PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
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	
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	
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 <.05).	NG-Nitroarginine Methyl Ester	47-53	nitric oxide synthase 3	Homo sapiens	86-90	
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	
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	
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	
12471479-23	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	
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	
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	
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	
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	
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	
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	
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	
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	
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	
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	
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	
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	
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	
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	
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	
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	
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	
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	
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	
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	
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	
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	
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	
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	
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	
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	
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	
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	
27927230-11	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	
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	
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	
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	
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	
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.	NG-Nitroarginine Methyl Ester	114-120	nitric oxide synthase 3	Homo sapiens	39-43	
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	
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	
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	
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	
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	
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	
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.	NG-Nitroarginine Methyl Ester	260-266	nitric oxide synthase 3	Homo sapiens	4-8	
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	
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	
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	
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	
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	
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	
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	
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	
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	
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	
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	
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	
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	
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	
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	
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	
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	
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	
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	
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	
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	
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	
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	
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	
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	
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	
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	
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	
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