ライフサイエンスコーパス: iNOS

1 iNOS expression and NO were associated with reversible n

2 iNOS siRNA and 1400W, a selective iNOS inhibitor, abolis

3 iNOS was measured in central and peripheral lung biopsie

4 iNOS(+) PCs are induced in the course of human H. pylori

5 f action of compound 30 for targeting COX-2, iNOS, and VGSC was investigated by using substance P, l-

6 of catabolic markers including IL-6, COX-2, iNOS, MMP-3, MMP-9, MMP-13 and ADAMTS-4 in IL-1beta-trea

7 macrophages expressed high TNFalpha, IL-23 & iNOS and lower IL-10 & CD163.

8 gh IL-10 & CD163 and lower TNFalpha, IL-23 & iNOS irrespective of macroscopic inflammation.

9 Expression of HIF-1alpha/HIF-2alpha/iNOS and VEGF were reduced, despite an increased hypoxic

10 s for expressions of pro-inflammatory (IL-6, iNOS, ICAM-1) and pro-fibrogenic (Col1, alpha-SMA, TIMP-

11 ver, lung-specific inhibition of iNOS with a iNOS-specific inhibitor, N6-(1-iminoethyl)-L-lysine, dih

12 ormal role for IRF8 expression in activating iNOS expression in MDSCs when they are generated under p

13 h 273-fold and 2822-fold selectivity against iNOS and eNOS, respectively.

14 hibited (IFN-gamma + LPS)-induced TNF-alpha, iNOS, and CXCL10 production by rat aMvarphis.

15 The levels of both bronchial and alveolar iNOS are increased in uncontrolled as compared to contro

16 g its mRNA, and siRNA for iNOS and 1400W, an iNOS blocker, inhibited tadalafil stimulation of CSE exp

17 tumour cell-conditioned media as well as an iNOS activity-dependent increase in EGFR activity in tum

18 -(1-iminoethyl)-L-lysine dihydrochloride, an iNOS inhibitor, significantly enhances M1 macrophage pol

19 by administration of S-methylisothiourea, an iNOS inhibitor.

20 e conclude that ATRA enhances both Arg-1 and iNOS expression in IFN-gamma-treated DCs, resulting in a

21 on and express high levels of Arginase 1 and iNOS.

22 uires NO production, and that HIF-1alpha and iNOS are linked by a positive feedback loop that amplifi

23 , IL-17, GITR, NF-kappaB, COX-2, STAT-3, and iNOS and increased the anti-inflammatory mediators such

24 y increased cardiac NF-kappaB activation and iNOS expression.

25 tent in vitro CB1R antagonist activities and iNOS inhibitory activities.

26 o-inflammatory genes IL-1beta, TNF-alpha and iNOS.

27 ed in CB1 receptor (CB1R) binding assays and iNOS activity assays.

28 by decreasing the levels of MCP1, CXCL9, and iNOS, but increasing the levels of IL-10, LIGHT, CCL1, a

29 tion of nNOS over related isoforms (eNOS and iNOS) is therapeutically desirable.

30 of immunosuppressive factors arginase I and iNOS.

31 dysfunction, perilymphatic inflammation and iNOS expression, and that weight loss via dietary modifi

32 dly decreased perilymphatic inflammation and iNOS expression.

33 es, Wnt7a inhibited IL-1beta-induced MMP and iNOS gene expression.

34 y molecules (p-p65, ICAM-1, Cox-2, MMP3, and iNOS), pro-inflammatory cytokines (TNF-alpha, IL-1beta,

35 ppaBalpha, nuclear translocation of p65, and iNOS expression.

36 ificantly reduced NO and IL-6 production and iNOS expression in activated macrophages.

37 ge macrophages were stimulated in vitro, and iNOS expression and NO production were investigated.

38 ophages and with anti-CD163 for M2, and anti-iNOS for M1 macrophages.

39 ls of suppressive molecules, including Arg1, iNOS, ROS, PDL-1 and P-STAT3, and stronger suppression o

40 nitric oxide synthase 2 (NOS2, also known as iNOS) originating from the glioma cells as a driving sti

41 decreased pro-oxidant enzyme levels, such as iNOS and gp91-phox, thereby decreasing net oxygen radica

42 onses, including cytokine release as well as iNOS activation.

