ライフサイエンスコーパス: COX-1

1 COX-1 and COX-2 are approximately 60% identical in amino

2 COX-1 and COX-2 are both targets of nonselective nonster

3 COX-1 and COX-2 are found in abundance on the luminal su

4 COX-1 is a constitutive enzyme involved in physiological

5 COX-1 is constitutively expressed and stable, whereas CO

6 COX-1 is constitutively expressed in many types of cells

7 COX-1(-/-), COX-2(-/-), and wild-type (WT) mice were stu

8 ally modified mice lacking functional COX-1 (COX-1(-/-)), as well as airway tissue from "aspirin-sens

9 xygenase reaction cycle of cyclooxygenase 1 (COX-1) is abstraction of the pro-S hydrogen atom of the

10 developed a novel assay of cyclooxygenase-1 (COX-1) acetylation in platelets isolated from volunteers

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

12 e synthase (NOS) and NOS3, cyclooxygenase-1 (COX-1) and COX-2, and hypoxia-inducing factor-1 alpha (H

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

14 ate inhibition of platelet cyclooxygenase-1 (COX-1) by aspirin.

15 mine oxidase B (MAO-B) and cyclooxygenase-1 (COX-1) enzyme through molecular docking and experimental

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

17 le (P6), a known selective cyclooxygenase-1 (COX-1) inhibitor, was used to design a new series of 3,4

18 stion of aspirin and other cyclooxygenase-1 (COX-1) inhibitors induces exacerbations of airway diseas

19 d by platelets from AA via cyclooxygenase-1 (COX-1) mediates thrombosis.

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

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

22 at simultaneously inhibits cyclooxygenase-1 (COX-1), COX-2, and fatty acid amide hydrolase (FAAH).

23 example, inhibition of the cyclooxygenase-1 (COX-1)-prostaglandin system within the VL-PAG alters spi

24 sion, but has no effect on cyclooxygenase-1 (COX-1).

25 f P. guajava showed 56.4% (COX-2) and 44.1% (COX-1) inhibitory activity, respectively.

26 tration and to show cyclooxygenase-1 and -2 (COX-1 and -2) immunoreactivities, respectively, in the p

27 2, commonly called cyclooxygenases-1 and -2 (COX-1 and -2), catalyze the committed step in prostaglan

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

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

30 ons show that despite the presence of COX-2, COX-1 is functionally predominant in the airways and exp

31 mL, these compounds inhibited LPO by 11-87%, COX-1 and -2 enzymes by 0-35% and 0-82% and growth of hu

32 COX blocker and the effect is mimicked by a COX-1, but not COX-2, antagonist, suggesting that astroc

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

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

35 ex in fully awake mice, we reveal that acute COX-1 inhibition reduces resting arteriole diameter but

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

37 most promising compounds were active against COX-1 in intact ovarian carcinoma cells (OVCAR-3).

38 arly, oligodeoxynucleotide-antisense against COX-1 or COX-2, but not oligodeoxynucleotide-mismatch, d

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

40 By univariate analysis, COX-1-dependent assays, including serum thromboxane B(2)

41 onstitutive cyclooxygenase enzyme (COX-2 and COX-1, respectively).

42 ction measured by serum thromboxane B(2) and COX-1-independent platelet function measured by PFA-100

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

44 sirable thyroid hormone receptor binding and COX-1 inhibition activity.

45 COX-1, COX-2 messenger RNA expressions, and COX-1, COX-2, eNOS protein expressions.

46 ted COX-1 in an MyD88-dependent fashion, and COX-1 deficiency increased PGE(2) production after LPS.

47 METHODS AND COX-1>COX-2 mice developed systolic hypertension relativ

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

49 induction, DPPH free radical scavenging, and COX-1 and COX-2 inhibitory activities and the 4'-sulfate

50 ate inhibited NFkappaB induction, as well as COX-1 and COX-2 activities.

