ライフサイエンスコーパス: iNOS

1 iNOS expressions increased in P group and L-100 signific

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 proinflammatory marker (TNF-alpha, IL-1beta, iNOS, and IL-6) expression using an MSC-macrophage cocul

6 nflammatory molecules, namely TNF, IL-1beta, iNOS, caspase-1 as well as the activation and morphologi

7 downregulated mRNA expressions of IL-1beta, iNOS, COX-2, and TIMP-1 when compared to vehicle alone i

8 conducted to detect nitric oxide synthase 2 (iNOS) expressing M1 polarized and CD163(+) M2 polarized

9 rkers (i.e. NF-kappaB, Ikappa-Balpha, COX-2, iNOS), histological damage, disease activity index (DAI)

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

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

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

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

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

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

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

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

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

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

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

21 -(1-iminoethyl)-L-lysine dihydrochloride, an iNOS inhibitor, significantly enhances M1 macrophage pol

22 raction of CD68(+) macrophage (P = 0.03) and iNOS(+) (P = 0.007) immunolabeling fractions than cultur

23 und that NADPH oxidase 5 (NOX5), mPGES-1 and iNOS were significantly increased in BE mucosa.

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

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

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

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

28 macrophage, IFN-gamma(+), TNF-alpha(+), and iNOS(+) immunolabeling fractions increased from stage I

29 macrophage, IFN-gamma(+), TNF-alpha(+), and iNOS(+) immunolabeling fractions increases.

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

31 NA expression levels of IL-6, IL-1 beta, and iNOS were significantly increased in the Lig group but w

32 ual-targeting inhibition of hepatic CB1R and iNOS improves diabetic dyslipidemia in mice with diet-in

33 ed on the concomitant inhibition of CB1R and iNOS represents a promising therapeutic strategy for the

34 ally restricted hybrid inhibitor of CB1R and iNOS.

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

36 d by pharmacological microglia depletion and iNOS inhibition.

37 of immunosuppressive factors arginase I and iNOS.

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

39 dly decreased perilymphatic inflammation and iNOS expression.

40 specificities of antral mucosal iNOS(+) and iNOS(-) PC in H. pylori infection, we sequenced rearrang

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

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

43 We conclude that NOX5, mPGES1 and iNOS may be reversible after PPI treatment.

44 lso significantly increased NOX5, mPGES1 and iNOS mRNA expression.

45 ent significantly decreased NOX5, mPGES1 and iNOS.

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

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

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

49 nducible NOS (iNOS) variants (nNOS W409F and iNOS K82A and V346I) and computational methods to study

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

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

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

53 10) but not proinflammatory markers, such as iNOS and TNF.

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

55 ss therapy response within PDAC and blocking iNOS/NO signaling may improve radiotherapy outcomes.

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

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

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

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

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

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

62 IL-12(+)CD38(+) iNOS(+) M (M1M ) located in the bacterial translocation

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

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

65 table in radiotherapy-activated tumor cells, iNOS expression and nitric oxide (NO) secretion were sig

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

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

68 he proinflammatory cytokines IL-6beta, COX2, iNOS, and IL-6 in the in vitro assays at much lower conc

69 he expression of pro-inflammatory cytokines, iNOS, IL6, and IL1beta, compared to unmodified extract d

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

71 in P group and L-100 significantly decreased iNOS levels.

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

73 restrict bacteria within IFN-gamma-dependent iNOS(+) granulomas and prevent dissemination.

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

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

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

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

78 ession of the l-citrulline-generating (i.e., iNOS) and l-citrulline-using (i.e., Ass1) enzymes in key

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

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

81 Two L-arginine catalytic enzymes, iNOS and arginase 1, are well-characterized hallmark mol

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

83 anization postinfection, including extensive iNOS(+) granuloma formation.

84 aging were stained immunohistochemically for iNOS.

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

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

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

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

89 All specific Ig originated from iNOS(+) PC.

90 d the related increase in LDLR resulted from iNOS inhibition via an mTOR complex 1-dependent mechanis

91 ed significantly higher levels of IFN-gamma, iNOS, and TNF-alpha gene transcripts in their livers tha

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

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

94 ses long-term survival and leads to a higher iNOS(+)/CD206(+) TAM ratio compared to irradiation alone

95 n eNOS, and murine and (in some cases) human iNOS.

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

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

98 inase-I (ARG1) expression and an increase in iNOS, MHCII, and CD40 expression.

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

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

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

102 tion of immune effector molecules, including iNOS, by suppressing IFN-gamma-JAK-STAT1 transcription-f

103 ith decreased CD31 and eNOS and an increased iNOS and COX2 expression.

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

105 a from radiotherapy-activated CAFs increased iNOS/NO signaling in tumor cells through NF-kappaB, whic

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

107 We observed increased iNOS expression concurrent with increased prolidase phos

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

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

110 ing results showed that the ligation-induced iNOS expression was also decreased by HES.

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

112 N-gamma plus TNF-alpha restimulation-induced iNOS expression as a model of MSC activation, because IF

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

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

115 in kinase (AMPK), Akt and eNOS, and inhibits iNOS and NADPH oxidase isoform 4 (NOX4), all of which ar

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

117 nitrite/nitrate, IL-6 and TNF-alpha levels, iNOS expression and MDA accumulation in the small intest

118 ) CD8 T cells, and increased M1 macrophages (iNOS(hi), arginase(lo), and IL10(lo)); the use of macrop

119 mice showed accumulation of M1 macrophages (iNOS-positive) in the liver.

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

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

122 , CCL3, CXCL10) and oxidative stress marker (iNOS) in the brain which was reversed through intraperit

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

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

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

126 Ig genes and specificities of antral mucosal iNOS(+) and iNOS(-) PC in H. pylori infection, we sequen

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

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

129 In summary, mucosal iNOS(+) PC producing H. pylori-specific Ig accumulate in

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

131 ing macrophage infiltration, or neutralizing iNOS.

