ライフサイエンスコーパス: COX-2

1 ne acid amidase (NAAA), or cyclooxygenase 2 (COX-2).

2 iosynthesis rather than expression levels of COX-2.

3 idualization via up-regulation of HB-EGF and COX-2.

4 cal inhibition or shRNA-mediated ablation of COX-2.

5 olin, and thereby inhibits the expression of COX-2.

6 o the activation of ERK and up-regulation of COX-2.

7 electrostatic profile of the side pocket of COX-2.

8 omplex with 5'-UUUAA-3' originating from the COX-2 3'-UTR.

9 Two novel compounds with high affinity to COX-2 (6k = 70 nM, 8e = 60 nM) have a fluoro substituent

10 ral targets including PTGS2, which codes for COX-2, a key enzyme in prostaglandin biosynthesis, and A

11 Inhibition of COX-2 abrogated the induction of CCL2/MCP-1 expression b

12 tes is transient, appears to be dependent on COX-2 activation and does not result in a full productiv

13 se Sertoli cells, evidence of binding at the COX-2 active site, and implications for endocrine disrup

14 nces were in line with the downregulation of COX-2 activity by the inhibitors.

15 In addition, pharmacological inhibition of COX-2 activity diminished levels of COX-2 metabolites du

16 Paracrine macrophage Cox-2 activity drives growth and progression of Apc (Min

17 TDO2 expression was increased by neuronal COX-2 activity, and overexpression of hippocampal TDO2 p

18 that PGE2 receptor EP2 is a key mediator of COX-2 activity-initiated cAMP signaling in Neuro-2a and

19 hisker stimulation involve cyclooxygenase-2 (COX-2) activity and activation of the prostaglandin E2 (

20 or selective inhibitors of cyclooxygenase-2 (COX-2) activity can induce or exacerbate salt-sensitive

21 ndothelial dysfunction: implications for the COX-2/ADMA axis.

22 rugs which directly target cyclooxygenase-2 (COX-2), an enzyme mainly responsible for induction of in

23 s induce the expression of cyclooxygenase 2 (COX-2), an enzyme that catalyzes rate-limiting steps in

24 species (ROS) and inhibit cyclooxygenase-2 (COX-2), an enzyme that is overexpressed in breast CSCs.

25 Specific inhibitors of COX-2 and 5-LOX decreased formation of HKD2 and HKE2 Pla

26 For one of the test compounds, IC50 for COX-2 and 5-LOX was 1 and 1.5 nM, respectively.

27 TE, and LTB4 as the principal metabolites of COX-2 and 5-LOX, respectively.

28 udies of the compounds in the active site of COX-2 and 5-LOX.

29 COX-2 and beta1-integrin were co-expressed in NSCLC tiss

30 e (AMPK) and decreased inflammatory markers (COX-2 and IL-1beta) and apoptotic markers (poly(ADP-ribo

31 ificantly reduced P4-PRWT transrepression of COX-2 and IL-8 Notably, GATAD2B expression was significa

32 eta induction of the NF-kappaB target genes, COX-2 and IL-8 P4-PRWT transrepression occurred at the l

33 equivalent recruitment of PRWT and PRmDBD to COX-2 and IL-8 promoters, suggesting that PR inhibitory

34 nt of NF-kappaB p65 and RNA polymerase II to COX-2 and IL-8 promoters.

35 nhanced recruitment of endogenous GATAD2B to COX-2 and IL-8 promoters.

36 ular consequences mediated by blocking renal COX-2 and increased ADMA.

37 te prostaglandin E2 (PGE2) through inducible COX-2 and microsomal PGE2 synthase 1 (mPGES-1) (1).

38 Levels of IL-1RI positively correlated with COX-2 and mPGES-1 expression in both NM-C and NP-AERD fi

39 educing the capacity of IL-1beta to increase COX-2 and mPGES-1 expression, which results in low PGE2

40 cancer cells independently of its effects on COX-2 and NF-kappaB.

41 The inflammatory mediators, COX-2 and PGE2, played a key role in this effect, as ind

42 esulted in rapid and increased production of COX-2 and PGE2.

43 n arginate can act to simultaneously inhibit COX-2 and preserve the NO pathway.