51 This was true in wild-type as well as COX-1(-/-) and COX-2(-/-) mice.

52 was only slight enhancement of NE-associated COX-1 and there was no change in COX-1/COX-2 levels in a

53 Adv-COPI treatment selectively augmented COX-1 and PGIS protein expression in the renal proximal

54 ated no PGE(2) release in the lungs, because COX-1 and COX-2 in alveolar macrophages were subcellular

55 -1/COX-2 and PGD2 synthase, and also between COX-1 and thromboxane A2 synthase.

56 es lining the cyclooxygenase channel between COX-1 and COX-2.

57 imental endpoints were not different between COX-1(-/-) and WT mice; however, the percentage of IL-9(

58 ing between COX-2 and PGE2 synthase, between COX-1/COX-2 and PGD2 synthase, and also between COX-1 an

59 oxazoles in order to improve its biochemical COX-1 selectivity and antiplatelet efficacy.

60 as inhibited by aspirin, SC560, which blocks COX-1 selectively, but not by rofecoxib, which is a sele

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

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

63 ed COX-1 and up-regulated expression of both COX-1 and COX-2 as well as their products PGE(2), PGF(2a

64 stronger C-nociceptor input were affected by COX-1 inhibition to a greater extent than those with wea

65 120 is required for high affinity binding by COX-1 but not COX-2, suggesting that hydrophobic interac

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

67 llographic results obtained with a celecoxib/COX-1 complex show how celecoxib can bind to one of the

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

69 l PGE(2) synthase-1 (mPGES1), which converts COX-1/COX-2-derived PGH(2) to PGE(2).

70 nal-regulated kinases ERK1/2, cyclooxygenase COX-1 (but not COX-2) and prostacyclin receptors.

71 Cyclooxygenase (COX-1/COX-2)-catalyzed eicosanoid formation plays a key

72 activity of the inflammatory cyclooxygenases COX-1 and COX-2, these findings suggest that downstream

73 Cyclooxygenases (COX-1 and COX-2) are N-glycosylated, endoplasmic reticul

74 of arachidonic acid (AA) by cyclooxygenases (COX-1 and COX-2) followed by metabolism of endoperoxide

75 ed by two isoenzyme groups, cyclooxygenases (COX-1 and COX-2) and terminal prostaglandin E synthases

76 ugh the activation of PLA2, cyclooxygenases (COX-1 and -2) and prostaglandins and at least TXA2, may

77 The cyclooxygenases (COX-1 and COX-2) are membrane-associated heme-containing

78 The cyclooxygenases (COX-1 and COX-2) generate prostaglandin H(2) from arachi

79 The cyclooxygenases (COX-1 and COX-2) oxygenate arachidonic acid (AA) in the

80 Two cyclooxygenases, COX-1 and COX-2, catalyze the initial step in the metabo

81 activity in vitro, inhibiting cycloxygenase (COX-1/2) activity.

82 induced NFkappaB activity, cylcooxygenases (COX-1 and COX-2), aromatase, nitric oxide production in

83 rs in humans, as well as platelet depletion, COX-1 knockdown, and COX-2 deletion in mice, revealed th

84 tification of the role that DRG cell-derived COX-1 and COX-2 play in the development of inflammatory

85 ntributed substantially to clinical disease; COX-1-/- mice were fully resistant to disease, whereas C

86 nt, would shift the inactive, NE-dissociated COX-1/COX-2 to active, NE-associated forms.

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

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

89 synthesized in reactions catalyzed by either COX-1 or COX-2.

90 Although loss of either COX-1 or COX-2 increases the disease severity, surprisin

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

92 8%, 63%, 81% and 43%, cyclooxygenase enzymes COX-1 by 55%, 33%, 43% and 24% and COX-2 by 65%, 55%, 77

93 Cyclooxygenase enzymes (COX-1 and COX-2) catalyze the conversion of arachidonic

94 exhibits homology to cyclooxygenase enzymes (COX-1 and COX-2).