43 se (iNOS) expression and NO release, because iNOS inhibition is neuroprotective.

44 nts showed a significant correlation between iNOS expression levels and expression of the mTOR pathwa

45 Both iNOS and arginase-1 expression were reduced in peritonea

46 that the PKR inhibitor C16 ameliorates both iNOS amplification and disease-induced phenotypic breakd

47 changer regulatory factor 2 (NHERF2) bridges iNOS with CFTR, forming CFTR-NHERF2-iNOS macromolecular

48 t that fine-tunes the expression of IL-12 by iNOS in macrophages, potentially enabling versatile resp

49 in the animal models of fibrosis mediated by iNOS inhibition and CB1R antagonism.

50 A family of proteins S-nitrosylated by iNOS-S100A8/A9 were revealed by proteomic analysis.

51 Although NO produced by iNOS is thought to have direct bactericidal activity aga

52 tiation, an effect that could be reversed by iNOS overexpression.

53 In summary, covalent modification of TSC2 by iNOS-derived NO is associated with impaired TSC2/TSC1 di

54 or 7 days) increased Ly6C(high) and CD11b(+)/iNOS(high) leukocytes and up-regulated levels of eNOS gl

55 entiated into FcgammaRIII(+)PD-L2(-)CD209a(-)iNOS(+) macrophages upon microbial stimulation.

56 ponent-specifically, the balance of CD68(+), iNOS(+) M1- and CD68(+), CD163(+) M2-like macrophages as

57 manner, leading to attenuation of host cell iNOS/NO-mediated anti-microbial capacity.

58 s to recruit RNA PolII, and as a consequence iNOS transcription does not proceed.

59 ctivation of pulmonary Rtp801 and consequent iNOS/NO-induced nitration of lung proteins, that otherwi

60 (iNOS) in cell culture as well as decreased iNOS and reactive oxygen species levels in EAE.

61 (gp91(phox) knockout [KO]), iNOS-deficient (iNOS KO), and C57BL/6 wild-type mice were orally infecte

62 Because we did not detect iNOS(+) PCs in three distinct infectious diseases, this

63 hat deficiency in IRF8 results in diminished iNOS expression in both mature CD11b(+)Gr1(-) and immatu

64 inhibition or silencing of SETD1B diminished iNOS expression in tumor-induced MDSCs.

65 Both central and distal iNOS levels may reflect responsiveness to steroid treatm

66 In tumor-bearing mice, elevated iNOS expression is a hallmark of myeloid-derived suppres

67 NOS inhibitor or knockout of Nos2, encoding iNOS, significantly ameliorates CHS.

68 th iNOS(+/+) BM, suggesting that endothelial iNOS suppresses iNOS expression in leukocytes and vice v

69 inase II expression while actually enhancing iNOS induction in LPS-stimulated cells.

70 hione peroxidase and GR activities and eNOS, iNOS and TNF-alpha levels (p<0.05).

71 mparative model, we found that MCF-7 express iNOS upon cytokine stimulation while MDA-MB-231 do not.

72 Thus, IgA(+) PCs expressing iNOS are described for the first time, to our knowledge,

73 aging were stained immunohistochemically for iNOS.

74 ibited increased protein and mRNA levels for iNOS, arginase I, and arginase II; although the inductio

75 flow cytometric analyses of lymphocytes for iNOS expression and activity.

76 ession by increasing its mRNA, and siRNA for iNOS and 1400W, an iNOS blocker, inhibited tadalafil sti

77 2-D/E motif was necessary and sufficient for iNOS-S100A8/A9-mediated S-nitrosylation.

78 In addition, we found iNOS gene induction in macrophages that are cultured in

79 These results suggest that NO derived from iNOS in activated macrophages suppresses M1 macrophage p

80 NO derived from iNOS mediates nitration of tyrosine residues in IRF5 pro

81 monoacetate salt, and 3) RA-DCs derived from iNOS(-/-) mice exhibited near complete loss of tolerogen

82 transnitrosylase activity, shuttling NO from iNOS to the target protein, whereas S100A8 and S100A9 co

83 Furthermore, iNOS MDSCs largely lost their ability to protect islet a

84 Furthermore, iNOS(+/+) mice transplanted with iNOS(-/-) BM had large

85 RIII(+)PD-L2(+)CD209a(+) moDCs but generated iNOS(+) macrophages more efficiently.

86 ncreased shear stress-induced NO generation, iNOS expression and eNOS expression compared with normal

87 rophage expression of the inflammatory genes iNOS and COX-2 occurs via PI3K- and Akt-dependent transl

88 Further, we identify iNOS as a potential mediator of immune suppression that

89 (18)F-NOS can be used to image iNOS activity in acute lung inflammation in humans and m

90 Imaging iNOS expression may be useful as an inflammation biomark

91 s and may be a useful PET tracer for imaging iNOS expression in inflammatory lung disease.