44 We show that COX-2 and prostaglandin E2 are required for C1P-mediated

45 eased by atorvastatin via S-nitrosylation of COX-2 and reduced by COX-2 inhibitors.

46 studies also uncover a relationship between COX-2 and semaphorin 7a expression and suggest that sema

47 address the mechanisms driving constitutive COX-2 and suggest that by targeting transcription it may

48 cells showed a dramatic increase in S100A4, COX-2 and the alteration of 30 tumor-related genes as me

49 upregulation of the proinflammatory proteins COX-2 and TNF-alpha.

50 n of inflammatory proteins cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS).

51 have shown that the enzyme cyclooxygenase-2 (COX-2) and its prostanoid products, prostaglandin E2 (PG

52 oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) and reduced cisplatin-mediated apoptosis.

53 ir impact on expression of cyclooxygenase 2 (COX-2) and resultant prostaglandin E2 (PGE2) production.

54 Elevated cyclooxygenase-2 (COX-2) and the associated inflammation within the brain

55 easing the levels of NF-kappaB, AKT, ERK1/2, COX-2, and 5-lipoxygenase.

56 IL-1beta-induced IL-1RI, COX-2, and mPGES-1 expression levels were also lower in

57 Alterations in IL-1RI, COX-2, and mPGES-1 expression that were found in NP-AERD

58 COX-1 and COX-2 are found in abundance on the luminal surfaces of

59 roxisomes did not affect the upregulation of COX-2 at the mRNA level, but it reduced the half-life of

60 ar type II (ATII) cell-specific knockdown of COX-2 (AT2CC(-/-)), to examine the role of ATII cell-der

61 upstream of luciferase cDNA to characterize COX-2 basal transcriptional regulation in cortical neuro

62 molecular modeling studies revealed that the COX-2 binding pocket can accommodate most of the pestici

63 ld serve as ligands of the cyclooxygenase-2 (COX-2) binding pocket.

64 uprofen sodium for inhibition of mouse/human COX-2, but only ibuprofen arginate served as a substrate

65 Specific inhibition of COX-2 by celecoxib, promoted apoptosis through activatio

66 ered, and biopsy specimens were analyzed for COX-2 by IHC.

67 sustained upregulation of TNF-alpha-induced COX-2 by IL-17A in ASM cells and show that is not via in

68 COX-2 can be regulated at transcriptional, post-transcri

69 ignificant Golgi residence time during which COX-2 can function catalytically.

70 GE2) has emerged as a principal mediator for COX-2 cascade-driven gliomagenesis.

71 Cyclooxygenase enzymes (COX-1 and COX-2) catalyze the conversion of arachidonic acid to pr

72 Two cyclooxygenases, COX-1 and COX-2, catalyze the initial step in the metabolism of ar

73 Cyclooxygenase-2 (COX-2) catalyzes the oxygenation of arachidonic acid (AA

74 se-2 (PGHS-2), also called cyclooxygenase-2 (COX-2), converts arachidonic acid to PGH2 PGHS-2 is a co

75 Similarly, 92% of COX-2-deficient mice developed anastomotic leakage (P =

76 allosteric site prevented the inhibition of COX-2-dependent 2-AG oxygenation by substrate-selective

77 ammatory mediators IDO, IL-10, and PGE2 in a COX-2-dependent manner.

78 a di-endoperoxide intermediate formed in the COX-2-dependent oxygenation of 5S-hydroxyeicosatetraenoi

79 IL-1beta, COX-2-dependent PGE2 activated the PI3-K/AKT and p38 sig

80 expression of DUSP2 led to overproduction of COX-2-derived prostaglandin E2, which promoted cancer st

81 n (ATX) in pregnant mice leads to HB-EGF and COX-2 down-regulation near embryos and attenuates decidu

82 observed that pharmacological inhibition of COX-2 dramatically increased NO production, causing a re

83 somes that correlated with the regulation of COX-2 during the late phase of LPS activation in macroph

84 life of COX-2 protein, which was restored by COX-2 enzyme inhibitors but not by proteasomal and lysos

85 NSAIDs) inhibit cyclooxygenase-1 (COX-1) and COX-2 enzymes.

86 Targeting the COX-2/EP1/PKC/MAPK/E2F-1/FoxC2/beta1-integrin pathway mi

87 ion of the PGE2-signaling pathway (including COX-2, EP2, EP4) in endometriosis lesions, dorsal root g

88 present that GAS inactivates both COX-1 and COX-2 equally.