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

96 tro, murine B cells constitutively expressed COX-1 and up-regulated expression of both COX-1 and COX-

97 orts a role for the constitutively expressed COX-1 in inflammation-induced activation of the HPA axis

98 extensively investigated, but relatively few COX-1-selective inhibitors have been described.

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

100 ess airway inflammation and blood assays for COX-1 and COX-2 activity to assess enzyme inhibition.

101 e studied using human whole blood assays for COX-1 and COX-2 inhibition in vitro, and results showed

102 OX-1 biology in vivo and promising leads for COX-1-targeted therapeutic agents.

103 ith an IC50 of 60 nM relative to 6000 nM for COX-1.

104 NA levels for COX-2 and mPGES-1, but not for COX-1 or cPGES.

105 As this is a critical residue for COX-1 catalysis, nitration at this site results in enzym

106 Bronchi from COX-1(-/-) mice were hyperresponsive to bronchoconstrict

107 iction in tissue from wild-type but not from COX-1(-/-) mice.

108 n mice, niacin-induced flushing results from COX-1-dependent formation of PGD(2) and PGE(2) followed

109 Furthermore, sera from COX-1 inhibitor-treated mice were dramatically less effe

110 genetically modified mice lacking functional COX-1 (COX-1(-/-)), as well as airway tissue from "aspir

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

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

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

114 irubin-3'-monoxime were tested against human COX-1.

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

116 pression of COX-2 in WT mice and of COX-1 in COX-1>COX-2 mice in the inner renal medulla.

117 -associated COX-1 and there was no change in COX-1/COX-2 levels in alveolar epithelial cells followin

118 Secondary end points were differences in COX-1 and -2 expressions; oxidized DNA bases; and marker

119 dues that manifest the enantioselectivity in COX-1.

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

121 , but borreliacidal activity was restored in COX-1 inhibitor-treated mice administered IL-17.

122 al studies showed that CDP-choline increased COX-1 and -2 immunoreactivities in the posterior hypotha

123 by PFA-100 collagen-ADP CT, but not indirect COX-1-dependent assays (arachidonic acid-stimulated plat

124 olac tromethamine, ibuprofen, indomethacin), COX-1-selective (SC-560), or COX-2-selective (SC-236) NS

125 Lead compounds did not inhibit COX-1 or COX-2 but blocked the AKR1C3 mediated productio

126 higher than the concentrations that inhibit COX-1 activity.

127 antiinflammatory drugs (NSAIDs) that inhibit COX-1 and COX-2 and NSAIDs designed to be selective for

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

129 Aspirin (10 mg/kg; i.v.) inhibited COX-1, measured as blood thromboxane and COX-2, measured

130 ed anti-inflammatory potential by inhibiting COX-1 and 12-LOX pathway products synthesis.

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

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

133 Interestingly, COX-1 expression is enhanced in ECs of brain PVC-deplete

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

135 ly that under physiological conditions it is COX-1 and not COX-2 that drives prostacyclin production

136 tion of the cyclooxygenase (COX) isoenzymes, COX-1 and COX-2, affect memory function and synaptic pla

137 Importantly, infection of mice lacking COX-1, but not COX-2, activity resulted in a defect in I

138 -2-picrylhydrazyl), and inhibition of 5-LOX, COX-1-2, and inducible nitric oxide synthase (iNOS) enzy

139 JWH-015 decreased mesenteric COX-1, COX-2 messenger RNA expressions, and COX-1, COX-2

140 data demonstrate that progressive microglial COX-1 expression and prostaglandin synthesis can underpi

141 Clinical data show that mixed COX-1/COX-2 inhibitors such as aspirin, but not COX-2 se

142 ng 15-LOX (IC(50), 55 mug/ml), with moderate COX-1 (IC(50), 66 mug/ml) and COX-2 (IC(50), 119 mug/ml)

143 ving a Golgi targeting signal but not native COX-1 exhibited efficient catalytic coupling to mPGES-1.

