ライフサイエンスコーパス: NO synthase

1 ors IL-1beta, IL-6, TNF-alpha, and inducible NO synthase.

2 unable to produce IFN-gamma or the inducible NO synthase.

3 monocyte-derived DCs that express inducible NO synthase.

4 ceptor-gamma coactivator-1alpha and neuronal NO Synthase.

5 othelium, in which they activate endothelial NO synthase.

6 the inducible or 'immunological' isoform of NO synthase.

7 y abolished by genetic deletion of inducible NO synthase.

8 retinas of transgenic mice lacking neuronal NO synthase.

9 ain, and uncoupled endothelial nitric oxide (NO) synthase.

10 /-) mouse mutants have reduced expression of NO synthase 1 (NOS1).

11 emonstrate that the low-output nitric oxide (NO) synthase 1 (NOS1 or nNOS) plays a critical role in t

12 Nitric oxide (NO) generated by inducible NO synthase 2 (NOS2) affects cellular iron homeostasis,

13 ases production of nitric oxide (NO) through NO synthase 2 (Nos2) and reactive oxygen species (ROS),

14 LPS induces the expression of NO synthase 2 (nos2) in macrophages.

15 stimulated in the presence of AqH expressed NO synthase 2 (NOS2) protein, nitrite concentrations in

16 (l-Arg), through the enzymes arginase 1 and NO synthase 2 (NOS2), is well documented as a major MDSC

17 Previous studies suggested that inducible NO synthase 2 (NOS2/iNOS) is required for normal IgA Ab

18 M. tuberculosis-infected macrophages induced NO synthase 2 and inhibited arginase 1 gene expression.

19 levels, with increased IL-10 production and NO synthase 2 expression.

20 ressor 1, was required for repression of the NO synthase 2 promoter.

21 and by down-regulating IL-12, TNF-alpha, and NO synthase 2.

22 xide (NO) production by the inducible enzyme NO synthase-2 (NOS2) plays major functions in host defen

23 d IL-12/IL-23p40), but whereas inhibition of NO synthase-2 has marginal effects, IL-12/IL-23p40 neutr

24 and IL-1beta cytokines, as well as inducible NO synthase-2 in bmMPhis, and also impaired the phagocyt

25 (MSP), inhibits the expression of inducible NO synthase, a marker of classically activated macrophag

26 O had reduced insulin-stimulated endothelial NO synthase activation (mean [SEM] wild type 170% [25%],

27 g to inhibition of inducible macrophage-type NO synthase activation in CD11b+ cells.

28 diac VEGF expression and Akt and endothelial NO synthase activation were observed by comparing B-trea

29 es of the lipoprotein, including endothelial NO synthase activation, NO production, and anti-inflamma

30 bility resulting from higher endothelial Akt/NO synthase activation, reduced c-Jun amino terminal kin

31 ation of both the cytochrome c reductase and NO synthase activities of eNOS.

32 NO synthase activity, evidenced in Pf-infected RBCs, ind

33 NO levels were not reduced by inhibition of NO-synthase activity.

34 ere dependent on NO production via inducible NO synthase and activation of protein kinase G.

35 erived suppressor cells expressing inducible NO synthase and arginase 1 are induced.

36 zed, in part, by the expression of inducible NO synthase and arginase I (Arg1) in M1 versus M2 activa

37 f oxidative stress and complement (inducible NO synthase and C3) and downregulation of specific recep

38 L-6, IL-12, IL-23, or enzymes like inducible NO synthase and cyclooxygenase 2, was reduced.

39 nce of B2R-induced activation of endothelial NO synthase and cyclooxygenase.

40 macrophages that highly expressed inducible NO synthase and decreased M2 macrophages that expressed

41 ere delayed in their production of inducible NO synthase and had reduced expression of MHC I and II.

42 p65 NF-kappaB phosphorylation and inducible NO synthase and ICAM-1 expression.

43 A-binding activity, and subsequent inducible NO synthase and ICAM-1 expression.

44 ne (ADMA) limits NO production by inhibiting NO synthase and is increased in adult SM.

45 ribing actual NO production from endothelial NO synthase and its various protein partners.

