Ignet

Gene Information

Gene symbol: NOS1

Gene name: nitric oxide synthase 1 (neuronal)

HGNC ID: 7872

Synonyms: nNOS

Related Genes

#	Gene Symbol	Number of hits
1	ADIPOQ	1 hits
2	AGT	1 hits
3	AOF2	1 hits
4	AVP	1 hits
5	CASP3	1 hits
6	CAV1	1 hits
7	CYBA	1 hits
8	EDN1	1 hits
9	HBB	1 hits
10	HMOX2	1 hits
11	IFNG	1 hits
12	IL1B	1 hits
13	IL1R1	1 hits
14	IL1RAPL2	1 hits
15	INS	1 hits
16	INSR	1 hits
17	MAPK1	1 hits
18	MMP2	1 hits
19	MMP9	1 hits
20	NOS2A	1 hits
21	NOS3	1 hits
22	OXTR	1 hits
23	PDPK1	1 hits
24	PLCG1	1 hits
25	PRKCA	1 hits
26	PTGS2	1 hits
27	PTHR1	1 hits
28	RAMP1	1 hits
29	REN	1 hits
30	SON	1 hits
31	TNF	1 hits
32	VASP	1 hits

Related Sentences

#	PMID	Sentence
1	21907990	Insulin stimulated nitric oxide synthase (NOS) activity in human vein endothelial cells from G/G (n=4, p=0.03) but not the G/A (n=5, p=0.83) genotype.
2	21907990	Variability at the SH2B1 obesity locus is associated with MI in diabetic patients and with reduced insulin-stimulated NOS activity in human endothelial cells.
3	21995824	Both ERK and arginase have been reported to affect the expression and activity of nitric oxide synthase (NOS) and consequently penile erection.
4	7540553	Hyperglycemia is likely to be the mechanism of NOS inhibition since insulin treatment reversed this abnormality.
5	8779862	Although IL-1 beta and TNF-alpha are themselves capable of inducing NO synthase (NOS) in glia, the specific factors mediating LPS induction of NOS in brain have not been identified.
6	8779862	To determine whether LPS induction of NOS in brain cells is mediated by IL-1 or TNF-alpha, acting alone or in concert, the effects of IL-1-receptor antagonist (IL-1Ra) and of TNF-soluble receptor (TNFsRp55), presented individually and in combination, on LPS-induced NOS activity were tested.
7	8779862	TNF-alpha alone induced NO production weakly as compared with IL-1, but combined submaximal concentrations of IL-1 beta (1 nM) and TNF-alpha (10 nM) induced NOS synergistically.
8	8779862	The results indicate that LPS induction of NOS activity in brain cells is mediated in part by both IL-1 beta and TNF-alpha.
9	9781316	Inhibition of NOS activity blunts contraction-stimulated glucose transport but has no effect on insulin-stimulated glucose transport.
10	10637124	When tissues are incubated in the presence of endothelin 1 (ET-1) (10(-7) M), NOS activity is higher in C pancreas, while the ET-receptor antagonist bosentan (B) decreases NOS levels in D but not in C tissues.
11	10810880	In contrast, exposure of glycated HDL induced a marked decrease of Cu2+Zn(2+)-SOD, catalase, and endothelial NOS as well as a slight increase of p22 phox in HAEC in term of both protein and mRNA expression, suggesting that increased formation of reactive oxygen species such as O2- and OH radical participate in the deterioration for the function of vascular endothelial cells in diabetic patients.
12	10969153	Acetylcholine-induced relaxation was largely due to nitric oxide (NO)-mediated relaxation; however, a small but significant portion of relaxation in aortic rings from temocapril-treated diabetic rats was resistant to inhibition by the nitric oxide synthase (NOS) inhibitor, L-nitroarginine.
13	10976915	Furthermore, treatment with synthetic inhibitors of phosphatidylinositol-3 kinase (PI3-kinase), nitric oxide synthase (NOS), and cyclic guanosine monophosphate (cGMP) all blocked insulin's effect on MBP activation.
14	11087959	The expression of the neuronal nitric oxide synthase (nNOS) gene in the paraventricular (PVN) and supraoptic nuclei (SON) in rats with lithium (Li)-induced polyuria was examined by using in situ hybridization histochemistry.
15	11087959	These results suggest that Li-induced diabetes insipidus may activate nNOS in the PVN and SON without change of the thyroid axis.