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

133 on of pro-inflammatory cytokines such as NO, iNOS, IL-6, and TNF-alpha in RAW264.7 cells administrate

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

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

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

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

138 with neuronal NOS (nNOS) and inducible NOS (iNOS) variants (nNOS W409F and iNOS K82A and V346I) and

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

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

141 The activity of iNOS and production of NO(-) by macrophages following st

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

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

144 s known to stimulate beta-cell expression of iNOS and production of the free radical nitric oxide.

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

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

147 Expression of iNOS messenger RNA was significantly increased in livers

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

149 The expression of iNOS was examined by immunohistochemistry.

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

151 sue activation of NFkappaB and expression of iNOS, 2 signaling pathways previously demonstrated to be

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

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

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

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

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

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

158 Subsequently, inhibition of iNOS decreased prolidase phosphorylation and reduced coc

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

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

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

162 manner, as well as the expression levels of iNOS and COX-2.

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

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

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

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

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

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

169 Moreover, high number of iNOS(+) M1-like macrophages combined with high number of

170 High number of iNOS(+) M1-like macrophages, both in the center of the t

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

172 nish phagocytosis and decrease production of iNOS and cytokines.

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

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

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

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

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

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

179 Pharmacological or genetic suppression of iNOS, or cardiomyocyte-restricted overexpression of XBP1

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

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

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

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

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

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

186 This protection requires low micromolar, or iNOS-derived, levels of nitric oxide.

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

190 e (inducible nitric oxide synthase-positive [iNOS(+)]) responses were evaluated in the lymph nodes an

191 Because of its potent iNOS suppression, low SREBP induction, and activation of

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

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

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

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

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

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

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

199 the CB1R-inactive stereoisomer that retains iNOS inhibitory activity, and JD-5037, a peripherally re

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

201 patients with VOC included IL-10 signaling, iNOS signaling, IL-6 signaling, and B cell signaling.

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 L-3 and IL-6), and reduced oxidative stress (iNOS and NO) in LPS activated murine macrophages (RAW 26

206 , CXCL10) and indicator of oxidative stress (iNOS).

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

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

211 phages that expressed inducible NO synthase (iNOS) drove peripheral expression of Hmp, allowing regen

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

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

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

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

216 anuloma formation and inducible NO synthase (iNOS) induction, increased dissemination of bacteria thr

217 n, mucosal PC express inducible NO synthase (iNOS), which positively correlates with clearance of exp

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

233 ot loops of inducible nitric oxide synthase (iNOS) and human agouti-related protein (AGRP) were synth

234 pression of inducible nitric oxide synthase (iNOS) and induction of sterol regulatory element-binding

235 activity of inducible nitric oxide synthase (iNOS) and S-nitrosylation of the endonuclease inositol-r

236 tivation of inducible nitric oxide synthase (iNOS) are associated with nonalcoholic steatohepatitis p

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

238 arginine by inducible Nitric Oxide Synthase (iNOS) enzyme.

239 OX-1-2, and inducible nitric oxide synthase (iNOS) enzymes (p < 0.05).

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

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

242 o stimulate inducible nitric oxide synthase (iNOS) expression and production of micromolar levels of

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

244 PGES)-1 and inducible nitric oxide synthase (iNOS) expression.

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

246 duction and inducible nitric oxide synthase (iNOS) gene expression was evident.

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

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

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

250 her ASS1 or inducible nitric oxide synthase (iNOS) in KSHV-transformed cells suppresses growth prolif

251 y increased inducible nitric oxide synthase (iNOS) in the tumor tissues.

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

253 probed the inducible nitric oxide synthase (iNOS) mediated phosphorylation of prolidase since mRNA l

254 , IL-6, and inducible nitric oxide synthase (iNOS) messenger (m)RNAs in the gingiva were determined b

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

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

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

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

259 e levels of inducible nitric oxide synthase (iNOS), bone morphogenetic protein (BMP)-2, matrix metall

260 , IL-6, and inducible nitric oxide synthase (iNOS), but not TNF-alpha.

261 (IL)-1beta, inducible nitric oxide synthase (iNOS), cyclooxygenase (COX)-2, matrix metalloproteinase

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

263 ry markers: Inducible Nitric Oxide Synthase (iNOS), Interleukin 1beta (IL-1beta) and Tumor Necrosis F

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

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

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

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

268 mediated by inducible nitric oxide synthase (iNOS), transforming growth factor beta (TGF-beta), NADPH

269 (GBPs) and inducible nitric oxide synthase (iNOS), which we found to inhibit R. parkeri.

270 vival in an inducible nitric oxide synthase (iNOS)-dependent manner.

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

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

273 h expressed inducible nitric oxide synthase (iNOS).

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

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

276 immunity is inducible nitric oxide synthase (iNOS).

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

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

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

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

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

282 We report that iNOS-driven dysregulation of the IRE1alpha-XBP1 pathway

283 These data show the important role that iNOS/NO signaling plays in the effectiveness of radiothe

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

285 The iNOS expression was enhanced in LPS-trained MSCs, 3 d af

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

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

288 PepNats derived from the iNOS DINNN hot loop and the AGRP RFF hot spot sequence y

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

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

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

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

293 ing SOCS box protein 2 (SPSB2) that binds to iNOS, and selective ligands for AGRP-binding melanocorti

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

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

296 ls, pancreatic tumor growth was delayed when iNOS inhibition was combined with radiotherapy.

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

298 In wild-type mice, most bacteria are within iNOS(+) granulomas, but in T-bet(-/-) mice, most bacteri

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