92 ntly attenuated when MDSCs were deficient in iNOS.

93 There were no differences, however, in iNOS mRNA levels in total BAL cells in uncontrolled as c

94 ifferent MAPK family members are involved in iNOS and arginase expression following LPS stimulation.

95 ses (MAPK) have been shown to participate in iNOS induction following lipopolysaccharide (LPS) stimul

96 nt TLR2 activation of macrophages results in iNOS induction via a novel ROS- and cathepsin-dependent

97 tion of proinflammatory cytokines, including iNOS, TNF-alpha, and IL-6.

98 mall ka, CyrillicB-dependent genes including iNOS, and that iNOS-dependent NO production was required

99 dominated dermal inflammation, and increased iNOS and IL-6 expression compared with control mice.

100 ro stimulation with leukotriene D4 increased iNOS mRNA levels and NO production in cultured BAL macro

101 (low) MDSCs, likely as a result of increased iNOS production.

102 ntiation, innate immune activation increases iNOS generation of NO to S-nitrosylate RING1A, a key mem

103 Further, ANIT-induced iNOS expression, liver fibrosis, and bile duct hyperplas

104 entiated the expression of IFN-gamma-induced iNOS, 2) suppressive function in RA-DCs was blocked by t

105 l inhibited lipopolysaccharide (LPS)-induced iNOS and COX-2 expression in the BV2 mouse microglia cel

106 Sulindac induced iNOS and Hsp70, late-phase IPC markers in the RPE cells.

107 gregate progenitor activity for inflammatory iNOS(+) macrophages or moDCs.

108 brin(ogen)-alphaMbeta2 interaction inhibited iNOS induction in macrophages stimulated with IFNgamma i

109 xidase-deficient (gp91(phox) knockout [KO]), iNOS-deficient (iNOS KO), and C57BL/6 wild-type mice wer

110 In 1 volunteer with low-level iNOS staining in BAL cells, the mean HUs increased by 7%

111 II induction in LPS-stimulated macrophages, iNOS induction by LPS is dependent on p38 activation.

112 gA-producing plasma cells (PCs) as one major iNOS(+) cell population in H. pylori-infected patients a

113 The nitroxidative stress marker iNOS, but not CYP2E1, was significantly elevated only in

114 gh IRF8 was silenced in tumor-induced MDSCs, iNOS expression was significantly elevated in tumor-indu

115 s capable of suppressing macrophage-mediated iNOS production resulting in mitigation of local skin de

116 and expressed the proinflammatory mediators iNOS, MCP-1 and IL-1beta.

117 regulation of oncogenic signaling molecules (iNOS, STAT3/pSTAT3, Src/pSrc).

118 Moreover, iNOS activity and PGE2 content, which were increased by

119 To characterize mucosal iNOS-producing leukocytes, biopsy specimens from H. pylo

120 Furthermore, numbers of mucosal iNOS(+) PCs were elevated in individuals who had cleared

121 nfirmed in mouse model by expressing mutated iNOS that is not targeted by Sal-1 in mice colon.

122 ing macrophage infiltration, or neutralizing iNOS.

123 d not suppress the cytokine-induced NFkappaB-iNOS-NO pathway but attenuated calcium leakage from endo

124 bridges iNOS with CFTR, forming CFTR-NHERF2-iNOS macromolecular complexes that potentiate CFTR chann

125 NOS) uncoupling and increased inducible NOS (iNOS) activity amplify vascular oxidative stress.

126 y augmented the expression of inducible NOS (iNOS) but not endothelial NOS.

127 , endothelial NOS (eNOS), and inducible NOS (iNOS) enzymes.

