregulation of angiotensin-converting enzyme (ACE) and AT1 receptors.	NG-Nitroarginine Methyl Ester	118-124	nitric oxide synthase 3	Homo sapiens	229-233
26672612-3	2016	Serial passaging from P1 to P4 (replicative senescence) and treatment of P1 endothelial cells with the eNOS inhibitor L-NAME (premature senescence) promoted acquisition of markers of senescence, enhanced ROS formation, decreased eNOS expression, and upregulation of angiotensin-converting enzyme (ACE) and AT1 receptors.	ros	204-207	nitric oxide synthase 3	Homo sapiens	103-107
26672612-5	2016	WS1442 prevented SA-beta-gal activity, the downregulation of eNOS, and oxidative stress in P3 cells.	WS 1442	0-6	nitric oxide synthase 3	Homo sapiens	61-65
26672612-6	2016	These findings indicate that the impairment of eNOS-derived nitric oxide formation favors a pro-oxidant response triggering the local angiotensin system, which, in turn, promotes endothelial senescence.	Nitric Oxide	60-72	nitric oxide synthase 3	Homo sapiens	47-51
29979511-3	2016	As L-arginine acts as the substrate of endothelial nitric oxide synthase (eNOS), arginine supplementation can enhance NO formation.	Arginine	3-13	nitric oxide synthase 3	Homo sapiens	39-72
29979511-3	2016	As L-arginine acts as the substrate of endothelial nitric oxide synthase (eNOS), arginine supplementation can enhance NO formation.	Arginine	3-13	nitric oxide synthase 3	Homo sapiens	74-78
29979511-3	2016	As L-arginine acts as the substrate of endothelial nitric oxide synthase (eNOS), arginine supplementation can enhance NO formation.	Arginine	5-13	nitric oxide synthase 3	Homo sapiens	39-72
29979511-3	2016	As L-arginine acts as the substrate of endothelial nitric oxide synthase (eNOS), arginine supplementation can enhance NO formation.	Arginine	5-13	nitric oxide synthase 3	Homo sapiens	74-78
27777063-8	2016	Moreover, either LY294002 or TFP abolished the liraglutide-induced upregulation of GTPCH1 and eNOS protein levels.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	17-25	nitric oxide synthase 3	Homo sapiens	94-98
29104725-7	2017	These findings suggest that NOS3 polymorphisms and physical training are important interacting variables to consider in evaluating redox status, nitric oxide availability and production, and BP control.	Nitric Oxide	145-157	nitric oxide synthase 3	Homo sapiens	28-32
27906429-9	2016	The frequency of TT, TC, and CC genotypes for the eNOS-786C polymorphism in the first group was 52.9%, 34.2%, and 12.9% respectively; in the second group, this was 46.4%, 42%, and 11.6%, and in the controls, 48.3%, 46.7%, and 5%.	Technetium	21-23	nitric oxide synthase 3	Homo sapiens	50-54
27613099-8	2016	eNOS gene haplotypes GCB, TCB (G-allele of 894G/T, C-allele -786T/C, B-allele of Intron 4b/4a respectively) were associated with high nitrite/nitrate levels compared to GTB in both FDRS and CHD patients (p &lt; 0.01).	Nitrites	134-141	nitric oxide synthase 3	Homo sapiens	0-4
27613099-8	2016	eNOS gene haplotypes GCB, TCB (G-allele of 894G/T, C-allele -786T/C, B-allele of Intron 4b/4a respectively) were associated with high nitrite/nitrate levels compared to GTB in both FDRS and CHD patients (p &lt; 0.01).	Nitrates	142-149	nitric oxide synthase 3	Homo sapiens	0-4
27613099-8	2016	eNOS gene haplotypes GCB, TCB (G-allele of 894G/T, C-allele -786T/C, B-allele of Intron 4b/4a respectively) were associated with high nitrite/nitrate levels compared to GTB in both FDRS and CHD patients (p &lt; 0.01).	s-(p-nitrobenzyl)glutathione	169-172	nitric oxide synthase 3	Homo sapiens	0-4
27658784-8	2016	PD123319 as a special inhibitor of AT2R was able to effectively decreased the levels of inflammatory cytokines and endothelial nitric oxide synthase (eNOS) activity, but only partially attenuate the effect of celastrol on AnII mediated HepG2 cell proliferation.	PD 123319	0-8	nitric oxide synthase 3	Homo sapiens	115-148
27845713-4	2016	Previous research has shown that 5-methyltetrahydrofolate, the product of the reaction catalysed by MTHFR, appears to be a positive allosteric modulator of endothelial nitric oxide synthase (eNOS) and may thus increase the production of nitric oxide, a potent vasodilator.	5-methyltetrahydrofolate	33-57	nitric oxide synthase 3	Homo sapiens	156-189
27660293-14	2016	Last, silencing CSE by siRNA significantly increased endothelial nitric oxide synthase phosphorylation at threonine 495 levels in human cardiac microvascular endothelial cells.	Threonine	106-115	nitric oxide synthase 3	Homo sapiens	53-86
26345518-0	2016	Polymorphisms of ABCC5 and NOS3 genes influence doxorubicin cardiotoxicity in survivors of childhood acute lymphoblastic leukemia.	Doxorubicin	48-59	nitric oxide synthase 3	Homo sapiens	27-31
27613870-5	2016	We found that S1179D substitution in CaM-free eNOS had multiple effects; it increased the rate of flavin reduction, altered the conformational equilibrium of the reductase domain, and increased the rate of its conformational transitions.	4,6-dinitro-o-cresol	98-104	nitric oxide synthase 3	Homo sapiens	46-50
27593859-0	2016	Arginase Inhibition Restores Peroxynitrite-Induced Endothelial Dysfunction via L-Arginine-Dependent Endothelial Nitric Oxide Synthase Phosphorylation.	Peroxynitrous Acid	29-42	nitric oxide synthase 3	Homo sapiens	100-133
27593859-0	2016	Arginase Inhibition Restores Peroxynitrite-Induced Endothelial Dysfunction via L-Arginine-Dependent Endothelial Nitric Oxide Synthase Phosphorylation.	Arginine	79-89	nitric oxide synthase 3	Homo sapiens	100-133
27593859-1	2016	PURPOSE: Peroxynitrite plays a critical role in vascular pathophysiology by increasing arginase activity and decreasing endothelial nitric oxide synthase (eNOS) activity.	Peroxynitrous Acid	9-22	nitric oxide synthase 3	Homo sapiens	120-153
27593859-1	2016	PURPOSE: Peroxynitrite plays a critical role in vascular pathophysiology by increasing arginase activity and decreasing endothelial nitric oxide synthase (eNOS) activity.	Peroxynitrous Acid	9-22	nitric oxide synthase 3	Homo sapiens	155-159
27593859-8	2016	The decreased eNOS phosphorylation at Ser1177 and the increased at Thr495 by SIN-1 were restored with arginase inhibitor and L-arginine.	Arginine	125-135	nitric oxide synthase 3	Homo sapiens	14-18
27813552-6	2016	The Asp298 and 4a alleles of the eNOS gene were found to be significantly associated with increased levels of urea and creatinine, and a decreased glomerular filtration rate in FD patients, and this association behaved in a co-dominant fashion.	Urea	110-114	nitric oxide synthase 3	Homo sapiens	33-37
27696828-0	2016	Structural Studies of a Complex Between Endothelial Nitric Oxide Synthase and Calmodulin at Physiological Calcium Concentration.	Calcium	106-113	nitric oxide synthase 3	Homo sapiens	40-73
27813552-6	2016	The Asp298 and 4a alleles of the eNOS gene were found to be significantly associated with increased levels of urea and creatinine, and a decreased glomerular filtration rate in FD patients, and this association behaved in a co-dominant fashion.	Creatinine	119-129	nitric oxide synthase 3	Homo sapiens	33-37
27283108-1	2016	BACKGROUND: Endothelial nitric oxide (NO) synthase (eNOS) has been implicated in the development of bicuspid aortic valve (BAV) and with differential expression in the ascending aorta of BAV patients.	nitric	24-30	nitric oxide synthase 3	Homo sapiens	52-56
32263632-4	2016	The results showed that the ionic products from SPS bioceramics significantly stimulated the proliferation, alkaline phosphate (ALP) activity and osteogenesis-related gene expression (Runx2, ALP, OCN, OPN) of rBMSCs as well as the proliferation and angiogenesis-related gene expression (VEGF, KDR, eNOS, HIF 1alpha) of HUVECs.	Sodium phenolsulfonate	48-51	nitric oxide synthase 3	Homo sapiens	298-302
27174595-7	2016	The compound stimulated cystathionine gamma-lyase (CSE) expression and endothelial NO synthase (eNOS) activity to produce H2S and NO.	Hydrogen Sulfide	122-125	nitric oxide synthase 3	Homo sapiens	96-100
27572151-2	2016	In uterine artery endothelial cells (UAECs), ATP activates endothelial nitric oxide synthase in a pregnancy (P)-specific manner that is dependent on Cx43 function.	Adenosine Triphosphate	45-48	nitric oxide synthase 3	Homo sapiens	59-92
27572151-3	2016	Caveolar subcellular domain partitioning plays key roles in ATP-induced endothelial nitric oxide synthase activation and nitric oxide production.	Adenosine Triphosphate	60-63	nitric oxide synthase 3	Homo sapiens	72-105
27572151-12	2016	These data demonstrate rapid ATP-stimulated repartitioning of Cx43 to the caveolae, where endothelial nitric oxide synthase resides and plays an important role in nitric oxide-mediated increasing uterine blood flow during pregnancy.	Adenosine Triphosphate	29-32	nitric oxide synthase 3	Homo sapiens	90-123
27557897-6	2016	Moreover, the mutant homozygous and heterozygous eNOS genotype together were significantly associated with higher TC, LDLc, (P &lt; 0.001), and TG (P = 0.001).	Technetium	114-116	nitric oxide synthase 3	Homo sapiens	49-53
27557897-6	2016	Moreover, the mutant homozygous and heterozygous eNOS genotype together were significantly associated with higher TC, LDLc, (P &lt; 0.001), and TG (P = 0.001).	Thioguanine	144-146	nitric oxide synthase 3	Homo sapiens	49-53
27174595-8	2016	Blocking CSE and/or eNOS suppressed both H2S and NO generation as well as the proangiogenic effect of ZYZ-803.	Hydrogen Sulfide	41-44	nitric oxide synthase 3	Homo sapiens	20-24
27174595-8	2016	Blocking CSE and/or eNOS suppressed both H2S and NO generation as well as the proangiogenic effect of ZYZ-803.	zyz-803	102-109	nitric oxide synthase 3	Homo sapiens	20-24
27174595-9	2016	Sirtuin-1 (SIRT1), CSE, and/or eNOS small interfering RNA (siRNA) suppressed the angiogenic effect of ZYZ-803-induced SIRT1 expression, VEGF, and cyclic guanosine 5"-monophosphate (cGMP) levels.	zyz-803	102-109	nitric oxide synthase 3	Homo sapiens	31-35
27394657-1	2016	Nitric oxide (NO) produced by endothelial nitric oxide synthase (eNOS) activates signaling pathways responsible for smooth muscle cell relaxation, leading to vasodilation and thus plays an important role in controlling vascular homeostasis, thrombosis and inflammation.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	30-63
27394657-1	2016	Nitric oxide (NO) produced by endothelial nitric oxide synthase (eNOS) activates signaling pathways responsible for smooth muscle cell relaxation, leading to vasodilation and thus plays an important role in controlling vascular homeostasis, thrombosis and inflammation.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	65-69
27378570-9	2016	Co-administration of L-NAME and GYY4137 attenuated the cardioprotection afforded by GYY4137, associated with attenuated phosphorylation of eNOS.	NG-Nitroarginine Methyl Ester	21-27	nitric oxide synthase 3	Homo sapiens	139-143
27610041-0	2016	Nafamostat mesilate promotes endothelium-dependent vasorelaxation via the Akt-eNOS dependent pathway.	nafamostat	0-19	nitric oxide synthase 3	Homo sapiens	78-82
27610030-0	2016	Dexmedetomidine inhibits vasoconstriction via activation of endothelial nitric oxide synthase.	Dexmedetomidine	0-15	nitric oxide synthase 3	Homo sapiens	60-93
27610030-2	2016	The present study tested the hypothesis that DEX inhibits vascular tension in human pulmonary arteries through the endothelial nitric oxide synthase (eNOS) mediated production of nitric oxide (NO).	Dexmedetomidine	45-48	nitric oxide synthase 3	Homo sapiens	115-148
27378570-9	2016	Co-administration of L-NAME and GYY4137 attenuated the cardioprotection afforded by GYY4137, associated with attenuated phosphorylation of eNOS.	GYY 4137	32-39	nitric oxide synthase 3	Homo sapiens	139-143
27378570-10	2016	LY294002 totally abrogated the infarct-limiting effect of GYY4137 and inhibited Akt, eNOS and GSK-3beta phosphorylation.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	0-8	nitric oxide synthase 3	Homo sapiens	85-89
27583345-3	2016	Also in high glucose condition monomeric adiponectin increased eNOS and above kinases phosphorylation with similar patterns but at lower extent.	Glucose	13-20	nitric oxide synthase 3	Homo sapiens	63-67
27699157-2	2016	The aim of the present study was to investigate the association of eNOS G894T genetic polymorphism and plasma levels of nitric oxide (NO) with CAD risk in an Iranian population.	Nitric Oxide	120-132	nitric oxide synthase 3	Homo sapiens	67-71
26462844-5	2016	Altered serum levels of CTSD and SIRT1 were measured by enzyme-linked immunosorbent assay, and eNOS activity was assessed by the conversion of 14(C)-L-arginine to 14(C)-L-citrulline.	14(c)-l-arginine	143-159	nitric oxide synthase 3	Homo sapiens	95-99
27490528-6	2016	Both the mix of urolithins at 5 muM and urolithin B-glucuronide at 15 muM activated eNOS expression.	urolithins	16-26	nitric oxide synthase 3	Homo sapiens	84-88
27490528-6	2016	Both the mix of urolithins at 5 muM and urolithin B-glucuronide at 15 muM activated eNOS expression.	urolithin b-glucuronide	40-63	nitric oxide synthase 3	Homo sapiens	84-88
27235860-6	2016	Rather than affecting eNOS expression and uncoupling, PGC-1alpha inhibited AngII-induced decrease of eNOS serine 1177 phosphorylation through activation of PI3K/Akt signaling.	Serine	106-112	nitric oxide synthase 3	Homo sapiens	101-105
26959555-1	2016	Asymmetric dimethylarginine (ADMA) induces the mitochondrial translocation of endothelial nitric oxide synthase (eNOS) through the nitration-mediated activation of Akt1.	dimethylarginine	11-27	nitric oxide synthase 3	Homo sapiens	78-111
26959555-1	2016	Asymmetric dimethylarginine (ADMA) induces the mitochondrial translocation of endothelial nitric oxide synthase (eNOS) through the nitration-mediated activation of Akt1.	N,N-dimethylarginine	29-33	nitric oxide synthase 3	Homo sapiens	78-111
26940040-1	2016	OBJECTIVE: To prospectively investigate the association of endothelial nitric oxide synthase (eNOS) G894T gene polymorphism with responsiveness to a selective alpha1 -blocker in men with benign prostatic hyperplasia related lower urinary tract symptoms (BPH/LUTS), as nitric oxide has recently gained increasing recognition as an important neurotransmitter of functions in the lower urinary tract.	Nitric Oxide	71-83	nitric oxide synthase 3	Homo sapiens	94-98
27490694-0	2016	AP-1 Inhibition by SR 11302 Protects Human Hepatoma HepG2 Cells from Bile Acid-Induced Cytotoxicity by Restoring the NOS-3 Expression.	SR 11302	19-27	nitric oxide synthase 3	Homo sapiens	117-122
27490694-0	2016	AP-1 Inhibition by SR 11302 Protects Human Hepatoma HepG2 Cells from Bile Acid-Induced Cytotoxicity by Restoring the NOS-3 Expression.	Bile Acids and Salts	69-78	nitric oxide synthase 3	Homo sapiens	117-122
27490694-1	2016	The harmful effects of bile acid accumulation occurring during cholestatic liver diseases have been associated with oxidative stress increase and endothelial nitric oxide synthase (NOS-3) expression decrease in liver cells.	Bile Acids and Salts	23-32	nitric oxide synthase 3	Homo sapiens	146-186
27490694-2	2016	We have previously reported that glycochenodeoxycholic acid (GCDCA) down-regulates gene expression by increasing SP1 binding to the NOS-3 promoter in an oxidative stress dependent manner.	Glycochenodeoxycholic Acid	33-59	nitric oxide synthase 3	Homo sapiens	132-137
27490694-2	2016	We have previously reported that glycochenodeoxycholic acid (GCDCA) down-regulates gene expression by increasing SP1 binding to the NOS-3 promoter in an oxidative stress dependent manner.	Glycochenodeoxycholic Acid	61-66	nitric oxide synthase 3	Homo sapiens	132-137
27490694-5	2016	Specific inhibition of AP-1 by the retinoid SR 11302 counteracted the cytotoxic effects induced by GCDCA while promoting NOS-3 expression recovery and cyclin D1 reduction.	Retinoids	35-43	nitric oxide synthase 3	Homo sapiens	121-126
27490694-8	2016	Our data provide direct evidence for the involvement of AP-1 in the NOS-3 expression regulation during cholestasis and define a critical role for NOS-3 in regulating the expression of cyclin D1 during the cell damage induced by bile acids.	Bile Acids and Salts	228-238	nitric oxide synthase 3	Homo sapiens	146-151
27279530-2	2016	Nitric oxide (NO), which is derived from endothelial nitric oxide synthase (eNOS), provides crucial signals for angiogenesis in the tumor microenvironment.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	41-74
27279530-2	2016	Nitric oxide (NO), which is derived from endothelial nitric oxide synthase (eNOS), provides crucial signals for angiogenesis in the tumor microenvironment.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	76-80
27279530-3	2016	Tetrahydrobiopterin (BH4) is an essential cofactor eNOS and represents a critical determinant of NO production.	sapropterin	0-19	nitric oxide synthase 3	Homo sapiens	51-55
27279530-3	2016	Tetrahydrobiopterin (BH4) is an essential cofactor eNOS and represents a critical determinant of NO production.	sapropterin	21-24	nitric oxide synthase 3	Homo sapiens	51-55
27279530-5	2016	Supplemental DAHP treatment decreased K-ras mRNA transcripts, inhibition of phosphorylation of eNOS and Akt, inhibition of guanosine triphosphate cyclohydrolase (GTPCH), and decreased significantly NO synthesis, and then inhibited angiogenesis, compared with the results observed in the saline group.	2,4-diaminohypoxanthine	13-17	nitric oxide synthase 3	Homo sapiens	95-99
27279530-8	2016	In addition, DAHP downregulates eNOS and Akt protein expression, corresponding to decreased eNOS phosphorylation at Ser1177 and Akt phosphorylation, compared with the saline control.	2,4-diaminohypoxanthine	13-17	nitric oxide synthase 3	Homo sapiens	32-36
27279530-8	2016	In addition, DAHP downregulates eNOS and Akt protein expression, corresponding to decreased eNOS phosphorylation at Ser1177 and Akt phosphorylation, compared with the saline control.	2,4-diaminohypoxanthine	13-17	nitric oxide synthase 3	Homo sapiens	92-96
27486304-1	2016	Sickle cell anemia (SCA) patients have vascular complications, and polymorphisms in endothelin-1 (ET-1) and endothelial nitric oxide synthase (eNOS) genes were associated with ET-1 and nitric oxide disturbance.	Nitric Oxide	120-132	nitric oxide synthase 3	Homo sapiens	143-147
27486304-5	2016	We suggest that eNOS and ET-1 gene polymorphisms can influence SCA pathophysiology and that eNOS variant in SCA patients might be important to nitric oxide activity and vascular alteration.	Nitric Oxide	143-155	nitric oxide synthase 3	Homo sapiens	92-96
27435826-3	2016	The role of Akt in tBHQ-induced eNOS phosphorylation was examined in human umbilical vein endothelial cells (HUVEC) or in mice.	2-tert-butylhydroquinone	19-23	nitric oxide synthase 3	Homo sapiens	32-36
27463705-0	2016	Estrogen Receptor Signaling and the PI3K/Akt Pathway Are Involved in Betulinic Acid-Induced eNOS Activation.	betulinic acid	69-83	nitric oxide synthase 3	Homo sapiens	92-96
27463705-6	2016	Short-term incubation of EA.hy 926 cells with BA resulted in eNOS phosphorylation at the serine 1177 residue in a concentration- and time-dependent manner with a half-maximal effective concentration of 0.57 microM.	betulinic acid	46-48	nitric oxide synthase 3	Homo sapiens	61-65
27463705-6	2016	Short-term incubation of EA.hy 926 cells with BA resulted in eNOS phosphorylation at the serine 1177 residue in a concentration- and time-dependent manner with a half-maximal effective concentration of 0.57 microM.	Serine	89-95	nitric oxide synthase 3	Homo sapiens	61-65
27463705-8	2016	BA-induced eNOS phosphorylation and NO production was completely blocked by pretreatment with ICI 182,780, and was attenuated by pretreatment with the PI3K inhibitors wortmannin and LY294002.	betulinic acid	0-2	nitric oxide synthase 3	Homo sapiens	11-15
27463705-8	2016	BA-induced eNOS phosphorylation and NO production was completely blocked by pretreatment with ICI 182,780, and was attenuated by pretreatment with the PI3K inhibitors wortmannin and LY294002.	Wortmannin	167-177	nitric oxide synthase 3	Homo sapiens	11-15
27463705-8	2016	BA-induced eNOS phosphorylation and NO production was completely blocked by pretreatment with ICI 182,780, and was attenuated by pretreatment with the PI3K inhibitors wortmannin and LY294002.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	182-190	nitric oxide synthase 3	Homo sapiens	11-15
27463705-9	2016	These results indicate that fast non-genomic effects of ER with downstream signaling through the PI3K/Akt pathway and consecutive eNOS phosphorylation at serine 1177 are involved in BA-induced eNOS activation.	Serine	154-160	nitric oxide synthase 3	Homo sapiens	130-134
27463705-9	2016	These results indicate that fast non-genomic effects of ER with downstream signaling through the PI3K/Akt pathway and consecutive eNOS phosphorylation at serine 1177 are involved in BA-induced eNOS activation.	Serine	154-160	nitric oxide synthase 3	Homo sapiens	193-197
27463705-9	2016	These results indicate that fast non-genomic effects of ER with downstream signaling through the PI3K/Akt pathway and consecutive eNOS phosphorylation at serine 1177 are involved in BA-induced eNOS activation.	betulinic acid	182-184	nitric oxide synthase 3	Homo sapiens	130-134
27463705-9	2016	These results indicate that fast non-genomic effects of ER with downstream signaling through the PI3K/Akt pathway and consecutive eNOS phosphorylation at serine 1177 are involved in BA-induced eNOS activation.	betulinic acid	182-184	nitric oxide synthase 3	Homo sapiens	193-197
27410748-4	2016	The first is rapid activation of calcium, which results in formation of calcium-calmodulin complexes, followed by recruitment of eNOS from caveolae.	Calcium	33-40	nitric oxide synthase 3	Homo sapiens	129-133
27410748-9	2016	Among several experimentally observed features, the model predicts a highly nonlinear, biphasic transient behavior of eNOS activation and NO production: a rapid initial activation due to the very rapid influx of calcium into the cytosol (occurring within 1-5 min) is followed by a sustained period of activation due to protein kinases.	Calcium	212-219	nitric oxide synthase 3	Homo sapiens	118-122
27106139-10	2016	Because PKC activity also relies on endoplasmic reticulum (ER) calcium release, we used thapsigargin and xestospongin C, BAPTA, and PKC inhibitors, which caused significant decreases in MEJ eNOS-P after PE.	Thapsigargin	88-100	nitric oxide synthase 3	Homo sapiens	190-194
27417628-1	2016	The arginine metabolite asymmetric dimethylarginine (ADMA) is a competitive inhibitor and uncoupler of endothelial nitric oxide synthase (eNOS), an enzyme that acts in multifarious ways to promote cardiovascular health.	Arginine	4-12	nitric oxide synthase 3	Homo sapiens	103-136
27417628-1	2016	The arginine metabolite asymmetric dimethylarginine (ADMA) is a competitive inhibitor and uncoupler of endothelial nitric oxide synthase (eNOS), an enzyme that acts in multifarious ways to promote cardiovascular health.	Arginine	4-12	nitric oxide synthase 3	Homo sapiens	138-142
27417628-1	2016	The arginine metabolite asymmetric dimethylarginine (ADMA) is a competitive inhibitor and uncoupler of endothelial nitric oxide synthase (eNOS), an enzyme that acts in multifarious ways to promote cardiovascular health.	dimethylarginine	35-51	nitric oxide synthase 3	Homo sapiens	103-136
27417628-1	2016	The arginine metabolite asymmetric dimethylarginine (ADMA) is a competitive inhibitor and uncoupler of endothelial nitric oxide synthase (eNOS), an enzyme that acts in multifarious ways to promote cardiovascular health.	dimethylarginine	35-51	nitric oxide synthase 3	Homo sapiens	138-142
27417628-1	2016	The arginine metabolite asymmetric dimethylarginine (ADMA) is a competitive inhibitor and uncoupler of endothelial nitric oxide synthase (eNOS), an enzyme that acts in multifarious ways to promote cardiovascular health.	N,N-dimethylarginine	53-57	nitric oxide synthase 3	Homo sapiens	103-136
27417628-1	2016	The arginine metabolite asymmetric dimethylarginine (ADMA) is a competitive inhibitor and uncoupler of endothelial nitric oxide synthase (eNOS), an enzyme that acts in multifarious ways to promote cardiovascular health.	N,N-dimethylarginine	53-57	nitric oxide synthase 3	Homo sapiens	138-142
27417628-3	2016	Fortunately, the suppressive impact of ADMA on eNOS activity can be offset by increasing intracellular arginine levels with supplemental citrulline.	N,N-dimethylarginine	39-43	nitric oxide synthase 3	Homo sapiens	47-51
27417628-3	2016	Fortunately, the suppressive impact of ADMA on eNOS activity can be offset by increasing intracellular arginine levels with supplemental citrulline.	Arginine	103-111	nitric oxide synthase 3	Homo sapiens	47-51
27417628-5	2016	Supplemental citrulline could be a practical option for primary or secondary prevention of cardiovascular events and mortality, as it is inexpensive, has a mild flavor, and is well tolerated in doses (3-6 g daily) that can influence eNOS activity.	Citrulline	13-23	nitric oxide synthase 3	Homo sapiens	233-237
26663724-10	2016	Treatment with etaftorone decreased expression of inducible NOS and XOR in kidneys, whereas it increased the expression of endothelial NOS.	etaftorone	15-25	nitric oxide synthase 3	Homo sapiens	123-138
27106139-10	2016	Because PKC activity also relies on endoplasmic reticulum (ER) calcium release, we used thapsigargin and xestospongin C, BAPTA, and PKC inhibitors, which caused significant decreases in MEJ eNOS-P after PE.	xestospongin C	105-119	nitric oxide synthase 3	Homo sapiens	190-194
27106139-10	2016	Because PKC activity also relies on endoplasmic reticulum (ER) calcium release, we used thapsigargin and xestospongin C, BAPTA, and PKC inhibitors, which caused significant decreases in MEJ eNOS-P after PE.	1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid	121-126	nitric oxide synthase 3	Homo sapiens	190-194
27106139-12	2016	We hypothesize that local lipid composition of the MEJ primes PKC and eNOS-P for stimulation by PE, allowing for compartmentalized function of eNOS in the blood vessel wall.	Phenylephrine	96-98	nitric oxide synthase 3	Homo sapiens	70-74
27106139-12	2016	We hypothesize that local lipid composition of the MEJ primes PKC and eNOS-P for stimulation by PE, allowing for compartmentalized function of eNOS in the blood vessel wall.	Phenylephrine	96-98	nitric oxide synthase 3	Homo sapiens	143-147
27184745-1	2016	Endothelial nitric oxide synthase (eNOS) plays an essential role in the regulation of endothelial function and acts as a master regulator of vascular tone and homeostasis through the generation of the gasotransmitter nitric oxide (NO).	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	35-39
27089822-3	2016	The aim of this study was to evaluate the production of endothelial nitric oxide synthase (eNOS), nitrite and hypoxia inducible factor alpha (HIF-alpha) in HUVECs (human umbilical vein endothelial cells) activated by heme in response to simvastatin, hydroxyurea (HU), and ascorbic acid therapies.	Heme	217-221	nitric oxide synthase 3	Homo sapiens	56-89
27175806-5	2016	The results demonstrated that high salt medium significantly increased the concentration of ADMA, the expression of protein arginine methyltransferase 1 (PRMT-1) and RhoA, and the activity of ROCK, and downregulated the expression of eNOS.	salt medium	35-46	nitric oxide synthase 3	Homo sapiens	234-238