46 s required for HDL activation of endothelial NO synthase and migration in cultured endothelial cells

47 IN) is an interaction partner of endothelial NO synthase and modulates its subcellular localization,

48 athways; one required calcium stimulation of NO synthase and NO/cGMP/protein kinase G II-dependent ac

49 N-beta and subsequent synthesis of inducible NO synthase and production of NO.

50 Endothelial NO synthase and Ser-1177-phosphorylated endothelial NO s

51 Although the altered function of endothelial NO synthase and the overproduction of reactive oxygen sp

52 armacodynamic profile depends on endothelial NO synthase and xanthine oxidoreductase -catalyzed reduc

53 drobiopterin (BH4), an obligate cofactor for NO synthases and aromatic amino acid hydroxylases.

54 bivolol protects the heart via nitric oxide (NO) synthase and NO-dependent signaling in an in vivo mo

55 ir down-regulatory effect on iNOS (inducible NO synthase) and COX (cyclooxygenase)-2 gene expression

56 express Arg1 (arginase) and Nos2 (inducible NO synthase) and suppress CD4(+) T cell proliferation, i

57 ltiple mechanisms, including PGE2, inducible NO synthase, and arginase.

58 increased expression of TNF-alpha, inducible NO synthase, and CCR2, CD11b(+)/Ly6C(lo) macrophages wer

59 lms revealed increased arginase-1, inducible NO synthase, and IL-10 expression, key mediators of MDSC

60 -33, thymic stromal lymphopoietin, inducible NO synthase, and MUC5ac in lung tissues.

61 le, IL-1beta, IL-6, TNF-alpha, and inducible NO synthase, and this effect is antagonized by coinjecti

62 an essential co-factor for the nitric-oxide (NO) synthases, and in its absence these enzymes produce

63 TRPV-1 channels; (3) 10 mm l-NAME to inhibit NO synthase; and (4) combined 20 mm capsazepine + 10 mm

64 duced by activated iNKT cells, and inducible NO synthase, arginase-1, and IL-10 produced by MDSCs, co

65 ine kinase 3 ligand, c-kit ligand, inducible NO synthase, arginase-1, TNF-alpha, cyclo-oxygenase 2, v

66 fect which was completely restored following NO synthase blockade (6.2 +/- 1.3 mmHg (ml min(-1))(-1))

67 duced changes in TD contractility similar to NO synthase blockade and prevented the relaxation induce

68 o control levels during fetal treatment with NO synthase blockade.

69 efence to hypoxaemia following nitric oxide (NO) synthase blockade.

70 as it was eliminated by pretreatment with an NO synthase blocker, TRIM.

71 Vasodilator responses after inhibition of NO synthase blunted acetylcholine responses in KK and le

72 h the endothelial (eNOS) and neuronal (nNOS) NO synthases, but the differential roles of these NOS is

73 e paralleled by reduced expression of type 2 NO synthase by lesional CD11b(+) cells.

74 (GCH) I increased levels of the endothelial NO synthase cofactor, tetrahydrobiopterin, in an EC-spec

75 ologic inhibitors of inducible nitric oxide (NO) synthase completely eliminated suppressor function.

76 ial GCH overexpression increased endothelial NO synthase coupling and enhanced the proliferative capa

77 dian clock, Bmal1, can influence endothelial NO synthase coupling and reactive oxygen species levels

78 activity, resulting in improved endothelial NO synthase coupling and reduced vascular O(2)(.-).

79 impact of the circadian clock on endothelial NO synthase coupling and vascular reactive oxygen specie

80 ugh tetrahydrobiopterin-mediated endothelial NO synthase coupling.

81 biopterin-mediated endothelial nitric oxide (NO) synthase coupling in patients with coronary artery d

82 models of nitroso-redox imbalance, neuronal NO synthase-deficient (NOS1(-/-)) mice and spontaneously

83 otype due to double neuronal and endothelial NO synthase deletion (dNOS(-/-)) or human sickle hemoglo

84 erodimer, induces IL-12-dependent, inducible NO synthase-dependent, T-reg-sensitive antileishmanial p

85 cytokines by CD11+ cells, and to endothelial NO synthase-derived NO by d7EB cells, leading to inhibit

86 disease immunology, inducible nitric oxide (NO) synthase-derived NO is believed to function primaril

87 Blocking arginase and inducible NO synthase did not restore B lymphopoiesis, indicating

88 te Leishmania major, expression of inducible NO synthase does not confer a cell-intrinsic ability to

89 l)imidazole (TRIM), an inhibitor of neuronal NO synthase, eliminated the light-evoked increase in S-n

90 dependently of IGF and increased endothelial NO synthase (eNOS) activity in arterial segments ex vivo

91 timulated and hypoxia-stimulated endothelial NO synthase (eNOS) activity.