128 Tadalafil rapidly augmented inducible NOS (iNOS) expression by increasing its mRNA, and siRNA for i

129 ot accompanied by TNFalpha or inducible NOS (iNOS) expression.

130 creased production of TNF and inducible NOS (iNOS) in the lungs.

131 factor kappaB and consequent inducible NOS (iNOS)-mediated overproduction of NO, which in combinatio

132 , endothelial NOS (eNOS), and inducible NOS (iNOS).

133 Activation of iNOS to produce reactive nitrogen species was not necess

134 at an increase of expression and activity of iNOS in cardiomyocytes by VCP is an essential mechanisti

135 is consistent with the known association of iNOS overexpression and poor prognosis in melanoma and o

136 Blockade with a combination of iNOS/NO and VISTA caused additive or synergistic abrogat

137 To examine the relative contribution of iNOS in resident brain cells and peripheral leukocytes i

138 PCS effected downregulation of iNOS protein expression (27%), NO production (20%), ROS

139 xpression was enhanced in the endothelium of iNOS(+/+) mice transplanted with iNOS(-/-) BM and in leu

140 s study was to investigate the expression of iNOS in bronchoalveolar lavage (BAL) cells and tissue fr

141 ced MDSCs, suggesting that the expression of iNOS is regulated by an IRF8-independent mechanism under

142 Expression of iNOS messenger RNA was significantly increased in livers

143 hibited, dose-dependently, the expression of iNOS mRNA and protein, resulting in a decreased NO produ

144 Expression of iNOS was increased in central airway tissue and the alve

145 Expression of iNOS, ARG2, arginine synthetic enzymes, and mitochondria

146 hich showed significantly more expression of iNOS.

147 neutralization increased the expressions of iNOS and phospho-STAT1 in the IMQ-treated skin, but it d

148 s) or siRNA knockdown (in BJ fibroblasts) of iNOS nearly abolished transdifferentiation, an effect th

149 The PKR-mediated hyperinduction of iNOS decreases cell survival in mouse embryonic fibrobla

150 s an inflammatory cell-dependent increase of iNOS, guanosine triphosphate cyclohydrolase I, tetrahydr

151 el protein levels, the essential inducers of iNOS in myeloid cells.

152 o regulates the transcriptional induction of iNOS and COX-2 in response to EMCV infection by a mechan

153 hereby inhibited TLR4-triggered induction of iNOS gene expression.

154 G mouse and by pharmacological inhibition of iNOS in isolated cardiac myocytes, we reveal that an inc

155 etion as well as pharmacologic inhibition of iNOS prevented ATII-induced endothelial dysfunction.

156 Blocking of CCL2 or the inhibition of iNOS significantly increased titer of the virus lacking

157 However, lung-specific inhibition of iNOS with a iNOS-specific inhibitor, N6-(1-iminoethyl)-L

158 mentally using pharmacological inhibitors of iNOS or by compounds that locally deplete skin macrophag

159 the Keap1/Nrf2/ARE pathway and inhibitors of iNOS.

160 anted with iNOS(-/-) BM and in leukocytes of iNOS(-/-) mice with iNOS(+/+) BM, suggesting that endoth

161 However, levels of iNOS in BAL macrophages were not reflected by alveolar N

162 Bronchoalveolar lavage cell mRNA levels of iNOS or iNOS expression in central and alveolar tissue d

163 pendently increased the expression levels of iNOS, CX3CR1, CD206, phospho-STAT1 and phospho-STAT3 pro

164 tidylic acid induced nuclear localization of iNOS, and its binding to, and nitrosylation of, the epig

165 onsistent with the identification of mRNA of iNOS as a target of Sal-1 in both human and mice.

166 delivery significantly reduced the number of iNOS(+) M1 macrophages and increased the expression of a

167 hese cells by upregulating the production of iNOS and arginase, as well as MMP-9 and VEGF.

168 ing the m20.1 and an increased production of iNOS by inflammatory monocytes was observed.

169 A by H-89 largely restored the production of iNOS in CyaA-treated murine macrophages.

170 cells, and to cause significant reduction of iNOS production.

171 Key differences in regulation of iNOS expression impair the translation from mouse models

172 s directly responsible for the repression of iNOS in MDA-MB-231.