89 rafficking between the ER and Golgi retarded COX-2 ERAD.

90 Patients with COX-2 expression >/= 2, performance status of 0 to 2, an

91 Moreover, constitutive COX-2 expression and luciferase activity were detected i

92 ppaB pathway leading to the up-regulation of COX-2 expression and recruitment of inflammatory macroph

93 ed with increased dysplasia, epithelial cell Cox-2 expression and submucosal tumour invasion, as well

94 Conclusion COX-2 expression by IHC failed to select patients who co

95 l survival in patients with moderate to high COX-2 expression by immunohistochemistry (IHC).

96 Constitutive COX-2 expression depended on spontaneous but not evoked

97 ology, chemotherapy regimen, and incremental COX-2 expression did not demonstrate any advantage for C

98 with the Cox-2 inhibitor NS398 could inhibit Cox-2 expression during noise overstimulation; and could

99 ed lipopolysaccharide (LPS)-induced iNOS and COX-2 expression in the BV2 mouse microglia cell line an

100 Instead, COX-2 expression in the kidney but not other regions col

101 in the kidney and other sites, constitutive COX-2 expression is a sterile response, independent of c

102 Although it is known that COX-2 expression is regulated by miRNAs, there are no da

103 Constitutive COX-2 expression is therapeutically important because NS

104 Because adult hepatocytes fail to induce COX-2 expression regardless of the proinflammatory stimu

105 However, the pathways driving constitutive COX-2 expression remain poorly understood.

106 tic activity regulates constitutive neuronal COX-2 expression via Sp1 and CREB protein-dependent tran

107 Transgenic macrophage Cox-2 expression was associated with increased dysplasia

108 lbicans-infected cPLA2alpha(+/+)macrophages, COX-2 expression was blocked by IP, EP2, and EP4 recepto

109 ptopodin and nephrin expression, and reduced COX-2 expression, after injury.

110 ymorphism in humans, associated with reduced COX-2 expression, was associated with higher anastomotic

111 e immunity through induction of IL-1beta and COX-2 expression.

112 ppaB axis abrogated the lipolysis-stimulated COX-2 expression.

113 by honokiol inhibition of cyclooxygenase-2 (COX-2) expression and PGE2 production in the UVB-exposed

114 activity and the increased cyclooxygenase 2 (COX-2) expression as well as the mutagenic effect in bys

115 y investigated the role of cyclooxygenase-2 (COX-2) expression by donor and host cells in muscle-deri

116 heir thousands-fold higher cyclooxygenase-2 (COX-2) expression than immune cells.

117 ent and require cells that express 5-LOX and COX-2 for their biosynthesis.

118 ASM cells and show that is not via increased COX-2 gene expression.

119 otic leakage and a human polymorphism of the COX-2 gene resulting in low COX-2 levels.

120 of the proximal promoter region of the mouse COX-2 gene upstream of luciferase cDNA to characterize C

121 between the groups (hazard ratio, 1.046 for COX-2 >/= 4).

122 COX-2 has a C-terminal STEL sequence, which is an ineffi

123 s of NIHL; and pharmacological inhibition of Cox-2 has considerable therapeutic potential in NIHL.

124 se Tumor overexpression of cyclooxygenase-2 (COX-2) has been associated with worse outcome in non-sma

125 Cyclooxygenase-2 (COX-2) has been implicated in cell invasion in non-small

126 Wildtype, COX-2 knockout and COX-2 heterozygous mice were subjected to a model of col

127 e selective inhibitors with high affinity to COX-2 (IC50 ranging from 20-2500 nM and negligible inhib

128 We observed that sustained COX-2/IKK2 expression caused histological abnormalities

129 ry drugs (NSAIDs) have been shown to inhibit COX-2 in a substrate-selective manner, with the binding

130 , and did not modify the genic expression of COX-2 in animals with EP (P >0.05).