92 in nitric oxide (NO) release and endothelial NO synthase (eNOS) activity.

93 oE3 binding to ApoER2 stimulates endothelial NO synthase (eNOS) and endothelial cell migration, and i

94 oxide (NO) donor administration; endothelial NO synthase (eNOS) and neuronal NO synthase (nNOS) mRNA,

95 modulate inflammation, including endothelial NO synthase (eNOS) and NO bioavailability, are unknown.

96 we quantified the expression of endothelial NO synthase (eNOS) and phosphorylated eNOS.

97 relationship between the loss of endothelial NO synthase (eNOS) and tau phosphorylation in neuronal t

98 dhesion using mice deficient for endothelial NO synthase (eNOS) because their NO metabolite levels ar

99 the role of IL-17 in regulating endothelial NO synthase (eNOS) expression in human vascular endothel

100 the impact of H2S deficiency on endothelial NO synthase (eNOS) function, NO production, and ischemia

101 rtic VEC, but not VIC, expressed endothelial NO synthase (eNOS) in both porcine and human valves, whi

102 Nitric oxide (NO) derived from endothelial NO synthase (eNOS) is an integral mediator of vascular c

103 The activity of endothelial NO synthase (eNOS) is triggered by calmodulin (CaM) bind

104 thelial cells, which express the endothelial NO synthase (eNOS) isoform, constitutively produced the

105 ose tissue of wild-type (WT) and endothelial NO synthase (eNOS) knockout (eNOS(-/-)) mice after a swi

106 Inhibition of endothelial isoform of NO synthase (eNOS) or PKG-I abolishes the H(2)S-stimulat

107 endothelium, insulin stimulates endothelial NO synthase (eNOS) to generate the antiatherosclerotic s

108 n transgenic mice overexpressing endothelial NO synthase (eNOS) was studied.

109 ely, by exposing wild-type (WT), endothelial NO synthase (eNOS)(-/-) and inducible NO synthase (iNOS)

110 1) and a significantly decreased endothelial NO synthase (eNOS), mRNA, and protein levels.

111 ]i transients, activation of the endothelial NO synthase (eNOS), phosphorylation of PECAM-1 and VEGFR

112 xide (NO), which is derived from endothelial NO synthase (eNOS), provides crucial signals for angioge

113 ligand-binding, which activates endothelial NO synthase (eNOS), regulates the prosurvival program of

114 ar whether it can be produced by endothelial NO synthase (eNOS), which is present in RBCs, and whethe

115 y the lowered bioavailability of endothelial NO synthase (eNOS)-derived NO, is a critical inducer of

116 nitric oxide (NO) production by endothelial NO synthase (eNOS).

117 ctly phosphorylates and inhibits endothelial NO synthase (eNOS).

118 phosphorylation of endothelial nitric oxide (NO) synthase (eNOS) at Thr497 (eNOS(pThr497)) by protein

119 177-phosphorylated endothelial nitric oxide (NO) synthase (eNOS) were significantly greater in the Tg

120 Endothelial cell nitric-oxide (NO) synthase (eNOS), the enzyme responsible for synthesi

121 nducible NO synthase protein suggesting that NO synthase enzymatic activity was compromised within th

122 hether protein expression or dimerization of NO synthase enzymes (neuronal [nNOS] and endothelial [eN

123 , NO, produced by the host via the inducible NO synthase, exerts critical antibacterial effects while

124 enous NO synthesis reduces neurite growth in NO-synthase-expressing B2, but has only minor effects on

125 ivated killer DCs was dependent on inducible NO synthase expression and NO production.

126 otype as evidenced by decreases in inducible NO synthase expression concomitant with robust arginase-

127 duced a marked increase in hepatic inducible NO synthase expression in C56BL/6 mice, but not in IRF-1

128 on and required down-regulation of inducible NO synthase expression to exert its protective effects.

