ライフサイエンスコーパス: COX

1 COX activity levels and COX-dependent respiration were l

2 COX inhibitors are also frequent cofactors in anaphylaxi

3 COX-2 inhibition reduces inflammation and pain.

4 COX-2 inhibitors have been associated with colonic anast

5 COX-2 inhibitors should preferably be avoided during doc

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

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

8 rived from the activity of cyclooxygenase-1 (COX-1) and COX-2.

9 e the duration of platelet cyclooxygenase-1 (COX-1) inhibition.

10 ve eicosanoid generated by cyclooxygenase-1 (COX-1) turnover during platelet activation that can stim

11 Cyclooxygenase-1 (COX-1), a biomarker for neuroinflammation, is implicated

12 xpected on-target actions, we found that: 1) COX or 15-LOX-1 inhibitors elevate inflammatory leukotri

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

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

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

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

17 2, commonly called cyclooxygenases-1 and -2 (COX-1 and -2), catalyze the committed step in prostaglan

18 a-amylase, lipase, cyclooxygenases-1 and -2 (COX-1/COX-2), and lipoxygenase was determined.

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

20 either cyclooxygenase-1 or cyclooxygenase-2 (COX-1 or COX-2).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

41 Administration of a COX-1-selective antagonist to mice completely prevented

42 oroethoxy)-1H-1,2,4-triazole ((11)C-PS13), a COX-1 PET neuroimaging radiopharmaceutical, in OvCa xeno

43 was available for ILC2 activation and that a COX product(s) inhibited IL-33 release.

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

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

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

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

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

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

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

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

52 Additionally, COX-1 is allosterically inhibited up to 50% by common FA

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

54 s in PGC-1alpha expression (0.61+/-0.07) and COX IV activity (0.70+/-0.10) relative to normal; P=0.01

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

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

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

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

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

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

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

62 ain and the oxidative markers PGC1-alpha and COX IV, were not altered in the dKO mice compared with w

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

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

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

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

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

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

69 COX activity levels and COX-dependent respiration were lower in amiCOX19 plants

70 lammatory pathways, namely, 12-LO, 5-LO, and COX.

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

72 ctron transport chain complexes) markers and COX IV (cytochrome C oxidase) activity in myocardium fro

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

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

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

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

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

78 per lobes and had lower COX2/COX4-ratios and COX/SDH-ratios (all p < 0.001).

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

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

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

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

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

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

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

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

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

88 acid to prostaglandin endoperoxide H(2) Both COX isoforms are sequence homodimers that function as co

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

90 through the irreversible inhibition of both COX isoforms.

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

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

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

94 urther design and optimization of conjugated COX reagents for imaging of malignant or inflammatory ti

95 In contrast, COX-1 was dispensable for FcepsilonRI-driven CysLT produ

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

97 the enzyme group, including cyclooxygenase (COX), lipoxygenase (LOX), or cytochrome P450 (CYP).

98 lammatory drugs that inhibit cyclooxygenase (COX)-1 and COX-2, increases heart failure risk.

99 itric oxide synthase (iNOS), cyclooxygenase (COX)-2, matrix metalloproteinase (MMP)-9 and tissue inhi

100 The effects of cyclooxygenase (COX) inhibition and PG assays indicate that PGs contribu

101 bosis by inhibiting platelet cyclooxygenase (COX)-1 activity and the production of thromboxane (Tx)A(

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

103 p to a serine residue in the cyclooxygenase (COX) active site.

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

105 The cyclooxygenase (COX) metabolic pathway regulates immune responses and in

106 5-lipoxygenase (5-LO) or the cyclooxygenase (COX) pathways, very few compounds selectively inhibiting

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

108 d leukotrienes by targeting cyclooxygenases (COXs), 5-lipoxygenase (LOX), or the 5-LOX-activating pro

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

110 ytochrome c-oxidase/succinate dehydrogenase [COX/SDH]-ratio) was depressed in ILD (median = 0.10,) co

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

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

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

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

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

116 001), as was the expression of mtDNA-encoded COX-subunit-2 protein normalized for the nucleus-encoded

117 2 protein normalized for the nucleus-encoded COX-subunit-4 (COX2/COX4-ratio; ILD-median = 0.6; contro