173 ibition and siRNA-mediated gene silencing of iNOS suppressed melanoma proliferation and in vivo growt

174 ylori infection, but the cellular sources of iNOS are ill defined.

175 e exposed to acid resulted in suppression of iNOS in alveolar macrophages.

176 infected gp91(phox) KO mice than in those of iNOS KO and C57BL/6 mice.

177 s activated and regulates the translation of iNOS and COX-2 through the mammalian target of rapamycin

178 in a manner that promotes the translation of iNOS and COX-2.

179 Upregulation of iNOS has been observed in human Helicobacter pylori infe

180 chronic melioidosis revealed upregulation of iNOS in tissue, consistent with the expression of IFN-ga

181 bition of B cells was ~50% dependent each on iNOS/NO and the MDSC-expressed negative-checkpoint regul

182 clast numbers (P <0.05) but had no effect on iNOS, IL-1beta, or bax levels.

183 ists of NFkappaB (nuclear factor kappa B) or iNOS activity, NO synthesis and induce endothelial cell

184 oalveolar lavage cell mRNA levels of iNOS or iNOS expression in central and alveolar tissue did not r

185 WT or iNOS MDSCs were cotransplanted with islet allografts und

186 ginine-dependent production of nitric oxide (iNOS(-/-)) were infected with the DeltaArcA mutant, cuta

187 ipid peroxidation (4-HNE), and nitric oxide (iNOS) - were significantly increased in WT mice, but onl

188 ed rats, such as: 1) inducible nitric oxide (iNOS) activity (LPS: 90.18 +/- 36.51 pmol/minute/mg prot

189 ivation, IKBalpha degradation, NFkappaB-p65, iNOS and COX-2 expression were determined by Western blo

190 in obese animals and decreases perilymphatic iNOS and inflammatory cell accumulation.

191 r endotoxin in 6 volunteers who had positive iNOS staining in BAL cells.

192 Surprisingly, postischemic iNOS expression was enhanced in the endothelium of iNOS(

193 A p38 inhibitor completely prevented iNOS expression while it only attenuated arginase II ind

194 the expression of proinflammatory proteins (iNOS, IL-6, TNFalpha, IL-1beta, and CXCL1) while increas

195 , we tested whether (18)F-NOS could quantify iNOS expression from endotoxin-induced lung inflammation

196 Thus, H2S recruits iNOS to generate NO to inhibit high glucose-induced NOX4

197 al inhibition of ROS and cathepsin B reduced iNOS expression.

198 allenged IFNgamma-deficient mice had reduced iNOS induction, bile duct hyperplasia, and liver fibrosi

199 with BAY 11-7082 or BBG also down-regulated iNOS, nitrotyrosine, and poly-ADP-ribosyl polymerase exp

200 inhibition in Akt2(-/-) macrophages restored iNOS expression.

201 iNOS siRNA and 1400W, a selective iNOS inhibitor, abolished the ameliorative effects of Na

202 8 nM), and showed strong inhibition of SPSB2-iNOS interaction in macrophage cell lysates.

203 yclic peptidomimetic inhibitors of the SPSB2-iNOS interaction constrained by organic linkers to impro

204 ens, suggesting that inhibitors of the SPSB2-iNOS interaction have potential as novel anti-infectives

205 g the key sequence motif mediating the SPSB2-iNOS interaction, which binds to the iNOS binding site o

206 We show that PI3K regulates EMCV-stimulated iNOS and COX-2 expression by two independent mechanisms.

207 cal analysis confirmed that Sal-1 suppressed iNOS expression in vitro and in vivo, thus reducing the

208 tion assay revealed that IFNalpha suppressed iNOS transcription through inhibiting the binding of Sta

209 suggesting that endothelial iNOS suppresses iNOS expression in leukocytes and vice versa.

210 ting Salmonella survival through suppressing iNOS induction was confirmed in mouse model by expressin

211 iral genes, including inducible NO synthase (iNOS) and cyclooxygenase (COX)-2.

212 uppressed LPS-induced inducible NO synthase (iNOS) and promoted M2 polarization, whereas miR-146a inh

213 Arginase1 (Arg1) and inducible NO synthase (iNOS) dynamic in monocytes/macrophages (mono/MPhi), whic

214 phocytes that inhibit inducible NO synthase (iNOS) expression and protect intracellular larvae.