129 LPS-stimulated inducible NO synthase expression was 3- to 6-fold higher in the li

130 K-1/2 and p65/RelA (NF-kappaB) and inducible NO synthase expression, suggesting that AnxA1 may be inv

131 sion, higher IL-12 production, and inducible NO synthase expression.

132 D40-induced p38MAPK activation and inducible NO synthase expression.

133 of IFN-gammaR but was independent of induced NO synthase expression.

134 ase inhibition) without changing endothelial NO synthase expression/activation (Ser 1177 phosphorylat

135 of tetrahydropteridines that is unrelated to NO synthase function and not limited to endothelial cell

136 isoform-specific regulation of the inducible NO synthase gene by HIF-1alpha, and the arginase1 gene b

137 a, which is dependent in part on endothelial NO synthase-generated NO.

138 ssion levels of the arginase-1 and inducible NO synthase genes, which characterize MDSCs, were upregu

139 , are regulated through concerted actions of NO synthase/GSNOR and that aberrant denitrosylation impa

140 cal macrophage activation markers, inducible NO synthase, IL-12, and TNF-alpha, as well as the proinf

141 0 also inhibited the expression of inducible NO synthase in activated astroglia.

142 c oxide (NO) and the expression of inducible NO synthase in activated microglia.

143 with concomitant downregulation of inducible NO synthase in APCs in vitro and in vivo.

144 logical mechanisms that regulate endothelial NO synthase in endothelial regeneration remain unclear.

145 mmatory genes (IL-6, IL-1beta) and inducible NO synthase in response to H. pylori.

146 ation and Golgi translocation of endothelial NO synthase in response to the M3R agonist carbachol wer

147 videnced by enhanced expression of inducible NO synthase in the lungs of H99gamma-immunized mice comp

148 factors IFN-gamma, TNF-alpha, and inducible NO synthase in the TME merely 4 d postinfection, before

149 species produced by inducible nitric oxide (NO) synthase in an NRAMP1(r) murine model of acute syste

150 d by the endothelial and neuronal isoform of NO synthase, in delayed preconditioning NO is synthesize

151 locked by NO scavenging, while inhibition of NO synthases increased M-current, suggesting that tonic

152 ocker; and (iii) two inhibitors of inducible NO synthase, indicating that KCa3.1 activity and excessi

153 After NO synthase inhibition (L-NAME), thrombin contracted age

154 aximum) during saline infusion (control) and NO synthase inhibition (NG-monomethyl-L-arginine; L-NMMA

155 rier failure, yet D-Pro-angiotensin-(1-7) or NO synthase inhibition blocked this effect.

156 +/- 3 years) healthy males, with and without NO synthase inhibition via intra-arterial infusion of N(

157 EDD (greater DeltaFBF(ACh) with endothelial NO synthase inhibition) without changing endothelial NO

158 l arteries, K(Ca)2.3 loss is associated with NO synthase inhibition, but is restored if TP receptors

159 was only partially reversed by non-selective NO synthase inhibition.

160 /-) eyes was more sensitive to nitric oxide (NO) synthase inhibition than controls, suggesting that e

161 donor (SNAP), NO substrate (l-arginine), and NO synthase inhibitor (l-NAME) on bladder afferent nerve

162 ut not by an mGluR1 antagonist (LY367385) or NO synthase inhibitor (l-NAME).

163 Using the NO synthase inhibitor and Arabidopsis (Arabidopsis thali

164 C57Bl/6 mice were treated with the NO synthase inhibitor L-N(G)-nitroarginine methyl ester

165 rhythmic effects of CO were abolished by the NO synthase inhibitor l-NAME, and reversed by ranolazine

166 of As(2)O(3)-induced T(reg) depletion by the NO synthase inhibitor N(G)-nitro-l-arginine methyl ester

167 binaltorphimine (norBNI) or the nonselective NO synthase inhibitor Nomega-nitro-L-arginine methyl est

168 and without 2 weeks of treatment with L-NIO (NO synthase inhibitor), sepiapterin (precursor of tetrah

169 th Ringer solution (control), a non-specific NO synthase inhibitor, a non-selective COX inhibitor or

170 d type, but is rescued by the presence of an NO synthase inhibitor.