27175806-7	2016	These results indicated that ADMA has a key role in high salt-mediated activation of the RhoA/ROCK pathway and inhibition of eNOS biosynthesis.	N,N-dimethylarginine	29-33	nitric oxide synthase 3	Homo sapiens	125-129
26508575-6	2016	NOS3 is highly expressed in the central nervous system (including cerebellum), neurons and endothelial cells, and is one of three enzymes that converts l-arginine to the neurotransmitter NO.	Arginine	152-162	nitric oxide synthase 3	Homo sapiens	0-4
27175806-0	2016	High salt medium activates RhoA/ROCK and downregulates eNOS expression via the upregulation of ADMA.	high salt medium	0-16	nitric oxide synthase 3	Homo sapiens	55-59
27184745-4	2016	Endothelial dysfunction is linked to eNOS uncoupling, which consists of a switch from the generation of NO to the generation of superoxide anions and hydrogen peroxide.	Superoxides	128-145	nitric oxide synthase 3	Homo sapiens	37-41
27184745-4	2016	Endothelial dysfunction is linked to eNOS uncoupling, which consists of a switch from the generation of NO to the generation of superoxide anions and hydrogen peroxide.	Hydrogen Peroxide	150-167	nitric oxide synthase 3	Homo sapiens	37-41
27018249-0	2016	Tirofiban induces vasorelaxation of the coronary artery via an endothelium-dependent NO-cGMP signaling by activating the PI3K/Akt/eNOS pathway.	Tirofiban	0-9	nitric oxide synthase 3	Homo sapiens	130-134
27374449-1	2016	Endothelial nitric oxide synthase (eNOS) is a major enzyme responsible for nitric oxide (NO) production.	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	35-39
27345001-1	2016	OBJECTIVE: Asymmetric dimethylarginine (ADMA) is an endogenous inhibitor of endothelial nitric oxide synthase.	dimethylarginine	22-38	nitric oxide synthase 3	Homo sapiens	76-109
27345001-1	2016	OBJECTIVE: Asymmetric dimethylarginine (ADMA) is an endogenous inhibitor of endothelial nitric oxide synthase.	N,N-dimethylarginine	40-44	nitric oxide synthase 3	Homo sapiens	76-109
27264087-4	2016	The study hypothesizes that L-AME, incorporated into PCU, functions as a bioactive porogen, releasing upon contact with blood to interact with endothelial nitric oxide synthase (eNOS) present in blood.	arginine methyl ester	28-33	nitric oxide synthase 3	Homo sapiens	143-176
27018249-0	2016	Tirofiban induces vasorelaxation of the coronary artery via an endothelium-dependent NO-cGMP signaling by activating the PI3K/Akt/eNOS pathway.	Cyclic GMP	88-92	nitric oxide synthase 3	Homo sapiens	130-134
27018249-5	2016	Further study showed that incubation of human umbilical venous endothelial cells (HUVECs) with tirofiban increased NO production, which was ascribed to the increased eNOS phosphorylation.	Tirofiban	95-104	nitric oxide synthase 3	Homo sapiens	166-170
27018249-9	2016	These findings suggest that tirofiban induces vasorelaxation via an endothelium-dependent NO-cGMP signaling through the activation of the Akt/eNOS/sGC pathway.	Tirofiban	28-37	nitric oxide synthase 3	Homo sapiens	142-146
27018249-9	2016	These findings suggest that tirofiban induces vasorelaxation via an endothelium-dependent NO-cGMP signaling through the activation of the Akt/eNOS/sGC pathway.	Cyclic GMP	93-97	nitric oxide synthase 3	Homo sapiens	142-146
27170438-3	2016	Estradiol induces endothelial NO synthase (eNOS) activation to increase NO production; however, it is unknown if eNOS regulation is dependent on both ERs.	Estradiol	0-9	nitric oxide synthase 3	Homo sapiens	43-47
26906511-9	2016	In addition, folic acid decreased protein expressions of NOX4 and p-ERK1/2, while it increased the protein expression of eNOS in HUVECs.	Folic Acid	13-23	nitric oxide synthase 3	Homo sapiens	121-125
27072494-0	2016	Exenatide exerts direct protective effects on endothelial cells through the AMPK/Akt/eNOS pathway in a GLP-1 receptor-dependent manner.	Exenatide	0-9	nitric oxide synthase 3	Homo sapiens	85-89
27072494-6	2016	In human umbilical vein endothelial cells, exendin-4 (a form of exenatide) significantly increased NO production, endothelial NO synthase (eNOS) phosphorylation, and GTP cyclohydrolase 1 (GTPCH1) level in a dose-dependent manner.	Exenatide	64-73	nitric oxide synthase 3	Homo sapiens	139-143
27072494-8	2016	Furthermore, exendin-4 reversed homocysteine-induced endothelial dysfunction by decreasing sICAM-1 and reactive oxygen species (ROS) levels and upregulating NO production and eNOS phosphorylation.	Homocysteine	32-44	nitric oxide synthase 3	Homo sapiens	175-179
27072494-11	2016	The effect may be mediated through activation of AMPK/PI3K-Akt/eNOS pathway via a GLP-1R/cAMP-dependent mechanism.	Cyclic AMP	89-93	nitric oxide synthase 3	Homo sapiens	63-67
26906511-12	2016	NAC, DPI, and U0126 increased the protein expression of eNOS.	Acetylcysteine	0-3	nitric oxide synthase 3	Homo sapiens	56-60
27081912-8	2016	Pre-treatment with L-NAME attenuated the inhibitory effects of polydatin on cell proliferation, inhibited the expression of SIRT1 and the phosphorylation of eNOS.	NG-Nitroarginine Methyl Ester	19-25	nitric oxide synthase 3	Homo sapiens	157-161
26906511-12	2016	NAC, DPI, and U0126 increased the protein expression of eNOS.	3-aminodiphenyleneiodium	5-8	nitric oxide synthase 3	Homo sapiens	56-60
26906511-12	2016	NAC, DPI, and U0126 increased the protein expression of eNOS.	U 0126	14-19	nitric oxide synthase 3	Homo sapiens	56-60
27081912-0	2016	Polydatin inhibits the oxidative stress-induced proliferation of vascular smooth muscle cells by activating the eNOS/SIRT1 pathway.	polydatin	0-9	nitric oxide synthase 3	Homo sapiens	112-116
27060172-12	2016	Further, serum eNOS was found to be significantly lower in women with RIF when compared with RIS (P &lt; 0.05), indicating possible impairment in nitric oxide production.	Nitric Oxide	146-158	nitric oxide synthase 3	Homo sapiens	15-19
27081912-10	2016	Taken together, these findings suggest that, polydatin inhibited the oxidative stress-induced proliferation of VMSCs by activating the eNOS/SIRT1 pathway.	polydatin	45-54	nitric oxide synthase 3	Homo sapiens	135-139
27081912-6	2016	The results showed that polydatin inhibited VSMC proliferation and the level of reactive oxygen species, increased the expression of Kip1/p27, SIRT1 and eNOS, whereas the expression of cyclin B1, Cdk1 and c-myc was decreased.	polydatin	24-33	nitric oxide synthase 3	Homo sapiens	153-157
27060232-0	2016	Endothelial nitric oxide synthase tagSNPs influence the effects of enalapril in essential hypertension.	Enalapril	67-76	nitric oxide synthase 3	Homo sapiens	0-33
25410796-4	2016	In this report, we provide data showing that PbCl2 treatment depresses the expressions of the three distinct NOS isoforms: neuronal nitric oxide synthase (nNOS), endothelial NOS (eNOS), and inducible NOS (iNOS) on both transcriptional and translational levels in MCF-7 cells.	lead chloride	45-50	nitric oxide synthase 3	Homo sapiens	162-177
27058899-0	2016	eNOS polymorphisms and clinical outcome in advanced HCC patients receiving sorafenib: final results of the ePHAS study.	Sorafenib	75-84	nitric oxide synthase 3	Homo sapiens	0-4
27058899-1	2016	Sorafenib may reduce endothelial nitric oxide synthase (eNOS) activity by inhibiting vascular endothelial growth factor receptors (VEGF-R), leading to a decrease in nitric oxide production.	Sorafenib	0-9	nitric oxide synthase 3	Homo sapiens	21-54
27058899-1	2016	Sorafenib may reduce endothelial nitric oxide synthase (eNOS) activity by inhibiting vascular endothelial growth factor receptors (VEGF-R), leading to a decrease in nitric oxide production.	Sorafenib	0-9	nitric oxide synthase 3	Homo sapiens	56-60
27058899-1	2016	Sorafenib may reduce endothelial nitric oxide synthase (eNOS) activity by inhibiting vascular endothelial growth factor receptors (VEGF-R), leading to a decrease in nitric oxide production.	Nitric Oxide	33-45	nitric oxide synthase 3	Homo sapiens	56-60
27058899-8	2016	Our results suggest that haplotype HT1 in the eNOS gene may be capable of identifying a subset of HCC patients who are resistant to sorafenib.	Sorafenib	132-141	nitric oxide synthase 3	Homo sapiens	46-50
27168827-3	2016	The 27-bp VNTR and G894T polymorphisms of the eNOS gene were genotyped using polymerase chain reaction (PCR) and PCR-restriction fragment length polymorphism, respectively, followed by agarose gel electrophoresis and DNA sequencing.	Sepharose	185-192	nitric oxide synthase 3	Homo sapiens	46-50
27060232-3	2016	While clinically relevant NOS3 polymorphisms were previously shown to affect the antihypertensive responses to enalapril, no study has tested the hypothesis that NOS3 tagSNPs influence the antihypertensive effects of this drug.	Enalapril	111-120	nitric oxide synthase 3	Homo sapiens	26-30
27060232-4	2016	We examined whether the NOS3 tagSNPs rs3918226, rs3918188, and rs743506, and their haplotypes, affect the antihypertensive responses to enalapril in 101 patients with essential hypertension.	Enalapril	136-145	nitric oxide synthase 3	Homo sapiens	24-28
27060232-7	2016	We compared the effects of NOS3 tagSNPs on changes in blood pressure after enalapril treatment.	Enalapril	75-84	nitric oxide synthase 3	Homo sapiens	27-31
27060232-13	2016	Our findings suggest that NOS3 tagSNPs influence the effects of enalapril in essential hypertension.	Enalapril	64-73	nitric oxide synthase 3	Homo sapiens	26-30
27091343-0	2016	Asymmetric Dimethylarginine Limits the Efficacy of Simvastatin Activating Endothelial Nitric Oxide Synthase.	dimethylarginine	11-27	nitric oxide synthase 3	Homo sapiens	74-107
25809076-4	2016	As eNOS produces nitric oxide (NO) and NAD(P)Hoxidase produces superoxide anions (O2 (-) , quenching NO) we propose that the eNOS/NAD(P)Hoxidase protein ratio is a marker of vasodilator capacity.	Superoxides	82-84	nitric oxide synthase 3	Homo sapiens	3-7
25809076-4	2016	As eNOS produces nitric oxide (NO) and NAD(P)Hoxidase produces superoxide anions (O2 (-) , quenching NO) we propose that the eNOS/NAD(P)Hoxidase protein ratio is a marker of vasodilator capacity.	Superoxides	82-84	nitric oxide synthase 3	Homo sapiens	125-129
27513240-0	2016	eNOS gene polymorphisms in paraffin-embedded tissues of prostate cancer patients.	Paraffin	27-35	nitric oxide synthase 3	Homo sapiens	0-4
26719362-4	2016	Diverse signaling events are responsible for effects of nitrated fatty acid, including activating peroxisome proliferator-activated receptor-dependent gene expression, suppressing NF-kappaB-induced inflammation, inhibiting oxidative stress, and increasing both endothelial nitric oxide synthase- and Nrf2-dependent gene regulation.	nitrated fatty acid	56-75	nitric oxide synthase 3	Homo sapiens	261-294
25809076-4	2016	As eNOS produces nitric oxide (NO) and NAD(P)Hoxidase produces superoxide anions (O2 (-) , quenching NO) we propose that the eNOS/NAD(P)Hoxidase protein ratio is a marker of vasodilator capacity.	Nitric Oxide	17-29	nitric oxide synthase 3	Homo sapiens	3-7
25809076-4	2016	As eNOS produces nitric oxide (NO) and NAD(P)Hoxidase produces superoxide anions (O2 (-) , quenching NO) we propose that the eNOS/NAD(P)Hoxidase protein ratio is a marker of vasodilator capacity.	Nitric Oxide	17-29	nitric oxide synthase 3	Homo sapiens	125-129
25809076-4	2016	As eNOS produces nitric oxide (NO) and NAD(P)Hoxidase produces superoxide anions (O2 (-) , quenching NO) we propose that the eNOS/NAD(P)Hoxidase protein ratio is a marker of vasodilator capacity.	Superoxides	63-80	nitric oxide synthase 3	Homo sapiens	125-129
27091343-0	2016	Asymmetric Dimethylarginine Limits the Efficacy of Simvastatin Activating Endothelial Nitric Oxide Synthase.	Simvastatin	51-62	nitric oxide synthase 3	Homo sapiens	74-107
27091343-1	2016	BACKGROUND: Asymmetric dimethylarginine (ADMA), an endogenous inhibitor of endothelial nitric oxide synthase (eNOS), is considered a risk factor for the pathogenesis of cardiovascular diseases.	dimethylarginine	23-39	nitric oxide synthase 3	Homo sapiens	75-108
27091343-1	2016	BACKGROUND: Asymmetric dimethylarginine (ADMA), an endogenous inhibitor of endothelial nitric oxide synthase (eNOS), is considered a risk factor for the pathogenesis of cardiovascular diseases.	N,N-dimethylarginine	41-45	nitric oxide synthase 3	Homo sapiens	75-108
26866567-3	2016	Nitric oxide (NO), which has a role on varicocele pathophysiology, is synthesized by endothelial nitric oxide synthase gene (NOS3).	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	85-118
26853630-3	2016	Endothelial nitric oxide synthase (eNOS) generates nitric oxide, which is responsible to endothelium-dependent vasodilation.	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	35-39
26853630-4	2016	The impact of glyLDL on the expression and activity of eNOS in vascular endothelial cells (EC) remains unknown.	glyldl	14-20	nitric oxide synthase 3	Homo sapiens	55-59
26866567-3	2016	Nitric oxide (NO), which has a role on varicocele pathophysiology, is synthesized by endothelial nitric oxide synthase gene (NOS3).	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	125-129
26853630-5	2016	The present study investigated the effect of glyLDL on the levels of protein, mRNA and activity of eNOS in cultured human umbilical vein EC.	glyldl	45-51	nitric oxide synthase 3	Homo sapiens	99-103
26853630-6	2016	The results demonstrated that incubation of EC with physiological concentrations of glyLDL significantly reduced the abundances of eNOS protein in EC with the maximal inhibition at 100mug/ml for 24h.	glyldl	84-90	nitric oxide synthase 3	Homo sapiens	131-135
27036881-1	2016	BACKGROUND: Non-viral-based gene modification of adult stem cells with endothelial nitric oxide synthase (eNOS) may enhance production of nitric oxide and promote angiogenesis.	Nitric Oxide	83-95	nitric oxide synthase 3	Homo sapiens	106-110
26853630-8	2016	Blocking antibody against the receptor for advanced glycation end products (RAGE) prevented glyLDL-induced downregulation of eNOS in EC.	glyldl	92-98	nitric oxide synthase 3	Homo sapiens	125-129
26853630-10	2016	Farnesyl-transferase inhibitor-276, an H-Ras antagonist, normalized glyLDL-induced downregulation of eNOS and prevented glyLDL-induced upregulation of H-Ras in EC membrane.	glyldl	68-74	nitric oxide synthase 3	Homo sapiens	101-105
26853630-11	2016	Treatment with 4-phenylbutyric acid, an endoplasmic reticulum (ER) stress antagonist, prevented glyLDL-induced eNOS downregulation in EC.	4-phenylbutyric acid	15-35	nitric oxide synthase 3	Homo sapiens	111-115
26853630-11	2016	Treatment with 4-phenylbutyric acid, an endoplasmic reticulum (ER) stress antagonist, prevented glyLDL-induced eNOS downregulation in EC.	glyldl	96-102	nitric oxide synthase 3	Homo sapiens	111-115
26853630-13	2016	ER stress induced by glyLDL is possibly involved in eNOS downregulation.	glyldl	21-27	nitric oxide synthase 3	Homo sapiens	52-56
26924495-7	2016	Fluctuating glucose, but not constant high glucose, significantly decreased the endothelial nitric oxide synthase (eNOS) phosphorylation level at Ser-1177 without affecting total eNOS expression, which was prevented by astaxanthin as well as by the anti-oxidant NAC.	Glucose	12-19	nitric oxide synthase 3	Homo sapiens	80-113
26924495-7	2016	Fluctuating glucose, but not constant high glucose, significantly decreased the endothelial nitric oxide synthase (eNOS) phosphorylation level at Ser-1177 without affecting total eNOS expression, which was prevented by astaxanthin as well as by the anti-oxidant NAC.	Serine	146-149	nitric oxide synthase 3	Homo sapiens	80-113
26924495-7	2016	Fluctuating glucose, but not constant high glucose, significantly decreased the endothelial nitric oxide synthase (eNOS) phosphorylation level at Ser-1177 without affecting total eNOS expression, which was prevented by astaxanthin as well as by the anti-oxidant NAC.	astaxanthine	219-230	nitric oxide synthase 3	Homo sapiens	80-113
26729266-10	2016	In a human PASMC line, immunoblot analysis showed the following: (1) eNOS expression, (2) Ser(1177) phosphorylation by U46619 and H2O2, and (3) Akt activation (Ser(473) phosphorylation) by U46619.	pasmc	11-16	nitric oxide synthase 3	Homo sapiens	69-73
27036881-9	2016	MC-eNOS vectors showed higher transfection efficiency (21 +- 3 %) compared to P-eNOS (9 +- 1 %) and also generated higher NO levels.	Methylcholanthrene	0-2	nitric oxide synthase 3	Homo sapiens	3-7
27036881-10	2016	In vitro capillary tubule formation assays showed both MC-eNOS and P-eNOS gene-modified rBMSCs formed longer (14.66 +- 0.55 mm and 13.58 +- 0.68 mm, respectively) and a greater number of tubules (56.33 +- 3.51 and 51 +- 4, respectively) compared to controls, which was reduced with the NOS inhibitor L-NAME.	Methylcholanthrene	55-57	nitric oxide synthase 3	Homo sapiens	58-62
27036881-10	2016	In vitro capillary tubule formation assays showed both MC-eNOS and P-eNOS gene-modified rBMSCs formed longer (14.66 +- 0.55 mm and 13.58 +- 0.68 mm, respectively) and a greater number of tubules (56.33 +- 3.51 and 51 +- 4, respectively) compared to controls, which was reduced with the NOS inhibitor L-NAME.	NG-Nitroarginine Methyl Ester	300-306	nitric oxide synthase 3	Homo sapiens	69-73
27036881-11	2016	In an in vitro wound healing assay, MC-eNOS transfected cells showed greater migration which was also reversed by L-NAME treatment.	Methylcholanthrene	36-38	nitric oxide synthase 3	Homo sapiens	39-43
27036881-11	2016	In an in vitro wound healing assay, MC-eNOS transfected cells showed greater migration which was also reversed by L-NAME treatment.	NG-Nitroarginine Methyl Ester	114-120	nitric oxide synthase 3	Homo sapiens	39-43
27036881-12	2016	Finally, gene expression analysis in MC-eNOS transfected cells showed significant upregulation of the endothelial-specific marker CD31 and enhanced expression of VEGFA and FGF-2 and their corresponding receptors PDGFRalpha and FGFR2, respectively.	Methylcholanthrene	37-39	nitric oxide synthase 3	Homo sapiens	40-44
26660642-14	2016	serelaxin infusion increased basal NOS activity, associated with increased endothelial NOS (eNOS) expression.	serelaxin protein, human	0-9	nitric oxide synthase 3	Homo sapiens	75-90
26890696-0	2016	Ivabradine Prevents Low Shear Stress Induced Endothelial Inflammation and Oxidative Stress via mTOR/eNOS Pathway.	Ivabradine	0-10	nitric oxide synthase 3	Homo sapiens	100-104
26824621-0	2016	Danggui Buxue Tang, Chinese Herbal Decoction Containing Astragali Radix and Angelicae Sinensis Radix, Induces Production of Nitric Oxide in Endothelial Cells: Signaling Mediated by Phosphorylation of Endothelial Nitric Oxide Synthase.	Nitric Oxide	124-136	nitric oxide synthase 3	Homo sapiens	200-233
26824621-6	2016	The Danggui Buxue Tang-induced phosphorylation of endothelial nitric oxide synthase and Akt kinase in human umbilical vein endothelial cells were fully blocked by treatment with an endothelial nitric oxide synthase inhibitor (L-NAME), a PI3K/Akt inhibitor (LY294002), and a Ca(2+) chelator (BAPTA-AM).	NG-Nitroarginine Methyl Ester	226-232	nitric oxide synthase 3	Homo sapiens	50-83
26824621-6	2016	The Danggui Buxue Tang-induced phosphorylation of endothelial nitric oxide synthase and Akt kinase in human umbilical vein endothelial cells were fully blocked by treatment with an endothelial nitric oxide synthase inhibitor (L-NAME), a PI3K/Akt inhibitor (LY294002), and a Ca(2+) chelator (BAPTA-AM).	NG-Nitroarginine Methyl Ester	226-232	nitric oxide synthase 3	Homo sapiens	181-214
26824621-6	2016	The Danggui Buxue Tang-induced phosphorylation of endothelial nitric oxide synthase and Akt kinase in human umbilical vein endothelial cells were fully blocked by treatment with an endothelial nitric oxide synthase inhibitor (L-NAME), a PI3K/Akt inhibitor (LY294002), and a Ca(2+) chelator (BAPTA-AM).	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	257-265	nitric oxide synthase 3	Homo sapiens	50-83
26824621-6	2016	The Danggui Buxue Tang-induced phosphorylation of endothelial nitric oxide synthase and Akt kinase in human umbilical vein endothelial cells were fully blocked by treatment with an endothelial nitric oxide synthase inhibitor (L-NAME), a PI3K/Akt inhibitor (LY294002), and a Ca(2+) chelator (BAPTA-AM).	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	257-265	nitric oxide synthase 3	Homo sapiens	181-214
26824621-6	2016	The Danggui Buxue Tang-induced phosphorylation of endothelial nitric oxide synthase and Akt kinase in human umbilical vein endothelial cells were fully blocked by treatment with an endothelial nitric oxide synthase inhibitor (L-NAME), a PI3K/Akt inhibitor (LY294002), and a Ca(2+) chelator (BAPTA-AM).	1,2-bis(2-aminophenoxy)ethane N,N,N',N'-tetraacetic acid acetoxymethyl ester	291-299	nitric oxide synthase 3	Homo sapiens	50-83
26824621-6	2016	The Danggui Buxue Tang-induced phosphorylation of endothelial nitric oxide synthase and Akt kinase in human umbilical vein endothelial cells were fully blocked by treatment with an endothelial nitric oxide synthase inhibitor (L-NAME), a PI3K/Akt inhibitor (LY294002), and a Ca(2+) chelator (BAPTA-AM).	1,2-bis(2-aminophenoxy)ethane N,N,N',N'-tetraacetic acid acetoxymethyl ester	291-299	nitric oxide synthase 3	Homo sapiens	181-214
27326226-8	2016	While beta-blockers generally provide comparable blood pressure reductions, only nebivolol demonstrated enhanced vasodilation and blood flow by increasing the expression of endothelial nitric oxide synthase and therefore increasing nitric oxide release from the endothelium.	Nebivolol	81-90	nitric oxide synthase 3	Homo sapiens	173-206
26896473-2	2016	We hypothesized that supplementation with tetrahydrobiopterin (BH4) would recouple endothelial nitric oxide synthase and thus improve endothelial function and consequently reduce aortic stiffness.	sapropterin	42-61	nitric oxide synthase 3	Homo sapiens	83-116
26896473-2	2016	We hypothesized that supplementation with tetrahydrobiopterin (BH4) would recouple endothelial nitric oxide synthase and thus improve endothelial function and consequently reduce aortic stiffness.	sapropterin	63-66	nitric oxide synthase 3	Homo sapiens	83-116
26890696-2	2016	Since endothelial nitric oxide synthase (eNOS) is a crucial enzyme in maintaining endothelial activity, we aimed to investigate the impact of ivabradine in low shear stress (LSS) induced inflammation and endothelial injury and the role of eNOS played in it.	Ivabradine	142-152	nitric oxide synthase 3	Homo sapiens	41-45
26890696-10	2016	It would appear that ivabradine diminish ROS generation by provoking mTORC2/Akt phosphorylation and repressing mTORC1 induced eNOS-Thr495 activation.	Ivabradine	21-31	nitric oxide synthase 3	Homo sapiens	126-130
26890696-11	2016	These results together suggest that LSS induced endothelial inflammation and oxidative stress are suppressed by ivabradine via mTORC2/Akt activation and mTORC1/eNOS reduction.	Ivabradine	112-122	nitric oxide synthase 3	Homo sapiens	160-164
26864067-1	2016	INTRODUCTION: In this study, we investigated the association between -786T/C polymorphism of the endothelial nitric oxide (NOS3) gene in which thymidine is replaced by a cytosine at nucleotide -786 (rs 2070744) and coronary collateral circulation (CCC) in patients with stable coronary artery disease.	Nitric Oxide	109-121	nitric oxide synthase 3	Homo sapiens	123-127
26864067-1	2016	INTRODUCTION: In this study, we investigated the association between -786T/C polymorphism of the endothelial nitric oxide (NOS3) gene in which thymidine is replaced by a cytosine at nucleotide -786 (rs 2070744) and coronary collateral circulation (CCC) in patients with stable coronary artery disease.	Thymidine	143-152	nitric oxide synthase 3	Homo sapiens	123-127
26864067-1	2016	INTRODUCTION: In this study, we investigated the association between -786T/C polymorphism of the endothelial nitric oxide (NOS3) gene in which thymidine is replaced by a cytosine at nucleotide -786 (rs 2070744) and coronary collateral circulation (CCC) in patients with stable coronary artery disease.	Cytosine	170-178	nitric oxide synthase 3	Homo sapiens	123-127
26628675-8	2016	Nicotinamide adenine dinucleotide phosphate oxidase subunit p47(phox) knockdown or 5,6,7,8-tetrahydrobiopterin supplementation attenuated endothelial nitric oxide synthase uncoupling and enhanced in vivo endothelial repair capacity of early EPCs from PHAs.	sapropterin	83-110	nitric oxide synthase 3	Homo sapiens	138-171
26750873-1	2016	Betulinic acid (BA) is a naturally occurring pentacyclic triterpene that attenuates vascular diseases and atherosclerosis, but the mechanism by which it stimulates endothelial nitric oxide synthase (eNOS) is unclear.	betulinic acid	0-14	nitric oxide synthase 3	Homo sapiens	164-197
26750873-1	2016	Betulinic acid (BA) is a naturally occurring pentacyclic triterpene that attenuates vascular diseases and atherosclerosis, but the mechanism by which it stimulates endothelial nitric oxide synthase (eNOS) is unclear.	betulinic acid	16-18	nitric oxide synthase 3	Homo sapiens	164-197
26893661-1	2016	The aim of the present study was to observe the effects of sevoflurane on the antioxidant capacity, endothelial nitric oxide synthase (eNOS) content and lifespan of erythrocytes.	Sevoflurane	59-70	nitric oxide synthase 3	Homo sapiens	100-133
26497187-10	2016	), eNOS inhibitor, abrogated the ameliorative potential of linagliptin.	Linagliptin	59-70	nitric oxide synthase 3	Homo sapiens	3-7
27215040-2	2016	Nitric oxide (NO) is regulated by endothelial nitric oxide synthase (eNOS) enzyme which is one of the isoenzymes of NO synthase (NOS).	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	34-67
26497187-12	2016	which elicits that ameliorative potential of linagliptin was through eNOS signaling cascade and it may be concluded that linagliptin 3 mg/kg, i.p.	Linagliptin	45-56	nitric oxide synthase 3	Homo sapiens	69-73
27251500-4	2016	Lepidoside, caffeic acid and methylsuccinic acid caused the highest up-regulated expression of endothelial nitric oxide synthase at the protein level with caffeic acid and ferulic acid showing strong inhibitory effects on inducible nitric oxide synthase (iNOS) expression.	Lepidoside	0-10	nitric oxide synthase 3	Homo sapiens	95-128
26656590-1	2016	Endothelial nitric oxide synthase (eNOS) is the major source of nitric oxide (NO) production in blood vessels.	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	35-39
26746999-7	2016	Consistently, testosterone enhanced the phosphorylation of AKT and nitric oxide synthase 3.	Testosterone	14-26	nitric oxide synthase 3	Homo sapiens	67-90
26746999-10	2016	CONCLUSIONS: Testosterone protects cardiomyocytes against senescence caused by doxorubicin at least in part by modulating telomere binding factor 2 via a pathway involving the androgen receptor, phosphatidylinositol 3 kinase, AKT, and nitric oxide synthase 3.	Testosterone	13-25	nitric oxide synthase 3	Homo sapiens	235-258
26916914-6	2016	Esculetin reduced the phosphorylation of VEGFR-2 and the downstream signaling of VEGFR-2, including ERK1/2 and eNOS/Akt pathways.	esculetin	0-9	nitric oxide synthase 3	Homo sapiens	111-115
27251500-4	2016	Lepidoside, caffeic acid and methylsuccinic acid caused the highest up-regulated expression of endothelial nitric oxide synthase at the protein level with caffeic acid and ferulic acid showing strong inhibitory effects on inducible nitric oxide synthase (iNOS) expression.	caffeic acid	12-24	nitric oxide synthase 3	Homo sapiens	95-128