131 ges, we demonstrated that stromal macrophage Cox-2 in colorectal (but not small intestinal) adenomas

132 The contribution of the COX-2 in IH-induced enhanced tumor malignancy was assess

133 ion of the prostaglandin biosynthetic enzyme COX-2 in lymphatics, a response thought to facilitate me

134 es the transcriptional induction of iNOS and COX-2 in response to EMCV infection by a mechanism that

135 periments demonstrate that the activation of COX-2 in response to increased sodium flux is mediated t

136 n CRC progression, and implicated a role for COX-2 in STIM1-mediated CRC metastasis.

137 , a robust ER retention signal, concentrated COX-2 in the ER where it was stable and slowly glycosyla

138 study, we investigated the possible role of Cox-2 in the mechanisms of NIHL and the therapeutic effe

139 sed risk of heart attacks caused by blocking COX-2 in the vasculature and/or kidney, with our recent

140 8, CCL3, CCL4, VCAM-1, and cyclooxygenase 2 (COX-2) in cerebral MVECs.

141 diet induces expression of cyclooxygenase-2 (COX-2) in macrophages, resulting in enhanced levels of p

142 arin-binding (HB-) EGF and cyclooxygenase-2 (COX-2) in the uterine epithelium contributes to decidual

143 s initiated by endothelial cyclooxygenase-2 (COX-2), increased by atorvastatin via S-nitrosylation of

144 nsteroidal anti-inflammatory drug inhibiting COX-2, increased anastomotic leakage compared to vehicle

145 y after 312 of the planned 322 patients with COX-2 index >/= 2 were randomly assigned.

146 n progression-free survival in patients with COX-2 index >/= 4 with hazard ratio of 0.645 with approx

147 COX-2-induced PGE2 production is essential for intestina

148 tive expression elsewhere or to inflammatory COX-2 induction at any site.

149 ti-inflammatory mechanism of action, through COX-2 inhibition by the phenolic acids identified.

150 ession did not demonstrate any advantage for COX-2 inhibition.

151 to identify patients who could benefit from COX-2 inhibition.

152 ct patients who could benefit from selective COX-2 inhibition.

153 ent studies have suggested cyclooxygenase-2 (COX-2) inhibition could represent a novel treatment appr

154 nt with ketamine or ketamine combined with a Cox-2 inhibitor (parecoxib).

155 rs and a newly developed substrate-selective COX-2 inhibitor (SSCI) reduce a variety of stress-induce

156 fen arginate provides, in one preparation, a COX-2 inhibitor and NOS substrate that could act to nega

157 B (CALGB) 30203, we found that the selective COX-2 inhibitor celecoxib in addition to chemotherapy in

158 Importantly, treatment with the COX-2 inhibitor celecoxib significantly inhibited the gr

159 Analogues of the sulfonamide-containing COX-2 inhibitor Celecoxib were prepared and evaluated.

160 her, our observations support the use of the COX-2 inhibitor celecoxib, in combination with paclitaxe

161 tudy, the administration of the preferential COX-2 inhibitor Meloxicam via histidine-tryptophan-ketog

162 we demonstrated that pre-treatment with the Cox-2 inhibitor NS398 could inhibit Cox-2 expression dur

163 ms of NIHL and the therapeutic effect of the Cox-2 inhibitor NS398 on NIHL using a mouse model.

164 ek and were treated daily with the selective COX-2 inhibitor parecoxib (25 mg/kg) or vehicle (control

165 Treatment with ketamine + COX-2 inhibitor prevented these bladder dysfunctions.

166 t utilization of either an ENaC blocker or a COX-2 inhibitor results in a marked reduction in scarrin

167 bset received 200 mg of celecoxib (selective COX-2 inhibitor) before repeating laser Doppler flowmetr

168 mg of indomethacin (non-selective COX-1 and COX-2 inhibitor), and another HS group subset received 2

169 am), preferential (Meloxicam), and selective COX-2 inhibitors (Parecoxib).

170 We show that traditional COX-2 inhibitors and a newly developed substrate-selecti

171 R-Profens are substrate selective COX-2 inhibitors and block the oxygenation of endocannab

172 Selective COX-2 inhibitors are non-steroidal anti-inflammatory dru

173 es for the development of (18)F-radiolabeled COX-2 inhibitors for imaging purposes with positron emis

174 COX-2 inhibitors have been associated with colonic anast

175 Exploratory analyses of studies that used COX-2 inhibitors have demonstrated potentially superior

176 These data emphasize that COX-2 inhibitors should be avoided after colonic surgery

177 ial utility of SSCIs, as well as traditional COX-2 inhibitors, as novel treatment approaches for stre

178 the allosteric effects of FAs and allosteric COX-2 inhibitors, including naproxen and flurbiprofen.

