ライフサイエンスコーパス: COX

1 COX subunit VIIa polypeptide 2-like protein (COX7AR) is

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

3 COX-2 inhibitors have been associated with colonic anast

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

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

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

7 ory drugs (NSAIDs) inhibit cyclooxygenase-1 (COX-1) and COX-2 enzymes.

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

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

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

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

12 8, CCL3, CCL4, VCAM-1, and cyclooxygenase 2 (COX-2) in cerebral MVECs.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

32 5-lipoxygenase (5-LOX) and cyclooxygenase-2 (COX-2) pathways.

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

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

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

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

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

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

39 (VDAC), and cytochrome c oxidase subunit 4 (COX IV).

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

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

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

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

44 We hypothesized that prostacyclin (a COX-derived product) may directly mediate cutaneous vaso

45 ing that the worms can synthesize PGE2 via a COX-independent pathway.

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

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

48 s or small interfering RNAs (siRNAs) against COX-1 and COX-2, significantly reduced PGE2 production,

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

50 o increase Ecat activity; and (c) allosteric COX inhibitors act by preventing FA binding to Eallo and

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

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

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

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

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

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

57 Decreased expression of SDH-A and COX-I demonstrated that cryptolepine treatment reduced m

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

59 of the cerebral vessels by releasing ATP and COX-1 derivatives.

60 dentifies a functional link between EETs and COX and identifies ct-8,9-E-11-HET as an angiogenic lipi

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

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

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

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

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

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

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

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

69 age induction by NSAIDs via COX-mediated and COX-independent processes.

70 Mass removal and COX-1 inhibition followed a nonlinear correlation and mi

71 However, inhibiting both sEH and COX led to a dramatic decrease in tumor growth, suggesti

72 the sites of action of these pesticides are COX enzymes.

73 adults because ageing is known to attenuate COX-dependent heat loss responses.

74 ed in older adults because ageing attenuates COX-dependent cutaneous vasodilatation and sweating.

75 rodegeneration in animal models, and because COX- and 5-LOX-derived eicosanoids are thought to contri

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

77 lar to those of analgesics intended to block COX enzymes.

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

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

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

81 We further present that GAS inactivates both COX-1 and COX-2 equally.

82 We previously reported that both COX and 5-LO metabolites increase during progression in

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

84 tributed to downstream metabolites formed by COX.

85 tivating platelet-derived lipid generated by COX-1 is presented that can activate or prime human neut

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

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

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

89 as observed in both models due to a combined COX and copper deficiency that resulted in a dilated car

90 e a problem in cytochrome c oxidase complex (COX) assembly.

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

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

93 Constitutive COX-2 expression is therapeutically important because NS

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

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

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

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

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

99 ing to Eallo and/or Ecat thereby controlling COX activities.

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

101 Cyclooxygenase (COX) contributes to the regulation of cutaneous vasodila

102 Cyclooxygenase (COX)-2 has been shown to be involved in regulating basal

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

104 ammatory effects by blocking cyclooxygenase (COX)-2.

105 acid (ARA) is metabolized by cyclooxygenase (COX) and cytochrome P450 to produce proangiogenic metabo

106 this study was to analyze if cyclooxygenase (COX) inhibitors could improve the early posttransplant o

107 mammalian enzymes including cyclooxygenase (COX) and lipoxygenase (LOX) has revealed far lower value

108 harmacological inhibition of cyclooxygenase (COX)-2 abrogates intestinal adenoma development at early

109 the proinflammatory protein cyclooxygenase (COX)-2 and the proinflammatory cytokines TNF-alpha, IL-6

110 ture of T. suis with several cyclooxygenase (COX) inhibitors that inhibit mammalian prostaglandin syn

111 nts and/or inhibitors of the cyclooxygenase (COX) and 5-lipoxygenase (5-LOX) pathways.

112 uced the vitalization of the cyclooxygenase (COX) and prostaglandin E2 (PGE2) pathway.

113 taglandins I2 and E2 through cyclooxygenase (COX)-1 and regulates gene expression by increasing cAMP.

114 We analyzed whether cyclooxygenase (COX)-2 signaling regulates this vasculogenic process.

115 an macrophages compared with cyclooxygenase (COX) inhibitors.

116 eroxide synthase 1 (PTGS1 or cyclooxygenase [COX] 1) and PTGS1 (COX2), other factors are involved.

117 including PGs, produced by cyclooxygenases (COX), and leukotrienes, produced by 5-lipoxygenase (5-LO

118 Cyclooxygenases (COXs) and their final product, prostaglandin E2 (PGE2),

119 thases (PGHSs), also called cyclooxygenases (COXs), convert arachidonic acid (AA) to PGH2.

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

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

122 Prostaglandin (PG) D2 is the dominant COX product of mast cells and is an effector of aspirin-

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

124 C2s are recruited to the nasal mucosa during COX-1 inhibitor-induced reactions in patients with AERD,

125 peripheral blood and the nasal mucosa during COX-1 inhibitor-induced reactions in patients with AERD.

126 gs, which inhibit the cyclooxygenase enzymes COX-1 and COX-2, reduce the risk of developing Alzheimer

127 on model to an in vitro bioassay to evaluate COX-1 inhibition.

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

129 and DeltaG of -19.2 +/- 0.06 kJ mol(-1) for COX-1.

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

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

132 tude of the PKIE measured in macrophages for COX and LOX oxygenation of AA is similar to KIEs determi

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

134 leads to a massive increase in the PKIE for COX oxygenation of AA.