27251500-4	2016	Lepidoside, caffeic acid and methylsuccinic acid caused the highest up-regulated expression of endothelial nitric oxide synthase at the protein level with caffeic acid and ferulic acid showing strong inhibitory effects on inducible nitric oxide synthase (iNOS) expression.	methylsuccinic acid	29-48	nitric oxide synthase 3	Homo sapiens	95-128
27251500-4	2016	Lepidoside, caffeic acid and methylsuccinic acid caused the highest up-regulated expression of endothelial nitric oxide synthase at the protein level with caffeic acid and ferulic acid showing strong inhibitory effects on inducible nitric oxide synthase (iNOS) expression.	caffeic acid	155-167	nitric oxide synthase 3	Homo sapiens	95-128
27251500-4	2016	Lepidoside, caffeic acid and methylsuccinic acid caused the highest up-regulated expression of endothelial nitric oxide synthase at the protein level with caffeic acid and ferulic acid showing strong inhibitory effects on inducible nitric oxide synthase (iNOS) expression.	ferulic acid	172-184	nitric oxide synthase 3	Homo sapiens	95-128
26909517-14	2016	Selenium reversed the homocysteine-induced reduction of NO release, and increased the expression and phosphoylation of endothelial nitric oxide synthetase (eNOS) in a dose-dependent manner.	Selenium	0-8	nitric oxide synthase 3	Homo sapiens	119-154
26909517-14	2016	Selenium reversed the homocysteine-induced reduction of NO release, and increased the expression and phosphoylation of endothelial nitric oxide synthetase (eNOS) in a dose-dependent manner.	Selenium	0-8	nitric oxide synthase 3	Homo sapiens	156-160
26909517-15	2016	Moreover, selenium enhanced AKT phosphorylation, and selenium-induced phosphorylation and expression of eNOS were inhibited by AKT inhibition.	Selenium	53-61	nitric oxide synthase 3	Homo sapiens	104-108
27516196-2	2016	This response is preceded by an early decline in basal nitric oxide (NO) levels, dependent on a signaling leading to inhibition of the constitutive isoform of NO synthase (cNOS).	Nitric Oxide	55-67	nitric oxide synthase 3	Homo sapiens	172-176
27563480-0	2016	Impact of Rosuvastatin Treatment on HDL-Induced PKC-betaII and eNOS Phosphorylation in Endothelial Cells and Its Relation to Flow-Mediated Dilatation in Patients with Chronic Heart Failure.	Rosuvastatin Calcium	10-22	nitric oxide synthase 3	Homo sapiens	63-67
27563480-4	2016	Recent studies demonstrated that HDL stimulates NO production due to eNOS phosphorylation at Ser(1177), dephosphorylation at Thr(495), and diminished phosphorylation of PKC-betaII at Ser(660).	Serine	93-96	nitric oxide synthase 3	Homo sapiens	69-73
27563480-5	2016	The aim of this study was to elucidate the impact of rosuvastatin on HDL mediated eNOS and PKC-betaII phosphorylation and its relation to endothelial function.	Rosuvastatin Calcium	53-65	nitric oxide synthase 3	Homo sapiens	82-86
27516196-3	2016	This process requires critical levels of arachidonic acid (AA), generated by Ca&amp;lt;sup&amp;gt;2+&amp;lt;/sup&amp;gt;-dependent activation of cytosolic phospholipase A2, and is mediated by the downstream tyrosine kinase-dependent phosphorylation of cNOS.	Arachidonic Acid	41-57	nitric oxide synthase 3	Homo sapiens	252-256
26759218-2	2016	Asymmetric dimethylarginine (ADMA), an endogenous inhibitor of endothelial nitric oxide synthase (eNOS), is considered as a marker of endothelial dysfunction.	dimethylarginine	11-27	nitric oxide synthase 3	Homo sapiens	63-96
26759218-2	2016	Asymmetric dimethylarginine (ADMA), an endogenous inhibitor of endothelial nitric oxide synthase (eNOS), is considered as a marker of endothelial dysfunction.	N,N-dimethylarginine	29-33	nitric oxide synthase 3	Homo sapiens	63-96
26204498-2	2016	The nitric oxide (NO) synthase type III (NOS-3) overexpression induces cell death in hepatoblastoma cells.	Nitric Oxide	4-16	nitric oxide synthase 3	Homo sapiens	41-46
27994632-6	2016	We further demonstrated that both isoflavonoids significantly increased nitric oxide (NO) production and upregulated the activities and expressions of endothelial NOS (eNOS) and neuronal NOS (nNOS).	isoflavonoids	34-47	nitric oxide synthase 3	Homo sapiens	151-166
26682233-7	2016	Additionally, Akt/eNOS activity and NO production were downregulated in high glucose-stimulated EPCs.	Glucose	77-84	nitric oxide synthase 3	Homo sapiens	18-22
26662566-4	2016	Despite unaltered endothelial nitric oxide synthase (eNOS) levels, serine1177-phosphorylated eNOS, the active form of eNOS, progressively decreased with time.	serine1177	67-77	nitric oxide synthase 3	Homo sapiens	93-97
26662566-4	2016	Despite unaltered endothelial nitric oxide synthase (eNOS) levels, serine1177-phosphorylated eNOS, the active form of eNOS, progressively decreased with time.	serine1177	67-77	nitric oxide synthase 3	Homo sapiens	93-97
26662566-6	2016	This also coincided with decreased interaction of eNOS with actin nucleating proteins like myristoylated alanine-rich C kinase substrate and Rac1, which plays a role in modulating the cytoskeleton and helps position eNOS in a favorable cytosolic position for active enzymatic activity.	Alanine	105-112	nitric oxide synthase 3	Homo sapiens	50-54
26662566-6	2016	This also coincided with decreased interaction of eNOS with actin nucleating proteins like myristoylated alanine-rich C kinase substrate and Rac1, which plays a role in modulating the cytoskeleton and helps position eNOS in a favorable cytosolic position for active enzymatic activity.	Alanine	105-112	nitric oxide synthase 3	Homo sapiens	216-220
26682233-9	2016	Furthermore, treatment with CoQ10 reduced reactive oxygen species, enhanced eNOS/Akt activity, and increased HO-1 expression in high glucose-treated EPCs.	coenzyme Q10	28-33	nitric oxide synthase 3	Homo sapiens	76-80
26682233-12	2016	CoQ10 reduced high glucose-induced EPC apoptosis and dysfunction through upregulation of eNOS, HO-1 through the AMPK pathway.	Glucose	19-26	nitric oxide synthase 3	Homo sapiens	89-93
27594770-5	2016	Immunohistochemistry and western blotting showed that atorvastatin increased the expression of cellular adhesion molecules (CAMs) but decreased the expression of endothelial nitric oxide synthase (eNOS); these effects of atorvastatin were blocked by ALOX15 overexpression.	Atorvastatin	54-66	nitric oxide synthase 3	Homo sapiens	162-195
27594770-5	2016	Immunohistochemistry and western blotting showed that atorvastatin increased the expression of cellular adhesion molecules (CAMs) but decreased the expression of endothelial nitric oxide synthase (eNOS); these effects of atorvastatin were blocked by ALOX15 overexpression.	Atorvastatin	221-233	nitric oxide synthase 3	Homo sapiens	162-195
26682008-1	2016	Nitric oxide synthase (eNOS/NOS3) is responsible for the endothelial synthesis of nitric oxide (NO( )).	Nitric Oxide	82-94	nitric oxide synthase 3	Homo sapiens	28-32
26590088-7	2016	The latter was blocked by treating the cells with 60 microM L-NAME (but not D-NAME) as well as by 30 microM sepiapterin, a precursor of tetrahydrobiopterin that is required for proper function of endothelial nitric oxide synthase (eNOS).	NG-Nitroarginine Methyl Ester	60-66	nitric oxide synthase 3	Homo sapiens	196-229
26590088-7	2016	The latter was blocked by treating the cells with 60 microM L-NAME (but not D-NAME) as well as by 30 microM sepiapterin, a precursor of tetrahydrobiopterin that is required for proper function of endothelial nitric oxide synthase (eNOS).	sepiapterin	108-119	nitric oxide synthase 3	Homo sapiens	196-229
26590088-7	2016	The latter was blocked by treating the cells with 60 microM L-NAME (but not D-NAME) as well as by 30 microM sepiapterin, a precursor of tetrahydrobiopterin that is required for proper function of endothelial nitric oxide synthase (eNOS).	sapropterin	136-155	nitric oxide synthase 3	Homo sapiens	196-229
26655728-2	2016	Nitric oxide (NO) generated by vascular endothelial NO synthase (eNOS) plays a critical role in the NO/ cyclic guanosine 5"-monophosphate (cGMP)-mediated pulmonary vascular function.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	65-69
26655728-2	2016	Nitric oxide (NO) generated by vascular endothelial NO synthase (eNOS) plays a critical role in the NO/ cyclic guanosine 5"-monophosphate (cGMP)-mediated pulmonary vascular function.	cyclic guanosine 5"-monophosphate	104-137	nitric oxide synthase 3	Homo sapiens	65-69
26802937-7	2016	DHA reversed the TNF-alpha-mediated reduction of endothelial nitric oxide synthase (NOS3) gene expression.	Docosahexaenoic Acids	0-3	nitric oxide synthase 3	Homo sapiens	49-82
26802937-7	2016	DHA reversed the TNF-alpha-mediated reduction of endothelial nitric oxide synthase (NOS3) gene expression.	Docosahexaenoic Acids	0-3	nitric oxide synthase 3	Homo sapiens	84-88
26655728-2	2016	Nitric oxide (NO) generated by vascular endothelial NO synthase (eNOS) plays a critical role in the NO/ cyclic guanosine 5"-monophosphate (cGMP)-mediated pulmonary vascular function.	Cyclic GMP	139-143	nitric oxide synthase 3	Homo sapiens	65-69
26655728-3	2016	Here we examined whether internalization of a fifteen amino acid (KRFNSISCSSWRRKR) synthetic peptide (P3) enhances the catalytic activity of eNOS via caveolae/eNOS dissociation leading to NO release and increased cGMP production in pulmonary artery endothelial cells (EC).	Cyclic GMP	213-217	nitric oxide synthase 3	Homo sapiens	141-145
26655728-8	2016	P3- mediated activation of eNOS was abolished by intracellular Ca(2+) chelator 1,2-bis(2-aminophenooxy)ethane-N,N,N",N"- tertraacetic acid-AM (BAPTA-AM), PI3K inhibition, or by siRNA-mediated Cav-1 suppression.	1,2-bis(2-aminophenooxy)ethane-n,n,n",n"- tertraacetic acid-am	79-141	nitric oxide synthase 3	Homo sapiens	27-31
26655728-8	2016	P3- mediated activation of eNOS was abolished by intracellular Ca(2+) chelator 1,2-bis(2-aminophenooxy)ethane-N,N,N",N"- tertraacetic acid-AM (BAPTA-AM), PI3K inhibition, or by siRNA-mediated Cav-1 suppression.	1,2-bis(2-aminophenoxy)ethane N,N,N',N'-tetraacetic acid acetoxymethyl ester	143-151	nitric oxide synthase 3	Homo sapiens	27-31
26645254-1	2016	BACKGROUND AND PURPOSE: The Efficacy of Nitric Oxide in Stroke (ENOS) trial found that transdermal glyceryl trinitrate (GTN, a nitric oxide donor) lowered blood pressure but did not improve functional outcome in patients with acute stroke.	Nitric Oxide	40-52	nitric oxide synthase 3	Homo sapiens	64-68
26645254-0	2016	Glyceryl Trinitrate for Acute Intracerebral Hemorrhage: Results From the Efficacy of Nitric Oxide in Stroke (ENOS) Trial, a Subgroup Analysis.	Nitroglycerin	0-19	nitric oxide synthase 3	Homo sapiens	109-113
26645254-1	2016	BACKGROUND AND PURPOSE: The Efficacy of Nitric Oxide in Stroke (ENOS) trial found that transdermal glyceryl trinitrate (GTN, a nitric oxide donor) lowered blood pressure but did not improve functional outcome in patients with acute stroke.	Nitroglycerin	99-118	nitric oxide synthase 3	Homo sapiens	64-68
26645254-0	2016	Glyceryl Trinitrate for Acute Intracerebral Hemorrhage: Results From the Efficacy of Nitric Oxide in Stroke (ENOS) Trial, a Subgroup Analysis.	Nitric Oxide	85-97	nitric oxide synthase 3	Homo sapiens	109-113
26645254-1	2016	BACKGROUND AND PURPOSE: The Efficacy of Nitric Oxide in Stroke (ENOS) trial found that transdermal glyceryl trinitrate (GTN, a nitric oxide donor) lowered blood pressure but did not improve functional outcome in patients with acute stroke.	Nitroglycerin	120-123	nitric oxide synthase 3	Homo sapiens	64-68
26645254-1	2016	BACKGROUND AND PURPOSE: The Efficacy of Nitric Oxide in Stroke (ENOS) trial found that transdermal glyceryl trinitrate (GTN, a nitric oxide donor) lowered blood pressure but did not improve functional outcome in patients with acute stroke.	Nitric Oxide	127-139	nitric oxide synthase 3	Homo sapiens	64-68
26404526-0	2015	Phosphocreatine protects endothelial cells from oxidized low-density lipoprotein-induced apoptosis by modulating the PI3K/Akt/eNOS pathway.	Phosphocreatine	0-15	nitric oxide synthase 3	Homo sapiens	126-130
26656861-5	2015	Compared with lactate production-negative VSA patients, the lactate production-positive counterparts were more likely to be nonsmoker female diabetics with -786T/C eNOS polymorphism (61% vs 31%, P&lt;0.001, 62% vs 34%, P&lt;0.001, 24% vs 14%, P=0.016, and 25% vs 15%, P=0.018, respectively).	Lactic Acid	60-67	nitric oxide synthase 3	Homo sapiens	164-168
26656861-6	2015	Multivariable logistic regression analysis identified female sex, diabetes mellitus, and -786T/C eNOS polymorphism to correlate with lactate production (odds ratio 3.51, 95% CI 2.16 to 5.70, P&lt;0.001; odds ratio 2.53, 95% CI 1.38 to 4.65, P=0.003; and odds ratio 1.85, 95% CI 1.02 to 3.35, P=0.044, respectively).	Lactic Acid	133-140	nitric oxide synthase 3	Homo sapiens	97-101
26656861-8	2015	CONCLUSIONS: The results indicated that female sex, diabetes, and mutation in -786T/C eNOS gene correlate with ACh-provoked myocardial ischemia in patients with coronary spasm.	Acetylcholine	111-114	nitric oxide synthase 3	Homo sapiens	86-90
26653547-12	2015	Expression of human endothelial nitric oxide synthase is associated with genistein supplementation.	Genistein	73-82	nitric oxide synthase 3	Homo sapiens	20-53
26390975-1	2015	Endothelial nitric oxide synthase (eNOS, NOS3) is responsible for producing nitric oxide (NO)--a key molecule that can directly (or indirectly) act as a vasodilator and anti-inflammatory mediator.	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	35-39
26390975-1	2015	Endothelial nitric oxide synthase (eNOS, NOS3) is responsible for producing nitric oxide (NO)--a key molecule that can directly (or indirectly) act as a vasodilator and anti-inflammatory mediator.	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	41-45
26527496-9	2015	It is our hypothesis that, in hypoxic stress, a key player in initiating this imbalance is the enzyme, protein arginine methyltransferase-1 (PRMT1) which indirectly affects eNOS activity by increased production of asymmetric dimethylarginine (ADMA), a NOS-inhibitor.	dimethylarginine	225-241	nitric oxide synthase 3	Homo sapiens	173-177
26393424-0	2015	CCN1 acutely increases nitric oxide production via integrin alphavbeta3-Akt-S6K-phosphorylation of endothelial nitric oxide synthase at the serine 1177 signaling axis.	Nitric Oxide	23-35	nitric oxide synthase 3	Homo sapiens	99-132
26393424-0	2015	CCN1 acutely increases nitric oxide production via integrin alphavbeta3-Akt-S6K-phosphorylation of endothelial nitric oxide synthase at the serine 1177 signaling axis.	Serine	140-146	nitric oxide synthase 3	Homo sapiens	99-132
26475965-4	2015	KEY FINDINGS: Non-cytotoxic PPF treatment was found to significantly upregulate inducible nitric oxide synthase (NOS2) but downregulate constitutive NOS3 expression.	Propofol	28-31	nitric oxide synthase 3	Homo sapiens	149-153
26527496-9	2015	It is our hypothesis that, in hypoxic stress, a key player in initiating this imbalance is the enzyme, protein arginine methyltransferase-1 (PRMT1) which indirectly affects eNOS activity by increased production of asymmetric dimethylarginine (ADMA), a NOS-inhibitor.	N,N-dimethylarginine	243-247	nitric oxide synthase 3	Homo sapiens	173-177
26498523-0	2015	beta-Amyrin induces angiogenesis in vascular endothelial cells through the Akt/endothelial nitric oxide synthase signaling pathway.	beta-amyrin	0-11	nitric oxide synthase 3	Homo sapiens	79-112
26335399-4	2015	Neuronal (nNOS, NOS1) and endothelial (eNOS, NOS3) are constitutive calcium-dependent forms of the enzyme that regulate neural and vascular function respectively.	Calcium	68-75	nitric oxide synthase 3	Homo sapiens	45-49
26476183-7	2015	By down-regulating S1P1 receptor expression, the S1P1-specific antisense oligonucleotides significantly inhibited E2-induced activation of Akt/eNOS in ECs.	Oligonucleotides	73-89	nitric oxide synthase 3	Homo sapiens	143-147
26560496-0	2015	Serine 1179 Phosphorylation of Endothelial Nitric Oxide Synthase Increases Superoxide Generation and Alters Cofactor Regulation.	Serine	0-6	nitric oxide synthase 3	Homo sapiens	31-64
26560496-0	2015	Serine 1179 Phosphorylation of Endothelial Nitric Oxide Synthase Increases Superoxide Generation and Alters Cofactor Regulation.	Superoxides	75-85	nitric oxide synthase 3	Homo sapiens	31-64
26188706-2	2015	However, some genes have been linked to their formation, as in the case of NOS3 gene which encodes the endothelial nitric oxide synthase responsible for producing nitric oxide.	Nitric Oxide	115-127	nitric oxide synthase 3	Homo sapiens	75-79
26414244-0	2015	Folic Acid Promotes Recycling of Tetrahydrobiopterin and Protects Against Hypoxia-Induced Pulmonary Hypertension by Recoupling Endothelial Nitric Oxide Synthase.	Folic Acid	0-10	nitric oxide synthase 3	Homo sapiens	127-160
26409042-1	2015	Caveolin-1 (Cav-1), the homo-oligomeric coat protein of cholesterol-rich caveolae signalosomes, regulates signaling proteins including endothelial nitric oxide synthase (eNOS).	Cholesterol	56-67	nitric oxide synthase 3	Homo sapiens	135-168
25812766-11	2015	The combination also increased nitric oxide production by NOS1 and NOS3 via mAChR activation, concomitantly with an up-regulation of NOS3 expression.	Nitric Oxide	31-43	nitric oxide synthase 3	Homo sapiens	67-71
26134126-7	2015	In in vitro experiments by using human aortic endothelial cells, bilirubin augmented eNOS and Akt phosphorylation, cell proliferation, cell migration and tube formation.	Bilirubin	65-74	nitric oxide synthase 3	Homo sapiens	85-89
26823875-10	2015	Interactions were existed between NOS3 gene polymorphisms and oxygen therapy duration.	Oxygen	62-68	nitric oxide synthase 3	Homo sapiens	34-38
26265282-8	2015	Two genes, SLCO2A1 and NOS3, (involved with prostaglandin reuptake/metabolism and nitric oxide production, respectively) were consistently decreased in "non-Caucasian" DA.	Prostaglandins	44-57	nitric oxide synthase 3	Homo sapiens	23-27
25663485-4	2015	We demonstrated that BPA markedly induces endothelial cell proliferation, migration and tube formation by activating endothelial nitric oxide synthase.	bisphenol A	21-24	nitric oxide synthase 3	Homo sapiens	117-150
25663485-5	2015	BPA-induced nitric oxide generation appeared to be associated with the X-linked inhibitor of apoptosis protein (XIAP), which competes with endothelial nitric oxide synthase for caveolin-1.	bisphenol A	0-3	nitric oxide synthase 3	Homo sapiens	139-172
25663485-5	2015	BPA-induced nitric oxide generation appeared to be associated with the X-linked inhibitor of apoptosis protein (XIAP), which competes with endothelial nitric oxide synthase for caveolin-1.	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	139-172
26351364-7	2015	A guanosine 3",5"-cyclic monophosphate (cGMP) antagonist reversed KMUP-1-induced ROCK II reduction, indicating cGMP/eNOS involvement.	Cyclic GMP	2-38	nitric oxide synthase 3	Homo sapiens	116-120
26351364-7	2015	A guanosine 3",5"-cyclic monophosphate (cGMP) antagonist reversed KMUP-1-induced ROCK II reduction, indicating cGMP/eNOS involvement.	Cyclic GMP	40-44	nitric oxide synthase 3	Homo sapiens	116-120
26351364-7	2015	A guanosine 3",5"-cyclic monophosphate (cGMP) antagonist reversed KMUP-1-induced ROCK II reduction, indicating cGMP/eNOS involvement.	KMUP 1	66-72	nitric oxide synthase 3	Homo sapiens	116-120
26265282-8	2015	Two genes, SLCO2A1 and NOS3, (involved with prostaglandin reuptake/metabolism and nitric oxide production, respectively) were consistently decreased in "non-Caucasian" DA.	Nitric Oxide	82-94	nitric oxide synthase 3	Homo sapiens	23-27
26265282-11	2015	Because decreased SLCO2A1 and NOS3 expression can lead to increased prostaglandin and decreased nitric oxide concentrations, we speculate that prostaglandin-mediated vasodilation may play a more dominant role in maintaining the "non-Caucasian" patent DA, making it more likely to close when inhibited by indomethacin.	Prostaglandins	68-81	nitric oxide synthase 3	Homo sapiens	30-34
26265282-11	2015	Because decreased SLCO2A1 and NOS3 expression can lead to increased prostaglandin and decreased nitric oxide concentrations, we speculate that prostaglandin-mediated vasodilation may play a more dominant role in maintaining the "non-Caucasian" patent DA, making it more likely to close when inhibited by indomethacin.	Nitric Oxide	96-108	nitric oxide synthase 3	Homo sapiens	30-34
26265282-11	2015	Because decreased SLCO2A1 and NOS3 expression can lead to increased prostaglandin and decreased nitric oxide concentrations, we speculate that prostaglandin-mediated vasodilation may play a more dominant role in maintaining the "non-Caucasian" patent DA, making it more likely to close when inhibited by indomethacin.	Prostaglandins	143-156	nitric oxide synthase 3	Homo sapiens	30-34
23319464-0	2015	eNOS transfection of adipose-derived stem cells yields bioactive nitric oxide production and improved results in vascular tissue engineering.	Nitric Oxide	65-77	nitric oxide synthase 3	Homo sapiens	0-4
26385052-0	2015	Pharmacogenetic influence of eNOS gene variant on endothelial and glucose metabolism responses to L-arginine supplementation: Post hoc analysis of the L-arginine trial.	Arginine	151-161	nitric oxide synthase 3	Homo sapiens	29-33
26385052-0	2015	Pharmacogenetic influence of eNOS gene variant on endothelial and glucose metabolism responses to L-arginine supplementation: Post hoc analysis of the L-arginine trial.	Glucose	66-73	nitric oxide synthase 3	Homo sapiens	29-33
26385052-1	2015	OBJECTIVE: To evaluate whether variants of the eNOS gene are associated with endothelial and metabolic responses to L-arginine (L-arg) supplementation.	Arginine	116-126	nitric oxide synthase 3	Homo sapiens	47-51
26385052-0	2015	Pharmacogenetic influence of eNOS gene variant on endothelial and glucose metabolism responses to L-arginine supplementation: Post hoc analysis of the L-arginine trial.	Arginine	98-108	nitric oxide synthase 3	Homo sapiens	29-33
26385052-1	2015	OBJECTIVE: To evaluate whether variants of the eNOS gene are associated with endothelial and metabolic responses to L-arginine (L-arg) supplementation.	Arginine	116-121	nitric oxide synthase 3	Homo sapiens	47-51
26385052-2	2015	MATERIAL AND METHODS: We examined a single nucleotide polymorphism of the eNOS gene (rs753482-A&gt;C) to investigate the effects of this variant on endothelial function (EF), colony-forming unit-endothelial cell (CFU-EC) number, asymmetric-dimethylarginine (ADMA) level, insulin sensitivity index (ISI), and insulin secretion (IS) in a post hoc analysis of the L-arg trial.	dimethylarginine	240-256	nitric oxide synthase 3	Homo sapiens	74-78
26385052-2	2015	MATERIAL AND METHODS: We examined a single nucleotide polymorphism of the eNOS gene (rs753482-A&gt;C) to investigate the effects of this variant on endothelial function (EF), colony-forming unit-endothelial cell (CFU-EC) number, asymmetric-dimethylarginine (ADMA) level, insulin sensitivity index (ISI), and insulin secretion (IS) in a post hoc analysis of the L-arg trial.	N,N-dimethylarginine	258-262	nitric oxide synthase 3	Homo sapiens	74-78
26385052-2	2015	MATERIAL AND METHODS: We examined a single nucleotide polymorphism of the eNOS gene (rs753482-A&gt;C) to investigate the effects of this variant on endothelial function (EF), colony-forming unit-endothelial cell (CFU-EC) number, asymmetric-dimethylarginine (ADMA) level, insulin sensitivity index (ISI), and insulin secretion (IS) in a post hoc analysis of the L-arg trial.	Arginine	361-366	nitric oxide synthase 3	Homo sapiens	74-78
26133666-6	2015	Fenofibrate and ER niacin also improved the impaired HDL ability to induce the expression of endothelial nitric oxide synthase and NO production (+10% and +8%, respectively).	Fenofibrate	0-11	nitric oxide synthase 3	Homo sapiens	93-126
26517550-1	2015	Nitric oxide (NO), an important endogenous pulmonary vasodilator is synthetized by the endothelial NO synthase (NOS3).	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	112-116
28989705-4	2015	In addition, evaluation of HAEC phenotype at confluence indicated significant differences in the gene expression of NOS3, thrombomodulin, and E-selectin on the PEG-Scl2-2 hydrogels relative to PEG-collagen controls.	Polyethylene Glycols	160-163	nitric oxide synthase 3	Homo sapiens	116-120
28989705-5	2015	At the protein level, however, only NOS3 was significantly different between the PEG-Scl2-2 and PEG-collagen surfaces.	Polyethylene Glycols	81-84	nitric oxide synthase 3	Homo sapiens	36-40
28989705-5	2015	At the protein level, however, only NOS3 was significantly different between the PEG-Scl2-2 and PEG-collagen surfaces.	Polyethylene Glycols	96-99	nitric oxide synthase 3	Homo sapiens	36-40
26416428-9	2015	Levels of phosphorylated Akt, anti-apoptotic Bcl-xL, pro-apoptotic Bax and endothelial nitric oxide synthase (NOS) were re-regulated after combined oxygen and melatonin delivery, whereas neuronal and inducible NOS, which were increased by oxygen treatment, were not influenced by melatonin.	Oxygen	148-154	nitric oxide synthase 3	Homo sapiens	75-108
26416428-9	2015	Levels of phosphorylated Akt, anti-apoptotic Bcl-xL, pro-apoptotic Bax and endothelial nitric oxide synthase (NOS) were re-regulated after combined oxygen and melatonin delivery, whereas neuronal and inducible NOS, which were increased by oxygen treatment, were not influenced by melatonin.	Melatonin	159-168	nitric oxide synthase 3	Homo sapiens	75-108
26296888-1	2015	Citrulline formation by both human neuronal nitric-oxide synthase (nNOS) and mouse macrophage inducible NOS was inhibited by the hydrogen sulfide (H2S) donor Na2S with IC50 values of ~2.4 10(-5) and ~7.9 10(-5) m, respectively, whereas human endothelial NOS was hardly affected at all.	Citrulline	0-10	nitric oxide synthase 3	Homo sapiens	242-257
26296888-1	2015	Citrulline formation by both human neuronal nitric-oxide synthase (nNOS) and mouse macrophage inducible NOS was inhibited by the hydrogen sulfide (H2S) donor Na2S with IC50 values of ~2.4 10(-5) and ~7.9 10(-5) m, respectively, whereas human endothelial NOS was hardly affected at all.	Hydrogen Sulfide	129-145	nitric oxide synthase 3	Homo sapiens	242-257
26296888-1	2015	Citrulline formation by both human neuronal nitric-oxide synthase (nNOS) and mouse macrophage inducible NOS was inhibited by the hydrogen sulfide (H2S) donor Na2S with IC50 values of ~2.4 10(-5) and ~7.9 10(-5) m, respectively, whereas human endothelial NOS was hardly affected at all.	Hydrogen Sulfide	147-150	nitric oxide synthase 3	Homo sapiens	242-257
26296888-1	2015	Citrulline formation by both human neuronal nitric-oxide synthase (nNOS) and mouse macrophage inducible NOS was inhibited by the hydrogen sulfide (H2S) donor Na2S with IC50 values of ~2.4 10(-5) and ~7.9 10(-5) m, respectively, whereas human endothelial NOS was hardly affected at all.	sodium sulfide	158-162	nitric oxide synthase 3	Homo sapiens	242-257
26268592-12	2015	ZFP580 also enhanced eNOS expression, and eNOS inhibition suppressed differentiation.	zfp580	0-6	nitric oxide synthase 3	Homo sapiens	21-25
26242202-10	2015	Finally, both GRalpha overexpression and 5-aza-2-deoxycytidine treatment eliminated the differences between sensitivity groups to DEX-mediated downregulation of endothelial nitric oxide synthase (NOS3), and upregulation of plasminogen activator inhibitor 1 (SERPINE1).	Decitabine	41-62	nitric oxide synthase 3	Homo sapiens	161-194
