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 clooxygenase-1 or cyclooxygenase-2 (COX-1 or COX-2).

3 in PGE2 synthesis-namely, cyclooxygenase-2 (COX-2).

4 as well as the expression levels of iNOS and COX-2.

5 ) block PG synthesis by inhibiting COX-1 and COX-2.

6 the activity of cyclooxygenase-1 (COX-1) and COX-2.

7 uman leukocytes activated with LPS to induce COX-2.

8 cyclooxygenase and peroxidase activities of COX-2.

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

10 iosynthesis rather than expression levels of COX-2.

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

12 ndirectly evaluate their effect on COX-1 and COX-2.

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

14 xpression of contraction-associated-protein, COX-2.

15 BCL6 with the concomitant down regulation of COX-2.

16 y determined by EPR, and inhibition of COX-1/COX-2.

17 e model of IUI by upregulating expression of COX-2.

18 This increase was associated with elevated COX-2 (17.9-fold; P = 0.008) and reduced 15-hydroxyprost

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

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

21 through the constriction at the mouth of the COX-2 active site, resulting in displacement and disorde

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

23 the detection of oxygen-dependent changes in COX-2 activity that are independent of protein expressio

24 Directly monitoring COX-2 activity within its native environment poses an ex

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

26 Here we show that acetylated COX-2 also retains COX activity, forming predominantly 1

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

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

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

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

31 in vitro for their ability to inhibit COX-1, COX-2 and 5-LOX.

32 unds confirmed their interaction with NF-kB, COX-2 and 5-LOX.

33 the gene expression of inflammation markers (COX-2 and IL-1beta).

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

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

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

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

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

39 Although Cox-2 and its enzymatic product PGE2 play major roles in

40 oducts of aspirin therapy via acetylation of COX-2 and may contribute to its antiplatelet and other p

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

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

43 Since COX-2 and PGE(2) signaling can impact colon cancer cell

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

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

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

47 Pharmacological abrogation of both the COX-2 and sEH pathways by PTUPB prevented the debris-sti

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

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

50 of pro-inflammatory markers (IL-6, IL-1beta, COX-2 and TNF-alpha) decreased.

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

52 ijacks the proinflammatory cyclooxygenase-2 (COX-2) and 5-lipoxygenase (5-LO) pathways and concurrent

53 pathways, specifically the cyclooxygenase-2 (COX-2) and 5-lipoxygenase (5-LOX) pathways, participate

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

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

56 prostaglandin-endoperoxide synthase 2 (Ptgs2/Cox-2) and prostaglandin E synthase (Ptges/mPGES-1) was

57 ological abrogation of the cyclooxygenase-2 (COX-2) and soluble epoxide hydrolase (sEH) pathways prev

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

59 eviously demonstrated that cyclooxygenase-2 (COX-2) and the prostaglandin E receptor, prostanoid E re

60 ase, lipase, cyclooxygenases-1 and -2 (COX-1/COX-2), and lipoxygenase was determined.

61 the protumorigenic factor cyclooxygenase-2 (COX-2), and that COX-2 inhibition enhances responsivenes

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

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

64 e NMDA receptor, cytosolic phospholipase A2, COX-2, and mPGES-1 increases P-gp protein expression and

65 the indomethacin parent compound against WT COX-2, and the R120A substitution reduced the time depen

66 egulated mRNA expressions of IL-1beta, iNOS, COX-2, and TIMP-1 when compared to vehicle alone in the

67 ant PGE2 receptor mediating the induction of COX-2 at parturition, which can be attenuated by simulta

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

69 n T cell infiltration and the EPHA2/TGF-beta/COX-2 axis is supported by independent clinical data, th

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

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

72 cat but indirectly and incompletely inhibits COX-2 by binding Eallo.

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

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

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

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

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

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

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

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

81 GE(2) in CRC has been shown to occur through COX-2-dependent mechanisms; however, loss of the PGE(2)-

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

83 g platelet COX-1 inhibition while preserving COX-2-dependent vascular thromboresistance.

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

85 on expression of COL1A1, CTGF, alpha-SMA and COX-2 did not differ between TNBS rats and controls.

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

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

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

89 ical models or pharmacological inhibition of COX-2 elicited the transformation of this immunosuppress

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

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

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

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

94 PPBC progression including tumor-associated COX-2 expression and fibroblast-mediated collagen deposi

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

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

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

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

99 This feed-forward induction of COX-2 expression by PGE2 is mediated via its receptors c

100 uction of CREB and STAT3 phosphorylation and COX-2 expression by PGE2 or EP2 stimulation, which was a

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

102 es of these 2 receptors in the regulation of COX-2 expression in amnion fibroblasts remain to be dete

103 rtisol, both well-demonstrated stimulants of COX-2 expression in amnion fibroblasts, increased EP2 bu

104 nsient increases in CREB phosphorylation and COX-2 expression in amnion fibroblasts.