135 c lipid, suggesting a physiological role for COX metabolites of EETs.

136 regioisomers were found to be substrates for COX, based on oxygen consumption and product formation.

137 The likely source of copper used for COX biogenesis is a labile pool found in the mitochondri

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

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

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

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

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

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

144 ppaB translocation inhibitor), or ibuprofen (COX inhibitor) suppressed molecular changes and inhibite

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

146 esent in Cox1p assembly intermediates and in COX.

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

148 ction was preceded by a temporal decrease in COX activity and copper levels in the longer-lived Sco1s

149 ion (hpi), with only a transient increase in COX-1 levels seen at 24 hpi.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

165 eletion consistently resulted in an isolated COX deficiency in these cells, and copper addition to th

166 However, the key COX product(s) responsible for restraining indomethacin-

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

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

169 o indicated the presence of Cox16p in mature COX and in supercomplexes consisting of COX and the bc1

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

171 t COX7AR is a stress-inducible mitochondrial COX subunit that facilitates human breast cancer maligna

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

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

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

175 nounsaturated fatty acids (FAs) that are not COX substrates differentially regulate PGHS-1 versus PGH

176 lypeptide 2-like protein (COX7AR) is a novel COX subunit that was recently found to be involved in mi

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

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

179 several Cox1p assembly intermediates and of COX.

180 e essential for the activity and assembly of COX.

181 ture COX and in supercomplexes consisting of COX and the bc1 complex.

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

183 The enzyme downstream of COX-1 that synthesizes PgE2 (microsomal prostaglandin E

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

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

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

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

188 Expression of COX is assisted by some two dozen ancillary proteins tha

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

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

191 that Cox16p is only present in a fraction of COX.

192 ion channel in macrophages, independently of COX enzymes.

193 NSAID inhibition of COX enzymes, along with luminal aggressors, results in e

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

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

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

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

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

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

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

201 iosynthesis rather than expression levels of COX-2.

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

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

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

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

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

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

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

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

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

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

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

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

214 Targeting of COX-1/2 using nonsteroidal anti-inflammatory drugs (NSAI

215 amples and decreased in blood at the time of COX-1 inhibitor reactions in 12 patients with AERD.

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

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

218 n, with possible implications for the use of COX and LOX pathway inhibitors for lung cancer therapy.

219 However, medical use of COX inhibitors in glioblastoma treatment has been limite

220 ompound was devoid of inhibitory activity on COX isozymes and blocked AKR1C3 mediated production of T

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

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

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

224 InC. albicans-infected cPLA2alpha(-/-)or COX-1(-/-)macrophages, expression ofI l10,Nr4a2, and Ptg

225 nfected but not uninfected cPLA2alpha(-/-)or COX-1(-/-)macrophages.

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

227 ith essential roles in cytochrome c oxidase (COX) assembly and the regulation of copper homeostasis.

228 Cytochrome c oxidase (COX) was initially purified more than 70 years ago.

229 ed for the activity of cytochrome c oxidase (COX), the terminal electron-accepting complex of the mit

230 Cytochrome c oxidase (COX), the terminal enzyme of the mitochondrial respirato

231 embly of mitochondrial cytochrome c oxidase (COX).

232 Mitochondrial cytochrome oxidase (COX) catalyzes the last step in the respiratory pathway.

233 Platelet COX-1 suppression by low-dose aspirin and the kinetics o

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

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

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

237 From data generated by purified COX isoforms and chemical oxidation, we propose that DXA

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

239 of cytochrome c oxidase, which have reduced COX, were protected from CS-induced pulmonary inflammati

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

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

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

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

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

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

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

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

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

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

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

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

252 crease in astrocyte [Ca(2+)]i and stimulates COX-1 activity.

253 calcium signaling, which in turn stimulates COX-1 activity and generates downstream PgE2 production.

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

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

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

257 ors NS-398 and celecoxib or siRNAs targeting COXs, inhibited PSaV replication.

258 77 may represent more effective therapy than COX inhibitors in treating uveitis and ocular diseases w

259 As a result, we now appreciate that COX relies on its redox-active metal centers (heme a and

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

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

262 rm HKs from exogenous 5S-HETE, implying that COX-1 is not involved.

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

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

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

266 anti-inflammatory drugs (NSAIDs) such as the COX-1/2 inhibitor indomethacin and the COX-2-specific in

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

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

269 This study identified a pivotal role for the COX/PGE2 pathway in the regulation of NO production duri

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

271 However, the COX inhibitors used were shown to cause relevant hepatot

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

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

274 the Cox1 subunit with its assembly into the COX enzyme and in a manner that involves the Cox14 and C

275 ms involved in the altered regulation of the COX pathway in patients with AERD.

276 Inhibition of the COX pathway with indomethacin resulted in delayed worm e

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

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

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

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

281 ProPol was associated with activation of the COX/PGE2 pathway.

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

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

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

285 wever, the precise mechanism(s) by which the COX/PGE2 pathway regulates sapovirus replication remains

286 o major products formed from 8,9-EET in this COX pathway were confirmed by chemical synthesis: ct-8,9

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

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

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

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

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

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

293 Using COX inhibitors, a sequential increase of posttransplanta

294 trointestinal damage induction by NSAIDs via COX-mediated and COX-independent processes.

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

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

297 This study explores the fate of EETs with COX, the angiogenic activity of the primary metabolites

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

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

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