16	11160605	Quantitative measurement of cytosolic NOS activity indicated no significant calcium-dependent (nNOS) activity in control or diabetic arteries, or calcium-independent (iNOS) activity in control arteries.
17	11426340	Eight weeks later the animals were killed, the distal part of the vagina was removed, and smooth muscle strips were prepared for functional organ bath experiments and for measurement of nitric oxide synthase (NOS) activity.
18	11798595	The changes of creatinine clearance rate (Ccr), nitric oxide(NO), nitric oxide synthase (NOS) and endothelin(ET) in the plasma and renal cortical tissue, membrane protein kinase C(PKC) in the renal glomeruli were observed.
19	11973412	Muscarinic agonists produce endothelium-dependent vasodilatation in the presence of nitric oxide synthase (NOS) inhibition.
20	14510866	Stimulated levels of cGMP accumulation were completely abrogated by NOS inhibitor, indicating NO involvement in the effects of insulin and lyso-PC.
21	15149729	We have also established that the neuronal isoform of constitutive NO synthase (nNOS) is expressed in beta-cells and modulates insulin secretion.
22	15149729	In this study, we explored the kinetics of glucose- and arginine-stimulated insulin release in perifused isolated islets as well as the effect of N-omega-nitro-L-arginine methyl ester (L-NAME), a NOS inhibitor, to get insight into the possible mechanisms responsible for the arginine hypersensitivity observed in vitro in this and other models of type 2 diabetes.
23	15010356	Plasma renin activity was significantly reduced in nNOS -/- mice on a mixed genetic background and in COX-2 -/- mice on either BALB/c or C57/BL6 congenic backgrounds.
24	15010356	In COX-2 -/- mice, nNOS mRNA expression in the kidney, determined by real-time RT-PCR, was upregulated throughout the postnatal periods, ranging from postnatal day (PND) 3 to PND 60.
25	15010356	The induction of nNOS protein expression and NOS activity in COX-2 -/- mice was localized to macula densa cells using immunohistochemistry and NADPH-diaphorase staining methods, respectively.
26	15010356	Therefore, these findings reveal that the absence of either COX-2 or nNOS is associated with suppressed renin secretion.
27	15562034	We determined nitric oxide synthase (NOS) activity in skeletal muscle of 10 type 2 diabetic (hemoglobin A(1C) = 6.8 +/- 0.1%) and 11 control subjects under basal conditions and during an 80 mU/m(2).min euglycemic insulin clamp performed with vastus lateralis muscle biopsies before and after 4 h of insulin.
28	15562034	In response to insulin, NOS activity increased 2.5-fold in controls after 4 h (934 +/- 282 pmol/min.mg protein, P < 0.05 vs. basal), whereas insulin failed to stimulate NOS activity in diabetics (86 +/- 28 pmol/min.mg protein, P = NS from basal).
29	15562034	In controls, insulin-stimulated NOS activity correlated inversely with fasting plasma insulin concentration (r = -0.58, P = 0.05) and positively with Rd (r = 0.71, P = 0.03).
30	15562034	In control and diabetic groups collectively, Rd correlated with insulin-stimulated NOS activity (r = 0.52, P = 0.02).
31	15562034	We conclude that basal and insulin-stimulated muscle NOS activity is impaired in well-controlled type 2 diabetic subjects, and the defect in insulin-stimulated NOS activity correlates closely with the severity of insulin resistance.
32	15774613	Plasma levels of nitrite ions have been used as an index of nitric oxide synthase (NOS) activity in vivo.
33	15933265	Hypoxia also reduced hENT1 protein and mRNA levels, effects unaltered by N(omega)-nitro-l-arginine methyl ester (l-NAME, nitric oxide synthase [NOS] inhibitor) or PD-98059 (inhibitor of mitogen-activated protein kinase kinase 1 and 2 [MEK1/2]).
