ライフサイエンスコーパス: NO synthase

1 retinas of transgenic mice lacking neuronal NO synthase.

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

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

4 monocyte-derived DCs that express inducible NO synthase.

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

6 othelium, in which they activate endothelial NO synthase.

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

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

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

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

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

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

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

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

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

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

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

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

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

20 es persisting in Arg1-deficient mice favored NO synthase 2-negative areas and mainly resided in myelo

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

22 We also found that rs2297518 in NOS (NO synthase) 2 (odds ratio, 2.25 [95% CI, 1.21-4.19]; P=

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

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

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

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

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

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

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

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

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

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

33 f S-nitrosylation by inducible nitric oxide (NO) synthase, an important effector of innate immunity,

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

49 pithelial transfer of exosomal nitric oxide (NO) synthase and nitric oxide was measured by using ELIS

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

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

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

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

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

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

56 -33, thymic stromal lymphopoietin, inducible NO synthase, and MUC5ac in lung tissues.

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

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

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

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

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

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

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

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

65 lial growth factor activation of endothelial NO synthase by altering endothelial NO synthase phosphor

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

67 everely immunocompromised- SCID or inducible NO synthase-, CD40-, or IL-12-deficient mice, indicating

68 g cancer progression due to reduction of the NO synthase cofactor, BH(4), under oxidative stress.

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

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

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

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

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

74 ugh tetrahydrobiopterin-mediated endothelial NO synthase coupling.

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

76 HtyOle inhibited the expression of inducible NO synthase, cyclooxygenase-2 and interleukin-1beta.

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

78 Erythrocytes isolated from endothelial NO synthase-deficient mice exhibited a reduced potency t

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

96 ivated protein kinase (MAPK) and endothelial NO synthase (eNOS) in EA.hy926 cells treated with condit

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

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

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

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

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

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

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

104 stically, higher Abeta42 reduced endothelial NO synthase (eNOS), cyclic GMP (cGMP), and protein kinas

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

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

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

108 on in aECs is independent of the endothelial NO synthase (eNOS)-mediated NO pathway.

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

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

111 by (i) increased phosphorylated endothelial NO synthase (eNOS)/eNOS protein expression with adropin

112 d to activation of endothelial nitric oxide (NO) synthase (eNOS) and increased production of NO and r

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

114 177-phosphorylated endothelial nitric oxide (NO) synthase (eNOS) were significantly greater in the Tg

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

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

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

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

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

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

121 285222 treatment enhanced dermis endothelial NO synthase expression and plasma NO levels of diabetic

122 aB, and a concomitant reduction in inducible NO synthase expression and production of TNF and IL-6 co

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

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

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

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

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

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

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

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

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

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

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

134 properties of a heme chaperone for inducible NO synthase, here we investigated whether heme delivery

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

136 0 also inhibited the expression of inducible NO synthase in activated astroglia.

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

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

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

140 o antagonizes the production of NO by type 2 NO synthase in myeloid cells and thereby impedes the con

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

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

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

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

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

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

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

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

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

150 +/- 3 years) healthy males, with and without NO synthase inhibition via intra-arterial infusion of N(

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

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

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

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

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

156 tylcholine, alone and in combination with an NO synthase inhibitor (L-NAME), a superoxide scavenger (

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

158 Using the NO synthase inhibitor and Arabidopsis (Arabidopsis thali

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

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

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

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

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

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

165 ished by pretreatment with the nitric oxide (NO) synthase inhibitor l-N (G)-nitro-l-arginine methyl e

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

167 ZIP and by treatment with the nitric oxide (NO)-synthase inhibitor L-NAME.

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

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

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

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

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

173 tivated macrophages that expressed inducible NO synthase (iNOS) drove peripheral expression of Hmp, a

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

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

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

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

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

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

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

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

182 deficient granuloma formation and inducible NO synthase (iNOS) induction, increased dissemination of

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

199 lori infection, mucosal PC express inducible NO synthase (iNOS), which positively correlates with cle

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

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

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

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

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

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

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

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

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

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

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

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

212 ncrease fetal growth in pregnant endothelial NO synthase knockout (eNOS(-/-) ) mice, which exhibit hy

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

214 one; 100 um) increased SMC death, inhibiting NO synthase (l-NAME, 100 um) or scavenging peroxynitrite

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

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

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

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

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

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

221 els are elevated by the activity of neuronal NO synthase (nNOS) following Ca(2+) entry through extras

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

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

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

225 Neuronal NO synthase (nNOS) is activated by Ca(2+)/calmodulin to

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

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

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

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

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

231 Neuronal NO(*) Synthase (nNOS) was examined for levels and locali

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

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

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

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

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

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

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

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

240 To determine the role of NO synthase (NOS) isoforms in NO generation following ex

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

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

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

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

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

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

247 lium-dependent vasodilation due to uncoupled NO synthase (NOS).

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

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

250 Here, we analyzed NO synthases (NOS) in four different species of placozoa

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

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

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

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

255 2 and its partner, endothelial nitric oxide (NO) synthase (NOS [eNOS]), mediate bacterial entry.

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

257 We provide evidence that a NO-synthase (NOS) is involved in the generation of the e

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

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

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

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

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

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

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

265 Nitric oxide (NO) synthases (NOSs) catalyze the formation of NO from l

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

267 Inhibiting NO synthase or scavenging peroxynitrite reduced SMC deat

268 ne-1-oxyl 3-oxide or following inhibition of NO synthase or the NO receptor soluble guanylate cyclase

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

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

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

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

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

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

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

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

277 othelial NO synthase by altering endothelial NO synthase phosphorylation.

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

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

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

281 Smyd2 and H3K27 trimethylation at inducible NO synthase promoter by Ezh2 to suppress their expressio

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 c or pharmacological inhibition of inducible NO synthase reduces DNA accessibility and suppresses ind

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

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

291 c or pharmacological inhibition of inducible NO synthase together with the Tandem Mass Tag approach,

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

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

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

297 Effects of IgG on endothelial NO synthase were assessed in human aortic endothelial ce

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