26242202-10	2015	Finally, both GRalpha overexpression and 5-aza-2-deoxycytidine treatment eliminated the differences between sensitivity groups to DEX-mediated downregulation of endothelial nitric oxide synthase (NOS3), and upregulation of plasminogen activator inhibitor 1 (SERPINE1).	Decitabine	41-62	nitric oxide synthase 3	Homo sapiens	196-200
26499181-4	2015	In the blood vessel wall, NO is produced mainly from l-arginine by the enzyme endothelial nitric oxide synthase (eNOS) but it can also be released non-enzymatically from S-nitrosothiols or from nitrate/nitrite.	Arginine	53-63	nitric oxide synthase 3	Homo sapiens	78-111
26242202-10	2015	Finally, both GRalpha overexpression and 5-aza-2-deoxycytidine treatment eliminated the differences between sensitivity groups to DEX-mediated downregulation of endothelial nitric oxide synthase (NOS3), and upregulation of plasminogen activator inhibitor 1 (SERPINE1).	Dexamethasone	130-133	nitric oxide synthase 3	Homo sapiens	161-194
26242202-10	2015	Finally, both GRalpha overexpression and 5-aza-2-deoxycytidine treatment eliminated the differences between sensitivity groups to DEX-mediated downregulation of endothelial nitric oxide synthase (NOS3), and upregulation of plasminogen activator inhibitor 1 (SERPINE1).	Dexamethasone	130-133	nitric oxide synthase 3	Homo sapiens	196-200
26428638-6	2015	L-arginine acts to increase the production of nitric oxide and Pycnogenol( ) activates the endothelial nitric oxide synthase and it is a potent antioxidant and inhibitor of inducible nitric oxide synthase.	Arginine	0-10	nitric oxide synthase 3	Homo sapiens	91-124
26428638-6	2015	L-arginine acts to increase the production of nitric oxide and Pycnogenol( ) activates the endothelial nitric oxide synthase and it is a potent antioxidant and inhibitor of inducible nitric oxide synthase.	pycnogenols	63-73	nitric oxide synthase 3	Homo sapiens	91-124
26187788-7	2015	Elevated serum homocysteine and vitamin B12 levels were associated with MTHFR 677C&gt;T and eNOS intron 4a/b polymorphisms.	Homocysteine	15-27	nitric oxide synthase 3	Homo sapiens	92-96
26091577-3	2015	Asymmetric dimethyl arginine (ADMA), endogenous inhibitor of endothelial nitric oxide synthase (eNOS), also represents one of the critical regulators of pulmonary vascular functions.	dimethylarginine	11-28	nitric oxide synthase 3	Homo sapiens	61-94
26091577-3	2015	Asymmetric dimethyl arginine (ADMA), endogenous inhibitor of endothelial nitric oxide synthase (eNOS), also represents one of the critical regulators of pulmonary vascular functions.	dimethylarginine	11-28	nitric oxide synthase 3	Homo sapiens	96-100
26091577-3	2015	Asymmetric dimethyl arginine (ADMA), endogenous inhibitor of endothelial nitric oxide synthase (eNOS), also represents one of the critical regulators of pulmonary vascular functions.	N,N-dimethylarginine	30-34	nitric oxide synthase 3	Homo sapiens	61-94
26091577-3	2015	Asymmetric dimethyl arginine (ADMA), endogenous inhibitor of endothelial nitric oxide synthase (eNOS), also represents one of the critical regulators of pulmonary vascular functions.	N,N-dimethylarginine	30-34	nitric oxide synthase 3	Homo sapiens	96-100
26091577-6	2015	It was discovered for the first time that ADMA induced the activation of signal transducer and activator of transcription 3 (STAT3) and stabilization of hypoxia inducible factor 1alpha (HIF-1alpha) in both types of cells, associated with drastic alternations in normal cellular functions (e.g., nitric oxide production, cell proliferation/Ca(2+) concentration, production of pro-inflammatory mediators, and expression of eNOS, DDAH1, and ICAM-1).	N,N-dimethylarginine	42-46	nitric oxide synthase 3	Homo sapiens	421-425
26116711-9	2015	Similarly, exercise-induced changes in whole blood expression of VEGF, endothelial nitric oxide synthase and phosphatidylinositol 3-kinase R2 were blunted after NAC.	Acetylcysteine	161-164	nitric oxide synthase 3	Homo sapiens	71-104
26512245-1	2015	OBJECTIVE: To find out whether dexamethasone induces an uncoupling of the endothelial nitric oxide synthase (eNOS).	Dexamethasone	31-44	nitric oxide synthase 3	Homo sapiens	74-107
26187788-7	2015	Elevated serum homocysteine and vitamin B12 levels were associated with MTHFR 677C&gt;T and eNOS intron 4a/b polymorphisms.	Vitamin B 12	32-43	nitric oxide synthase 3	Homo sapiens	92-96
26187788-8	2015	The ApoE and eNOS -786T&gt;C polymorphisms were associated with increased serum vitamin B12 levels.	Vitamin B 12	80-91	nitric oxide synthase 3	Homo sapiens	13-17
26187788-11	2015	CONCLUSIONS: The present study suggests that the genotypes and haplotypes of MTHFR 677C&gt;T and eNOS intron 4a/b polymorphisms are potential serum biomarkers in the pathophysiological processes of ischemic stroke, by modulating homocysteine and vitamin B12 levels.	Homocysteine	229-241	nitric oxide synthase 3	Homo sapiens	97-101
26187788-11	2015	CONCLUSIONS: The present study suggests that the genotypes and haplotypes of MTHFR 677C&gt;T and eNOS intron 4a/b polymorphisms are potential serum biomarkers in the pathophysiological processes of ischemic stroke, by modulating homocysteine and vitamin B12 levels.	Vitamin B 12	246-257	nitric oxide synthase 3	Homo sapiens	97-101
26008990-0	2015	Pterostilbene, an Active Constituent of Blueberries, Stimulates Nitric Oxide Production via Activation of Endothelial Nitric Oxide Synthase in Human Umbilical Vein Endothelial Cells.	pterostilbene	0-13	nitric oxide synthase 3	Homo sapiens	106-139
26304753-0	2015	Role of phosphatase activity of soluble epoxide hydrolase in regulating simvastatin-activated endothelial nitric oxide synthase.	Simvastatin	72-83	nitric oxide synthase 3	Homo sapiens	94-127
26152729-11	2015	However, preservation of cAMP by ascorbate was found to depend on both the production of nitric oxide by endothelial nitric-oxide synthase, which ascorbate is known to activate, and the subsequent generation cGMP by guanylate cyclase.	Cyclic AMP	25-29	nitric oxide synthase 3	Homo sapiens	105-138
26152729-11	2015	However, preservation of cAMP by ascorbate was found to depend on both the production of nitric oxide by endothelial nitric-oxide synthase, which ascorbate is known to activate, and the subsequent generation cGMP by guanylate cyclase.	Ascorbic Acid	33-42	nitric oxide synthase 3	Homo sapiens	105-138
26152729-11	2015	However, preservation of cAMP by ascorbate was found to depend on both the production of nitric oxide by endothelial nitric-oxide synthase, which ascorbate is known to activate, and the subsequent generation cGMP by guanylate cyclase.	Nitric Oxide	89-101	nitric oxide synthase 3	Homo sapiens	105-138
26152729-11	2015	However, preservation of cAMP by ascorbate was found to depend on both the production of nitric oxide by endothelial nitric-oxide synthase, which ascorbate is known to activate, and the subsequent generation cGMP by guanylate cyclase.	Ascorbic Acid	146-155	nitric oxide synthase 3	Homo sapiens	105-138
26304753-11	2015	These findings suggest that sEH phosphatase activity negatively regulates simvastatin-activated eNOS by impeding the Akt-AMPK-eNOS signaling cascade.	Simvastatin	74-85	nitric oxide synthase 3	Homo sapiens	96-100
26304753-11	2015	These findings suggest that sEH phosphatase activity negatively regulates simvastatin-activated eNOS by impeding the Akt-AMPK-eNOS signaling cascade.	Simvastatin	74-85	nitric oxide synthase 3	Homo sapiens	126-130
26304753-4	2015	Simvastatin, a clinical lipid-lowering drug, also has a pleiotropic effect on eNOS activation.	Simvastatin	0-11	nitric oxide synthase 3	Homo sapiens	78-82
26304753-5	2015	However, whether sEH phosphatase is involved in simvastatin-activated eNOS activity remains elusive.	Simvastatin	48-59	nitric oxide synthase 3	Homo sapiens	70-74
26304753-6	2015	We investigated the role of sEH phosphatase activity in simvastatin-mediated activation of eNOS in endothelial cells (ECs).	Simvastatin	56-67	nitric oxide synthase 3	Homo sapiens	91-95
26304753-8	2015	In addition, pharmacological inhibition of sEH phosphatase or overexpressing the inactive phosphatase domain of sEH enhanced simvastatin-induced NO bioavailability, tube formation and phosphorylation of eNOS, Akt, and AMP-activated protein kinase (AMPK).	Simvastatin	125-136	nitric oxide synthase 3	Homo sapiens	203-207
26304753-9	2015	In contrast, overexpressing the phosphatase domain of sEH limited the simvastatin-increased NO biosynthesis and eNOS phosphorylation at Ser1179.	Simvastatin	70-81	nitric oxide synthase 3	Homo sapiens	112-116
26304753-10	2015	Simvastatin evoked epidermal growth factor receptor-c-Src-increased Tyr phosphorylation of sEH and formation of an sEH-Akt-AMPK-eNOS complex, which was abolished by the c-Src kinase inhibitor PP1 or c-Src dominant-negative mutant K298M.	Simvastatin	0-11	nitric oxide synthase 3	Homo sapiens	128-132
26297582-15	2015	The impairment of the PI3K/AKT/eNOS pathway after physiological insulin treatment could contribute to detrimental effects on cardiovascular homeostasis under high glucose conditions, and might shift toward the activation of certain mitogenic effectors, such as ERK1/2, p38 and JNK, the only ones that respond to physiological insulin treatment in high glucose.	Glucose	163-170	nitric oxide synthase 3	Homo sapiens	31-35
26297582-15	2015	The impairment of the PI3K/AKT/eNOS pathway after physiological insulin treatment could contribute to detrimental effects on cardiovascular homeostasis under high glucose conditions, and might shift toward the activation of certain mitogenic effectors, such as ERK1/2, p38 and JNK, the only ones that respond to physiological insulin treatment in high glucose.	Glucose	352-359	nitric oxide synthase 3	Homo sapiens	31-35
26297582-4	2015	AKT phosphorylates eNOS at Ser1177, resulting in increased nitric oxide production and vasodilation.	Nitric Oxide	59-71	nitric oxide synthase 3	Homo sapiens	19-23
25913239-10	2015	Taken together, YLF-466D is capable of inhibiting platelet aggregation by activating AMPK and its downstream eNOS-cGMP-PKG signaling axis.	Cyclic GMP	114-118	nitric oxide synthase 3	Homo sapiens	109-113
26297582-9	2015	RESULTS: In normal glucose, the active phosphorylated forms of AKT, eNOS, ERK1/2, p38 and JNK were increased in insulin treated cells, in a dose-dependent manner.	Glucose	19-26	nitric oxide synthase 3	Homo sapiens	68-72
26284388-9	2015	The mRNA levels of endothelial markers platelet endothelial cell adhesion molecule-1 (PECAM-1/CD31) and endothelial nitric oxide synthase (eNOS), were significantly upregulated in about 2 folds by PGE2 detected with Q-PCR assay.	Dinoprostone	197-201	nitric oxide synthase 3	Homo sapiens	104-137
26286023-1	2015	Endothelial nitric oxide synthase (eNOS) catalyzes the conversion of l-arginine and molecular oxygen into l-citrulline and nitric oxide (NO), a gaseous second messenger that influences cardiovascular physiology and disease.	Arginine	69-79	nitric oxide synthase 3	Homo sapiens	0-33
26286023-1	2015	Endothelial nitric oxide synthase (eNOS) catalyzes the conversion of l-arginine and molecular oxygen into l-citrulline and nitric oxide (NO), a gaseous second messenger that influences cardiovascular physiology and disease.	Arginine	69-79	nitric oxide synthase 3	Homo sapiens	35-39
26286023-1	2015	Endothelial nitric oxide synthase (eNOS) catalyzes the conversion of l-arginine and molecular oxygen into l-citrulline and nitric oxide (NO), a gaseous second messenger that influences cardiovascular physiology and disease.	Oxygen	94-100	nitric oxide synthase 3	Homo sapiens	0-33
26286023-1	2015	Endothelial nitric oxide synthase (eNOS) catalyzes the conversion of l-arginine and molecular oxygen into l-citrulline and nitric oxide (NO), a gaseous second messenger that influences cardiovascular physiology and disease.	Oxygen	94-100	nitric oxide synthase 3	Homo sapiens	35-39
26286023-1	2015	Endothelial nitric oxide synthase (eNOS) catalyzes the conversion of l-arginine and molecular oxygen into l-citrulline and nitric oxide (NO), a gaseous second messenger that influences cardiovascular physiology and disease.	Citrulline	106-118	nitric oxide synthase 3	Homo sapiens	0-33
26286023-1	2015	Endothelial nitric oxide synthase (eNOS) catalyzes the conversion of l-arginine and molecular oxygen into l-citrulline and nitric oxide (NO), a gaseous second messenger that influences cardiovascular physiology and disease.	Citrulline	106-118	nitric oxide synthase 3	Homo sapiens	35-39
26286023-1	2015	Endothelial nitric oxide synthase (eNOS) catalyzes the conversion of l-arginine and molecular oxygen into l-citrulline and nitric oxide (NO), a gaseous second messenger that influences cardiovascular physiology and disease.	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	35-39
26286023-2	2015	Several mechanisms regulate eNOS activity and function, including phosphorylation at Ser and Thr residues and protein-protein interactions.	Serine	85-88	nitric oxide synthase 3	Homo sapiens	28-32
26286023-2	2015	Several mechanisms regulate eNOS activity and function, including phosphorylation at Ser and Thr residues and protein-protein interactions.	Threonine	93-96	nitric oxide synthase 3	Homo sapiens	28-32
26286023-4	2015	SDF2 knockdown impaired agonist-stimulated NO synthesis and decreased the phosphorylation of eNOS at Ser(1177), a key event required for maximal activation of eNOS.	Serine	101-104	nitric oxide synthase 3	Homo sapiens	93-97
26286023-4	2015	SDF2 knockdown impaired agonist-stimulated NO synthesis and decreased the phosphorylation of eNOS at Ser(1177), a key event required for maximal activation of eNOS.	Serine	101-104	nitric oxide synthase 3	Homo sapiens	159-163
26286023-5	2015	Conversely, SDF2 overexpression dose-dependently increased NO synthesis through a mechanism involving Akt and calcium (induced with ionomycin), which increased the phosphorylation of Ser(1177) in eNOS.	Calcium	110-117	nitric oxide synthase 3	Homo sapiens	196-200
26286023-5	2015	Conversely, SDF2 overexpression dose-dependently increased NO synthesis through a mechanism involving Akt and calcium (induced with ionomycin), which increased the phosphorylation of Ser(1177) in eNOS.	Ionomycin	132-141	nitric oxide synthase 3	Homo sapiens	196-200
26286023-5	2015	Conversely, SDF2 overexpression dose-dependently increased NO synthesis through a mechanism involving Akt and calcium (induced with ionomycin), which increased the phosphorylation of Ser(1177) in eNOS.	Serine	183-186	nitric oxide synthase 3	Homo sapiens	196-200
25536367-5	2015	The objective of this study was to determine whether starting L-citrulline after the onset of pulmonary hypertension inhibits disease progression and improves NO production by recoupling endothelial NO synthase (eNOS).	Citrulline	62-74	nitric oxide synthase 3	Homo sapiens	212-216
25536367-11	2015	When started after disease onset, oral L-citrulline treatment improves NO production by recoupling eNOS and inhibits the further development of chronic hypoxia-induced pulmonary hypertension in newborn piglets.	Citrulline	39-51	nitric oxide synthase 3	Homo sapiens	99-103
25536367-10	2015	NO production and eNOS dimer-to-monomer ratios were greater in pulmonary arteries from L-citrulline-treated than from untreated hypoxic animals but were lower than in normoxic controls.	Citrulline	87-99	nitric oxide synthase 3	Homo sapiens	18-22
25728347-0	2015	Propranolol induces regression of hemangioma cells via the down-regulation of the PI3K/Akt/eNOS/VEGF pathway.	Propranolol	0-11	nitric oxide synthase 3	Homo sapiens	91-95
26367737-0	2015	Piceatannol, a natural hydroxylated analog of resveratrol, promotes nitric oxide release through phosphorylation of endothelial nitric oxide synthase in human endothelial cells.	3,3',4,5'-tetrahydroxystilbene	0-11	nitric oxide synthase 3	Homo sapiens	116-149
26367737-0	2015	Piceatannol, a natural hydroxylated analog of resveratrol, promotes nitric oxide release through phosphorylation of endothelial nitric oxide synthase in human endothelial cells.	Resveratrol	46-57	nitric oxide synthase 3	Homo sapiens	116-149
26367737-0	2015	Piceatannol, a natural hydroxylated analog of resveratrol, promotes nitric oxide release through phosphorylation of endothelial nitric oxide synthase in human endothelial cells.	Nitric Oxide	68-80	nitric oxide synthase 3	Homo sapiens	116-149
25728347-13	2015	CONCLUSIONS: The current study demonstrated the antiangiogenic properties of propranolol in vitro and that the drug was able to induce the regression of hemangioma cells via the inhibition of cell cycle progression, invasion, and tube formation, concomitantly with decreased NO and VEGF levels through the down-regulation of the PI3K/Akt/eNOS/VEGF pathway.	Propranolol	77-88	nitric oxide synthase 3	Homo sapiens	338-342
25931146-1	2015	During the course of cholestatic liver diseases, the toxic effect of bile acids accumulation has been related to the decreased expression of endothelial nitric oxide synthase (NOS-3) and cellular oxidative stress increase.	Bile Acids and Salts	69-79	nitric oxide synthase 3	Homo sapiens	141-181
25931146-3	2015	In the human hepatocarcinoma cell line HepG2, cytotoxic response to GCDCA was characterized by the reduced activity of the respiratory complexes II+III, the increased expression and activation of the transcription factor Sp1, and a higher binding capacity of this at positions -1386, -632 and -104 of the NOS-3 promoter (pNOS-3).	Glycochenodeoxycholic Acid	68-73	nitric oxide synthase 3	Homo sapiens	305-310
25931146-10	2015	Thus, the identification of Sp1 as a potential negative regulator of NOS-3 expression represents a new mechanism by which the accumulation of bile acids causes a cytotoxic effect through the oxidative stress increase, and provides a new potential target in cholestatic liver diseases.	Bile Acids and Salts	142-152	nitric oxide synthase 3	Homo sapiens	69-74
25815690-7	2015	PA attenuated insulin-mediated insulin receptor substrate-1 (IRS-1) tyrosine phosphorylation, leading to decreased glucose uptake, and phosphorylation of eNOS, leading to a reduction in the production of NO.	Palmitic Acid	0-2	nitric oxide synthase 3	Homo sapiens	154-158
25902041-1	2015	The dysregulation of nitric oxide (NO) synthesis attributable to the abnormal expression/activity of endothelial NO synthase (eNOS) is considered to be a major characteristic of insulin-resistant states, as well as an essential contributor to the pathogenesis of cardiovascular diseases.	Nitric Oxide	21-33	nitric oxide synthase 3	Homo sapiens	101-124
25902041-1	2015	The dysregulation of nitric oxide (NO) synthesis attributable to the abnormal expression/activity of endothelial NO synthase (eNOS) is considered to be a major characteristic of insulin-resistant states, as well as an essential contributor to the pathogenesis of cardiovascular diseases.	Nitric Oxide	21-33	nitric oxide synthase 3	Homo sapiens	126-130
25708288-6	2015	Deficiency in farnesoid X receptor and G-protein-coupled bile acid receptor 1 genes alters the expression/activity of cystathione gamma-lyase and endothelial nitric oxide synthase, two genes involved in the synthesis of hydrogen sulfide and nitric oxide, i.e., two gaseous mediators that have been shown to be essential in maintaining the intestinal homeostasis.	Hydrogen Sulfide	220-236	nitric oxide synthase 3	Homo sapiens	146-179
25815690-1	2015	Growing evidence suggests that the elevation of free fatty acids, including palmitic acid (PA), are associated with inflammation and oxidative stress, which may be involved in endothelial dysfunction, characterized by the reduced bioavailability of nitric oxide (NO) synthesized from endothelial NO synthase (eNOS).	Fatty Acids, Nonesterified	48-64	nitric oxide synthase 3	Homo sapiens	309-313
25815690-1	2015	Growing evidence suggests that the elevation of free fatty acids, including palmitic acid (PA), are associated with inflammation and oxidative stress, which may be involved in endothelial dysfunction, characterized by the reduced bioavailability of nitric oxide (NO) synthesized from endothelial NO synthase (eNOS).	Palmitic Acid	76-89	nitric oxide synthase 3	Homo sapiens	309-313
25815690-1	2015	Growing evidence suggests that the elevation of free fatty acids, including palmitic acid (PA), are associated with inflammation and oxidative stress, which may be involved in endothelial dysfunction, characterized by the reduced bioavailability of nitric oxide (NO) synthesized from endothelial NO synthase (eNOS).	Palmitic Acid	91-93	nitric oxide synthase 3	Homo sapiens	309-313
25815690-8	2015	Pic effectively mitigated the inhibitory effects of PA on the insulin-mediated phosphorylation of IRS-1 and eNOS, which was not observed following inhibition of HO-1 activity.	3,3',4,5'-tetrahydroxystilbene	0-3	nitric oxide synthase 3	Homo sapiens	108-112
25815690-8	2015	Pic effectively mitigated the inhibitory effects of PA on the insulin-mediated phosphorylation of IRS-1 and eNOS, which was not observed following inhibition of HO-1 activity.	Palmitic Acid	52-54	nitric oxide synthase 3	Homo sapiens	108-112
25815690-9	2015	The results of the present study suggested that Pic may have the potential to prevent PA-induced impairment of insulin signaling and eNOS function, by inducing the expression of the anti-inflammatory and antioxidant, HO-1.	3,3',4,5'-tetrahydroxystilbene	48-51	nitric oxide synthase 3	Homo sapiens	133-137
25815690-9	2015	The results of the present study suggested that Pic may have the potential to prevent PA-induced impairment of insulin signaling and eNOS function, by inducing the expression of the anti-inflammatory and antioxidant, HO-1.	Palmitic Acid	86-88	nitric oxide synthase 3	Homo sapiens	133-137
25869503-0	2015	Roles of ROS and PKC-betaII in ionizing radiation-induced eNOS activation in human vascular endothelial cells.	Reactive Oxygen Species	9-12	nitric oxide synthase 3	Homo sapiens	58-62
26721349-2	2016	Recent evidence suggests that H2S may also modulate Na(+)- and Ca(2+)-permeable channels and intracellular Ca(2+) stores, but the influence of H2S on endothelial Ca(2+) dynamics and Ca(2+)-dependent activation of endothelial nitric oxide synthase (eNOS) is unclear.	Hydrogen Sulfide	30-33	nitric oxide synthase 3	Homo sapiens	213-246
25869503-3	2015	We found that ionizing radiation increased eNOS phosphorylation at Ser-1177 and dephosphorylation at Thr-495 in HUVECs in a dose-dependent (&lt;= 20 Gy) and time-dependent (6-72 h) manner.	Serine	67-70	nitric oxide synthase 3	Homo sapiens	43-47
25869503-7	2015	Furthermore, when the radiation-induced increase in reactive oxygen species (ROS) generation was prevented by the anti-oxidant N-acetyl-L-cysteine, eNOS Ser-1177 phosphorylation and Thr-495 dephosphorylation in irradiated HUVECs were significantly reduced.	Reactive Oxygen Species	52-75	nitric oxide synthase 3	Homo sapiens	148-152
25869503-7	2015	Furthermore, when the radiation-induced increase in reactive oxygen species (ROS) generation was prevented by the anti-oxidant N-acetyl-L-cysteine, eNOS Ser-1177 phosphorylation and Thr-495 dephosphorylation in irradiated HUVECs were significantly reduced.	Reactive Oxygen Species	77-80	nitric oxide synthase 3	Homo sapiens	148-152
25869503-7	2015	Furthermore, when the radiation-induced increase in reactive oxygen species (ROS) generation was prevented by the anti-oxidant N-acetyl-L-cysteine, eNOS Ser-1177 phosphorylation and Thr-495 dephosphorylation in irradiated HUVECs were significantly reduced.	Acetylcysteine	127-146	nitric oxide synthase 3	Homo sapiens	148-152
25869503-7	2015	Furthermore, when the radiation-induced increase in reactive oxygen species (ROS) generation was prevented by the anti-oxidant N-acetyl-L-cysteine, eNOS Ser-1177 phosphorylation and Thr-495 dephosphorylation in irradiated HUVECs were significantly reduced.	Serine	153-156	nitric oxide synthase 3	Homo sapiens	148-152
25869503-9	2015	Taken together, our results suggest that ionizing radiation-induced eNOS activation in human vascular endothelial cells is attributed to both the up-regulation of PKC-betaII and the increase in ROS generation which were independent of each other.	Reactive Oxygen Species	194-197	nitric oxide synthase 3	Homo sapiens	68-72
26084222-0	2015	Atorvastatin-induced endothelial nitric oxide synthase expression in endothelial cells is mediated by endoglin.	Atorvastatin	0-12	nitric oxide synthase 3	Homo sapiens	21-54
25963768-5	2015	Herein, we report for the first time that the hydrogen peroxide (H2O2), a redox signaling molecule, generated by these EHNs activates the endothelial nitric oxide synthase (eNOS) that promotes the nitric oxide (NO) production in a PI3K (phosphoinositide 3-kinase)/Akt dependent manner, eventually triggering angiogenesis.	Hydrogen Peroxide	46-63	nitric oxide synthase 3	Homo sapiens	138-171
25963768-5	2015	Herein, we report for the first time that the hydrogen peroxide (H2O2), a redox signaling molecule, generated by these EHNs activates the endothelial nitric oxide synthase (eNOS) that promotes the nitric oxide (NO) production in a PI3K (phosphoinositide 3-kinase)/Akt dependent manner, eventually triggering angiogenesis.	Hydrogen Peroxide	65-69	nitric oxide synthase 3	Homo sapiens	138-171
25699607-1	2015	Endothelial nitric oxide synthase (eNOS), an enzyme that generates nitric oxide, is a major determinant of endothelial function.	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	35-39
25631232-7	2015	The molecular mechanisms underlying H2 S/zofenoprilat-induced angiogenesis were dependent on Akt, eNOS and ERK1/2 cascades.	Hydrogen Sulfide	36-40	nitric oxide synthase 3	Homo sapiens	98-102
25631232-7	2015	The molecular mechanisms underlying H2 S/zofenoprilat-induced angiogenesis were dependent on Akt, eNOS and ERK1/2 cascades.	zofenoprilate	41-53	nitric oxide synthase 3	Homo sapiens	98-102
25631232-10	2015	CONCLUSIONS AND IMPLICATIONS: Zofenoprilat induced a constant production of H2 S that stimulated the angiogenic process through a KATP channel/Akt/eNOS/ERK1/2 pathway.	zofenoprilate	30-42	nitric oxide synthase 3	Homo sapiens	147-151
25631232-10	2015	CONCLUSIONS AND IMPLICATIONS: Zofenoprilat induced a constant production of H2 S that stimulated the angiogenic process through a KATP channel/Akt/eNOS/ERK1/2 pathway.	Hydrogen Sulfide	76-80	nitric oxide synthase 3	Homo sapiens	147-151
26084222-2	2015	Interestingly, atorvastatin (ATV) is able to increase both endoglin and eNOS expression and reduce plaque size beyond its lipid lowering effects but by unknown mechanisms.	Atorvastatin	15-27	nitric oxide synthase 3	Homo sapiens	72-76
26084222-2	2015	Interestingly, atorvastatin (ATV) is able to increase both endoglin and eNOS expression and reduce plaque size beyond its lipid lowering effects but by unknown mechanisms.	Atorvastatin	29-32	nitric oxide synthase 3	Homo sapiens	72-76
26084222-3	2015	We hypothesized whether inflammation modulates ATV-dependent induction of endoglin and eNOS expression in vitro in endothelial cells and whether ATV-induced eNOS expression is regulated via endoglin.	Atorvastatin	47-50	nitric oxide synthase 3	Homo sapiens	87-91
26084222-3	2015	We hypothesized whether inflammation modulates ATV-dependent induction of endoglin and eNOS expression in vitro in endothelial cells and whether ATV-induced eNOS expression is regulated via endoglin.	Atorvastatin	145-148	nitric oxide synthase 3	Homo sapiens	157-161