179 via S-nitrosylation of COX-2 and reduced by COX-2 inhibitors.

180 strength of stimulation and is reversible by COX-2 inhibitors.

181 ic oxide synthase (iNOS) and cyclooxygenase (COX-2) inhibitory activity than an equivalent mixture of

182 mode of action of compound 30 for targeting COX-2, iNOS, and VGSC was investigated by using substanc

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

184 lated by miRNAs, there are no data regarding COX-2 involvement in miRNA regulation.

185 e that the modulation of miRNA processing by COX-2 is a key event in insulin signaling in liver and h

186 COX-2 is a sequence homodimer, but the enzyme displays h

187 However, COX-2 is also constitutively expressed, in the absence o

188 We demonstrated that Cox-2 is constitutively expressed in the mouse cochlea,

189 COX-2 is generally considered inducible, but in glutamat

190 ermore, T cells in the FRC environment where Cox-2 is genetic inactivated are more sensitive and rapi

191 involved in physiological processes, whereas COX-2 is induced by a variety of stimuli.

192 In the brain, COX-2 is induced in neurons in response to excitatory sy

193 Our results suggest that Cox-2 is involved in the pathogenesis of NIHL; and pharm

194 COX-2 is localised to stromal cells (predominantly macro

195 Cyclooxygenase-2 (COX-2) is a key enzyme in gastrointestinal homeostasis.

196 Cyclooxygenase-2 (COX-2) is activated in response to ischemia and signific

197 Cyclooxygenase-2 (Cox-2) is an inducible enzyme involved in the synthesis

198 Cyclooxygenase-2 (COX-2) is an inducible enzyme that drives inflammation a

199 uced MDSCs formed significantly less bone in COX-2 knock-out (Cox-2KO) than in COX-2 wild-type (WT) m

200 Wildtype, COX-2 knockout and COX-2 heterozygous mice were subjecte

201 notype because only 46% of PGE2-administered COX-2 knockout mice developed anastomotic leakage (P = 0

202 ymorphism of the COX-2 gene resulting in low COX-2 levels.

203 ancer cells overexpressing cyclooxygenase-2 (COX-2) limited the cleavage of caspase-3 and HuR, which

204 In this way, IL-17A acts to amplify the COX-2-mediated effects of TNF-alpha and greatly enhances

205 ore, we tested the hypothesis that paracrine Cox-2-mediated signalling from macrophages drives adenom

206 beta1-integrin silencing suppressed COX-2-mediated tumour growth and cancer cell invasion in

207 ition of COX-2 activity diminished levels of COX-2 metabolites during lipolytic activation.

208 dicating less blood vessels, was observed in COX-2 mice (2 vessels/mm vs 6 vessels/mm in controls (P

209 tly be reversed by administration of PGE2 to COX-2 mice.

210 aling, namely IL-1 type I receptor (IL-1RI), COX-2, microsomal prostaglandin E synthase 1 (mPGES-1),

211 ion of AA and 2-AG at the allosteric site of COX-2 might result in differential regulation of the oxy

212 of its downstream targets cyclin D1, c-Myc, COX-2, MMP-7, MMP-14, and Claudin-1.

213 ls of inflammatory molecules (p-p65, ICAM-1, Cox-2, MMP3, and iNOS), pro-inflammatory cytokines (TNF-

214 thin the genus Sapovirus, markedly increased COX-2 mRNA and protein levels at 24 and 36 h postinfecti

215 ed that, cellular non-cleavable HuR controls COX-2 mRNA expression and enzymatic activity.

216 However, TNF-induced COX-2 mRNA expression and PGE2 secretion is repressed by

217 reatment with NF-kappaB inhibitor suppressed Cox-2 mRNA expression.