171 oups after incubation with the nitric oxide (NO) synthase inhibitor N(omega) -nitro-l-arginine methyl

172 as had upregulated inducible and endothelial NO synthase (iNOS and eNOS) and arginase (Arg1 and Arg2)

173 ory and antiviral genes, including inducible NO synthase (iNOS) and cyclooxygenase (COX)-2.

174 us cells expressing the inducible isoform of NO synthase (iNOS) and elevated levels of nitrotyrosine,

175 However, translation of inducible NO synthase (iNOS) and NO generation by H pylori-stimula

176 macrophages suppressed LPS-induced inducible NO synthase (iNOS) and promoted M2 polarization, whereas

177 oteins that may be involved, using inducible NO synthase (iNOS) as a model target.

178 NO produced by inducible NO synthase (iNOS) contributes to ischemic brain injury,

179 s disrupt the Arginase1 (Arg1) and inducible NO synthase (iNOS) dynamic in monocytes/macrophages (mon

180 L-10(+) T lymphocytes that inhibit inducible NO synthase (iNOS) expression and protect intracellular

181 FNs was exerted through inhibiting inducible NO synthase (iNOS) expression in IFNgamma and TNFalpha-s

182 XCL1 in LTB(4), NADPH oxidase, and inducible NO synthase (iNOS) expression in lungs and neutrophils,

183 sphate interfered with LPS-induced inducible NO synthase (iNOS) expression in RAW264.7 macrophages, w

184 The role of inducible NO synthase (iNOS) in allergic airway inflammation remai

185 ed levels of nitric oxide (NO) and inducible NO synthase (iNOS) in cell culture as well as decreased

186 led to downregulated expression of inducible NO synthase (iNOS) in human mesenchymal stem cells in vi

187 Enhanced levels of inducible NO synthase (iNOS) in infected lungs are observed during

188 the removal of NO by the use of an inducible NO synthase (iNOS) inhibitor or iNOS-deficient macrophag

189 Inducible NO synthase (iNOS) is a hallmark of chronic inflammation

190 Inducible NO synthase (iNOS) is involved in the production of NO f

191 Exemplifying this, ablation of inducible NO synthase (iNOS) protected effector-memory T (TEM) cel

192 production of nitric oxide (NO) by inducible NO synthase (iNOS) regulates many aspects of physiology

193 fection by upregulating epithelial inducible NO synthase (iNOS) transcription and NO production.

194 ophage arginase II (Arg2) inhibits inducible NO synthase (iNOS) translation, causes apoptosis, and re

195 Inducible NO synthase (iNOS) was significantly upregulated in the

196 Elevated levels of inducible NO synthase (iNOS) were also observed in the double-laye

197 helial NO synthase (eNOS)(-/-) and inducible NO synthase (iNOS)(-/-) lymphatic vessels to controlled

198 ation and production of TNF-alpha, inducible NO synthase (iNOS), cyclooxygenase-2, IL-1beta, and IL-1

199 this study, we show a key role of inducible NO synthase (iNOS), expressed by classically activated m

200 Inducible NO synthase (iNOS), however, was found to be a more sign

201 O), the end product of the inducible form of NO synthase (iNOS), is an important mediator of a variet

202 or necrosis factor (TNF)-alpha and inducible NO synthase (iNOS), these cells have been referred to as

203 in vitro activates the inducible isoform of NO synthase (iNOS), thus increasing the extracellular co

204 Inducible NO synthase (iNOS)-dependent production of NO is one of

205 cells and enhanced recruitment of inducible NO synthase (iNOS)-producing neutrophils to infected mus

206 for control of M. tuberculosis is inducible NO synthase (iNOS).

207 s regain virulence in mice lacking inducible NO synthase (iNOS).

208 asthma are suggested to be through inducible NO synthase (iNOS).

209 asthma are suggested to be through inducible NO synthase (iNOS).

210 the production of NO derived from inducible NO synthase (iNOS).