26084222-5	2015	By contrast, ATV treatment increased endoglin and eNOS protein expression, while preventing TNF-alpha-mediated downregulation of endoglin and eNOS protein levels.	Atorvastatin	13-16	nitric oxide synthase 3	Homo sapiens	50-54
26084222-5	2015	By contrast, ATV treatment increased endoglin and eNOS protein expression, while preventing TNF-alpha-mediated downregulation of endoglin and eNOS protein levels.	Atorvastatin	13-16	nitric oxide synthase 3	Homo sapiens	142-146
26084222-6	2015	Moreover, suppression of endoglin using small interfering RNA (siRNA), but not inhibition of TGF-beta signaling with SB431542, abrogated ATV-induced eNOS expression.	Atorvastatin	137-140	nitric oxide synthase 3	Homo sapiens	149-153
26084222-7	2015	These results suggest that ATV treatment prevents inflammation-reduced endoglin and eNOS expression in endothelial cells and that ATV-induced eNOS expression strongly depends on the proper expression of endoglin in HUVECs.	Atorvastatin	27-30	nitric oxide synthase 3	Homo sapiens	84-88
26084222-7	2015	These results suggest that ATV treatment prevents inflammation-reduced endoglin and eNOS expression in endothelial cells and that ATV-induced eNOS expression strongly depends on the proper expression of endoglin in HUVECs.	Atorvastatin	130-133	nitric oxide synthase 3	Homo sapiens	142-146
25838201-0	2015	Sevoflurane pretreatment attenuates TNF-alpha-induced human endothelial cell dysfunction through activating eNOS/NO pathway.	Sevoflurane	0-11	nitric oxide synthase 3	Homo sapiens	108-112
25057159-1	2015	Reduced production of nitric oxide due to rs1799983 single nucleotide polymorphism in nitric oxide synthase 3 gene (NOS3) may enhance the risk of coronary artery disease.	Nitric Oxide	22-34	nitric oxide synthase 3	Homo sapiens	86-109
25057159-1	2015	Reduced production of nitric oxide due to rs1799983 single nucleotide polymorphism in nitric oxide synthase 3 gene (NOS3) may enhance the risk of coronary artery disease.	Nitric Oxide	22-34	nitric oxide synthase 3	Homo sapiens	116-120
25838201-5	2015	Meanwhile, sevoflurane (1.5 and 2.5 MAC) significantly induced endothelial nitric oxide synthase (eNOS) phosphorylation and enhanced NO levels both intracellularly and in the cell culture medium.	Sevoflurane	11-22	nitric oxide synthase 3	Homo sapiens	63-96
25838201-5	2015	Meanwhile, sevoflurane (1.5 and 2.5 MAC) significantly induced endothelial nitric oxide synthase (eNOS) phosphorylation and enhanced NO levels both intracellularly and in the cell culture medium.	Sevoflurane	11-22	nitric oxide synthase 3	Homo sapiens	98-102
25838201-7	2015	Collectively, these data indicate that sevoflurane protects against TNF-alpha -induced vascular endothelium dysfunction through activation of eNOS/NO pathway and inhibition of NF-kappaB.	Sevoflurane	39-50	nitric oxide synthase 3	Homo sapiens	142-146
25938443-10	2015	In addition, P2X7 mediated both high glucose and palmitate-induced increase in reactive oxygen species levels and decrease in endothelial nitric oxide synthase.	Glucose	37-44	nitric oxide synthase 3	Homo sapiens	126-159
25938443-10	2015	In addition, P2X7 mediated both high glucose and palmitate-induced increase in reactive oxygen species levels and decrease in endothelial nitric oxide synthase.	Palmitates	49-58	nitric oxide synthase 3	Homo sapiens	126-159
25804308-6	2015	Furthermore, Ang II increased eNOS-Ser(1177) but decreased eNOS-Thr(495), indicating concomitant activation of eNOS.	Serine	35-38	nitric oxide synthase 3	Homo sapiens	30-34
25804308-6	2015	Furthermore, Ang II increased eNOS-Ser(1177) but decreased eNOS-Thr(495), indicating concomitant activation of eNOS.	Threonine	64-67	nitric oxide synthase 3	Homo sapiens	59-63
25804308-6	2015	Furthermore, Ang II increased eNOS-Ser(1177) but decreased eNOS-Thr(495), indicating concomitant activation of eNOS.	Threonine	64-67	nitric oxide synthase 3	Homo sapiens	59-63
25804308-7	2015	Intriguingly, ROS scavengers but not AT2R antagonist prevented Ang II-activation of eNOS.	ros	14-17	nitric oxide synthase 3	Homo sapiens	84-88
25804308-11	2015	Taken together, we demonstrate, for the first time, that Ang II upregulates nNOS protein expression and activity via AT1R/ROS/eNOS-dependent S-nitrosation and membrane translocation of AT2R.	ros	122-125	nitric oxide synthase 3	Homo sapiens	126-130
25917853-9	2015	CONCLUSIONS: Homozygosity for the G allele of the eNOS G894T polymorphism was associated with worse survival in systolic HF patients, especially in those treated with nitrates.	Nitrates	167-175	nitric oxide synthase 3	Homo sapiens	50-54
25712867-7	2015	Nitro-oxidative stress and cell death in NOS-3 overexpressing cells occurred with the expression increase of pro-apoptotic genes and a higher expression/activity of the enzymes adrenodoxin reductase mitochondrial (AR) and cathepsin D (CatD).	nitro	0-5	nitric oxide synthase 3	Homo sapiens	41-46
26419990-6	2015	The mRNA and protein expressions of eNOS and DDAH2 were uncorrelated under the effect of Hcy (r = 0.057 and 0.449, both P &gt; 0.05) and VEGF (r = 0.284 and 0.432, both P &gt; 0.05).	Homocysteine	89-92	nitric oxide synthase 3	Homo sapiens	36-40
26419990-7	2015	CONCLUSION: Recombinant adenovirus Ad-hVEGF165 could reverse Hcy-induced endothelial cells dysfunction via upregulating the expressions of eNOS and DDAH2.	Homocysteine	61-64	nitric oxide synthase 3	Homo sapiens	139-143
25920448-0	2015	Roles of miRNA-24 in regulating endothelial nitric oxide synthase expression and vascular endothelial cell proliferation.	mirna-24	9-17	nitric oxide synthase 3	Homo sapiens	32-65
25920448-1	2015	This study is to investigate the effect of miRNA-24 on endothelial nitric oxide synthase (eNOS) expression and vascular endothelial cell proliferation.	mirna-24	43-51	nitric oxide synthase 3	Homo sapiens	55-88
25920448-1	2015	This study is to investigate the effect of miRNA-24 on endothelial nitric oxide synthase (eNOS) expression and vascular endothelial cell proliferation.	mirna-24	43-51	nitric oxide synthase 3	Homo sapiens	90-94
25748584-1	2015	Nitric oxide (NO), produced by the enzyme endothelial nitric oxide synthase (eNOS), has critical roles in the regulation of vascular homeostasis and prevention of atherogenesis by inhibiting leukocytes, platelet activation, and smooth muscle cell proliferation.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	42-75
25588940-9	2015	As compared with the ox-LDL group, results of the PG high dose group showed that cell viability was significantly increased (P&lt;0.05), the level of NO release, expression of eNOS mRNA, densitometric value of eNOS protein expression, as well as the activities of SOD and GPx were all significantly higher (all P&lt;0.05).	Propyl Gallate	50-52	nitric oxide synthase 3	Homo sapiens	176-180
25588940-9	2015	As compared with the ox-LDL group, results of the PG high dose group showed that cell viability was significantly increased (P&lt;0.05), the level of NO release, expression of eNOS mRNA, densitometric value of eNOS protein expression, as well as the activities of SOD and GPx were all significantly higher (all P&lt;0.05).	Propyl Gallate	50-52	nitric oxide synthase 3	Homo sapiens	210-214
26131136-3	2015	They were intervened by heparin and the expression levels of soluble thrombomodulin (sTM) and serum activated protein C (APC) were detected by ELISA, the regulatory mechanism of heparin improving vascular endothelial cells injury induced by TNFalpha was detected by Western Blotting method, the methylation of histone in the gene promoter region of endothelial nitric oxide synthase (eNOS) and monocyte chemotactic protein-1 (MCP-1) were detected using chromatin immunoprecipitation method.	Heparin	178-185	nitric oxide synthase 3	Homo sapiens	349-382
25748584-1	2015	Nitric oxide (NO), produced by the enzyme endothelial nitric oxide synthase (eNOS), has critical roles in the regulation of vascular homeostasis and prevention of atherogenesis by inhibiting leukocytes, platelet activation, and smooth muscle cell proliferation.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	77-81
25733135-4	2015	In this review, we aim to place the genomic findings on components of the NO/cGMP pathway, namely endothelial nitric oxide synthase, soluble guanylyl cyclase and phosphodiesterase 5A, in context of preventive and therapeutic strategies for treating atherosclerosis and its sequelae.	Cyclic GMP	77-81	nitric oxide synthase 3	Homo sapiens	98-131
25892567-6	2015	Furthermore, delphinidins increase endothelial nitric oxide synthase expression and decreases expression of vaso-constrictory endothelin-1.	delphinidin	13-25	nitric oxide synthase 3	Homo sapiens	35-68
25581901-0	2015	Transient receptor potential vanilloid type 1 is vital for (-)-epigallocatechin-3-gallate mediated activation of endothelial nitric oxide synthase.	epigallocatechin gallate	59-89	nitric oxide synthase 3	Homo sapiens	113-146
25263733-9	2015	The expression of neuronal NOS, endothelial NOS, and inducible NOS decreased mainly in GNO3 group compared to the G group (P &lt; .05), with no difference compared to C group (P &gt; .05).	gno3	87-91	nitric oxide synthase 3	Homo sapiens	32-47
25601987-7	2015	Impaired effects of metformin on eNOS phosphorylation and NO production were reversed in cells transfected with constitutively active AMP-activated protein kinase.	Metformin	20-29	nitric oxide synthase 3	Homo sapiens	33-37
25848469-6	2015	Furthermore, therapeutic agents that are identified in increasing NO bioavailability through improvement of hepatic endothelial nitric oxide synthase (eNOS) activity and reduction in hepatic asymmetric dimethylarginine, an endogenous modulator of eNOS and a key mediator of elevated intrahepatic vascular tone in cirrhosis would be interesting therapeutic approaches in patients with endothelial dysfunction and portal hypertension in advanced liver diseases.	dimethylarginine	202-218	nitric oxide synthase 3	Homo sapiens	247-251
25797242-8	2015	Moreover, the aforementioned positive effects were abolished by blocking PI3K/Akt/eNOS pathway with LY-294002.	Lysine	100-102	nitric oxide synthase 3	Homo sapiens	82-86
25686009-5	2015	Nitric oxide levels were not modulated by the treatments, although eNOS was upregulated by cyanidin-3-glucoside, and superoxide production was decreased by both phenolic acids.	cyanidin-3-o-glucoside	91-111	nitric oxide synthase 3	Homo sapiens	67-71
25748432-5	2015	This effect was unaffected by the pretreatment with the pure estrogen receptor antagonist ICI 182,780, but was largely impaired by endothelial nitric oxide synthase (eNOS) inhibitor NG-nitro-L-arginine methyl ester (L-NAME) or by phosphoinositide 3-kinase (PI3K) inhibitor wortmannin (WM).	-nitro-l-arginine methyl ester	184-214	nitric oxide synthase 3	Homo sapiens	131-164
25748432-5	2015	This effect was unaffected by the pretreatment with the pure estrogen receptor antagonist ICI 182,780, but was largely impaired by endothelial nitric oxide synthase (eNOS) inhibitor NG-nitro-L-arginine methyl ester (L-NAME) or by phosphoinositide 3-kinase (PI3K) inhibitor wortmannin (WM).	NG-Nitroarginine Methyl Ester	216-222	nitric oxide synthase 3	Homo sapiens	131-164
25748432-5	2015	This effect was unaffected by the pretreatment with the pure estrogen receptor antagonist ICI 182,780, but was largely impaired by endothelial nitric oxide synthase (eNOS) inhibitor NG-nitro-L-arginine methyl ester (L-NAME) or by phosphoinositide 3-kinase (PI3K) inhibitor wortmannin (WM).	Wortmannin	273-283	nitric oxide synthase 3	Homo sapiens	131-164
25748432-5	2015	This effect was unaffected by the pretreatment with the pure estrogen receptor antagonist ICI 182,780, but was largely impaired by endothelial nitric oxide synthase (eNOS) inhibitor NG-nitro-L-arginine methyl ester (L-NAME) or by phosphoinositide 3-kinase (PI3K) inhibitor wortmannin (WM).	Wortmannin	285-287	nitric oxide synthase 3	Homo sapiens	131-164
25542418-1	2015	Physiological concentrations (1 muM) of 15 flavonoids were evaluated in human umbilical vein endothelial cells in the presence of hydrogen peroxide (H2O2) for their ability to affect endothelial nitric oxide synthase (eNOS) and endothelin-1 (ET-1) expression in order to establish the structural basis of their bioactivity.	Flavonoids	43-53	nitric oxide synthase 3	Homo sapiens	183-216
25555250-7	2015	The suppression of eNOS was significantly reversed by ROCK inhibitor Y-27632.	Y 27632	69-76	nitric oxide synthase 3	Homo sapiens	19-23
25555250-9	2015	In addition, blocking ERK1/2 or p38 MAPK by PD98059 and SB203580, respectively attenuated the OMVs-induced eNOS phosphorylation.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	44-51	nitric oxide synthase 3	Homo sapiens	107-111
25555250-9	2015	In addition, blocking ERK1/2 or p38 MAPK by PD98059 and SB203580, respectively attenuated the OMVs-induced eNOS phosphorylation.	SB 203580	56-64	nitric oxide synthase 3	Homo sapiens	107-111
25542418-1	2015	Physiological concentrations (1 muM) of 15 flavonoids were evaluated in human umbilical vein endothelial cells in the presence of hydrogen peroxide (H2O2) for their ability to affect endothelial nitric oxide synthase (eNOS) and endothelin-1 (ET-1) expression in order to establish the structural basis of their bioactivity.	Flavonoids	43-53	nitric oxide synthase 3	Homo sapiens	218-222
25542418-2	2015	Flavonoid effects on eNOS transcription factor Krupple like factor-2 (KLF-2) expression were also evaluated.	Flavonoids	0-9	nitric oxide synthase 3	Homo sapiens	21-25
25542418-4	2015	Notably, the more effective flavonoids for KLF-2 up-regulation resulted in the highest values for eNOS expression, showing that the increment of eNOS expression would take place through KLF-2 induction.	Flavonoids	28-38	nitric oxide synthase 3	Homo sapiens	98-102
25542418-4	2015	Notably, the more effective flavonoids for KLF-2 up-regulation resulted in the highest values for eNOS expression, showing that the increment of eNOS expression would take place through KLF-2 induction.	Flavonoids	28-38	nitric oxide synthase 3	Homo sapiens	145-149
25557764-8	2015	Thus an increase in Sirt4, Nrf2, Tfam, UCP1, eNOS, HO1 and STAT3 genes could profoundly affect mitochondrial function, cholesterol homeostasis, and fatty acid oxidation, suggesting that ASA could be beneficial beyond simply its ability to inhibit cyclooxygenase.	Cholesterol	119-130	nitric oxide synthase 3	Homo sapiens	45-49
25635941-1	2015	Rapid nitric oxide (NO) production via endothelial NO synthase (eNOS) activation represents a major signaling pathway for the cardiovascular protective effects of estrogens; however, the pathways after NO biosynthesis that estrogens use to function remain largely unknown.	Nitric Oxide	6-18	nitric oxide synthase 3	Homo sapiens	64-68
25635941-5	2015	We hypothesized that estradiol-17beta (E2beta) stimulates SNO of CFL1 via eNOS-derived NO and that E2beta-induced SNO-CFL1 mediates cytoskeleton remodeling in endothelial cells.	Estradiol	21-37	nitric oxide synthase 3	Homo sapiens	74-78
25635941-13	2015	Thus, SNO(Cys80) of cofilin-1 via eNOS-derived NO provides a novel pathway for mediating estrogen-induced endothelial cell cytoskeleton remodeling.	sno	6-9	nitric oxide synthase 3	Homo sapiens	34-38
26937388-6	2015	The expression of eNOS in HPAECs is reduced up to two thirds in the presence of DS.	Dermatan Sulfate	80-82	nitric oxide synthase 3	Homo sapiens	18-22
25663871-5	2015	Thus, the present study identified that metformin improves the function of IR endothelial cells, possibly through promoting eNOS protein expression and increasing the NO content.	Metformin	40-49	nitric oxide synthase 3	Homo sapiens	124-128
25557764-8	2015	Thus an increase in Sirt4, Nrf2, Tfam, UCP1, eNOS, HO1 and STAT3 genes could profoundly affect mitochondrial function, cholesterol homeostasis, and fatty acid oxidation, suggesting that ASA could be beneficial beyond simply its ability to inhibit cyclooxygenase.	Fatty Acids	148-158	nitric oxide synthase 3	Homo sapiens	45-49
25557764-8	2015	Thus an increase in Sirt4, Nrf2, Tfam, UCP1, eNOS, HO1 and STAT3 genes could profoundly affect mitochondrial function, cholesterol homeostasis, and fatty acid oxidation, suggesting that ASA could be beneficial beyond simply its ability to inhibit cyclooxygenase.	Aspirin	186-189	nitric oxide synthase 3	Homo sapiens	45-49
25666326-2	2015	Many researches evidenced that nitric oxide (NO)/endothelial nitric oxide synthase (eNOS) system plays a significant role in the occurrence and development of CVD.	Nitric Oxide	31-43	nitric oxide synthase 3	Homo sapiens	49-82
25705617-4	2015	Nitric oxide (NO) generated through the endothelial nitric oxide synthase (eNOS) acts a gas signaling mediator to promote mitochondrial biogenesis and bioenergetics, with a favorable impact in diverse chronic diseases of the elderly.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	40-73
25699114-4	2015	5-hydroxymethylcytosine, H3K9ac and Histone 2A (H2A).Zac at the NOS3 transcription start site directly correlated with NOS3 mRNA levels.	5-hydroxymethylcytosine	0-23	nitric oxide synthase 3	Homo sapiens	64-68
25699114-4	2015	5-hydroxymethylcytosine, H3K9ac and Histone 2A (H2A).Zac at the NOS3 transcription start site directly correlated with NOS3 mRNA levels.	5-hydroxymethylcytosine	0-23	nitric oxide synthase 3	Homo sapiens	119-123
25705617-4	2015	Nitric oxide (NO) generated through the endothelial nitric oxide synthase (eNOS) acts a gas signaling mediator to promote mitochondrial biogenesis and bioenergetics, with a favorable impact in diverse chronic diseases of the elderly.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	75-79
25410138-2	2015	The generation of reactive oxygen species from the vascular endothelium is strongly related to various enzymes, such as xanthine oxidase, endothelial nitric oxide synthase and nicotinamide-adenine dinucleotide phosphate oxidase.	Reactive Oxygen Species	18-41	nitric oxide synthase 3	Homo sapiens	138-171
24840719-11	2015	Chemerin can increase eNOS and Akt levels in HUVECs, and these results could be partly blocked by LY294002 and L-NAME.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	98-106	nitric oxide synthase 3	Homo sapiens	22-26
24840719-11	2015	Chemerin can increase eNOS and Akt levels in HUVECs, and these results could be partly blocked by LY294002 and L-NAME.	NG-Nitroarginine Methyl Ester	111-117	nitric oxide synthase 3	Homo sapiens	22-26
23836447-0	2015	Humic acid induces the endothelial nitric oxide synthase phosphorylation at Ser1177 and Thr495 Via Hsp90alpha and Hsp90beta upregulation in human umbilical vein endothelial cells.	Humic Substances	0-10	nitric oxide synthase 3	Homo sapiens	23-56
23836447-2	2015	We investigated the effect of HA on the regulation of endothelial nitric oxide (NO) synthase (eNOS) in human umbilical vein endothelial cells (HUVECs) to evaluate the involvement of eNOS and related factors in peripheral vascular impairment with HA exposure.	Nitric Oxide	66-78	nitric oxide synthase 3	Homo sapiens	94-98
23836447-9	2015	These results suggest that upregulation of eNOS phosphorylation at Ser1177 and eNOS phosphorylation at Thr495 produce NO and superoxide anions, respectively, resulting in generation of peroxynitrite, which causes impairment of vascular endothelial cells.	Superoxides	125-142	nitric oxide synthase 3	Homo sapiens	43-47
23836447-9	2015	These results suggest that upregulation of eNOS phosphorylation at Ser1177 and eNOS phosphorylation at Thr495 produce NO and superoxide anions, respectively, resulting in generation of peroxynitrite, which causes impairment of vascular endothelial cells.	Superoxides	125-142	nitric oxide synthase 3	Homo sapiens	79-83
23836447-9	2015	These results suggest that upregulation of eNOS phosphorylation at Ser1177 and eNOS phosphorylation at Thr495 produce NO and superoxide anions, respectively, resulting in generation of peroxynitrite, which causes impairment of vascular endothelial cells.	Peroxynitrous Acid	185-198	nitric oxide synthase 3	Homo sapiens	43-47
23836447-9	2015	These results suggest that upregulation of eNOS phosphorylation at Ser1177 and eNOS phosphorylation at Thr495 produce NO and superoxide anions, respectively, resulting in generation of peroxynitrite, which causes impairment of vascular endothelial cells.	Peroxynitrous Acid	185-198	nitric oxide synthase 3	Homo sapiens	79-83
24840719-5	2015	We also tested the effects of the phosphoinositide 3-kinase inhibitor LY294002 and the eNOS inhibitor L-NAME.	NG-Nitroarginine Methyl Ester	102-108	nitric oxide synthase 3	Homo sapiens	87-91
25966592-2	2015	The purpose of this study was to investigate the association of--86T&gt;C and E298D polymorphisms of the endothelial nitric oxide synthase(NOS3) gene with the risk of ce-ebral stroke (CS) in Russian inhabitants of Central Russia, as well as to evaluate the trigger effect of smoking on the risk of CS in carriers of genotypes NOS3.	Cesium	184-186	nitric oxide synthase 3	Homo sapiens	105-143
25406019-6	2015	Ca(2+) is involved in this pathway as intracellular Ca(2+) flux increased after ID, and thapsigargin activated NOS3 and increased VEGF-A mRNA expression.	Thapsigargin	88-100	nitric oxide synthase 3	Homo sapiens	111-115
25406019-8	2015	RYR inhibition using ryanodine at 10muM decreased ID-induced NOS3 activation, HIF-1alpha, and VEGF-A expression, whereas RYR activation with ryanodine at 1nM increased NOS3 activation and VEGF-A mRNA expression.	Ryanodine	21-30	nitric oxide synthase 3	Homo sapiens	61-65
25406019-8	2015	RYR inhibition using ryanodine at 10muM decreased ID-induced NOS3 activation, HIF-1alpha, and VEGF-A expression, whereas RYR activation with ryanodine at 1nM increased NOS3 activation and VEGF-A mRNA expression.	Ryanodine	141-150	nitric oxide synthase 3	Homo sapiens	168-172
25966592-2	2015	The purpose of this study was to investigate the association of--86T&gt;C and E298D polymorphisms of the endothelial nitric oxide synthase(NOS3) gene with the risk of ce-ebral stroke (CS) in Russian inhabitants of Central Russia, as well as to evaluate the trigger effect of smoking on the risk of CS in carriers of genotypes NOS3.	Cesium	184-186	nitric oxide synthase 3	Homo sapiens	139-143
25453767-0	2015	HMG-CoA reductase inhibitor rosuvastatin improves abnormal brain electrical activity via mechanisms involving eNOS.	Rosuvastatin Calcium	28-40	nitric oxide synthase 3	Homo sapiens	110-114
24943287-0	2015	The effects of endothelial nitric oxide synthase tagSNPs on nitrite levels and risk of hypertension and obesity in children and adolescents.	Nitrites	60-67	nitric oxide synthase 3	Homo sapiens	15-48
24943287-1	2015	Obesity and the nitric oxide synthase 3 (NOS3) gene polymorphisms are associated with nitrite levels and hypertension.	Nitrites	86-93	nitric oxide synthase 3	Homo sapiens	16-39
24943287-1	2015	Obesity and the nitric oxide synthase 3 (NOS3) gene polymorphisms are associated with nitrite levels and hypertension.	Nitrites	86-93	nitric oxide synthase 3	Homo sapiens	41-45
24943287-2	2015	However, no study has tested the hypothesis that NOS3 tagSNPs rs3918226, rs3918188, rs743506 and rs7830 affect nitrite levels and are associated with hypertension in childhood obesity.	Nitrites	111-118	nitric oxide synthase 3	Homo sapiens	49-53
25475491-2	2015	Several single nucleotide polymorphisms (SNP) in the endothelial nitric oxide gene (NOS3) have been previously associated with arterial hypertension.	Nitric Oxide	65-77	nitric oxide synthase 3	Homo sapiens	84-88
25056928-1	2015	Nitric oxide (NO) derived from endothelial NO synthase (eNOS) mediates vascular endothelial growth factor (VEGF)-stimulated endothelial cytoskeleton remodeling and migration; however, the underlying mechanisms are elusive.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	56-60
25477161-0	2015	A NOS3 polymorphism determines endothelial response to folate in children with type 1 diabetes or obesity.	Folic Acid	55-61	nitric oxide synthase 3	Homo sapiens	2-6
25477161-1	2015	OBJECTIVE: To determine the effect of polymorphisms in NOS3 and folate pathway enzymes on vascular function and folate status and endothelial response to folate in children with diabetes or obesity.	Folic Acid	112-118	nitric oxide synthase 3	Homo sapiens	55-59
25477161-1	2015	OBJECTIVE: To determine the effect of polymorphisms in NOS3 and folate pathway enzymes on vascular function and folate status and endothelial response to folate in children with diabetes or obesity.	Folic Acid	112-118	nitric oxide synthase 3	Homo sapiens	55-59
25477161-3	2015	The effect of NOS3 genotype on endothelial response to folate (5 mg) was assessed in 85 subjects with diabetes and 28 obese subjects who received active treatment during intervention trials.	Folic Acid	55-61	nitric oxide synthase 3	Homo sapiens	14-18
25477161-6	2015	The polymorphism in intron 4 of endothelial nitric oxide synthase altered endothelial response to folate significantly: in subjects with diabetes FMD improved by 6.4 +- 5% (insertion carriers) vs 2.3 +- 6.6% (deletion carriers), P = .01; in obese subjects FMD improved by 1.8 +- 5.4% (insertion carriers) and deteriorated by -3.2 +- 7.2% (deletion carriers), P = .05.	Folic Acid	98-104	nitric oxide synthase 3	Homo sapiens	32-65
25477161-8	2015	CONCLUSIONS: A NOS3 polymorphism predicts endothelial response to folate in children with diabetes or obesity, with implications for vascular risk and folate intervention studies.	Folic Acid	66-72	nitric oxide synthase 3	Homo sapiens	15-19
25477161-8	2015	CONCLUSIONS: A NOS3 polymorphism predicts endothelial response to folate in children with diabetes or obesity, with implications for vascular risk and folate intervention studies.	Folic Acid	151-157	nitric oxide synthase 3	Homo sapiens	15-19
25592012-0	2015	Effects of polymorphisms in endothelial nitric oxide synthase and folate metabolizing genes on the concentration of serum nitrate, folate, and plasma total homocysteine after folic acid supplementation: a double-blind crossover study.	Nitrates	122-129	nitric oxide synthase 3	Homo sapiens	28-61
25592012-0	2015	Effects of polymorphisms in endothelial nitric oxide synthase and folate metabolizing genes on the concentration of serum nitrate, folate, and plasma total homocysteine after folic acid supplementation: a double-blind crossover study.	Folic Acid	131-137	nitric oxide synthase 3	Homo sapiens	28-61
25592012-0	2015	Effects of polymorphisms in endothelial nitric oxide synthase and folate metabolizing genes on the concentration of serum nitrate, folate, and plasma total homocysteine after folic acid supplementation: a double-blind crossover study.	Homocysteine	156-168	nitric oxide synthase 3	Homo sapiens	28-61
25592012-0	2015	Effects of polymorphisms in endothelial nitric oxide synthase and folate metabolizing genes on the concentration of serum nitrate, folate, and plasma total homocysteine after folic acid supplementation: a double-blind crossover study.	Folic Acid	175-185	nitric oxide synthase 3	Homo sapiens	28-61
25592012-4	2015	The aim of this study was to investigate whether genetic polymorphisms in endothelial nitric oxide synthase (eNOS) and genes involved in folate metabolism affect the concentration of serum nitrate, serum folate, and plasma total homocysteine in healthy individuals after folic acid supplementation.	Nitrates	189-196	nitric oxide synthase 3	Homo sapiens	74-107