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

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

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

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

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

123 COX19 function is particularly important for COX assembly under iron deficiency.

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

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

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

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

128 ated blood from platelet-COX-1-ko and global-COX-1-ko mice produced similar eicosanoid profiles in vi

129 HETE was absent in both platelet- and global-COX-1-ko mice.

130 d a distinctly different profile from global-COX-1-ko or aspirin-treated control mice, notably signif

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

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

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

134 t promotes tumor cell seeding and identifies COX-1/TXA2 signaling as a target for the prevention of m

135 an artificial miRNA did not cause changes in COX activity levels or respiration in plants grown under

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

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

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

139 -genotype ECs, FSS elicited a marked rise in COX (cyclooxygenase)-2 and L-PGDS (lipocalin-type prosta

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

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

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

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

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

145 d naproxen) block PG synthesis by inhibiting COX-1 and COX-2.

146 e, naproxen directly and completely inhibits COX-1 by binding Ecat but indirectly and incompletely in

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

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

149 MC-intrinsic COX-1 amplifies IL-33-induced activation in the setting

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

151 -2-picrylhydrazyl), and inhibition of 5-LOX, COX-1-2, and inducible nitric oxide synthase (iNOS) enzy

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

153 uscle biopsies, cocoa improved mitochondrial COX (cytochrome c oxidase) activity (P=0.013), increased

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

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

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

157 Nevertheless, COX inhibition attenuated peak hyperaemia by ~30% in WE,

158 patients with AERD react to all nonselective COX inhibitors regardless of their chemical structure, t

159 c desensitization to aspirin by nonselective COX inhibitors in patients with AERD.

160 n response to administration of nonselective COX inhibitors is a cardinal feature of aspirin-exacerba

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

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

163 cyclooxygenase and peroxidase activities of COX-2.

164 several Cox1p assembly intermediates and of COX.

165 e essential for the activity and assembly of COX.

166 However, the angiogenic capacity of COX-deficient ECs is severely compromised under energeti

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

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

169 details about the biological consequences of COX allosterism and how ligand binding to Eallo modulate

170 es coexist, which differ in their content of COX subunits and COX7A2L/HIGD2A assembly factors.

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

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

173 substitution reduced the time dependence of COX inhibition.

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

175 PG) E synthase (S)-1, a target downstream of COX, regulates myocardial (M) ischemia/reperfusion (I/R)

176 ogenous PGH(2), implying that the effects of COX-1 required its catalytic function.

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

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

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

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

181 Unexpectedly, the constitutive function of COX-1 is required for IL-33 to activate group IVa cytoso

182 (11)C-PS13 shows promise for PET imaging of COX-1 in OvCa, and rapid translation for clinical cancer

183 m contribute to anaphylaxis independently of COX inhibitor intake is unclear.

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

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

186 s, and respiratory reactions on ingestion of COX-1 inhibitors.

187 Inhibition of COX-1 by low-dose aspirin prevents thrombosis.

188 eicosanoid profiles linked to inhibition of COX-1 in platelets and in the remainder of the cardiovas

189 Inhibition of COX-1 prevented IL-33-induced phosphorylation of extrace

190 educed lung metastasis through inhibition of COX-1 while the cancer cells remained intravascular and

191 ctivity determined by EPR, and inhibition of COX-1/COX-2.

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

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

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

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

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

197 rotein, which mediates membrane insertion of COX proteins, was also localized to cristae and reticula

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

199 xane A2 (TXA2) was the prostanoid product of COX-1 responsible for this antimetastatic effect.

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

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

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

203 or the first time data regarding the role of COX-1 inhibition in NIUA.

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

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

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

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

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

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

210 Investigating the mysteries of COXs anchored my scientific career.

211 of MC function and an aberrant dependency on COX-1-derived prostaglandin E(2) to maintain a tenuous h

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

213 vitro to indirectly evaluate their effect on COX-1 and COX-2.

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

215 FA tone of the milieu in which each operates-COX-1 in the endoplasmic reticulum and COX-2 in the Golg

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

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

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

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

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

221 between EGFL9 and the cytochrome c oxidase (COX) assembly factor COA3.