34	15933265	Hypoxia reduced endothelial NOS (eNOS) activity and eNOS phosphorylation at Ser(1177), but increased eNOS protein level.
35	16191353	Compared with the control, the iNOS expression increased and nNOS decreased in the 2 w of diabetes.
36	16191353	The former increased further while the latter nearly disappeared in the 20 w, indicating that the increasing production of NO in the retina of diabetic rats was related with the decrease of nNOS expression and the increase of iNOS expression.
37	16191353	In the diabetic rat models, the retinal damages are closely related with the increase of NO which results from the decrease of nNOS expression and increase of iNOS expression.
38	15967436	Non-diabetic and diabetic (treated with streptozotocin 65 mg kg(-1) body wt, i.p.) rats were injected with the nitric oxide synthase (NOS) inhibitor, L-NAME (50 mg kg(-1) body wt day(-1), x 10 days i.p.) or NOS substrate, L-arginine (200 mg kg(-1) body wt day(-1), x 10 days i.p.).
39	16256381	The effects of glibenclamide on cell viability were partially inhibited after treatment with N(G)-nitro-L-arginine methyl ester (L-NAME), inhibitor more selective for constitutive nitric oxide synthase, and in the presence of D600--a blocker of voltage-gated L-type Ca(2+) channels inhibited Ca(2+) influx into beta cells, whereas aminoguanidine (AG), a preferential inhibitor of inducible NOS, was significantly less effective.
40	16375869	After 12 weeks, immunostaining of wholemount preparations of ileum revealed that diabetes induced a significant shift (P < 0.001, chi-squared test for trend) towards increased neuronal cell body size in nNOS-immunoreactive neurons while HO2-immunoreactive neurons remained unaffected.
41	16508208	In conclusion, the overproduction of nNOS and COX-2 in the kidney of OLETF rats was confirmed, suggesting that the overproduction of nNOS and/or COX-2 does not affect the intrarenal RAS or iNOS production but does affect TGF.
42	16682803	The parameters studied were the mesenteric arteriolar reactivity (intravital microscopy), nitric oxide synthase (NOS) activity (conversion of L-arginine to L-citrulline), eNOS gene expression (RT-PCR), NO production (diaminofluorescein), reactive oxygen species (ROS) generation (intravital fluorescence microscopy) and Cu/Zn superoxide dismutase (SOD) activity (spectrophotometry) and gene expression (RT-PCR).
43	16682803	In contrast to males, however, insulin does not regulate NOS in the microcirculation of diabetic females.
44	17023679	Further, genetic or pharmacological inhibition of either NAD(P)H oxidase-derived O2*- or PKC-zeta or NOS abolished the effects of HOCl on eNOS dimers.
45	17094672	In the present study, increased nitric oxide synthase (NOS) enzyme activity in the aorta and decreased activity in the kidney tissue of streptozotocin-induced diabetic rats has been found in the early phase of the disease.
46	17890296	In addition, while a NO donor enhanced MMP2 and MMP9 activities, a NOS inhibitor reduced these activities in the maternal side of the placenta from control rats.
47	17890296	On the other hand, the NO donor did not modify MMP2 and MMP9 activities, while the NOS inhibitor reduced MMP9 activity in the fetal side of both control and diabetic placentas.
48	17962481	Mice were treated with a NOS inhibitor, N(G)-nitro-L-arginine methyl ester (L-NAME), which shows a preference for constitutive isoforms over iNOS.
49	18430992	Reduction in central insulin decreases neuronal nitric oxide synthase and increases inducible synthase activity.
50	18792879	More studies are required in order to certify the role of NOS inhibitors in insulin resistance and endothelial dysfunction.