25592012-4	2015	The aim of this study was to investigate whether genetic polymorphisms in endothelial nitric oxide synthase (eNOS) and genes involved in folate metabolism affect the concentration of serum nitrate, serum folate, and plasma total homocysteine in healthy individuals after folic acid supplementation.	Nitrates	189-196	nitric oxide synthase 3	Homo sapiens	109-113
25592012-4	2015	The aim of this study was to investigate whether genetic polymorphisms in endothelial nitric oxide synthase (eNOS) and genes involved in folate metabolism affect the concentration of serum nitrate, serum folate, and plasma total homocysteine in healthy individuals after folic acid supplementation.	Folic Acid	204-210	nitric oxide synthase 3	Homo sapiens	74-107
25592012-4	2015	The aim of this study was to investigate whether genetic polymorphisms in endothelial nitric oxide synthase (eNOS) and genes involved in folate metabolism affect the concentration of serum nitrate, serum folate, and plasma total homocysteine in healthy individuals after folic acid supplementation.	Folic Acid	204-210	nitric oxide synthase 3	Homo sapiens	109-113
25592012-4	2015	The aim of this study was to investigate whether genetic polymorphisms in endothelial nitric oxide synthase (eNOS) and genes involved in folate metabolism affect the concentration of serum nitrate, serum folate, and plasma total homocysteine in healthy individuals after folic acid supplementation.	Homocysteine	229-241	nitric oxide synthase 3	Homo sapiens	74-107
25592012-4	2015	The aim of this study was to investigate whether genetic polymorphisms in endothelial nitric oxide synthase (eNOS) and genes involved in folate metabolism affect the concentration of serum nitrate, serum folate, and plasma total homocysteine in healthy individuals after folic acid supplementation.	Homocysteine	229-241	nitric oxide synthase 3	Homo sapiens	109-113
25592012-10	2015	The individuals with three polymorphisms in eNOS gene had increased concentration of serum folate and decreased concentration of p-tHcy after folic acid supplementation.	Folic Acid	91-97	nitric oxide synthase 3	Homo sapiens	44-48
25592012-10	2015	The individuals with three polymorphisms in eNOS gene had increased concentration of serum folate and decreased concentration of p-tHcy after folic acid supplementation.	p-thcy	129-135	nitric oxide synthase 3	Homo sapiens	44-48
25592012-10	2015	The individuals with three polymorphisms in eNOS gene had increased concentration of serum folate and decreased concentration of p-tHcy after folic acid supplementation.	Folic Acid	142-152	nitric oxide synthase 3	Homo sapiens	44-48
25592012-13	2015	CONCLUSIONS: Polymorphisms in eNOS and folate genes affect the concentration of serum folate and p-tHcy but do not have any effect on the concentration of NO3 in healthy individuals after folic acid supplementation.	p-thcy	97-103	nitric oxide synthase 3	Homo sapiens	30-34
25592012-13	2015	CONCLUSIONS: Polymorphisms in eNOS and folate genes affect the concentration of serum folate and p-tHcy but do not have any effect on the concentration of NO3 in healthy individuals after folic acid supplementation.	Folic Acid	188-198	nitric oxide synthase 3	Homo sapiens	30-34
25453767-7	2015	However, the most pronounced anti-epileptic effect was observed in rosuvastatin-treated animals, which was associated with improved blood-brain barrier (BBB) integrity, increased expression of endothelial nitric oxide synthase (eNOS) mRNA and decreased expressions of pro-apoptotic p53, Bax and caspase-3 mRNAs.	Rosuvastatin Calcium	67-79	nitric oxide synthase 3	Homo sapiens	193-226
25453767-7	2015	However, the most pronounced anti-epileptic effect was observed in rosuvastatin-treated animals, which was associated with improved blood-brain barrier (BBB) integrity, increased expression of endothelial nitric oxide synthase (eNOS) mRNA and decreased expressions of pro-apoptotic p53, Bax and caspase-3 mRNAs.	Rosuvastatin Calcium	67-79	nitric oxide synthase 3	Homo sapiens	228-232
25453767-8	2015	Inhibition of eNOS activity with L-NG-Nitroarginine Methyl Ester (L-NAME) reversed the anti-epileptic effect of rosuvastatin significantly.	NG-Nitroarginine Methyl Ester	33-64	nitric oxide synthase 3	Homo sapiens	14-18
25453767-8	2015	Inhibition of eNOS activity with L-NG-Nitroarginine Methyl Ester (L-NAME) reversed the anti-epileptic effect of rosuvastatin significantly.	NG-Nitroarginine Methyl Ester	66-72	nitric oxide synthase 3	Homo sapiens	14-18
25453767-8	2015	Inhibition of eNOS activity with L-NG-Nitroarginine Methyl Ester (L-NAME) reversed the anti-epileptic effect of rosuvastatin significantly.	Rosuvastatin Calcium	112-124	nitric oxide synthase 3	Homo sapiens	14-18
25453767-10	2015	Here, we provide evidence that among HMG-CoA reductase inhibitors, rosuvastatin was the most effective statin on the reduction of epileptiform activity, which was associated with improved BBB permeability, increased expression of eNOS and decreased expressions of pro-apoptotic p53, Bax and caspase-3.	Rosuvastatin Calcium	67-79	nitric oxide synthase 3	Homo sapiens	230-234
25453767-11	2015	Our observation also revealed that the anti-epileptic effect of rosuvastatin was dependent on the increased expression level of eNOS.	Rosuvastatin Calcium	64-76	nitric oxide synthase 3	Homo sapiens	128-132
25854385-1	2015	Endothelial nitric oxide synthase (eNOS or NOS3) produces nitric oxide and genetic polymorphisms of NOS3 gene play significant roles in various processes of carcinogenesis.	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	43-47
26994413-1	2015	Nitric oxide (NO) synthesized by endothelial nitric oxide synthase (eNOS) enzyme is a critical regulator of cerebrovascular homeostasis.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	33-66
26994413-1	2015	Nitric oxide (NO) synthesized by endothelial nitric oxide synthase (eNOS) enzyme is a critical regulator of cerebrovascular homeostasis.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	68-72
25283600-3	2015	SDMA suppressed VEGF-induced endothelial nitric oxide synthase (eNOS) phosphorylation and nitric oxide production, but not VEGFR2 activation and signaling leading to eNOS activation.	symmetric dimethylarginine	0-4	nitric oxide synthase 3	Homo sapiens	29-62
26235577-8	2015	Treatment of HUVECs with H2O2 also down-regulated the phosphorylation of endothelial nitric oxide synthase (eNOS), decreased the level of nitric oxide in the culture medium, and inhibited the protein expression and enzymatic activity of silent information regulator 1 (SIRT1), while pretreatment with curcumin partly reversed these effects (all p&lt;0.05).	Hydrogen Peroxide	25-29	nitric oxide synthase 3	Homo sapiens	73-106
26273653-3	2015	The effect of Lipofundin MCT/LCT on acetylcholine-induced endothelial nitric oxide synthase (eNOS) phosphorylation in human umbilical vein endothelial cells (HUVECs) was investigated using western blotting.	Lipofundin	14-24	nitric oxide synthase 3	Homo sapiens	58-91
26273653-3	2015	The effect of Lipofundin MCT/LCT on acetylcholine-induced endothelial nitric oxide synthase (eNOS) phosphorylation in human umbilical vein endothelial cells (HUVECs) was investigated using western blotting.	Acetylcholine	36-49	nitric oxide synthase 3	Homo sapiens	58-91
25755737-6	2015	Furthermore, vaspin increased the production of NO and the effect of vaspin on EPCs can be diminished partly by the eNOS inhibitor (L-NAME).	NG-Nitroarginine Methyl Ester	132-138	nitric oxide synthase 3	Homo sapiens	116-120
26156267-3	2015	The latest data demonstrate that nitric oxide (NO) is induced by CIL through endothelial nitric oxide synthase (eNOS) activation via a cyclic-AMP (cAMP)/ protein kinase A (PKA)- and PI3K/Akt- dependent mechanism.	Nitric Oxide	33-45	nitric oxide synthase 3	Homo sapiens	77-110
26156267-3	2015	The latest data demonstrate that nitric oxide (NO) is induced by CIL through endothelial nitric oxide synthase (eNOS) activation via a cyclic-AMP (cAMP)/ protein kinase A (PKA)- and PI3K/Akt- dependent mechanism.	Cilostazol	65-68	nitric oxide synthase 3	Homo sapiens	77-110
27025039-1	2015	The objective of this study was to show the effect of H2S donor, NaHS on the endothelium-dependent vasorelaxation, free radical state and cNOS uncoupling in old rats.	Hydrogen Sulfide	54-57	nitric oxide synthase 3	Homo sapiens	138-142
25697563-4	2015	Nitric oxide (NO) produced by endothelial nitric oxide synthase (eNOS) is an important regulator of vascular function.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	30-63
25697563-4	2015	Nitric oxide (NO) produced by endothelial nitric oxide synthase (eNOS) is an important regulator of vascular function.	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	65-69
25634184-1	2015	Endothelial nitric oxide synthase (eNOS) is the catalyst of endothelial nitric oxide (NO) synthesis.	Nitric Oxide	12-24	nitric oxide synthase 3	Homo sapiens	35-39
24510253-13	2015	The effects of LPC on Akt/eNOS and Bcl-2/Bax activity were reversed by pravastatin.	Pravastatin	71-82	nitric oxide synthase 3	Homo sapiens	26-30
25878398-4	2015	Interestingly, the NOS3 -786TT genotype was associated with increased nitrite/nitrate levels only in IEI patients.	Nitrites	70-77	nitric oxide synthase 3	Homo sapiens	19-23
25878398-4	2015	Interestingly, the NOS3 -786TT genotype was associated with increased nitrite/nitrate levels only in IEI patients.	Nitrates	78-85	nitric oxide synthase 3	Homo sapiens	19-23
25878398-8	2015	Here, we first demonstrate that NOS3 -786T&gt;C variant affects nitrite/nitrate levels in IEI patients and that screening for NOS2A -2.5 kb (CCTTT) n polymorphism may be useful for differential diagnosis of various IEI.	Nitrites	64-71	nitric oxide synthase 3	Homo sapiens	32-36
25878398-8	2015	Here, we first demonstrate that NOS3 -786T&gt;C variant affects nitrite/nitrate levels in IEI patients and that screening for NOS2A -2.5 kb (CCTTT) n polymorphism may be useful for differential diagnosis of various IEI.	Nitrates	72-79	nitric oxide synthase 3	Homo sapiens	32-36
25531414-9	2014	Western blot showed that Flk1 and Nos3 were down-regulated in the DBDx-treated group.	dbdx	66-70	nitric oxide synthase 3	Homo sapiens	34-38
25320160-9	2015	CONCLUSION: We could replicate and extend previous findings showing altered NOx (-) levels in BPD and an influence of NOS3 rs2070744 on NOS3 expression and NOx (-) concentration.	nicotine 1-N-oxide	76-79	nitric oxide synthase 3	Homo sapiens	118-122
25320160-9	2015	CONCLUSION: We could replicate and extend previous findings showing altered NOx (-) levels in BPD and an influence of NOS3 rs2070744 on NOS3 expression and NOx (-) concentration.	nicotine 1-N-oxide	156-159	nitric oxide synthase 3	Homo sapiens	118-122
25201086-6	2014	The linear correlation between log (RIP/CEC) and the ratio of the coordination number (CN) of IS (=CNIS) and OS (=CNOS) complexes noted as CNIS/(CNIS + CNOS) suggested that the ratio of CN is very sensitive to Cs(+) adsorption species with variable RIP and CEC.	Cesium	210-212	nitric oxide synthase 3	Homo sapiens	114-118
24760600-9	2014	This study thus identifies NOS3 polymorphism-dependent sensitivity to the effects of physical training on plasma NO2.	Nitrogen Dioxide	113-116	nitric oxide synthase 3	Homo sapiens	27-31
25201086-6	2014	The linear correlation between log (RIP/CEC) and the ratio of the coordination number (CN) of IS (=CNIS) and OS (=CNOS) complexes noted as CNIS/(CNIS + CNOS) suggested that the ratio of CN is very sensitive to Cs(+) adsorption species with variable RIP and CEC.	Cesium	210-212	nitric oxide synthase 3	Homo sapiens	152-156
25419657-4	2014	This was accompanied with a partial disruption of the active endothelial nitric oxide synthase (eNOS)- dimer, leading to eNOS uncoupling and increased formation of reactive oxygen species (ROS).	Reactive Oxygen Species	164-187	nitric oxide synthase 3	Homo sapiens	61-94
24670328-1	2014	Our objective was to investigate whether the presence of Glu298Asp polymorphism in the endothelial NO synthase (eNOS) gene differentially affects the postprandial blood pressure response to dietary nitrate-rich beetroot bread.	Nitrates	198-205	nitric oxide synthase 3	Homo sapiens	112-116
24670328-7	2014	The beneficial diastolic blood pressure reduction was observed only in the T carriers of the Glu298Asp polymorphism in the eNOS gene after consumption of nitrate-rich beetroot bread.	Nitrates	154-161	nitric oxide synthase 3	Homo sapiens	123-127
25531191-7	2014	Activity of e-NOS in sperm was evaluated in parallel by measuring the quantity of L-citulline produced from L-arginine.	l-citulline	82-93	nitric oxide synthase 3	Homo sapiens	12-17
25531191-7	2014	Activity of e-NOS in sperm was evaluated in parallel by measuring the quantity of L-citulline produced from L-arginine.	Arginine	108-118	nitric oxide synthase 3	Homo sapiens	12-17
25243430-8	2014	Treatment with Y27632 restored ET-1-mediated eNOS activity (+61%) and stimulated NO production in the perinuclear region after LPS pretreatment.	Y 27632	15-21	nitric oxide synthase 3	Homo sapiens	45-49
25419657-4	2014	This was accompanied with a partial disruption of the active endothelial nitric oxide synthase (eNOS)- dimer, leading to eNOS uncoupling and increased formation of reactive oxygen species (ROS).	Reactive Oxygen Species	164-187	nitric oxide synthase 3	Homo sapiens	96-100
25419657-4	2014	This was accompanied with a partial disruption of the active endothelial nitric oxide synthase (eNOS)- dimer, leading to eNOS uncoupling and increased formation of reactive oxygen species (ROS).	Reactive Oxygen Species	189-192	nitric oxide synthase 3	Homo sapiens	61-94
25419657-4	2014	This was accompanied with a partial disruption of the active endothelial nitric oxide synthase (eNOS)- dimer, leading to eNOS uncoupling and increased formation of reactive oxygen species (ROS).	Reactive Oxygen Species	189-192	nitric oxide synthase 3	Homo sapiens	96-100
25419657-5	2014	The LPC 18:1-induced ROS formation was attenuated by the superoxide scavenger Tiron, as well as by the pharmacological inhibitors of eNOS, NADPH oxidases, flavin-containing enzymes and superoxide dismutase (SOD).	Reactive Oxygen Species	21-24	nitric oxide synthase 3	Homo sapiens	133-137
25419657-10	2014	We conclude that LPC 18:1 induces eNOS uncoupling and unspecific superoxide production.	lpc	17-20	nitric oxide synthase 3	Homo sapiens	34-38
25257463-0	2014	Berberine protects endothelial progenitor cell from damage of TNF-alpha via the PI3K/AKT/eNOS signaling pathway.	Berberine	0-9	nitric oxide synthase 3	Homo sapiens	89-93
25257463-3	2014	The aim of this study was to investigate whether berberine (BBR) can protect EPCs from the inhibition caused by TNF-alpha via the PI3K (Phosphatidyl Inositol 3-kinase) /AKT (Serine/threonine protein kinase B) /eNOS (endothelial Nitric Oxide synthase) signaling pathway.	Berberine	49-58	nitric oxide synthase 3	Homo sapiens	210-214
25257463-3	2014	The aim of this study was to investigate whether berberine (BBR) can protect EPCs from the inhibition caused by TNF-alpha via the PI3K (Phosphatidyl Inositol 3-kinase) /AKT (Serine/threonine protein kinase B) /eNOS (endothelial Nitric Oxide synthase) signaling pathway.	Berberine	49-58	nitric oxide synthase 3	Homo sapiens	216-249
25257463-3	2014	The aim of this study was to investigate whether berberine (BBR) can protect EPCs from the inhibition caused by TNF-alpha via the PI3K (Phosphatidyl Inositol 3-kinase) /AKT (Serine/threonine protein kinase B) /eNOS (endothelial Nitric Oxide synthase) signaling pathway.	Berberine	60-63	nitric oxide synthase 3	Homo sapiens	210-214
25257463-3	2014	The aim of this study was to investigate whether berberine (BBR) can protect EPCs from the inhibition caused by TNF-alpha via the PI3K (Phosphatidyl Inositol 3-kinase) /AKT (Serine/threonine protein kinase B) /eNOS (endothelial Nitric Oxide synthase) signaling pathway.	Berberine	60-63	nitric oxide synthase 3	Homo sapiens	216-249
25257463-9	2014	Blockade of PI3K by 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one (Ly294002) and blockade of eNOS by l-NAME (NG-Nitroarginine Methyl Ester) attenuates the effect of BBR.	NG-Nitroarginine Methyl Ester	104-110	nitric oxide synthase 3	Homo sapiens	96-100
25257463-10	2014	BBR can increase the level of PI3K/Akt/eNOS mRNA and the protein level of PI3K, p-Akt, eNOS and p-eNOS, which can be blocked by PI3K inhibitor (LY294002) and eNOS inhibitor (l-NAME).	Berberine	0-3	nitric oxide synthase 3	Homo sapiens	39-43
25239655-2	2014	NOS3 and NOS2 SNPs might modify plasma nitrite/nitrate (NOx) levels, sepsis development, hemodynamics and survival.	Nitrites	39-46	nitric oxide synthase 3	Homo sapiens	0-4
25257463-10	2014	BBR can increase the level of PI3K/Akt/eNOS mRNA and the protein level of PI3K, p-Akt, eNOS and p-eNOS, which can be blocked by PI3K inhibitor (LY294002) and eNOS inhibitor (l-NAME).	Berberine	0-3	nitric oxide synthase 3	Homo sapiens	87-91
25239655-2	2014	NOS3 and NOS2 SNPs might modify plasma nitrite/nitrate (NOx) levels, sepsis development, hemodynamics and survival.	Nitrates	47-54	nitric oxide synthase 3	Homo sapiens	0-4
25239655-2	2014	NOS3 and NOS2 SNPs might modify plasma nitrite/nitrate (NOx) levels, sepsis development, hemodynamics and survival.	nicotine 1-N-oxide	56-59	nitric oxide synthase 3	Homo sapiens	0-4
25239655-8	2014	Plasma NOx was higher in carriers of the T allele of the NOS3 (E298D) SNP (p = 0.006).	nicotine 1-N-oxide	7-10	nitric oxide synthase 3	Homo sapiens	57-61
25257463-10	2014	BBR can increase the level of PI3K/Akt/eNOS mRNA and the protein level of PI3K, p-Akt, eNOS and p-eNOS, which can be blocked by PI3K inhibitor (LY294002) and eNOS inhibitor (l-NAME).	Berberine	0-3	nitric oxide synthase 3	Homo sapiens	87-91
25257463-10	2014	BBR can increase the level of PI3K/Akt/eNOS mRNA and the protein level of PI3K, p-Akt, eNOS and p-eNOS, which can be blocked by PI3K inhibitor (LY294002) and eNOS inhibitor (l-NAME).	Berberine	0-3	nitric oxide synthase 3	Homo sapiens	87-91
25257463-10	2014	BBR can increase the level of PI3K/Akt/eNOS mRNA and the protein level of PI3K, p-Akt, eNOS and p-eNOS, which can be blocked by PI3K inhibitor (LY294002) and eNOS inhibitor (l-NAME).	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	144-152	nitric oxide synthase 3	Homo sapiens	39-43
25257463-10	2014	BBR can increase the level of PI3K/Akt/eNOS mRNA and the protein level of PI3K, p-Akt, eNOS and p-eNOS, which can be blocked by PI3K inhibitor (LY294002) and eNOS inhibitor (l-NAME).	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	144-152	nitric oxide synthase 3	Homo sapiens	87-91
25257463-10	2014	BBR can increase the level of PI3K/Akt/eNOS mRNA and the protein level of PI3K, p-Akt, eNOS and p-eNOS, which can be blocked by PI3K inhibitor (LY294002) and eNOS inhibitor (l-NAME).	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	144-152	nitric oxide synthase 3	Homo sapiens	87-91
25257463-10	2014	BBR can increase the level of PI3K/Akt/eNOS mRNA and the protein level of PI3K, p-Akt, eNOS and p-eNOS, which can be blocked by PI3K inhibitor (LY294002) and eNOS inhibitor (l-NAME).	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	144-152	nitric oxide synthase 3	Homo sapiens	87-91
25375125-2	2014	Previous work has demonstrated that the hyperoxia-induced vascular injury is mediated by dysfunction of endothelial nitric oxide synthase resulting in peroxynitrite formation.	Peroxynitrous Acid	151-164	nitric oxide synthase 3	Homo sapiens	104-137
26019598-7	2014	eNOS is a subgroup of this family of enzymes that catalyses the production of nitric oxide (NO) from L-arginine and oxygen, which leads to vascular relaxation by activating the guanylate cyclase.	Nitric Oxide	78-90	nitric oxide synthase 3	Homo sapiens	0-4
26019598-7	2014	eNOS is a subgroup of this family of enzymes that catalyses the production of nitric oxide (NO) from L-arginine and oxygen, which leads to vascular relaxation by activating the guanylate cyclase.	Arginine	101-111	nitric oxide synthase 3	Homo sapiens	0-4
26019598-7	2014	eNOS is a subgroup of this family of enzymes that catalyses the production of nitric oxide (NO) from L-arginine and oxygen, which leads to vascular relaxation by activating the guanylate cyclase.	Oxygen	116-122	nitric oxide synthase 3	Homo sapiens	0-4
25234816-6	2014	Atorvastatin also avoided striking alterations on cell monolayer structure triggered by both stimuli and enhanced NO reduction because of cocaine stimulation through disrupting interactions between endothelial nitric oxide synthase (eNOS) and caveolin-1, thus increasing eNOS bioavailability.	Atorvastatin	0-12	nitric oxide synthase 3	Homo sapiens	198-231
25234816-6	2014	Atorvastatin also avoided striking alterations on cell monolayer structure triggered by both stimuli and enhanced NO reduction because of cocaine stimulation through disrupting interactions between endothelial nitric oxide synthase (eNOS) and caveolin-1, thus increasing eNOS bioavailability.	Cocaine	138-145	nitric oxide synthase 3	Homo sapiens	198-231
25163536-7	2014	Inorganic nitrite drove cGMP-mediated inhibition of human platelet aggregation in vitro and nitrate inhibited platelet function in eNOS(-/-) mice in vivo in a model of thromboembolic radiolabeled platelet aggregation associated with an enhanced plasma nitrite concentration as compared with wild-type mice.	Nitrates	92-99	nitric oxide synthase 3	Homo sapiens	131-135
25244505-1	2014	In the vascular wall, reactive oxygen species (ROS) are produced by several enzyme systems including NADPH oxidase, xanthine oxidase, uncoupled endothelial nitric oxide synthase (eNOS) and the mitochondrial electron transport chain.	Reactive Oxygen Species	22-45	nitric oxide synthase 3	Homo sapiens	144-177
25244505-1	2014	In the vascular wall, reactive oxygen species (ROS) are produced by several enzyme systems including NADPH oxidase, xanthine oxidase, uncoupled endothelial nitric oxide synthase (eNOS) and the mitochondrial electron transport chain.	Reactive Oxygen Species	47-50	nitric oxide synthase 3	Homo sapiens	144-177
25130141-7	2014	Under conditions of beta-adrenoceptor inhibition, the endogenous generation of nitric oxide (NO) as well as the phosphorylation of endothelial nitric oxide synthase (eNOS) was decreased in embryoid bodies, whereas an increase in NO generation was observed with the NO donor S-nitroso-N-acetyl-D,L-penicillamine (SNAP).	snap	274-310	nitric oxide synthase 3	Homo sapiens	131-164
25130141-7	2014	Under conditions of beta-adrenoceptor inhibition, the endogenous generation of nitric oxide (NO) as well as the phosphorylation of endothelial nitric oxide synthase (eNOS) was decreased in embryoid bodies, whereas an increase in NO generation was observed with the NO donor S-nitroso-N-acetyl-D,L-penicillamine (SNAP).	snap	312-316	nitric oxide synthase 3	Homo sapiens	131-164
25163536-10	2014	The absence of eNOS leads to enhanced plasma nitrite levels following nitrate administration in vivo, which negatively impacts on platelet function.	Nitrites	45-52	nitric oxide synthase 3	Homo sapiens	15-19
25095760-6	2014	Overactivation of the N-Methyl-D-Aspartate receptor and peroxynitrite formation results in high levels of neuronal NOS (nNOS) and endothelial NOS (eNOS) which suggest that nNOS and eNOS are critical for pain hypersensitivity.	Peroxynitrous Acid	56-69	nitric oxide synthase 3	Homo sapiens	130-145
25163536-10	2014	The absence of eNOS leads to enhanced plasma nitrite levels following nitrate administration in vivo, which negatively impacts on platelet function.	Nitrates	70-77	nitric oxide synthase 3	Homo sapiens	15-19
25550859-4	2014	The effect of rhACE2 on phosphorylation eNOS level was also observed in the presence of LY294002 (10 mumol/L) (PI3K/AKT inhibitors).	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	88-96	nitric oxide synthase 3	Homo sapiens	40-44
25550859-8	2014	After HUVEC was intervened by PI3K/AKT pathway inhibitor LY294002, the expression level of phosphorylated eNOS was significantly lower than that in the rhACE2 30 min treatment group (P &lt; 0.05).	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	57-65	nitric oxide synthase 3	Homo sapiens	106-110
25550859-9	2014	rhACE2 may reduce the activity of Ang II inhibited endothelial cell eNOS, which can be blocked by PI3K/AKT pathway inhibitor LY294002, suggesting PI3K/AKT signaling pathway plays an important role in rhACE2"s promotion of the activity of endothelial cell eNOS.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	125-133	nitric oxide synthase 3	Homo sapiens	68-72
25550859-9	2014	rhACE2 may reduce the activity of Ang II inhibited endothelial cell eNOS, which can be blocked by PI3K/AKT pathway inhibitor LY294002, suggesting PI3K/AKT signaling pathway plays an important role in rhACE2"s promotion of the activity of endothelial cell eNOS.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	125-133	nitric oxide synthase 3	Homo sapiens	255-259
25095760-6	2014	Overactivation of the N-Methyl-D-Aspartate receptor and peroxynitrite formation results in high levels of neuronal NOS (nNOS) and endothelial NOS (eNOS) which suggest that nNOS and eNOS are critical for pain hypersensitivity.	Peroxynitrous Acid	56-69	nitric oxide synthase 3	Homo sapiens	147-151
25095760-6	2014	Overactivation of the N-Methyl-D-Aspartate receptor and peroxynitrite formation results in high levels of neuronal NOS (nNOS) and endothelial NOS (eNOS) which suggest that nNOS and eNOS are critical for pain hypersensitivity.	Peroxynitrous Acid	56-69	nitric oxide synthase 3	Homo sapiens	181-185
25197782-5	2014	Moreover, high glucose reduced the levels of endothelial nitric oxide synthase (eNOS) phosphorylation, nitric oxide (NO) production and intracellular cyclic guanosine monophosphate (cGMP).	Glucose	15-22	nitric oxide synthase 3	Homo sapiens	45-78
25063757-8	2014	In UAECs from pregnant and non-pregnant animals Ca(2+) responses and eNOS activation were sensitive to the phospholipase C/inositol 1,4,5-trisphosphate pathway inhibitors 2-aminoethoxydiphenylborane and U73122.	Inositol 1,4,5-Trisphosphate	123-151	nitric oxide synthase 3	Homo sapiens	69-73
25063757-8	2014	In UAECs from pregnant and non-pregnant animals Ca(2+) responses and eNOS activation were sensitive to the phospholipase C/inositol 1,4,5-trisphosphate pathway inhibitors 2-aminoethoxydiphenylborane and U73122.	2-aminoethoxydiphenylborane	171-198	nitric oxide synthase 3	Homo sapiens	69-73
24996290-3	2014	Statins are potent modulators of CYP3A4 2 enzyme and endothelial nitric oxide synthase (eNOS) functions in a number of cholesterol-independent, cardio protective actions in T2D.	Cholesterol	119-130	nitric oxide synthase 3	Homo sapiens	53-86
24446239-7	2014	Furthermore, here we show that capsaicin-induced CGRP release from mesenteric perivascular sensory nerves induces pannexin-1-formed channel opening, which in turn leads to reduction of pannexin-1 and endothelial nitric oxide synthase (eNOS) expression along the time.	Capsaicin	31-40	nitric oxide synthase 3	Homo sapiens	200-233
24996290-3	2014	Statins are potent modulators of CYP3A4 2 enzyme and endothelial nitric oxide synthase (eNOS) functions in a number of cholesterol-independent, cardio protective actions in T2D.	Cholesterol	119-130	nitric oxide synthase 3	Homo sapiens	88-92