218 tion of this pro-inflammatory enzyme because COX-2 mRNA gene expression is NF-kappaB-dependent, and u

219 ating VEGFR-3, was able to promote increased COX-2 mRNA levels in lymphatic endothelial cells, and ha

220 Inhibition of SGs clearance blocked COX-2 mRNA translation whereas blocking the assembly of

221 sing cellular HuR increased the half-life of COX-2 mRNA, promoted COX-2 protein expression and exhibi

222 as more potent in inducing cyclooxygenase-2 (COX-2) mRNA and protein expression.

223 nd immediate expression of cyclooxygenase-2 (COX-2) mRNA is observed in IL-1beta-stimulated OA chondr

224 st time assembly of SGs and sequestration of COX-2 mRNAs in human OA chondrocytes under pathological

225 A translation, in the delayed translation of COX-2 mRNAs in IL-1beta-stimulated OA chondrocytes.

226 Post-transcriptional regulation of COX-2 mRNAs translation by SGs indicates a role in IL-1b

227 bridization and RNA immunoprecipitation, the COX-2 mRNAs were found sequestered in SGs in IL-1beta-st

228 ndin E2 signaling cascade (phospholipase A2, COX-2, multidrug resistance protein 4, and G-protein-cou

229 AM-8138 restored the activity of COX-2 mutants that exhibited very poor 2-AG oxygenating

230 energic activation induced cyclooxygenase 2 (COX-2), not COX-1, expression in a manner that depended

231 xpression of the inflammatory genes iNOS and COX-2 occurs via PI3K- and Akt-dependent translational c

232 The present study investigated the effect of COX-2 on beta1-integrin expression and cell invasion in

233 To study the effects of COX-2 on colonic surgical wound healing.

234 ed by 5AR inhibition and opposing effects of COX-2 on the tissue-protective action of ERbeta.

235 Inhibiting COX-2 or microsomal prostaglandin E synthase-1 suppresse

236 gineered to express either cyclooxygenase-2 (COX-2) or IkappaB kinase-2 (IKK2), and TP53(+/+) or TP53

237 Using a transgenic C57Bl/6 mouse model of Cox-2 over-expression driven by the chicken lysozyme loc

238 COX-2 overexpression or Prostaglandin E2 (PGE2) treatmen

239 lished hypoxia-induced DUSP2 downregulation, COX-2 overexpression, cancer stemness, tumor growth, and

240 Cyclooxygenase-2 (COX-2) oxygenates arachidonic acid (AA) and its ester an

241 ostaglandin E2, indicating activation of the COX-2 pathway, was a negative prognostic factor.

242 through activation of the cyclooxygenase-2 (COX-2) pathway and the concomitant increases in prostagl

243 decidualization via the canonical HB-EGF and COX-2 pathways.

244 5-lipoxygenase (5-LOX) and cyclooxygenase-2 (COX-2) pathways.

245 via the infection-induced cyclooxygenase-2 (COX-2)/PGE2 axis and inducing its nuclear localization.

246 Cs of human lymphoid organs manifest similar COX-2/PGE2 hyperactivity and T cell suppression.

247 or the first time that IL-17A impacts on the COX-2/PGE2 pathway, molecules known to contribute to dis

248 This hyperactive COX-2/PGE2-induced suppression is evident during antigen

249 However, which EP receptor is the culprit of COX-2/PGE2-mediated neuronal inflammation and degenerati

250 Thus, ATII cell-derived COX-2 plays an important role in regulating basal airway

251 Concurrently, COX-2 positively impacts ERbeta action through its effec

252 prostaglandin E2 (PGE2), the most important COX-2 product in the intestine.

253 -aspartate receptor-dependent enhancement of COX-2 promoter activity.

254 factors CREB and Sp1 to the native neuronal COX-2 promoter was confirmed.

255 ated by mutating the CRE-binding site on the COX-2 promoter.

256 ctivate fibroblast via the cyclooxygenase 2 (COX-2)/prostaglandin E2 (PGE2) pathway.