144 AID-induced reactions, chemically nonrelated COX-1 inhibitors can be safely used.

145 s of indomethacin (10 mg/kg), a nonselective COX-1/COX-2 inhibitor, or NS398 [N-(2-cyclohexyloxy-4-ni

146 vation induced cyclooxygenase 2 (COX-2), not COX-1, expression in a manner that depended on activatio

147 microsomal PGE synthase-1 (mPGES-1) but not COX-1 in the Golgi apparatus.

148 s that the expression of COX-2 mRNA, but not COX-1 mRNA, was markedly reduced in the aortic tissues o

149 etylated by aspirin, however, COX-2 (but not COX-1) can form 15(R)-HETE, which is metabolized to aspi

150 t the selective inhibition of COX-2, but not COX-1, acutely prevented the suppression of hippocampal

151 vious studies have shown that COX-2, but not COX-1, can oxygenate endocannabinoid substrates, includi

152 tion of COX-2 and up-regulated COX-2 but not COX-1.

153 n peripheral tissue depends on activation of COX-1 and COX-2 in C-fibers, which contribute to the ind

154 These results suggest that activation of COX-1/PGI(2)/PPARdelta pathway is an important mechanism

155 ating activity and increased the activity of COX-1 toward 2-AG.

156 nce analysis demonstrated that the amount of COX-1 and COX-2, constitutively expressed in TRPV-1(+) c

157 reased expression of COX-2 in WT mice and of COX-1 in COX-1>COX-2 mice in the inner renal medulla.

158 aspirin to the substrate binding channel of COX-1 in vitro, exposure of volunteers to a single thera

159 roms, respectively, and a crystal complex of COX-1 with meloxicam at 2.4 angstroms.

160 Recent reports of a possible contribution of COX-1 in analgesia, neuroinflammation, or carcinogenesis

161 responses, but the relative contributions of COX-1 and COX-2 remain unclear.

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

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

164 In contrast, the expression of COX-1, hematopoietic-PGDS (H-PGDS), cytosolic-PGES (c-PG

165 h no significant change in the expression of COX-1.

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

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

168 r indomethacin or by genetic inactivation of COX-1 or PGI(2) synthase with small interfering (si)RNA.

169 ell proliferation induced by inactivation of COX-1 were rescued by the treatment with iloprost or the

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

171 Inhibition of COX-1 activity was completely removed.

172 PGF(2alpha) were suppressed by inhibition of COX-1 and COX-2, but not by selective inhibition of COX-

173 In vitro inhibition of COX-1 and/or COX-2 in murine B cells resulted in decreas

174 ecoxib does interfere with the inhibition of COX-1 by aspirin in vitro.

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

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

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

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

179 from 20-2500 nM and negligible inhibition of COX-1).

180 but not confined to inadequate inhibition of COX-1, are responsible for poor clinical outcomes in asp

181 gregation in vitro through the inhibition of COX-1-dependent thromboxane (TX) A2.

182 sulfide (E-DMSS) analogues for inhibition of COX-1.

183 s 1, 4, and 5 exhibit moderate inhibition of COX-1.

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

185 Isoxicam is a nonselective inhibitor of COX-1 and COX-2 whereas meloxicam displays some selectiv

186 and the effect of ketorolac (an inhibitor of COX-1 and COX-2) was negligible.

187 These findings support an involvement of COX-1 in bidirectional interplay between ECs and PVCs in

188 Functional involvement of COX-1 is indicated by the observation that central, but

189 Moreover, we characterized their kinetics of COX-1 inhibition.

190 rol human donors contained similar levels of COX-1 and COX-2 immunoreactivity.

191 BM(-/-) mice also had higher levels of COX-1 protein and more leukocytes in the infarct, but no

192 he present study, we detected high levels of COX-1 protein expression and PGI(2) biosynthesis in huma

193 Basal protein levels of COX-1, cPGES, and mPGES-2 were readily detected in whole

194 stinct cellular/subcellular localizations of COX-1-IR in the three cell types.