25198200-0	2014	Resveratrol ameliorates low shear stress-induced oxidative stress by suppressing ERK/eNOS-Thr495 in endothelial cells.	Resveratrol	0-11	nitric oxide synthase 3	Homo sapiens	85-89
25198200-2	2014	eNOS, a key enzyme in controlling nitric oxide (NO) release, has a crucial role in mediating oxidative stress, and resveratrol (RSV)-mediated eNOS also attenuates oxidative damage and suppresses endothelial dysfunction.	Nitric Oxide	34-46	nitric oxide synthase 3	Homo sapiens	0-4
25198200-2	2014	eNOS, a key enzyme in controlling nitric oxide (NO) release, has a crucial role in mediating oxidative stress, and resveratrol (RSV)-mediated eNOS also attenuates oxidative damage and suppresses endothelial dysfunction.	Resveratrol	115-126	nitric oxide synthase 3	Homo sapiens	142-146
25198200-2	2014	eNOS, a key enzyme in controlling nitric oxide (NO) release, has a crucial role in mediating oxidative stress, and resveratrol (RSV)-mediated eNOS also attenuates oxidative damage and suppresses endothelial dysfunction.	Resveratrol	128-131	nitric oxide synthase 3	Homo sapiens	142-146
25198200-11	2014	Of note, the activation effect of LSS on ERK/eNOS was markedly eliminated by RSV.	Resveratrol	77-80	nitric oxide synthase 3	Homo sapiens	45-49
25198200-12	2014	In conclusion, RSV exerts antioxidant effects by suppressing LSS-activated ERK/eNOS and may provide a potential therapeutic target for atherosclerosis.	Resveratrol	15-18	nitric oxide synthase 3	Homo sapiens	79-83
25174844-7	2014	Allicin also reduces the levels of malondialdehyde and increases the levels of superoxide dismutase, nitric oxide release and endothelial nitric oxide synthase mRNA, but has no significant effect on inducible nitric oxide synthase mRNA levels.	allicin	0-7	nitric oxide synthase 3	Homo sapiens	126-159
25112869-4	2014	Treating the cells with l-NAME, a selective inhibitor of constitutive nitric-oxide synthase (cNOS), can partially reverse the IkappaB reduction and inhibit the DNA binding activity as well as nuclear translocation of NF-kappaB after UVB radiation.	NG-Nitroarginine Methyl Ester	24-30	nitric oxide synthase 3	Homo sapiens	93-97
25112869-6	2014	The cNOS-mediated reduction of IkappaB is likely due to the imbalance of nitric oxide/peroxynitrite because treating the cells with lower (50 mum), but not higher (100-500 mum), concentration of S-nitroso-N-acetylpenicillamine (SNAP) can reverse the effect of l-NAME in partial restore IkappaB level post-UVB.	Nitric Oxide	73-85	nitric oxide synthase 3	Homo sapiens	4-8
25112869-6	2014	The cNOS-mediated reduction of IkappaB is likely due to the imbalance of nitric oxide/peroxynitrite because treating the cells with lower (50 mum), but not higher (100-500 mum), concentration of S-nitroso-N-acetylpenicillamine (SNAP) can reverse the effect of l-NAME in partial restore IkappaB level post-UVB.	Peroxynitrous Acid	86-99	nitric oxide synthase 3	Homo sapiens	4-8
25112869-6	2014	The cNOS-mediated reduction of IkappaB is likely due to the imbalance of nitric oxide/peroxynitrite because treating the cells with lower (50 mum), but not higher (100-500 mum), concentration of S-nitroso-N-acetylpenicillamine (SNAP) can reverse the effect of l-NAME in partial restore IkappaB level post-UVB.	S-Nitroso-N-Acetylpenicillamine	195-226	nitric oxide synthase 3	Homo sapiens	4-8
25112869-6	2014	The cNOS-mediated reduction of IkappaB is likely due to the imbalance of nitric oxide/peroxynitrite because treating the cells with lower (50 mum), but not higher (100-500 mum), concentration of S-nitroso-N-acetylpenicillamine (SNAP) can reverse the effect of l-NAME in partial restore IkappaB level post-UVB.	S-Nitroso-N-Acetylpenicillamine	228-232	nitric oxide synthase 3	Homo sapiens	4-8
25112869-6	2014	The cNOS-mediated reduction of IkappaB is likely due to the imbalance of nitric oxide/peroxynitrite because treating the cells with lower (50 mum), but not higher (100-500 mum), concentration of S-nitroso-N-acetylpenicillamine (SNAP) can reverse the effect of l-NAME in partial restore IkappaB level post-UVB.	NG-Nitroarginine Methyl Ester	260-266	nitric oxide synthase 3	Homo sapiens	4-8
25205851-0	2014	The coordination of S-sulfhydration, S-nitrosylation, and phosphorylation of endothelial nitric oxide synthase by hydrogen sulfide.	Hydrogen Sulfide	114-130	nitric oxide synthase 3	Homo sapiens	77-110
25205851-2	2014	A target protein for H(2)S is endothelial nitric oxide synthase (eNOS), an enzyme that generates nitric oxide (NO), which causes vasodilation.	(2)s	22-26	nitric oxide synthase 3	Homo sapiens	30-63
25012137-13	2014	Ticagrelor, but not clopidogrel, increased Akt and endothelial nitric oxide synthase phosphorylation.	Ticagrelor	0-10	nitric oxide synthase 3	Homo sapiens	51-84
25012137-15	2014	The protective effect of ticagrelor was dependent on adenosine-receptor activation with downstream upregulation of endothelial nitric oxide synthase and COX2 activity.	Ticagrelor	25-35	nitric oxide synthase 3	Homo sapiens	115-148
25061098-5	2014	In order to assess roles of NO production in survival and development of the ovine conceptus, we conducted an in vivo morpholino antisense oligonucleotide (MAO)-mediated knockdown trial of nitric oxide synthase-3 (NOS3) mRNA, the major isoform of NO synthase, in ovine conceptus trophectoderm (Tr).	Oligonucleotides	139-154	nitric oxide synthase 3	Homo sapiens	189-212
25061098-10	2014	Thus, the adverse effect of MAO-NOS3 to reduce NO generation and the transport of arginine and ornithine into conceptuses is central to an explanation for failure of normal development of MAO-NOS3, compared to control conceptuses.	Arginine	82-90	nitric oxide synthase 3	Homo sapiens	32-36
25061098-10	2014	Thus, the adverse effect of MAO-NOS3 to reduce NO generation and the transport of arginine and ornithine into conceptuses is central to an explanation for failure of normal development of MAO-NOS3, compared to control conceptuses.	Ornithine	95-104	nitric oxide synthase 3	Homo sapiens	32-36
25061098-12	2014	Our data suggest that NOS3 is the key enzyme for NO production by conceptus Tr and that this protein also regulates the availability of arginine in conceptus tissues for synthesis of polyamines that are essential for conceptus survival and development.	Arginine	136-144	nitric oxide synthase 3	Homo sapiens	22-26
25061098-12	2014	Our data suggest that NOS3 is the key enzyme for NO production by conceptus Tr and that this protein also regulates the availability of arginine in conceptus tissues for synthesis of polyamines that are essential for conceptus survival and development.	Polyamines	183-193	nitric oxide synthase 3	Homo sapiens	22-26
24909615-10	2014	In contrast to iNOS, endothelial NOS-driven cGMP-dependent signaling promoted mitochondrial function and survival of MG132-stressed cells.	Cyclic GMP	44-48	nitric oxide synthase 3	Homo sapiens	21-36
24909615-10	2014	In contrast to iNOS, endothelial NOS-driven cGMP-dependent signaling promoted mitochondrial function and survival of MG132-stressed cells.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	117-122	nitric oxide synthase 3	Homo sapiens	21-36
25089924-1	2014	Many pyrrolidine-based inhibitors highly selective for neuronal nitric oxide synthase (nNOS) over endothelial NOS (eNOS) exhibit dramatically different binding modes.	pyrrolidine	5-16	nitric oxide synthase 3	Homo sapiens	98-113
25133540-0	2014	Redox-sensitive induction of Src/PI3-kinase/Akt and MAPKs pathways activate eNOS in response to EPA:DHA 6:1.	Eicosapentaenoic Acid	96-99	nitric oxide synthase 3	Homo sapiens	76-80
25133540-0	2014	Redox-sensitive induction of Src/PI3-kinase/Akt and MAPKs pathways activate eNOS in response to EPA:DHA 6:1.	Docosahexaenoic Acids	100-103	nitric oxide synthase 3	Homo sapiens	76-80
25133540-3	2014	METHODS AND RESULTS: EPA:DHA 6:1 and 9:1 caused significantly greater endothelium-dependent relaxations in porcine coronary artery rings than EPA:DHA 3:1, 1:1, 1:3, 1:6, 1:9, EPA and DHA alone, and EPA:DHA 6:1 with a reduced EPA + DHA amount, which were inhibited by an eNOS inhibitor.	Eicosapentaenoic Acid	21-24	nitric oxide synthase 3	Homo sapiens	270-274
25133540-5	2014	EPA:DHA 6:1 induced phosphorylation of Src, Akt, p38 MAPK, ERK, JNK and eNOS; these effects were inhibited by MnTMPyP.	Docosahexaenoic Acids	4-7	nitric oxide synthase 3	Homo sapiens	72-76
25133540-7	2014	CONCLUSION: Omega-3 fatty acids cause endothelium-dependent NO-mediated relaxations in coronary artery rings, which are dependent on the EPA:DHA ratio and amount, and involve an intracellular activation of the redox-sensitive PI3-kinase/Akt and MAPKs pathways to activate eNOS.	Fatty Acids, Omega-3	12-31	nitric oxide synthase 3	Homo sapiens	272-276
24863258-1	2014	(6R)-5,6,7,8-Tetrahydro-L-biopterin (BH4) availability regulates nitric oxide and superoxide formation by endothelial nitric oxide synthase (eNOS).	sapropterin	37-40	nitric oxide synthase 3	Homo sapiens	106-139
25210424-6	2014	Increased ADMA may be responsible for the diminished eNOS activity found in these patients, which in turn contributes to the decrease in NO levels, which likely plays a role in the pathogenesis of AMD.	N,N-dimethylarginine	10-14	nitric oxide synthase 3	Homo sapiens	53-57
25092105-6	2014	In addition, we evaluated the effects of long-term treatment with isosorbide dinitrate, a NO donor, on the n/i/eNOS-/- mice with BLM-induced pulmonary fibrosis.	Isosorbide Dinitrate	66-86	nitric oxide synthase 3	Homo sapiens	111-115
24863258-1	2014	(6R)-5,6,7,8-Tetrahydro-L-biopterin (BH4) availability regulates nitric oxide and superoxide formation by endothelial nitric oxide synthase (eNOS).	Nitric Oxide	65-77	nitric oxide synthase 3	Homo sapiens	106-139
24863258-0	2014	Cell type-specific recycling of tetrahydrobiopterin by dihydrofolate reductase explains differential effects of 7,8-dihydrobiopterin on endothelial nitric oxide synthase uncoupling.	sapropterin	32-51	nitric oxide synthase 3	Homo sapiens	136-169
24863258-1	2014	(6R)-5,6,7,8-Tetrahydro-L-biopterin (BH4) availability regulates nitric oxide and superoxide formation by endothelial nitric oxide synthase (eNOS).	Superoxides	82-92	nitric oxide synthase 3	Homo sapiens	106-139
24863258-0	2014	Cell type-specific recycling of tetrahydrobiopterin by dihydrofolate reductase explains differential effects of 7,8-dihydrobiopterin on endothelial nitric oxide synthase uncoupling.	7,8-dihydrobiopterin	112-132	nitric oxide synthase 3	Homo sapiens	136-169
24863258-1	2014	(6R)-5,6,7,8-Tetrahydro-L-biopterin (BH4) availability regulates nitric oxide and superoxide formation by endothelial nitric oxide synthase (eNOS).	sapropterin	0-35	nitric oxide synthase 3	Homo sapiens	106-139
24928905-5	2014	Treatment of endothelial cells with VEGF or phorbol 12,13-dibutyrate (PDBu) activates PKD and increases eNOS Ser1179 phosphorylation.	Phorbol 12,13-Dibutyrate	44-68	nitric oxide synthase 3	Homo sapiens	104-108
23471592-6	2014	In agreement, our in vitro studies show that testosterone inhibits the gene expression of endothelial NO synthase (eNOS) after 48 hours.	Testosterone	45-57	nitric oxide synthase 3	Homo sapiens	115-119
23471592-7	2014	When the antioxidant seleno-L-methionine was added, the down-regulation of mRNA specific eNOS was partly abrogated.	Selenomethionine	21-40	nitric oxide synthase 3	Homo sapiens	89-93
23471592-9	2014	CONCLUSION: These results show that a supraphysiological dose of testosterone decreases the expression of eNOS and consequently the formation of NO, which could partly be explained by oxidative stress.	Testosterone	65-77	nitric oxide synthase 3	Homo sapiens	106-110
24928905-5	2014	Treatment of endothelial cells with VEGF or phorbol 12,13-dibutyrate (PDBu) activates PKD and increases eNOS Ser1179 phosphorylation.	Phorbol 12,13-Dibutyrate	70-74	nitric oxide synthase 3	Homo sapiens	104-108
24771066-6	2014	ZNF580 and eNOS downregulation induced by TGF-beta1 was blocked by the specific TGF-beta1 type I receptor ALK5 inhibitor, SB431542.	4-(5-benzo(1,3)dioxol-5-yl-4-pyridin-2-yl-1H-imidazol-2-yl)benzamide	122-130	nitric oxide synthase 3	Homo sapiens	11-15
25082887-0	2014	Beraprost sodium, a stable prostacyclin analogue, elicits dilation of isolated porcine retinal arterioles: roles of eNOS and potassium channels.	beraprost	0-16	nitric oxide synthase 3	Homo sapiens	116-120
25020117-3	2014	In human lung microvascular endothelial cells (HLMVEC), pretreatment with the nitric oxide synthase (NOS) inhibitor, ETU reduced the ability of LLO to increase microvascular cell permeability suggesting an endothelial nitric oxide synthase (eNOS)-dependent mechanism.	Ethylenethiourea	117-120	nitric oxide synthase 3	Homo sapiens	206-239
25077953-1	2014	Cardiovascular benefits from estradiol activation of nitric oxide endothelial production may depend on vascular wall and on estrogen receptor alpha (ESR1) and nitric oxide synthase (NOS3) polymorphisms.	Nitric Oxide	53-65	nitric oxide synthase 3	Homo sapiens	182-186
25020117-3	2014	In human lung microvascular endothelial cells (HLMVEC), pretreatment with the nitric oxide synthase (NOS) inhibitor, ETU reduced the ability of LLO to increase microvascular cell permeability suggesting an endothelial nitric oxide synthase (eNOS)-dependent mechanism.	Ethylenethiourea	117-120	nitric oxide synthase 3	Homo sapiens	241-245
25020117-6	2014	Expression of a phosphomimetic T495D eNOS (human isoform) resulted in increased superoxide and diminished nitric oxide (NO) production.	Superoxides	80-90	nitric oxide synthase 3	Homo sapiens	37-41
25020117-6	2014	Expression of a phosphomimetic T495D eNOS (human isoform) resulted in increased superoxide and diminished nitric oxide (NO) production.	Nitric Oxide	106-118	nitric oxide synthase 3	Homo sapiens	37-41
25020117-10	2014	Both hsp90 and caveolin-1 have been shown to influence eNOS uncoupling and a peptide mimicking the scaffolding domain of caveolin-1 blocked the ability of PKCalpha to stimulate eNOS-derived superoxide.	Superoxides	190-200	nitric oxide synthase 3	Homo sapiens	177-181
25020117-11	2014	Collectively, these results suggest that the G+ pore-forming toxins promote increased EC permeability via activation of PKCalpha, phosphorylation of eNOS-T495, loss of hsp90 and caveolin-1 binding which collectively promote eNOS uncoupling and the production of barrier disruptive superoxide.	Superoxides	281-291	nitric oxide synthase 3	Homo sapiens	224-228
24944642-8	2014	In addition, the plasma NOx concentration in the eNOS Glu/Glu homozygote carriers (129.66+-59.15 mumol/l) was significantly lower compared with the Asp allele carriers (169.84+- 55.18 mumol/l; P=0.010).	nicotine 1-N-oxide	24-27	nitric oxide synthase 3	Homo sapiens	49-53
24944642-8	2014	In addition, the plasma NOx concentration in the eNOS Glu/Glu homozygote carriers (129.66+-59.15 mumol/l) was significantly lower compared with the Asp allele carriers (169.84+- 55.18 mumol/l; P=0.010).	Glutamic Acid	54-57	nitric oxide synthase 3	Homo sapiens	49-53
24944642-8	2014	In addition, the plasma NOx concentration in the eNOS Glu/Glu homozygote carriers (129.66+-59.15 mumol/l) was significantly lower compared with the Asp allele carriers (169.84+- 55.18 mumol/l; P=0.010).	Glutamic Acid	58-61	nitric oxide synthase 3	Homo sapiens	49-53
24944642-8	2014	In addition, the plasma NOx concentration in the eNOS Glu/Glu homozygote carriers (129.66+-59.15 mumol/l) was significantly lower compared with the Asp allele carriers (169.84+- 55.18 mumol/l; P=0.010).	Aspartic Acid	148-151	nitric oxide synthase 3	Homo sapiens	49-53
24944642-10	2014	Therefore, the concordance of decreased SOD activity and NOx concentration, combined with genotypes of SOD3 Ala/Ala and/or eNOS Glu/Glu in hypertensive patients, may be useful in directing the antioxidant therapy of hypertension.	Glutamic Acid	128-131	nitric oxide synthase 3	Homo sapiens	123-127
24748593-2	2014	The present study was designed to evaluate the relationship between exercise training and NOS3 polymorphisms at -786T&gt;C, 894G&gt;T, and intron 4b/a on blood pressure (BP) using 24-h ambulatory BP monitoring (ABPM), nitrate/nitrite levels (NOx), and redox state.	Nitrates	218-225	nitric oxide synthase 3	Homo sapiens	90-94
24764294-0	2014	Endothelial nitric-oxide synthase (eNOS) is activated through G-protein-coupled receptor kinase-interacting protein 1 (GIT1) tyrosine phosphorylation and Src protein.	Tyrosine	125-133	nitric oxide synthase 3	Homo sapiens	0-33
24764294-0	2014	Endothelial nitric-oxide synthase (eNOS) is activated through G-protein-coupled receptor kinase-interacting protein 1 (GIT1) tyrosine phosphorylation and Src protein.	Tyrosine	125-133	nitric oxide synthase 3	Homo sapiens	35-39
24764294-6	2014	GIT1 was phosphorylated on tyrosine by Src, and Y293F and Y554F mutations reduced GIT1 phosphorylation as well as the ability of GIT1 to bind to and activate eNOS.	Tyrosine	27-35	nitric oxide synthase 3	Homo sapiens	158-162
24764294-7	2014	Akt phosphorylation activated eNOS (at Ser(1177)), and Akt also regulated the ability of Src to phosphorylate GIT1 as well as GIT1-eNOS association.	Serine	39-42	nitric oxide synthase 3	Homo sapiens	30-34
24764294-8	2014	These pathways were activated by endothelin-1 through the ETB receptor; inhibiting receptor-activated G-protein betagamma subunits blocked activation of Akt, GIT1 tyrosine phosphorylation, and ET-1-stimulated GIT1-eNOS association but did not affect Src activation.	Endothelin-1	193-197	nitric oxide synthase 3	Homo sapiens	214-218
24748593-2	2014	The present study was designed to evaluate the relationship between exercise training and NOS3 polymorphisms at -786T&gt;C, 894G&gt;T, and intron 4b/a on blood pressure (BP) using 24-h ambulatory BP monitoring (ABPM), nitrate/nitrite levels (NOx), and redox state.	Nitrites	226-233	nitric oxide synthase 3	Homo sapiens	90-94
24748593-2	2014	The present study was designed to evaluate the relationship between exercise training and NOS3 polymorphisms at -786T&gt;C, 894G&gt;T, and intron 4b/a on blood pressure (BP) using 24-h ambulatory BP monitoring (ABPM), nitrate/nitrite levels (NOx), and redox state.	nicotine 1-N-oxide	242-245	nitric oxide synthase 3	Homo sapiens	90-94
24748593-10	2014	The NOS3 polymorphism for intron 4 mitigated the beneficial effect of ET for systolic BP (nonpolymorphic group: -3.0% and polymorphic group: -0.6%) and diastolic BP (nonpolymorphic group: -3.2% and polymorphic group: -0.5%), but it was not associated with NOx level and redox state.	nicotine 1-N-oxide	256-259	nitric oxide synthase 3	Homo sapiens	4-8
24918290-0	2014	Eicosapentaenoic acid protects against palmitic acid-induced endothelial dysfunction via activation of the AMPK/eNOS pathway.	Eicosapentaenoic Acid	0-21	nitric oxide synthase 3	Homo sapiens	112-116
24940036-1	2014	PURPOSE: To analyze the association of polymorphisms of the endothelial nitric oxide synthase (NOS3) gene and nitric oxide (NO) levels with high-tension primary open-angle glaucoma (POAG) in an Egyptian population.	Nitric Oxide	72-84	nitric oxide synthase 3	Homo sapiens	95-99
24914683-0	2014	Adenosine prevents TNFalpha-induced decrease in endothelial mitochondrial mass via activation of eNOS-PGC-1alpha regulatory axis.	Adenosine	0-9	nitric oxide synthase 3	Homo sapiens	97-101
24914683-5	2014	The effects of adenosine were blocked by a nitric oxide synthase inhibitor, a soluble guanylate cyclase inhibitor, a morpholino antisense oligonucleotide to endothelial nitric oxide synthase (eNOS), or siRNA knockdown of the transcriptional coactivator, PGC-1alpha.	Adenosine	15-24	nitric oxide synthase 3	Homo sapiens	157-190
24914683-5	2014	The effects of adenosine were blocked by a nitric oxide synthase inhibitor, a soluble guanylate cyclase inhibitor, a morpholino antisense oligonucleotide to endothelial nitric oxide synthase (eNOS), or siRNA knockdown of the transcriptional coactivator, PGC-1alpha.	Adenosine	15-24	nitric oxide synthase 3	Homo sapiens	192-196
24914683-5	2014	The effects of adenosine were blocked by a nitric oxide synthase inhibitor, a soluble guanylate cyclase inhibitor, a morpholino antisense oligonucleotide to endothelial nitric oxide synthase (eNOS), or siRNA knockdown of the transcriptional coactivator, PGC-1alpha.	Oligonucleotides	138-153	nitric oxide synthase 3	Homo sapiens	192-196
24914683-6	2014	Incubation with exogenous NO, a GC activator, or a cGMP analog reversed the effect of eNOS knockdown, while the effect of NO was blocked by inhibition of GC.	Cyclic GMP	51-55	nitric oxide synthase 3	Homo sapiens	86-90
24914683-8	2014	TNFalpha also decreased expression of eNOS, cellular NO levels, and PGC-1alpha expression, which were reversed by adenosine.	Adenosine	114-123	nitric oxide synthase 3	Homo sapiens	38-42
24914683-11	2014	These effects were reversed by adenosine, an effect mediated by eNOS-synthesized NO, acting via soluble guanylate cyclase/cGMP to activate a mitochondrial biogenesis regulatory program under the control of PGC-1alpha.	Adenosine	31-40	nitric oxide synthase 3	Homo sapiens	64-68
24914683-11	2014	These effects were reversed by adenosine, an effect mediated by eNOS-synthesized NO, acting via soluble guanylate cyclase/cGMP to activate a mitochondrial biogenesis regulatory program under the control of PGC-1alpha.	Cyclic GMP	122-126	nitric oxide synthase 3	Homo sapiens	64-68
24914683-12	2014	These results support the existence of an adenosine-triggered, mito-and cytoprotective mechanism dependent upon an eNOS-PGC-1alpha regulatory pathway, which acts to preserve endothelial mitochondrial function and mass during inflammatory challenge.	Adenosine	42-51	nitric oxide synthase 3	Homo sapiens	115-119
24898615-0	2014	Sphingosine-1-phosphate promotes the differentiation of adipose-derived stem cells into endothelial nitric oxide synthase (eNOS) expressing endothelial-like cells.	sphingosine 1-phosphate	0-23	nitric oxide synthase 3	Homo sapiens	88-121
24918290-0	2014	Eicosapentaenoic acid protects against palmitic acid-induced endothelial dysfunction via activation of the AMPK/eNOS pathway.	Palmitic Acid	39-52	nitric oxide synthase 3	Homo sapiens	112-116
24918290-6	2014	EPA also restored the PA-mediated reduction of endothelial nitric oxide synthase (eNOS) and AMP-activated protein kinase (AMPK) phosphorylation.	Eicosapentaenoic Acid	0-3	nitric oxide synthase 3	Homo sapiens	47-80
24918290-6	2014	EPA also restored the PA-mediated reduction of endothelial nitric oxide synthase (eNOS) and AMP-activated protein kinase (AMPK) phosphorylation.	Eicosapentaenoic Acid	0-3	nitric oxide synthase 3	Homo sapiens	82-86
24918290-6	2014	EPA also restored the PA-mediated reduction of endothelial nitric oxide synthase (eNOS) and AMP-activated protein kinase (AMPK) phosphorylation.	Palmitic Acid	1-3	nitric oxide synthase 3	Homo sapiens	47-80
24918290-6	2014	EPA also restored the PA-mediated reduction of endothelial nitric oxide synthase (eNOS) and AMP-activated protein kinase (AMPK) phosphorylation.	Palmitic Acid	1-3	nitric oxide synthase 3	Homo sapiens	82-86
24918290-7	2014	Using AMPK siRNA and the specific inhibitor compound C, we found that EPA restored the PA-mediated inhibitions of eNOS and AKT activities via activation of AMPK.	Eicosapentaenoic Acid	70-73	nitric oxide synthase 3	Homo sapiens	114-118
24918290-7	2014	Using AMPK siRNA and the specific inhibitor compound C, we found that EPA restored the PA-mediated inhibitions of eNOS and AKT activities via activation of AMPK.	Palmitic Acid	71-73	nitric oxide synthase 3	Homo sapiens	114-118
24918290-9	2014	In summary, these results provide new insight into the possible molecular mechanisms by which EPA protects against atherogenesis via the AMPK/eNOS-related pathway.	Eicosapentaenoic Acid	94-97	nitric oxide synthase 3	Homo sapiens	142-146
24525631-6	2014	RESULTS: Ropivacaine and lidocaine attenuated TNFalpha-induced Src activation (half-maximal inhibitory concentration [IC50] = 8.611 x 10 M for ropivacaine; IC50 = 5.864 x 10 M for lidocaine) and endothelial nitric oxide synthase phosphorylation (IC50 = 7.572 x 10 M for ropivacaine; IC50 = 6.377 x 10 M for lidocaine).	Ropivacaine	9-20	nitric oxide synthase 3	Homo sapiens	195-228
24525631-6	2014	RESULTS: Ropivacaine and lidocaine attenuated TNFalpha-induced Src activation (half-maximal inhibitory concentration [IC50] = 8.611 x 10 M for ropivacaine; IC50 = 5.864 x 10 M for lidocaine) and endothelial nitric oxide synthase phosphorylation (IC50 = 7.572 x 10 M for ropivacaine; IC50 = 6.377 x 10 M for lidocaine).	Lidocaine	25-34	nitric oxide synthase 3	Homo sapiens	195-228
24952486-0	2014	Oxidized extracellular DNA suppresses nitric oxide production by endothelial NO synthase (eNOS) in human endothelial cells (HUVEC).	Nitric Oxide	38-50	nitric oxide synthase 3	Homo sapiens	65-88
24952486-0	2014	Oxidized extracellular DNA suppresses nitric oxide production by endothelial NO synthase (eNOS) in human endothelial cells (HUVEC).	Nitric Oxide	38-50	nitric oxide synthase 3	Homo sapiens	90-94
24380841-1	2014	Nitric oxide is a key signaling molecule in the heart and is produced endogenously by three isoforms of nitric oxide synthase, neuronal NOS (NOS1), endothelial NOS (NOS3), and inducible NOS (NOS2).	Nitric Oxide	0-12	nitric oxide synthase 3	Homo sapiens	165-169
24684492-0	2014	Association of nitric oxide synthase 3 (NOS3) 894 G&gt;T polymorphism with prognostic outcomes of anthracycline in Chinese patients with acute myeloid leukaemia.	Anthracyclines	98-111	nitric oxide synthase 3	Homo sapiens	15-38
24684492-0	2014	Association of nitric oxide synthase 3 (NOS3) 894 G&gt;T polymorphism with prognostic outcomes of anthracycline in Chinese patients with acute myeloid leukaemia.	Anthracyclines	98-111	nitric oxide synthase 3	Homo sapiens	40-44
24684492-1	2014	The aim of the present study was to investigate the influence of the nitric oxide synthase 3 (NOS3) 894 G&gt;T polymorphism on prognostic outcomes of anthracycline in Chinese patients with de novo intermediate-risk acute myeloid leukaemia (AML) and to examine the gene expression level in relation to genetic variation.	Anthracyclines	150-163	nitric oxide synthase 3	Homo sapiens	69-92
24684492-1	2014	The aim of the present study was to investigate the influence of the nitric oxide synthase 3 (NOS3) 894 G&gt;T polymorphism on prognostic outcomes of anthracycline in Chinese patients with de novo intermediate-risk acute myeloid leukaemia (AML) and to examine the gene expression level in relation to genetic variation.	Anthracyclines	150-163	nitric oxide synthase 3	Homo sapiens	94-98
24661939-5	2014	We hypothesized that WBPA (pGz) has neuroprotective and neurotherapeutic effects due to enhancement of biological pathways that include eNOS, BDNF and GDNF.	wbpa	21-25	nitric oxide synthase 3	Homo sapiens	136-140
24661939-5	2014	We hypothesized that WBPA (pGz) has neuroprotective and neurotherapeutic effects due to enhancement of biological pathways that include eNOS, BDNF and GDNF.	Methyl 2-O-[(S)-(Benzyloxy)(Hydroxy)phosphoryl]-3-Deoxy-3-{[(4-Methylphenyl)carbonyl]amino}-1-Thio-Beta-D-Galactopyranoside	27-30	nitric oxide synthase 3	Homo sapiens	136-140