51	19485884	Modulation of ENTs and NOS expression and activity in endothelium involves several signalling molecules, including protein kinase C, mitogen-activated protein kinases p42 and p44, calcium and phosphatidyl inositol 3 kinase.
52	19543853	In the 12-week-old GK rat aorta, a significant increase in norepinephrine-induced contraction and a significant decrease in acetylcholine-induced relaxation as well as significant increases in expression levels of muscarinic M(3) receptor and eNOS and a significant decrease in nNOS mRNAs were observed compared to age-matched controls.
53	19717727	In the diabetic group, various insulin-stimulated levels (nitric oxide production, phosphorylation of endothelial NOS at Ser(1177), of Akt at Thr(308), and of PDK-1 at Ser(241)) were significantly increased, whereas, in the HI-diabetic group, these levels were all decreased (vs. control aortas).
54	19734360	We found that basal and isoproterenol-induced VASP phosphorylation is entirely unchanged in cardiomyocytes isolated from either endothelial or neuronal nitric oxide synthase knockout mice.
55	19462315	The effect of AT(1) receptor blockade on NOS expression and activity in humans with early insulin resistance syndrome (INSR) has not been previously investigated.
56	19934009	Hypoglycemia increased hypothalamic constitutive NO synthase (NOS) activity and neuronal NOS (nNOS) but not endothelial NOS (eNOS) phosphorylation in rats.
57	18931023	Ovariectomized Wistar rats consuming a high-sodium diet received one of four treatments (n=7 per group): group 1, placebo pellets; group 2, E(2) (0 x 5 mg/pellet, 21-day release); group 3, NOS inhibitor, N(omega)-nitro-L-arginine-methyl-ester (L-NAME; 40 mg/kg per day for 14 days) plus Ang II (0 x 225 mg/kg per day on days 11-14); group 4, E(2) plus L-NAME/Ang II.
58	20721817	This conference report highlights selected presentations on NR2B subtype-selective NMDA receptor antagonists from Merck; selective neuronal nitric oxide synthase inhibitors from Northwestern University; novel GPR119 agonists, suchas GSK-1292263A (GlaxoSmithKline plc), PSN-821 ((OSI) Prosidion) and MBX-2982 (Metabolex Inc); a small-molecule Bcl inhibitor,navitoclax (Abbott Laboratories); and p53-targeting agents from sanofi-aventis and Ascenta Therapeutics Inc, including AT-219.
59	20854065	We studied the relationship between plasma adiponectin and skeletal muscle nitric oxide synthase (NOS) activity in type 2 diabetic (T2DM) patients.
60	20854065	We determined NOS activity in skeletal muscle of 7 T2DM and 8 nondiabetic control subjects under basal conditions and after a 4-h euglycemic insulin (80 mU/m2 x min) clamp.
61	20854065	Plasma adiponectin was decreased in T2DM (4.5 +/- 0.8 vs. 7.0 +/-1.0 microg/mL, P < 0.02) and correlated with insulin-stimulated NOS activity (r = 0.49, P < 0.05) and with Rd (r = 0.50, P < 0.05).
62	20854065	Decreased plasma adiponectin correlates with impaired insulin-stimulated NOS activity and severity of insulin resistance in T2DM.
63	20377540	Because the release of nitric oxide (NO) and atrial natriuretic peptide (ANP) is a function of the oxytocin receptor (OTR), we examined the effect of PH on gene and protein expression of OTR, NP (A, atrial; B, brain) and receptors (NPRs), nitric oxide synthases (NOS), interleukin (IL)-1?, IL-6 and tumour necrosis factor-? in the hypertrophied RV in a model of PH.
64	20819950	Angiotensin II (Ang II) enhances ROS production by activating NAD(P)H oxidase and uncoupling endothelial nitric oxide synthase (NOS).
65	20939847	In control and diabetic colons, we determined the total ganglion area (hematoxylin-eosin staining), changes in neuronal markers-protein gene product 9.5, peripherin, neuronal nitric oxide synthase (nNOS), neuropeptide Y (NPY), choline acetyl transferase (ChAT) and vasoactive intestinal peptide (by immunostaining), apoptosis (cleaved caspase-3 staining) and reduced glutathione levels.