195 suggest that a vasoconstrictor metabolite of COX-1 could play a role in this impaired tissue blood fl

196 Although celecoxib binding to one monomer of COX-1 does not affect the normal catalytic processing of

197 Rat islets constitutively expressed mRNAs of COX-1, COX-2, cPGES, and mPGES-1.

198 OX-1 and demonstrate that the side pocket of COX-1, previously thought to be sterically inaccessible,

199 E-DMSS analogues may be useful probes of COX-1 biology in vivo and promising leads for COX-1-targ

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

201 levant doses, which suppressed production of COX-1- and COX-2-derived prostaglandins and caused small

202 t relevant localization(s) and regulation of COX-1 expression is lacking.

203 gest that the coordinated down-regulation of COX-1 facilitates PGE(2) production after TLR-4 activati

204 scular reactivity and to clarify the role of COX-1 and COX-2 in normotensive subjects on a short-term

205 ent study demonstrates the important role of COX-1 derived vasoconstrictor metabolites in regulation

206 ring a HS diet suggests an important role of COX-1 derived vasoconstrictor metabolites in the regulat

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

208 We investigated the roles of COX-1 and COX-2 in the humoral immune response to infect

209 xychromanol to the substrate-binding site of COX-1.

210 nd other coxibs bind tightly to a subunit of COX-1.

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

212 However, the downstream targets of COX-1 signaling in EOC are not yet known.

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

214 rdioprotective effect of low-dose aspirin on COX-1 may be blunted when taken with coxibs.

215 rstand the structural impact of chirality on COX-1 selectivity, the crystal structures of ovine COX-1

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

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

218 cts nitration to alternative Tyr residues on COX-1, preserving catalytic activity.

219 s were found in inflamed joint tissues, only COX-1 contributed substantially to clinical disease; COX

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

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

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

223 ans-infected wild type and cPLA2alpha(-/-)or COX-1(-/-)macrophages.

224 than inhibition of platelet degranulation or COX-1 inhibition.

225 ent to explain aspirin's unique (among other COX-1 inhibitors) effectiveness in preventing atherothro

226 to the preferential inhibition of COX-2 over COX-1.

227 selectivity, the crystal structures of ovine COX-1 in complexes with an enantiomeric pair of these in

228 Increased generation of cyclo-oxygenase (COX-1 and COX-2)-derived vasoconstrictor factors and end

229 t (HS) diet on the role of cyclo-oxygenases (COX-1 and COX-2) and the vasoconstrictor prostaglandins,

230 Inhibition of VL-PAG COX-1 in anaesthetised rats increased firing thresholds

231 A-nociceptive information, even after VL-PAG COX-1 inhibition, whereas the encoding of C-nociceptor i

232 etermined the effect of inhibition of VL-PAG COX-1 on dorsal horn wide dynamic-range neurons evoked b

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

234 n mice, revealed that niacin evoked platelet COX-1-derived PGD(2) biosynthesis.

235 he ability of aspirin to inactivate platelet COX-1 will confound head-to-head comparisons of distinct

236 In contrast, indirect measures of platelet COX-1 (arachidonic acid-stimulated platelet markers, sho

237 2 (sTXB2), a validated biomarker of platelet COX-1 activity, and urinary prostacyclin metabolite (PGI

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

239 d 3d were more potent inhibitors of platelet COX-1 and aggregation than P6 (named 6) for their tighte

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

241 f coronary artery disease, residual platelet COX-1 function measured by serum thromboxane B(2) and CO

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

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

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

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

246 from wild-type mice contained predominantly COX-1 immunoreactivity and contracted in vitro in respon

247 a novel role for the substrate in protecting COX-1 from inactivation by nitration in pathophysiologic