24573174-6	2014	These effects were mimicked in part by endothelial nitric oxide synthase (eNOS) overexpression and abrogated by eNOS deficiency, demonstrating the importance of nitric oxide signaling in mediating the cardiac effects of exercise.	Nitric Oxide	51-63	nitric oxide synthase 3	Homo sapiens	74-78
24269521-0	2014	Telmisartan attenuates monocrotaline-induced pulmonary artery endothelial dysfunction through a PPAR gamma-dependent PI3K/Akt/eNOS pathway.	Telmisartan	0-11	nitric oxide synthase 3	Homo sapiens	126-130
24648521-5	2014	Herein, we identified and characterized a small 10-amino acid CAV subsequence (90-99) that accounted for the majority of eNOS association with Cav-1 (Kd = 49 nM), and computer modeling of CAV(90-99) docking to eNOS provides a rationale for the mechanism of eNOS inhibition by Phe-92.	Phenylalanine	276-279	nitric oxide synthase 3	Homo sapiens	121-125
24269521-7	2014	Immunoblotting results indicated lower levels of PPARgamma, p-Akt and p-eNOS in pulmonary arteries treated with MCT alone and levels were significantly restored by co-treatment with telmisartan.	Telmisartan	182-193	nitric oxide synthase 3	Homo sapiens	70-76
24269521-9	2014	In cultured HPAECs, treatment with telmisartan increased PPARgamma expression and promoted the phosphorylation of Akt and eNOS, thereby increasing the production of NO.	Telmisartan	35-46	nitric oxide synthase 3	Homo sapiens	122-126
24849208-11	2014	Moreover, nebivolol treatment significantly increased the phosphorylation of endothelial NOS (eNOS) and the expression of neuronal NOS (nNOS).	Nebivolol	10-19	nitric oxide synthase 3	Homo sapiens	77-92
24664541-3	2014	Here, we show that OLA-NO2 increased endothelial NO release by modulating activation of endothelial nitric oxide synthase (eNOS) in endothelial cells.	ola-no2	19-26	nitric oxide synthase 3	Homo sapiens	88-121
24827148-0	2014	Telmisartan activates endothelial nitric oxide synthase via Ser1177 phosphorylation in vascular endothelial cells.	Telmisartan	0-11	nitric oxide synthase 3	Homo sapiens	22-55
24827148-2	2014	Here, we examined whether telmisartan modulates eNOS function through its pleiotropic effect.	Telmisartan	26-37	nitric oxide synthase 3	Homo sapiens	48-52
24827148-4	2014	Similarly, telmisartan treatment of human umbilical vein endothelial cells significantly increased the phosphorylation levels of AMP-activated protein kinase (Thr172) and eNOS and the concentration of intracellular guanosine 3",5"-cyclic monophosphate (cGMP).	Telmisartan	11-22	nitric oxide synthase 3	Homo sapiens	171-175
24827148-5	2014	Furthermore, pretreatment with a p38 mitogen-activated protein kinase (p38 MAPK) inhibitor suppressed the increased phosphorylation level of eNOS and intracellular cGMP concentration.	Cyclic GMP	164-168	nitric oxide synthase 3	Homo sapiens	141-145
24827148-6	2014	These data show that telmisartan increases eNOS activity through Ser1177 phosphorylation in vascular endothelial cells mainly via p38 MAPK signaling.	Telmisartan	21-32	nitric oxide synthase 3	Homo sapiens	43-47
24797675-4	2014	In addition, it was revealed that the atheroprotective genes induced with pitavastatin, such as nitric oxide synthase 3 (NOS3) and thrombomodulin (THBD), were suppressed by KLF4 knockdown.	pitavastatin	74-86	nitric oxide synthase 3	Homo sapiens	96-119
24797675-4	2014	In addition, it was revealed that the atheroprotective genes induced with pitavastatin, such as nitric oxide synthase 3 (NOS3) and thrombomodulin (THBD), were suppressed by KLF4 knockdown.	pitavastatin	74-86	nitric oxide synthase 3	Homo sapiens	121-125
24405159-9	2014	Transfection studies with wild-type and mutant human eNOS confirmed the dual role of eNOS as a producer of superoxide anion (O2-) with SIN-1 treatment, and a producer of NO in the presence of DMPO.	Superoxides	107-123	nitric oxide synthase 3	Homo sapiens	53-57
24405159-9	2014	Transfection studies with wild-type and mutant human eNOS confirmed the dual role of eNOS as a producer of superoxide anion (O2-) with SIN-1 treatment, and a producer of NO in the presence of DMPO.	Superoxides	107-123	nitric oxide synthase 3	Homo sapiens	85-89
24405159-9	2014	Transfection studies with wild-type and mutant human eNOS confirmed the dual role of eNOS as a producer of superoxide anion (O2-) with SIN-1 treatment, and a producer of NO in the presence of DMPO.	Superoxides	125-128	nitric oxide synthase 3	Homo sapiens	53-57
24405159-9	2014	Transfection studies with wild-type and mutant human eNOS confirmed the dual role of eNOS as a producer of superoxide anion (O2-) with SIN-1 treatment, and a producer of NO in the presence of DMPO.	Superoxides	125-128	nitric oxide synthase 3	Homo sapiens	85-89
24405159-9	2014	Transfection studies with wild-type and mutant human eNOS confirmed the dual role of eNOS as a producer of superoxide anion (O2-) with SIN-1 treatment, and a producer of NO in the presence of DMPO.	5,5-dimethyl-1-pyrroline-1-oxide	192-196	nitric oxide synthase 3	Homo sapiens	53-57
24599126-8	2014	Treatment with the soluble guanylate cyclase activator BAY41-2272, a vasorelaxing agent that acts downstream of endothelial nitric oxide synthase (eNOS) by directly activating its soluble guanylyl cyclase receptor, rescued blood vessel function and tumor growth.	3-(4-Amino-5-cyclopropylpyrimidine-2-yl)-1-(2-fluorobenzyl)-1H-pyrazolo(3,4-b)pyridine	55-65	nitric oxide synthase 3	Homo sapiens	112-145
24571196-6	2014	RESULTS: Both the release of NO (determined by nitrite+nitrate concentration) and the expression of endothelial-type NO synthase (eNOS) were higher in mononuclear cells from ASA sensitive as compared with those from ASA-resistant patients.	Aspirin	174-177	nitric oxide synthase 3	Homo sapiens	100-128
24571196-6	2014	RESULTS: Both the release of NO (determined by nitrite+nitrate concentration) and the expression of endothelial-type NO synthase (eNOS) were higher in mononuclear cells from ASA sensitive as compared with those from ASA-resistant patients.	Aspirin	174-177	nitric oxide synthase 3	Homo sapiens	130-134
24571196-6	2014	RESULTS: Both the release of NO (determined by nitrite+nitrate concentration) and the expression of endothelial-type NO synthase (eNOS) were higher in mononuclear cells from ASA sensitive as compared with those from ASA-resistant patients.	Aspirin	216-219	nitric oxide synthase 3	Homo sapiens	130-134
24571196-7	2014	There was a positive correlation between either the release of NO and the expression of eNOS protein in mononuclear cells with the ability of ASA to inhibit platelet activity.	Aspirin	142-145	nitric oxide synthase 3	Homo sapiens	88-92
24414281-6	2014	Estradiol in particular mediates early and late endothelial nitric oxide synthase (eNOS) activation via interaction with estrogen receptors through both nongenomic and genomic mechanisms.	Estradiol	0-9	nitric oxide synthase 3	Homo sapiens	48-81
24414281-6	2014	Estradiol in particular mediates early and late endothelial nitric oxide synthase (eNOS) activation via interaction with estrogen receptors through both nongenomic and genomic mechanisms.	Estradiol	0-9	nitric oxide synthase 3	Homo sapiens	83-87
24414281-7	2014	In the vascular system, the primary endogenous source of nitric oxide (NO) generation is eNOS.	Nitric Oxide	57-69	nitric oxide synthase 3	Homo sapiens	89-93
24681424-3	2014	Human eNOS promoter was modified by inserting a Sp1 element at a -74 bp site and function of the modified promoter was investigated via a hypoxia model induced by cobalt chloride in human umbilical vein endothelial cells.	cobaltous chloride	163-178	nitric oxide synthase 3	Homo sapiens	6-10
24681424-5	2014	There was a correlation between the transcriptional activity of the Sp1-modified promoter and the level of eNOS expression with enhancement of nitric oxide production.	Nitric Oxide	143-155	nitric oxide synthase 3	Homo sapiens	107-111
24732179-4	2014	Compared with control group, cisplatin reduced endothelial nitric oxide synthase dimer/monomer ratio, activated protein kinase C and enhanced endothelial nitric oxide synthase-Thr495 phosphorylation, decreased nitric oxide production, augmented intercellular adhesion molecule 1 expression and monocyte-endothelial adhesion.	Cisplatin	29-38	nitric oxide synthase 3	Homo sapiens	47-80
24573187-4	2014	In addition, apelin-13 dose dependently stimulated the phosphorylation of AMP-activated protein kinase (AMPK) and endothelial nitric oxide synthase (eNOS) at Thr-172 and Ser-1179, respectively.	Threonine	158-161	nitric oxide synthase 3	Homo sapiens	114-147
24573187-4	2014	In addition, apelin-13 dose dependently stimulated the phosphorylation of AMP-activated protein kinase (AMPK) and endothelial nitric oxide synthase (eNOS) at Thr-172 and Ser-1179, respectively.	Serine	170-173	nitric oxide synthase 3	Homo sapiens	114-147
24732179-4	2014	Compared with control group, cisplatin reduced endothelial nitric oxide synthase dimer/monomer ratio, activated protein kinase C and enhanced endothelial nitric oxide synthase-Thr495 phosphorylation, decreased nitric oxide production, augmented intercellular adhesion molecule 1 expression and monocyte-endothelial adhesion.	Cisplatin	29-38	nitric oxide synthase 3	Homo sapiens	142-175
24732179-8	2014	Compared with control group, cisplatin and PMA, a protein kinase C activator, both increased endothelial nitric oxide synthase-Thr495 phosphorylation, while propofol and GFX, a protein kinase C inhibitor, both decreased cisplatin-induced endothelial nitric oxide synthase-Thr495 phosphorylation.	Cisplatin	29-38	nitric oxide synthase 3	Homo sapiens	93-126
24732179-8	2014	Compared with control group, cisplatin and PMA, a protein kinase C activator, both increased endothelial nitric oxide synthase-Thr495 phosphorylation, while propofol and GFX, a protein kinase C inhibitor, both decreased cisplatin-induced endothelial nitric oxide synthase-Thr495 phosphorylation.	Cisplatin	29-38	nitric oxide synthase 3	Homo sapiens	238-271
24732179-8	2014	Compared with control group, cisplatin and PMA, a protein kinase C activator, both increased endothelial nitric oxide synthase-Thr495 phosphorylation, while propofol and GFX, a protein kinase C inhibitor, both decreased cisplatin-induced endothelial nitric oxide synthase-Thr495 phosphorylation.	Tetradecanoylphorbol Acetate	43-46	nitric oxide synthase 3	Homo sapiens	93-126
24732179-8	2014	Compared with control group, cisplatin and PMA, a protein kinase C activator, both increased endothelial nitric oxide synthase-Thr495 phosphorylation, while propofol and GFX, a protein kinase C inhibitor, both decreased cisplatin-induced endothelial nitric oxide synthase-Thr495 phosphorylation.	Tetradecanoylphorbol Acetate	43-46	nitric oxide synthase 3	Homo sapiens	238-271
24732179-9	2014	Our data indicated that propofol, via reducing cisplatin-induced endothelial nitric oxide synthase uncoupling and endothelial nitric oxide synthase-Thr495 phosphorylation, restored nitric oxide production, intercellular adhesion molecule 1 expression and monocyte-endothelial interaction.	Propofol	24-32	nitric oxide synthase 3	Homo sapiens	65-98
24732179-9	2014	Our data indicated that propofol, via reducing cisplatin-induced endothelial nitric oxide synthase uncoupling and endothelial nitric oxide synthase-Thr495 phosphorylation, restored nitric oxide production, intercellular adhesion molecule 1 expression and monocyte-endothelial interaction.	Propofol	24-32	nitric oxide synthase 3	Homo sapiens	114-147
24732179-9	2014	Our data indicated that propofol, via reducing cisplatin-induced endothelial nitric oxide synthase uncoupling and endothelial nitric oxide synthase-Thr495 phosphorylation, restored nitric oxide production, intercellular adhesion molecule 1 expression and monocyte-endothelial interaction.	Cisplatin	47-56	nitric oxide synthase 3	Homo sapiens	65-98
24732179-9	2014	Our data indicated that propofol, via reducing cisplatin-induced endothelial nitric oxide synthase uncoupling and endothelial nitric oxide synthase-Thr495 phosphorylation, restored nitric oxide production, intercellular adhesion molecule 1 expression and monocyte-endothelial interaction.	Cisplatin	47-56	nitric oxide synthase 3	Homo sapiens	114-147
24518543-1	2014	We have previously shown that nectandrin B, a potent natural activator of AMP-activated protein kinase (AMPK) results in endothelium-dependent relaxation via endothelial nitric oxide synthase phosphorylation.	nectandrin-B	30-42	nitric oxide synthase 3	Homo sapiens	158-191
24755153-1	2014	BACKGROUND: Glutathionylation of endothelial nitric oxide synthase (eNOS) "uncouples" the enzyme, switching its function from nitric oxide (NO) to O2( -) generation.	Oxygen	147-149	nitric oxide synthase 3	Homo sapiens	33-66
24570151-4	2014	Several molecules with relevant functions in endothelial cells are localized in caveolae, including endothelial nitric oxide synthase (eNOS), which regulates the production of nitric oxide, and scavenger receptor class B type I (SR-BI), which plays a key role in the induction of eNOS activity mediated by high density lipoproteins (HDL).	Nitric Oxide	112-124	nitric oxide synthase 3	Homo sapiens	135-139
24447953-5	2014	Nitrite levels were enhanced by pretreatment with deltaV1-1 30 minutes before ACA possibly attributable to enhanced endothelial NOS protein levels.	Nitrites	0-7	nitric oxide synthase 3	Homo sapiens	116-131
24464923-7	2014	The results suggested a significant association between the -786T &gt; C polymorphism in NOS3 and cancer risk (CC vs. TT + CT; OR = 1.30, 95% CI = 1.07-1.57, P = 0.007) in total analysis.	tt + ct	118-125	nitric oxide synthase 3	Homo sapiens	89-93
24924461-0	2014	[Salidroside attenuates high glucose-induced apoptosis in human umbilical vein endothelial cells via activating the Ca(2)+/CaM/CAMKIIdelta/eNOS pathway].	rhodioloside	1-12	nitric oxide synthase 3	Homo sapiens	139-143
24924461-7	2014	Western blot was performed to detect the protein expressions of eNOS, active caspase-3 and eNOS ser 1177 phosphorylation.	Serine	96-99	nitric oxide synthase 3	Homo sapiens	91-95
24924461-8	2014	RESULTS: Comparing to the normal glucose group, high glucose treatment increased the cell damage, the level of NO and [Ca(2)+]i (P &lt; 0.05) , downregulated CAMKIIdelta, eNOS expression and eNOS ser 1177 phosphorylation (P &lt; 0.05), elevated the concentration of MDA and ROS (P &lt; 0.05) in HUVECs.	Glucose	53-60	nitric oxide synthase 3	Homo sapiens	171-175
24924461-8	2014	RESULTS: Comparing to the normal glucose group, high glucose treatment increased the cell damage, the level of NO and [Ca(2)+]i (P &lt; 0.05) , downregulated CAMKIIdelta, eNOS expression and eNOS ser 1177 phosphorylation (P &lt; 0.05), elevated the concentration of MDA and ROS (P &lt; 0.05) in HUVECs.	Glucose	53-60	nitric oxide synthase 3	Homo sapiens	191-195
24924461-11	2014	CONCLUSIONS: These findings suggeste that salidroside could attenuate high glucose induced apoptosis in HUVEC, partly through activating the Ca(2)+/CaM/CAMKIIdelta/eNOS pathway.	rhodioloside	42-53	nitric oxide synthase 3	Homo sapiens	164-168
24486907-1	2014	Exposure to pro-inflammatory cytokines, such as Angiotensin II, endothelin-1 or TNF leads to endothelial dysfunction, characterized by the reduced production of nitric oxide via endothelial nitric oxide synthase (eNOS).	Nitric Oxide	161-173	nitric oxide synthase 3	Homo sapiens	178-211
24486907-1	2014	Exposure to pro-inflammatory cytokines, such as Angiotensin II, endothelin-1 or TNF leads to endothelial dysfunction, characterized by the reduced production of nitric oxide via endothelial nitric oxide synthase (eNOS).	Nitric Oxide	161-173	nitric oxide synthase 3	Homo sapiens	213-217
24302629-1	2014	AIMS: Nitric oxide (NO) plays a key role in vascular homeostasis and is produced by endothelial NO synthase (eNOS), encoded by NOS3 gene.	Nitric Oxide	6-18	nitric oxide synthase 3	Homo sapiens	109-113
24760515-7	2014	The mRNA levels of VEGF-R1/2, VE-cadherin, Tie2, endothelial nitric oxide synthase, MMP9, and VEGF increased in EPCs treated with dextran.	Dextrans	130-137	nitric oxide synthase 3	Homo sapiens	49-82
24444496-9	2014	Furthermore, the expression of endothelial nitric oxide synthase (eNOS) and prostacyclin (PGI2) was significantly attenuated following treatment with TSH in dose- and time-dependent manner.	Thyrotropin	150-153	nitric oxide synthase 3	Homo sapiens	31-64
24302629-1	2014	AIMS: Nitric oxide (NO) plays a key role in vascular homeostasis and is produced by endothelial NO synthase (eNOS), encoded by NOS3 gene.	Nitric Oxide	6-18	nitric oxide synthase 3	Homo sapiens	127-131
24480876-0	2014	Shear-induced endothelial NOS activation and remodeling via heparan sulfate, glypican-1, and syndecan-1.	Heparitin Sulfate	60-75	nitric oxide synthase 3	Homo sapiens	14-29
24616589-1	2014	Tetrahydrobiopterin (BH4) is an essential cofactor in NO synthesis by endothelial nitric oxide synthase (eNOS) enzymes.	sapropterin	0-19	nitric oxide synthase 3	Homo sapiens	70-103
24616589-1	2014	Tetrahydrobiopterin (BH4) is an essential cofactor in NO synthesis by endothelial nitric oxide synthase (eNOS) enzymes.	sapropterin	21-24	nitric oxide synthase 3	Homo sapiens	70-103
24577926-2	2014	The aim of this study was to find if there is any correlation exists between ACS and hereditary genetic defect in endothelial nitric oxide synthase (ecNOS) gene as eNOS generates Nitric oxide in blood vessels and regulates the vascular tone hence directly affecting the cardiovascular function.	Nitric Oxide	179-191	nitric oxide synthase 3	Homo sapiens	114-147
24623205-4	2014	However, we found that participants older than 67 years who carried a combination of eNOS (Asp/Asp) genotype and ADRB2 glycine (Gly) allele were at a higher risk of having hypertension (p=0.029).	Aspartic Acid	91-94	nitric oxide synthase 3	Homo sapiens	85-89
24623205-4	2014	However, we found that participants older than 67 years who carried a combination of eNOS (Asp/Asp) genotype and ADRB2 glycine (Gly) allele were at a higher risk of having hypertension (p=0.029).	Aspartic Acid	95-98	nitric oxide synthase 3	Homo sapiens	85-89
24623205-5	2014	CONCLUSION: Our findings offer an opportunity for prediction of hypertension in elderly Lebanese individuals that carry a genetic combination of Asp/Asp genotype and Gly allele in eNOS and ADRB2 genes.	Glycine	166-169	nitric oxide synthase 3	Homo sapiens	180-184
24577926-2	2014	The aim of this study was to find if there is any correlation exists between ACS and hereditary genetic defect in endothelial nitric oxide synthase (ecNOS) gene as eNOS generates Nitric oxide in blood vessels and regulates the vascular tone hence directly affecting the cardiovascular function.	Nitric Oxide	179-191	nitric oxide synthase 3	Homo sapiens	149-154
24577926-2	2014	The aim of this study was to find if there is any correlation exists between ACS and hereditary genetic defect in endothelial nitric oxide synthase (ecNOS) gene as eNOS generates Nitric oxide in blood vessels and regulates the vascular tone hence directly affecting the cardiovascular function.	Nitric Oxide	179-191	nitric oxide synthase 3	Homo sapiens	164-168
24577926-3	2014	Single nucleotide polymorphism (SNP) (Glu 298 Asp) in ecNOS was determined in 280 subjects, from Southern Punjab (in Pakistan) population, including (160 ACS patients and 120 healthy controls) by PCR-RFLP method and genotype was correlated with various risk factors as well as with serum cholesterol and triglyceride levels.	Cholesterol	288-299	nitric oxide synthase 3	Homo sapiens	54-59
24577926-3	2014	Single nucleotide polymorphism (SNP) (Glu 298 Asp) in ecNOS was determined in 280 subjects, from Southern Punjab (in Pakistan) population, including (160 ACS patients and 120 healthy controls) by PCR-RFLP method and genotype was correlated with various risk factors as well as with serum cholesterol and triglyceride levels.	Triglycerides	304-316	nitric oxide synthase 3	Homo sapiens	54-59
25016868-8	2014	CONCLUSION: Sequoyitol alleviates high glucose-induced cell injuries in HUVECs via inhibiting oxidative stress and up-regulating eNOS expression.	5-O-methyl-myo-inositol	12-22	nitric oxide synthase 3	Homo sapiens	129-133
25016868-0	2014	[Effect of sequoyitol on expression of NOX4 and eNOS induced with glucose in human umbilical vein endothelial cells].	5-O-methyl-myo-inositol	11-21	nitric oxide synthase 3	Homo sapiens	48-52
24587005-5	2014	The defective vasorelaxation seems to stem from a faulty release of NO from platelets of HD patients and, it is associated with impairment of eNOS phosphorylation (Ser(1177)) and activity.	Serine	164-167	nitric oxide synthase 3	Homo sapiens	142-146
25016868-0	2014	[Effect of sequoyitol on expression of NOX4 and eNOS induced with glucose in human umbilical vein endothelial cells].	Glucose	66-73	nitric oxide synthase 3	Homo sapiens	48-52
24469026-4	2014	ADMA is an endogenous inhibitor of endothelial nitric oxide synthase.	N,N-dimethylarginine	0-4	nitric oxide synthase 3	Homo sapiens	35-68
24138560-8	2014	CONCLUSION: We conclude that H2S affects [Ca(2+)]i homeostasis that is mediated by H2S-evoked NO production via an endothelial nitric oxide synthase (eNOS)-NO-sGC-cyclic guanosine monophosphate-PKG-Gq-protein-PLC-IP3 pathway to induce Ca(2+) release, and this pathway is identical to the one we recently proposed for a sole effect of NO and the two gaseous molecules synergistically function to regulate Ca(2+) homeostasis.	Hydrogen Sulfide	29-32	nitric oxide synthase 3	Homo sapiens	115-148
24520999-6	2014	The net effect of NO in the kidney is to promote natriuresis and diuresis, along with renal adaptation to dietary salt intake.The eNOS gene has been considered a potential candidate gene for DN susceptibility.	Salts	114-118	nitric oxide synthase 3	Homo sapiens	130-134
24138560-8	2014	CONCLUSION: We conclude that H2S affects [Ca(2+)]i homeostasis that is mediated by H2S-evoked NO production via an endothelial nitric oxide synthase (eNOS)-NO-sGC-cyclic guanosine monophosphate-PKG-Gq-protein-PLC-IP3 pathway to induce Ca(2+) release, and this pathway is identical to the one we recently proposed for a sole effect of NO and the two gaseous molecules synergistically function to regulate Ca(2+) homeostasis.	Hydrogen Sulfide	83-86	nitric oxide synthase 3	Homo sapiens	115-148
24138560-8	2014	CONCLUSION: We conclude that H2S affects [Ca(2+)]i homeostasis that is mediated by H2S-evoked NO production via an endothelial nitric oxide synthase (eNOS)-NO-sGC-cyclic guanosine monophosphate-PKG-Gq-protein-PLC-IP3 pathway to induce Ca(2+) release, and this pathway is identical to the one we recently proposed for a sole effect of NO and the two gaseous molecules synergistically function to regulate Ca(2+) homeostasis.	Cyclic GMP	163-193	nitric oxide synthase 3	Homo sapiens	115-148
24520379-5	2014	This beneficial effect of nifedipine was associated with reduced reactive oxygen species (ROS) and increased endothelial nitric oxide synthase (eNOS) activity.	Nifedipine	26-36	nitric oxide synthase 3	Homo sapiens	109-142
24520379-5	2014	This beneficial effect of nifedipine was associated with reduced reactive oxygen species (ROS) and increased endothelial nitric oxide synthase (eNOS) activity.	Nifedipine	26-36	nitric oxide synthase 3	Homo sapiens	144-148
24520379-6	2014	Thus, nifedipine prevented high glucose-induced ROS generation and increased basal eNOS phosphorylation level at Ser-1177.	Nifedipine	6-16	nitric oxide synthase 3	Homo sapiens	83-87
24520379-6	2014	Thus, nifedipine prevented high glucose-induced ROS generation and increased basal eNOS phosphorylation level at Ser-1177.	Serine	113-116	nitric oxide synthase 3	Homo sapiens	83-87
24138560-8	2014	CONCLUSION: We conclude that H2S affects [Ca(2+)]i homeostasis that is mediated by H2S-evoked NO production via an endothelial nitric oxide synthase (eNOS)-NO-sGC-cyclic guanosine monophosphate-PKG-Gq-protein-PLC-IP3 pathway to induce Ca(2+) release, and this pathway is identical to the one we recently proposed for a sole effect of NO and the two gaseous molecules synergistically function to regulate Ca(2+) homeostasis.	Inositol 1,4,5-Trisphosphate	213-216	nitric oxide synthase 3	Homo sapiens	115-148
24520379-7	2014	Treatment with N (G)-nitro-L-arginine (L-NAME) and transfection of small interfering RNA (siRNA) targeting eNOS eliminated the anti-senscence effect of nifedipine.	Nifedipine	152-162	nitric oxide synthase 3	Homo sapiens	107-111
24520379-8	2014	These results demonstrate that nifedipine can prevent endothelial cell senescence in an eNOS-dependent manner.	Nifedipine	31-41	nitric oxide synthase 3	Homo sapiens	88-92
24505326-6	2014	The expression of MMP-2/9, extracellular inducer of matrix metalloproteinase (EMMPRIN), CD44, eNOS and E-cadherin were suppressed by alpha-solanine in PANC-1 cells.	alpha-solanine	133-147	nitric oxide synthase 3	Homo sapiens	94-98
24332564-6	2014	On one hand, Pin1 and eNOS not only inhibit Abeta production but also accelerate Abeta clearance, preventing Abeta deposition in cerebral microvessels.	UNII-042A8N37WH	44-49	nitric oxide synthase 3	Homo sapiens	22-26
24403014-4	2014	Our aim is to investigate the association Glu- 298Asp polymorphism of the endothelial nitric oxide synthase (eNOS) gene with serum nitric oxide levels and microalbuminuria in patients with GDM and healthy pregnancies.	Nitric Oxide	86-98	nitric oxide synthase 3	Homo sapiens	109-113
24573064-5	2014	One of the most studied eNOS gene polymorphisms is a c.894G&gt;T polymorphism that results in the conversion of Glu (GAG) to Asp (GAT) at position 298.	Glutamic Acid	112-115	nitric oxide synthase 3	Homo sapiens	24-28
24573064-5	2014	One of the most studied eNOS gene polymorphisms is a c.894G&gt;T polymorphism that results in the conversion of Glu (GAG) to Asp (GAT) at position 298.	Glycosaminoglycans	117-120	nitric oxide synthase 3	Homo sapiens	24-28
24573064-5	2014	One of the most studied eNOS gene polymorphisms is a c.894G&gt;T polymorphism that results in the conversion of Glu (GAG) to Asp (GAT) at position 298.	Aspartic Acid	125-128	nitric oxide synthase 3	Homo sapiens	24-28
24333161-3	2014	Tetrahydrobiopterin (BH4) is a co-factor of endothelial nitric oxide synthase (eNOS) which may easily become oxidized to the inactive form dihydrobiopterin (BH2).	sapropterin	0-19	nitric oxide synthase 3	Homo sapiens	44-77
24333161-3	2014	Tetrahydrobiopterin (BH4) is a co-factor of endothelial nitric oxide synthase (eNOS) which may easily become oxidized to the inactive form dihydrobiopterin (BH2).	sapropterin	21-24	nitric oxide synthase 3	Homo sapiens	44-77
24333161-3	2014	Tetrahydrobiopterin (BH4) is a co-factor of endothelial nitric oxide synthase (eNOS) which may easily become oxidized to the inactive form dihydrobiopterin (BH2).	7,8-dihydrobiopterin	139-155	nitric oxide synthase 3	Homo sapiens	44-77
24333161-3	2014	Tetrahydrobiopterin (BH4) is a co-factor of endothelial nitric oxide synthase (eNOS) which may easily become oxidized to the inactive form dihydrobiopterin (BH2).	bh2	157-160	nitric oxide synthase 3	Homo sapiens	44-77
26354377-7	2015	Plasma L-arginine decreased while ADMA, an endogenous endothelial nitric oxide synthase (eNOS) inhibitor, increased in Cd-exposed subjects.	N,N-dimethylarginine	34-38	nitric oxide synthase 3	Homo sapiens	54-87
26354377-7	2015	Plasma L-arginine decreased while ADMA, an endogenous endothelial nitric oxide synthase (eNOS) inhibitor, increased in Cd-exposed subjects.	Cadmium	119-121	nitric oxide synthase 3	Homo sapiens	54-87