66	18192221	Since superoxide production was suppressed by NOS inhibitor treatment, eNOS was implicated as a principal superoxide source.
67	20807334	Decreased expression and activity of constitutive NOS (cNOS), including endothelial NOS (eNOS) and neuronal NOS (nNOS), associated with enhanced inducible NOS (iNOS) expression and activity were observed in vehicle-treated diabetic rats.
68	20807334	Although PJ-34 had no effect on eNOS expression, it significantly prevented the decrease in nNOS expression and cNOS activity, and inhibited iNOS expression and activity in diabetic rats.
69	15075180	Increases in plasma renin concentration (PRC) in response to a 3-day infusion of bumetanide (50 mg.kg(-1).day(-1)) or an acute injection of furosemide (50 mg/kg ip) were not markedly altered in nNOS-/- mice.
70	15075180	In the isolated kidney preparation, bumetanide caused similar relative increases in renin secretion in kidneys of wild-type, nNOS-/-, and eNOS-/- mice.
71	15075180	Our data suggest that NO generated by macula densa nNOS does not play a specific mediator role in macula densa-dependent renin secretion.
72	16597606	In the kidney cortex, neuronal nitric oxide synthase (nNOS) is also localized to the MD, and interactions between intrarenal nNOS and COX-2 systems have been proposed.
73	16597606	Cortical nNOS expression also increased after protein loading, and inhibition of nNOS activity completely reversed high protein-induced cortical COX-2 elevation and hyperfiltration.
74	19458119	Analysis of specific NOS isoform activity revealed increased NOS1 and NOS2 activities in mTALs from STZ rats.
75	19458119	Western blot analysis detected no differences in NOS isoform expression, although phosphorylation of pThr(495)-NOS3 was significantly reduced in mTALs from STZ rats.
76	21261471	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.
77	20811799	IFNG-inducible KYN/pteridines inflammation cascade is characterized by up-regulation of nitric oxide synthase (NOS) activity (induced by KYN) and decreased formation of NOS cofactor, BH4, that results in uncoupling of NOS that shifting arginine from NO to superoxide anion production.
78	20363891	Thus in cav-1 deficiency states and HS diet MR blockade is associated with increased BP, enhanced vasoconstriction, and decreased NOS-mediated vascular relaxation and eNOS expression.
79	21620828	P-nNOS and RAMP1 expression were increased in segments from fenofibrate-treated rats, while nNOS expression remained unmodified.
80	21554376	These results suggest that sepiapterin inhibits uncoupling of NOS and improves LV function presumably by increasing iNOS-derived nitric oxide in the diabetic heart.
81	21847584	Pharmacological blockade of nNOS was unable to modify beta cell response to glucose in fa/fa rats and in islets from obese individuals, suggesting an abnormal control of insulin secretion by the enzyme.
82	18465682	We investigate muscle fiber composition, fiber-specific glycolytic and oxidative enzyme capacity and nitric oxide synthase (NOS) expression in skeletal muscle of patients with type 1 diabetes (T1D) compared to individuals with normal glucose tolerance (NGT).
83	21873498	Endothelium removal or pretreatment with N(?)-nitro-l-arginine methyl ester (blocker of NOS) or ODQ abolished Ach-induced relaxation in aorta of WT but had minimal effect in LSD1(+/-).
84	21972802	SalA treatment also reduced the serum malondialdehyde, the content of aortic advanced glycation end products (AGEs), and the nitric oxide synthase (NOS) activity as well as the expression of endothelial NOS protein in the rat aorta.
85	21663490	Nitric oxide synthase (NOS) activity was measured in kidney homogenates.