211 de treatment induced biogenesis of inducible NO synthase (iNOS)/NO and apoptosis through an NF-kappaB

212 , IFN-gamma-mediated expression of inducible NO synthase (iNOS)/TNF-alpha and NO/TNF-alpha release de

213 s factor-alpha, interleukin-1) and inducible NO synthase (iNOS); the former is dependent on c-Jun and

214 TGF-beta1 regulates inducible nitric oxide (NO) synthase (iNOS) both positively and negatively.

215 basal forebrain (BF) inducible nitric oxide (NO) synthase (iNOS)-dependent NO as a key homeostatic fa

216 creased levels of NO, namely production from NO synthases, intravascular nitrite reduction, release f

217 In these pathways, endothelial NO synthase is activated 1), via calcium release, 2), vi

218 udies have shown that the host nitric oxide (NO) synthase is active during colonization, suggesting t

219 cardiac myocytes contain several isoforms of NO synthases, it is unclear whether these can control re

220 Inducible NO synthase knockout mice exhibited significantly reduce

221 or CD4(+)Foxp3(+) phenotypes from inducible NO synthase knockout mice.

222 s in myoglobin and endothelial and inducible NO synthase knockout models suggest that only myoglobin

223 thmic effects of CO arise from activation of NO synthase, leading to NO-mediated nitrosylation of Na(

224 erebellum and brainstem, increased inducible NO synthase levels in the cerebellum and brainstem, and

225 icidal NO production is reliant on inducible NO synthase-mediated L-arginine metabolism in macrophage

226 tochrome P450 epoxygenases (fluconazole) and NO synthase (N(G)-monomethyl-l-arginine [L-NMMA]).

227 g cardiac myocytes, we identified a neuronal NO synthase (nNOS) as the most relevant source of intrac

228 that nitric oxide (NO) derived from neuronal NO synthase (nNOS) does not contribute to the hyperaemic

229 Nitric oxide (NO) synthesized by neuronal NO synthase (nNOS) has long been implicated in brain pla

230 itter NO, through the activation of neuronal NO synthase (nNOS) in these neurons.

231 Nitric oxide (NO) generated by neuronal NO synthase (nNOS) initiates penile erection, but has no

232 with these observations, studies in neuronal NO synthase (nNOS) knock-out (KO) mice confirmed that PD

233 endothelial NO synthase (eNOS) and neuronal NO synthase (nNOS) mRNA, phospho-eNOS protein, nNOS, and

234 ompanied by loss of stretch-induced neuronal NO synthase (nNOS) S1412 phosphorylation.

235 demonstrate that neurons containing neuronal NO synthase (nNOS), which are morphologically associated

236 ing NO production via activation of neuronal NO synthase (nNOS).

237 Neurons expressing nitric oxide (NO) synthase (nNOS) and thus capable of synthesizing NO

238 AO CB compared to sham, neural nitric oxide (NO) synthase (nNOS) expression and NO levels were suppre

239 NO-level, arginase, and NO synthase (NOS) activities were analyzed in saliva sam

240 caused increased blood flow independently of NO synthase (NOS) activity, suggesting involvement of pr

241 The individual and combined effects of NO synthase (NOS) and cyclooxygenase (COX) inhibition we

242 zolo-[4,3-a]-quinoxalin-1-one, inhibitors of NO synthase (NOS) and soluble guanylyl cyclase, respecti

243 a reduction in vascular NO, in part because NO synthase (NOS) becomes uncoupled when oxidative deple

244 cued by sepiapterin, the stable precursor of NO synthase (NOS) cofactor, tetrahydrobiopterin.

245 ynthesized de novo mainly from L-arginine by NO synthase (NOS) enzymes.

246 uce NO by assessing Fos co-localization with NO synthase (NOS) in recently mated male gerbils.

247 Nitric oxide (NO) produced by NO synthase (NOS) participates in diverse physiological

248 Nitric oxide (NO), produced by NO synthase (NOS), modulates the function of all retinal

249 Epigenetic regulation of NO synthase (NOS), the genes responsible for NO producti

250 consistently account for the biochemistry of NO synthase (NOS)-dependent signalling in many cell syst

251 S-nitrosylases can use NO synthase (NOS)-derived NO to modify selected cysteine

252 O) is generated from arginine and oxygen via NO synthase (NOS).

253 esis by inducible, endothelial, and neuronal NO synthase (NOS).

254 er local intra-brachial combined blockade of NO synthase (NOS; via N(G)-monomethyl-L-arginine: L-NMMA

255 ed protein levels of various isoforms of the NO synthases (NOS) and superoxide dismutase (SOD) enzyme

256 the mechanisms controlling the expression of NO synthases (NOS) in innate and adaptive immune cells,

257 lex electron transfer reactions catalyzed by NO synthases (NOS).