105 +) conditioned medium-dependent induction of Cox-2 expression in fibroblasts.

106 rs play different roles in the regulation of COX-2 expression in human amnion fibroblasts.

107 ort that AML-MSC cocultures greatly increase Cox-2 expression in MSC and PGE2 production in an ARC/IL

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

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

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

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

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

113 ent by increased levels of arachidonic acid, COX-2 expression, and PGE(2) synthesis.

114 urther shown to be associated with decreased Cox-2 expression, followed by a decrease in PGE(2) produ

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

116 asting increases in CREB phosphorylation and COX-2 expression, whereas an EP4 agonist induced only tr

117 calcineurin/NFATc1 activation and decreased COX-2 expression.

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

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

120 regulation of calcineurin/NFAT signaling and COX-2 expression.

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

122 din endoperoxide synthase 2 (PTGS2) (encodes COX-2) expression in a TGF-beta signaling-dependent mann

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

124 inally, we show that co-expression of SEMA7A/COX-2/FN predicts for poor prognosis in breast cancer pa

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

126 yclooxygenase activity of aspirin-acetylated COX-2 forms 15 R-prostaglandins that inhibit platelet ag

127 Deletion of COX-2 from the interstitial/mesangial lineage displayed

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

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

130 fgamma, Litaf, and Ptgs2 (Cyclooxygenases-2 (COX-2) gene) in chicken splenocytes.

131 The overexpression of cyclooxygenase 2 (COX-2) gene, also known as prostaglandin-endoperoxide sy

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

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

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

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

136 some allosterically active FAs positioned in COX-2 in a conformation lacking an interaction with Arg-

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

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

139 ecombinant IL-1alpha is sufficient to induce Cox-2 in fibroblasts and to inhibit transforming growth

140 K cells (MKalpha3(-)), induces expression of Cox-2 in fibroblasts in a time- and dose-dependent manne

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

142 rent liver diseases, but the significance of COX-2 in IRI is a matter of controversy.

143 Overexpressing COX-2 in the EBF1-deficient mice, however, partially res

144 rates-COX-1 in the endoplasmic reticulum and COX-2 in the Golgi apparatus.

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

146 8, CCL3, CCL4, VCAM-1, and cyclooxygenase 2 (COX-2) in cerebral MVECs.

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

148 Acetylated COX-2, in contrast, gains a new catalytic activity and f

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

150 rugs that inhibit cyclooxygenase (COX)-1 and COX-2, increases heart failure risk.

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

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

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

154 t the view of a protective effect of hepatic COX-2 induction and the consequent rise of derived prost

155 study was designed to elucidate the role of COX-2 induction in hepatocytes against liver IRI.

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

157 ic factor cyclooxygenase-2 (COX-2), and that COX-2 inhibition enhances responsiveness of tumors to ru

158 COX-2 inhibition reduces inflammation and pain.

159 his task following seizures were reversed by COX-2 inhibition, which prevented severe postictal hypox

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

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

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

163 es micrometastasis, while treatment with the COX-2 inhibitor celecoxib abrogates prolactin secretion

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

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

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

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

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

169 films that controllably deliver a non-opioid COX-2 inhibitor, etoricoxib, in vivo and in vitro as a m

170 ypoxia was prevented in animals treated by a COX-2 inhibitor, which experimentally separated seizures

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

172 COX-2 inhibitors have been associated with colonic anast

173 hus contribute to the documented efficacy of COX-2 inhibitors in cancer suppression.

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

175 COX-2 inhibitors should preferably be avoided during doc

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

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

178 tory markers (i.e. NF-kappaB, Ikappa-Balpha, COX-2, iNOS), histological damage, disease activity inde

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

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

181 eage cells shared characteristics with Ptgs2/COX-2-insufficient models, and mechanistic investigation

182 0% by common FAs like palmitic acid, whereas COX-2 is allosterically activated 2-fold by palmitic aci

183 COX-2 is also inhibited by COX-2-selective inhibitors.

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

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

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

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

188 Cyclooxygenase-2 (COX-2) is elevated in skin, dorsal root ganglia (DRG), a

189 Cyclooxygenase-2 (COX-2) is involved in different liver diseases, but the

190 lecular dynamic studies and the use of Y385F COX-2, it was observed that the breakage of the pentapep

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

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

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

194 nant or inflammatory tissues containing high COX-2 levels.