222 iated with the gain of cytochrome c oxidase (COX) function, and the COX subunit, COX4, was localized

223 s in the biogenesis of cytochrome c oxidase (COX) in yeast and humans.

224 an assembly factor of cytochrome c oxidase (COX) specifically in mouse ECs, providing a model for va

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

226 from bc(1) complex to cytochrome c oxidase (COX), and as a trigger of type II apoptosis when release

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

228 , NDU) and complex IV (cytochrome-c-oxidase, COX) of the mitochondrial electron transport chain have

229 LnCeVar-Survival performs COX regression analyses and produces survival curves for

230 2 (sTXB2), a validated biomarker of platelet COX-1 activity, and urinary prostacyclin metabolite (PGI

231 ntravascular and that inhibition of platelet COX-1 alone was sufficient to impair metastasis.

232 of 3 aspirin regimens in optimizing platelet COX-1 inhibition while preserving COX-2-dependent vascul

233 ry analysis demonstrated blood from platelet-COX-1-ko and global-COX-1-ko mice produced similar eicos

234 thway Analysis (IPA) predicted that platelet-COX-1-ko mice would be protected from thrombosis, formin

235 Here, we used platelet-COX-1-ko mice to define the platelet and non-platelet ei

236 Conversely, in vivo, platelet-COX-1-ko mice had a distinctly different profile from gl

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

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

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

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

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

242 Consequently, EGFL9 regulates COX activity and modulates cell metabolism, promoting a

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

244 e we show that acetylated COX-2 also retains COX activity, forming predominantly 15 R-configuration P

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

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

247 Some COX inhibitors (i.e. nonsteroidal anti-inflammatory drug

248 Interestingly, 3D tomography showed some COX-positive lamellar cristae were not connected to IBM.

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

250 Conversely, aspirin or lack of systemic COX-1 activity decreased the synthesis of anti-aggregato

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

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

253 In this study, we tested the hypothesis that COX inhibition augments Alternaria-induced pulmonary gro

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

255 Here we report that COX-1 and mPGES-1 mediate production of substantial amou

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

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

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

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

260 cytochrome c oxidase (COX) function, and the COX subunit, COX4, was localized predominantly to organi

261 ybrids are also able to efficiently bind the COX active site.

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

263 n murine models and clinical trials, but the COX isoform, downstream prostanoid, and cell compartment

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

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

266 access of arachidonic acid substrate in the COX-1 isoenzyme.

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

268 Inhibiting the COX signaling by aspirin significantly attenuated INFgam

269 e GPCR agonist AYPGKF in the presence of the COX inhibitor indomethacin, we found that PTPN7 KO mouse

270 eviously reported, the overall effect of the COX pathway on ILC2 function is inhibitory in Alternaria

271 The effect of the COX pathway on innate pulmonary inflammation induced by

272 The effects of the COX-1/2 inhibitor flurbiprofen, the hematopoietic prosta

273 uced ILC2 activation because blocking of the COX-1/2 or HPGDS enzymes or the CRTH2 receptor abolishes

274 otherapy, and dependent on inhibition of the COX-1/thromboxane A2 (TXA2) pathway.

275 Inhibition of the COX-1/TXA2 pathway in platelets decreased aggregation of

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

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

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

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

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

281 s supported by the in vitro finding that the COX product PGE(2) and the PGI(2) analogs cicaprost decr

282 M) while having a lesser affinity toward the COX pathway.

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

284 nist collagen-related peptide along with the COX inhibitor indomethacin did not result in phosphoryla

285 Mice were treated with the COX inhibitors indomethacin, flurbiprofen, or vehicle an

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

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

288 Thus, COXs are physiologically and pharmacologically regulated

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

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

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

292 A binding to Eallo also affects responses to COX inhibitors.

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

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

295 In vitro, COX activity, caspase-3 activity, and heme degradation i

296 0% by common FAs like palmitic acid, whereas COX-2 is allosterically activated 2-fold by palmitic aci

297 luence of PGs may be blunted by K(+) , while COX inhibition leads to compensatory increases in other

298 sensitivity reactions (CRs), associated with COX-1 inhibition, and selective reactions, associated wi

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

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