257 ignaling components in the cyclooxygenase-2 (COX-2)/prostaglandin E2 signaling cascade (phospholipase

258 ase (AERD), reduced expression/production of COX-2/prostaglandin (PG) E2 and diminished expression of

259 duces a robust and sustained upregulation of COX-2 protein and PGE2 secretion from airway smooth musc

260 reased the half-life of COX-2 mRNA, promoted COX-2 protein expression and exhibited enhanced tumor gr

261 No increase in COX-2 protein expression was observed during the persist

262 ophages (BMDMs) significantly down-regulates Cox-2 protein expression, whereas Cox-1 levels are signi

263 In addition, overexpressed COX-2 protein repressed the cleavage of caspase-3 and Hu

264 nd IL-17A acts to increase TNF-alpha-induced COX-2 protein stability as confirmed by cycloheximide ch

265 ersistence of SGs but enhanced expression of COX-2 protein was noted upon clearance of the SGs.

266 munofluorescence staining of SGs markers and COX-2 protein, RNA fluorescence in situ hybridization an

267 mRNA level, but it reduced the half-life of COX-2 protein, which was restored by COX-2 enzyme inhibi

268 te-selective inhibitors that bind rapidly to COX-2, quench tyrosyl radicals, and reduce higher oxidat

269 inhibit the cyclooxygenase enzymes COX-1 and COX-2, reduce the risk of developing Alzheimer's disease

270 provide insight into the cellular source of COX-2 related to these lung phenotypes.

271 tructures of each drug in complex with human COX-2 revealed that the inhibitor binds within the cyclo

272 was largely blocked by TG4-155, TG6-10-1 or COX-2 selective inhibitor celecoxib, but not by GW627368

273 These results suggest a crucial role for the COX-2 signaling pathway in the IH-exacerbated malignant

274 studies confirmed that paracrine macrophage Cox-2 signalling drives catenin-related transcription in

275 interfering RNAs (siRNAs) against COX-1 and COX-2, significantly reduced PGE2 production, as well as

276 malignancy was assessed using celecoxib as a COX-2 specific inhibitor in a murine model of OSA bearin

277 s the COX-1/2 inhibitor indomethacin and the COX-2-specific inhibitors NS-398 and celecoxib or siRNAs

278 but not by NSC-398, a specific inhibitor of COX-2, suggesting IDO as a mediator.

279 findings demonstrate that the inhibition of COX-2 suppresses vasculogenesis in endometriotic lesions

280 ng fibrosis; however, the cellular source of COX-2 that underlies these effects is unknown.

281 ed and regulates the translation of iNOS and COX-2 through the mammalian target of rapamycin complex

282 Cyclooxygenase-2 (COX-2) triggers pro-inflammatory processes that can aggr

283 This study suggested that COX-2 upregulates beta1-integrin expression and cell inv

284 duced macrophages, which blocked LPS-induced COX-2 upregulation in naive RAW264.7 cells and human pri

285 Instead, TNF-alpha-induced COX-2 upregulation is subject to regulation by the prote

286 ophage inflammatory protein 1beta secretion, COX-2 upregulation, and PGD2 generation in mast cells.

287 defined the biosynthetic roles of 5-LOX and COX-2, using inhibitors and incubations with exogenous s

288 f the novel inhibitors in the active side of COX-2 was calculated in silico using the protein-ligand

289 Specific knockdown of COX-2 was confirmed by real-time RT-PCR and Western blot

290 Herein, we demonstrated that COX-2 was induced and showed nuclear translocation in tw

291 oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) was decreased and the nuclear translocation of NF

292 EET substrate preference for both COX-1 and COX-2 were estimated as 8,9-EET > 5,6-EET > 11,12-EET, w

293 ion levels of the anti-inflammatory cytokine COX-2 were significantly inhibited by fractions P2-P5, w

294 The interactions of 30 with COX-2 were supported by isothermal calorimetry experimen

295 n driven by the chicken lysozyme locus (cLys-Cox-2), which directs integration site-independent, copy

296 asteride also induces cyclooxygenase type 2 (COX-2), which functions in a negative feedback loop in T

297 ppressed IL-1beta, IL-6, IL-8, TNF-alpha and COX-2, while PPH reduced LPS-induced IL-6 and TNF-alpha

298 ss bone in COX-2 knock-out (Cox-2KO) than in COX-2 wild-type (WT) mice.

299 Me) (30) reduced prostaglandin production of COX-2 with an IC50 of 60 nM relative to 6000 nM for COX-

300 but not small intestinal) adenomas from cLys-Cox-2 x Apc (Min/+) mice was associated with significant