258 -arginine (NOHA, 1) is the best substrate of NO synthases (NOS).

259 ling actions of NO(*) generated by mammalian NO(*) synthase (NOS) result from targeting of the haem m

260 2 and its partner, endothelial nitric oxide (NO) synthase (NOS [eNOS]), mediate bacterial entry.

261 that GLP-1 potently stimulates nitric oxide (NO) synthase (NOS) phosphorylation in endothelial cells,

262 Mice deficient in inducible NO synthase (NOS2(-/-)) exhibited reduced morbidity, red

263 een done in mouse models, in which inducible NO synthase (NOS2) and NO are important components of th

264 Inhibiting inducible NO synthase (NOS2), but not neuronal NOS (NOS1), partial

265 acrophages to induce the type 2 nitic oxide (NO) synthase (NOS2) that produces high levels of NO in t

266 e via a family of dedicated enzymes known as NO synthases (NOSes).

267 While NO synthases (NOSs) are also expressed in cardiac myocyt

268 nthesized in animals by structurally related NO synthases (NOSs), which contain NADPH/FAD- and FMN-bi

269 xide produced by the inducible nitric oxide (NO) synthase of macrophages.

270 ite were reduced in mice lacking endothelial NO synthase or treated with the xanthine oxidoreductase

271 with or without inhibitors of nitric oxide (NO) synthase or K(+) channels that mediate endothelium-d

272 Mice with transgenic endothelial NO synthase overexpression were protected against high-f

273 IL-1beta, IL-6, IL-12, IL-23, and inducible NO synthase owing to enhanced transcriptional activation

274 d competitive metabolism by the arginase and NO synthase pathways.

275 d keratinocyte proliferation via endothelial NO synthase phosphorylation and NO production.

276 ation of endothelial repair, and endothelial NO synthase phosphorylation were abrogated in C451A-ERal

277 signal-regulated kinase 1/2, and endothelial NO synthase phosphorylation, upregulation of cyclin D1,

278 horylation of Akt, endothelial nitric oxide (NO) synthase phosphorylation, and a 60% increase in NO g

279 ocyte-derived innate TNF-alpha and inducible NO synthase-producing DCs dominated the antibacterial re

280 logically produced NO from TNF and inducible NO synthase-producing dendritic cells can contribute to

281 ulature, to regulate coupling of endothelial NO synthase, production of superoxide, and maintenance o

282 echanism for reduced production of inducible NO synthase protein and its NO product.

283 hase and Ser-1177-phosphorylated endothelial NO synthase protein levels were upregulated in renal cor

284 onstrated comparable expression of inducible NO synthase protein suggesting that NO synthase enzymati

285 ng tetrahydrobiopterin-dependent endothelial NO synthase regulation in the endothelium is a rational

286 and blocked by pharmacological inhibitors of NO synthase, soluble guanylate cyclase, or cGMP-dependen

287 cent to macrophages that expressed inducible NO synthase, suggesting a potential protective role for

288 cells expressing MHC class II and inducible NO synthase, suggesting an induction of potent host-prot

289 Expression of inducible NO synthase, TGFbeta, NADPH oxidase, VEGF, and/or argina

290 nfection through several mechanisms, such as NO synthase, the respiratory burst, acidification, and a

291 such as IL-1alpha, IL-1beta, IL-6, inducible NO synthase, TNF, and reactive oxygen intermediate.

292 The F-BAR protein NO synthase traffic inducer (NOSTRIN) is an interaction

293 nsduction via JAK-STAT, escalating inducible NO synthase transcription levels and promoting accumulat

294 riming was critically required for inducible NO synthase upregulation, NO production, Rac activation,

295 tumor was moderately impaired when inducible NO synthase was inhibited and greatly impaired in the ab

296 Expression of inducible NO synthase was significantly upregulated in PGN+poly(I:

297 Additionally, gene expression of NO synthase was strongly diminished in infected IFN-gamm

298 0, matrix metalloproteinase 9, and inducible NO synthase, whereas mRNA and protein levels of IL-10, i

299 e expression of Rap1A, HSPB6, or endothelial NO synthase, which serve as PKA-activatable substrates,

300 Pharmacologic inhibition of NO synthase with L-N(G)-nitroarginine methyl ester (L-NA