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

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

197 The kinetic parameter K(cat)/K(m) for COX-2-mediated metabolism of the peptide (6.3 x 10(5) M(

198 the regulation of inflammatory responses and Cox-2-mediated PGE(2) production in the lung, and the at

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

200 Remarkably, COX-2 metabolized the pentapeptide into small fragments

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

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

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

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

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

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

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

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

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

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

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

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

213 We conclude that acetylation of Ser530 in COX-2 not only triggers formation of 15 R-HETE but also

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

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

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

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

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

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

220 which exhibited appreciable selectivity for COX-2, overcoming acetic acid- and formalin-induced pain

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

222 Cyclooxygenase-2 (COX-2) overexpression is prominent in inflammatory disea

223 In addition to arachidonic acid, COX-2 oxidizes the endocannabinoid 2-arachidonoylglycero

224 = 17) had interaction with cyclooxygenase-2 (COX-2), p65- nuclear factor kappa B, lipoxygenase-1 (LOX

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

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

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

228 5-lipoxygenase (5-LOX) and cyclooxygenase-2 (COX-2) pathways.

229 lly stimulatory relationship between PRR and COX-2/PGE(2) or Wnt/beta-catenin signaling in the renal

230 Inhibition of the COX-2/PGE(2) pathway by chemical inhibitors or knockdown

231 2) completely restored the inhibition of the COX-2/PGE(2) pathway in MDV replication.

232 r results reveal that MDV also activates the COX-2/PGE(2) pathway, which supports MDV replication by

233 ether, our data demonstrate that the FAS and COX-2/PGE(2) pathways play an important role in the repl

234 r findings uncover an important role for the COX-2/PGE(2)/EP4 signaling axis in oxaliplatin resistanc

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

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

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

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

239 d myofibroblasts and fewer cyclooxygenase 2 (Cox-2)-positive dermal cells than controls.

240 increased number of activated microglia and COX-2-positive cells induced by Al exposure.

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

242 Moreover, COX-2 proinflammatory state, as well as Nrf-2 antioxidan

243 Across multiple human cancers, COX-2, prolactin, and prolactin receptor show consistent

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

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

246 rpin RNA reduced MDV titers, suggesting that COX-2 promotes virus replication.

247 nt/beta-catenin signaling, cyclooxygenase-2 (COX-2)/prostaglandin E(2) (PGE(2) ) signaling, and the a

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

249 demonstrate that MDV infection activates the COX-2/prostaglandin E(2) (PGE(2)) pathway, as evident by

250 ine the outcome of drug-induced ICD and pose COX-2/prostaglandin E(2) blockade as a strategy to harne

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

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

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

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

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

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

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

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

259 xhibited higher inhibitory potency against a COX-2 R120A variant than against the WT enzyme.

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

261 Targeting IL6 or COX-2 reduced DNMT3B induction and improved chemo or PD1

262 Thus, inflammation resolution via dual COX-2/sEH inhibition is an approach to prevent carcinoge

263 In animal models, the dual COX-2/sEH inhibitor PTUPB delayed the onset of debris-st

264 Therefore, dual inhibition of COX-2/sEH may be an approach to suppress debris-stimulat

265 at the cardiovascular risk is not limited to COX-2 selective but also extended to non-selective NSAID

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

267 es was strictly associated with the usage of COX-2 selective NSAIDs.

268 acin amides and esters are cyclooxygenase-2 (COX-2)-selective inhibitors, providing a framework for t

269 Both compounds are COX-2-selective inhibitors with IC(50) values of 0.76 an

270 COX-2 is also inhibited by COX-2-selective inhibitors.

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

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

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

274 erated debris up-regulates cyclooxygenase-2 (COX-2), soluble epoxide hydrolase (sEH), ER stress-respo

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

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

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

278 s is induced by tumor cell production of the COX-2 synthetic product prostaglandin E2 (PGE2).

279 ors, providing a framework for the design of COX-2-targeted imaging and cancer chemotherapeutic agent

280 COX-2 was ~3-fold lower than for uninhibited COX-2, the catalytic efficiency for PG formation by the

281 At least in the case of COX-2, the enzyme becomes folded into a stable Eallo/Eca

282 In the present work, hepatocyte-specific COX-2 transgenic mice (hCOX-2-Tg) and their wild-type (W

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

284 constitutively express HPGDS and upregulate COX-2 upon IL-2, IL-25, and IL-33 plus thymic stromal ly

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

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

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

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

289 ry agents through enzyme inhibition, herein, COX-2 was provided with an alternate substrate.

290 the K(m) of arachidonic acid for acetylated COX-2 was ~3-fold lower than for uninhibited COX-2, the

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

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

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

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

295 econditioning-derived increase in endogenous COX-2, which is mainly localized in hepatocytes.

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

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

298 ent observations on the crystal complexes of COX-2 with two indomethacin-dansyl conjugates (compounds

299 tivity-based sensing approach for monitoring COX-2 within live cells with confocal microscopy and flo

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