215 ed through inhibiting inducible NO synthase (iNOS) expression in IFNgamma and TNFalpha-stimulated MSC

216 ered with LPS-induced inducible NO synthase (iNOS) expression in RAW264.7 macrophages, whereas inhibi

217 nitric oxide (NO) and inducible NO synthase (iNOS) in cell culture as well as decreased iNOS and reac

218 Inducible NO synthase (iNOS), however, was found to be a more significant contr

219 Inducible NO synthase (iNOS)-dependent production of NO is one of the factors l

220 ggested to be through inducible NO synthase (iNOS).

221 of M. tuberculosis is inducible NO synthase (iNOS).

222 ggested to be through inducible NO synthase (iNOS).

223 = 0.02) and inducible nitric oxide synthase (iNOS) (2.4 +/- 0.4-fold; p = 0.01) mRNA in cervical spin

224 h increased inducible nitric oxide synthase (iNOS) activity causes S-nitrosylation of a key UPR regul

225 Inducible nitric oxide synthase (iNOS) activity increases in acute and chronic inflammato

226 , including inducible nitric oxide synthase (iNOS) and arginase (ARG), are typical in asthmatic airwa

227 oduction of inducible nitric oxide synthase (iNOS) and arginase, as well as other suppressive mechani

228 Inducible nitric oxide synthase (iNOS) and B-cell lymphoma-2-associated X (bax) protein e

229 hibitors of inducible nitric oxide synthase (iNOS) and cathepsin B also reversed chlamydial killing.

230 higher NO, inducible nitric oxide synthase (iNOS) and cyclooxygenase (COX-2) inhibitory activity tha

231 TNF-alpha, inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) and reduced cisplatin

232 pression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) was decreased and the

233 pression of inducible nitric oxide synthase (iNOS) and enhanced killing of persistent pathogens, sugg

234 pression of inducible nitric oxide synthase (iNOS) and generation of high levels of nitric oxide.

235 creased the inducible nitric oxide synthase (iNOS) and tumor necrosis factor-alpha (TNF-alpha) levels

236 F1alpha and inducible nitric oxide synthase (iNOS) coordinates DC metabolism and function to limit DC

237 rilymphatic inducible nitric oxide synthase (iNOS) expression and accumulation of T cells and macroph

238 microglial inducible nitric oxide synthase (iNOS) expression and NO release, because iNOS inhibition

239 FV promotes inducible nitric oxide synthase (iNOS) expression in cultured glial cells and generated N

240 it p65; and inducible nitric oxide synthase (iNOS) expression.

241 inducible isoform of nitric oxide synthase (iNOS) from VCP TG mouse and by pharmacological inhibitio

242 Inducible nitric oxide synthase (iNOS) generates nitric oxide (NO) in myeloid cells that

243 ts cellular inducible nitric oxide synthase (iNOS) in a miRNA manner, leading to attenuation of host

244 oxidase and inducible nitric oxide synthase (iNOS) in a murine model of A. actinomycetemcomitans-indu

245 Inducible nitric oxide synthase (iNOS) is overexpressed in melanoma and other cancers, an

246 mmation and inducible nitric oxide synthase (iNOS) levels characterized the M1 response.

247 upregulate inducible nitric oxide synthase (iNOS) mRNA following Toll-like receptor (TLR) agonist tr

248 -gamma, and inducible nitric oxide synthase (iNOS) to vaccine efficacy.

249 as well as inducible nitric oxide synthase (iNOS) were significantly upregulated in the cecal tissue

250 nduction of inducible nitric oxide synthase (iNOS), a gene linked to bile duct hyperplasia and liver

251 Arginase-1, inducible nitric oxide synthase (iNOS), and transforming growth factor-beta and suppresse

252 nitrite and inducible nitric oxide synthase (iNOS), followed by induction of TNFalpha.

253 , including inducible nitric oxide synthase (iNOS), interleukin-6 (IL-6), and IL-1beta.

254 ing enzyme, inducible nitric oxide synthase (iNOS), is overexpressed under the plasma membrane and ge

255 N-gamma and inducible nitric oxide synthase (iNOS), known to mediate T-cell suppression by CD11b(+)Gr

256 o decreased inducible-nitric oxide synthase (iNOS), NO-production, and VEGF.