248 But 13'-carboxychromanol inhibits purified COX-1 and COX-2 much more potently than shorter side-cha

249 In contrast, LPS down-regulated COX-1 in an MyD88-dependent fashion, and COX-1 deficienc

250 rrow-derived leukocytes negatively regulates COX-1 expression, prostaglandin E(2) biosynthesis, and i

251 dv-COPI transfection, we evaluated the renal COX-1 and PGIS protein expression and PGI2 and prostagla

252 estradiol (0, 10, 20, and 30%) and/or SC560 (COX-1 inhibitor) or NS398 (COX-2 inhibitor) after intrap

253 Selective COX-1 inhibition with SC560 similarly increased gastric

254 3g, 3s, 3d were potent and selective COX-1 inhibitors that affected platelet aggregation in v

255 tive COX inhibitor (indomethacin), selective COX-1 (valeryl salicylate), or selective COX-2 (SC-236)

256 ceived 100 mg of indomethacin (non-selective COX-1 and COX-2 inhibitor), and another HS group subset

257 ot systemic, pretreatment with the selective COX-1 inhibitor SC-560 attenuated the early phase of LPS

258 r of COX-2 is desirable but difficult, since COX-1 and COX-2 ordinarily catalyze formation of an iden

259 more, transfection of PGI(2) synthase siRNA, COX-1 siRNA, or PPARdelta siRNA into EPCs decreased the

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

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

262 single NSAID with good tolerance to a strong COX-1 inhibitor and/or evidence by in vivo tests support

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

264 -switching in response to infection and that COX-1 is a critical, previously unrecognized regulator o

265 data are consistent with the conclusion that COX-1 drives vascular prostacyclin release and puts the

266 We previously established that COX-1 undergoes selective nitration on Tyr385 via a mech

267 In contrast, we and others have found that COX-1, not COX-2, is responsible for vascular prostacycl

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

269 genetic knockdown approaches indicated that COX-1, and not the COX-2 pathway, was responsible for th

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

271 Western blot analysis revealed that COX-1 was expressed by the cells, but there was no COX-2

272 t experiments fill this void in showing that COX-1 immunoreactivity (IR) and mRNA are detectable in i

273 These data suggest that COX-1 derived prostaglandins exert an inhibitory effect

274 inflammation, or carcinogenesis suggest that COX-1 is a potential therapeutic target.

275 The COX-1-specific inhibitor SC-560 provided significant pro

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

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

278 We now show that occupancy of the COX-1 active site with substrate protects against Tyr385

279 to one of the two available COX sites of the COX-1 dimer.

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

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

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

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

284 the thyroid hormone nuclear receptor or the COX-1 enzyme.

285 with adverse clinical outcomes, whereas the COX-1-independent assay, PFA-100 collagen-ADP CT <65 sec

286 enantiomer-selective interactions within the COX-1 side pocket region that stabilize drug binding and

287 between protein and substrate when bound to COX-1 are conserved in our COX-2 structures, with the on

288 h affinity binding of a neutral inhibitor to COX-1 and demonstrate that the side pocket of COX-1, pre

289 ion, permitting MC activation in response to COX-1 inhibition.

290 e was essential for their selectivity toward COX-1.

291 Unlike COX-1, mutating this residue to Ala, Phe, Pro, or Thr di

292 Here we have used COX-1- and COX-2-knockout mice to establish whether plas

293 r functional contribution was compared using COX-1-/- and COX-2-/- mice as well as isoform-specific i

294 ouplings were experimentally validated using COX-1 and COX-2 selective inhibitors.

295 contribution of prostanoids synthesized via COX-1, in particular PGI2, to inflammatory arthritis.

296 uced by pro-inflammatory challenges, whereas COX-1 is constitutively expressed.

297 n mainly in astroglia and microglia, whereas COX-1 expression was predominant in microglia and did no

298 tudy were to determine prospectively whether COX-1-dependent and other platelet function assays corre

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

300 ent and secondary structure predictions with COX-1 and experimental observations that governed the pl