257 tor (VEGF), inducible nitric oxide synthase (iNOS), nuclear factor-kappa B (NF-kappaB) and intercellu

258 IFN-gamma), inducible nitric oxide synthase (iNOS), or the phagocyte oxidase subunit p47.

259 absence of inducible nitric oxide synthase (iNOS), reactive oxygen species (ROS), and arginase 1 inh

260 amage in an inducible nitric oxide synthase (iNOS)-dependent manner.

261 xpressed in inducible nitric oxide synthase (iNOS)-positive myeloid cells in the substantia nigra in

262 immunity is inducible nitric oxide synthase (iNOS).

263 nduction of inducible nitric oxide synthase (iNOS).

264 y effect on inducible nitric oxide synthase (iNOS).

265 radation of inducible nitric oxide synthase (iNOS).

266 h expressed inducible nitric oxide synthase (iNOS).

267 (COX-2) and inducible nitric oxide synthase (iNOS).

268 d levels of inducible nitric oxide synthase (iNOS).

269 T cells by inducible nitric oxide synthase (iNOS)/nitric oxide (NO), but uniquely, inhibition of B c

270 control the inducible nitric oxide synthase (iNOS, NOS2).

271 pression of inducible nitric oxide synthase (iNOS; r = 0.9986, P < 0.0001).

272 lease and inducible nitric oxide synthetase (iNOS) expression.

273 icB-dependent genes including iNOS, and that iNOS-dependent NO production was required for a feedforw

274 The findings establish that iNOS in both neutrophils and endothelium mediates tissue

275 In this study, we found that iNOS broadly regulates the macrophage transcriptome duri

276 Accordingly, we hypothesized that iNOS-generated nitric oxide (NO) might enhance transdiff

277 erimental model of endotoxin shock show that iNOS deficiency results in more severe inflammation with

278 Here we show that iNOS-deficient mice display enhanced classically activat

279 ther cancers, and previous data suggest that iNOS and nitric oxide (NO) drive survival and proliferat

280 -MB-231 cells, both Oct-1 and Oct-2 bind the iNOS promoter, forming a higher-order complex which fail

281 In MCF-7 cells Oct-1 binds the iNOS promoter, recruits RNA PolII and triggers initiatio

282 essive function in RA-DCs was blocked by the iNOS inhibitor N(G)-monomethyl-l-arginine, monoacetate s

283 epithelial cells significantly increased the iNOS level but not the levels of various inflammatory cy

284 o Arginase-1, a functional antagonist of the iNOS pathway, and was confirmed by immunohistochemistry.

285 st potent cyclic peptidomimetic bound to the iNOS binding site of SPSB2 with low nanomolar affinity (

286 e SPSB2-iNOS interaction, which binds to the iNOS binding site on SPSB2 with a Kd of 4.4 nM, as shown

287 ory pathways compromise UPR function through iNOS-mediated S-nitrosylation of IRE1alpha, which contri

288 veloped a novel tracer for PET that binds to iNOS in vivo, (18)F-NOS.

289 n through inhibiting the binding of Stat1 to iNOS promoter.

290 similar to those of autologous transplanted iNOS(+/+) mice (39 +/- 4 mm(3); n = 14), indicating the

291 The molecular mechanisms underlying iNOS expression and regulation in tumor-induced MDSCs ar

292 Vascular iNOS-dependent NO formation was increased, whereas eNOS-

293 EPR spectroscopy revealed that both vascular iNOS- and eNOS-dependent NO formation were normalized in

294 tiated endothelial cells was associated with iNOS expression and NO elaboration.

295 esis in hyperlipidemic mice, coincident with iNOS-mediated oxidative stress.

296 BM and in leukocytes of iNOS(-/-) mice with iNOS(+/+) BM, suggesting that endothelial iNOS suppresse

297 othelium of iNOS(+/+) mice transplanted with iNOS(-/-) BM and in leukocytes of iNOS(-/-) mice with iN

298 urthermore, iNOS(+/+) mice transplanted with iNOS(-/-) BM had large infarcts (39 +/- 6 mm(3); n = 13)

299 Remarkably, parasites within iNOS(+) cells showed normal morphology and genome integr

300 led comparably with BrdU to parasites within iNOS(-) cells, suggesting that these parasites may be un