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(-/-) mice showed a significant reduction of microg

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

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

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

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

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

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

14 synthesis is controlled by cyclooxygenase-1 (COX-1) and COX-2, whose induction involves the STATs.

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

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

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 The mechanism by which cyclooxygenase-1 (COX-1), a heme- and tyrosyl radical-containing enzyme, c

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

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

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

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

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

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

27 ssette (i.e. del597-612 COX-2 and ins594-596 COX-1) are stable.

28 ssette, stabilizes both COX-2 and ins594-612 COX-1; nonetheless, COX mutants that are glycosylated at

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

30 reased levels of COX-1, but not COX-2, and a COX-1-selective inhibitor, SC-560, attenuates prostaglan

31 ibition of Ag-mediated DCF fluorescence by a COX-1 inhibitor (FR122047) and reduced DCF fluorescence

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

33 reated in vitro express catalytically active COX-1 and COX-2 that are localized in the NE and diffuse

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

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

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

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

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

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

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

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

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

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

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

45 Thus mBMMC and huMC generate ROS by 5-LO and COX-1 in response to FcepsilonRI aggregation; huMC gener

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

47 g a "balance" between COX-2-derived PGI2 and COX-1-derived platelet thromboxane is misplaced.

48 minimal thyroid hormone nuclear receptor and COX-1 binding.

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

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

51 n ConA treatment compared with wild-type and COX-1(-/-) mice.

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

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

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

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

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

57 -1/COX-2 and PGD2 synthase, and also between COX-1 and thromboxane A2 synthase.

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

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

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

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

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

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

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

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

66 ylsalicylic acid, a potent inhibitor of both COX-1 and COX-2, to inhibit rat Kv2.1 channels.

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

68 120 is required for high affinity binding by COX-1 but not COX-2, suggesting that hydrophobic interac

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

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

71 ted with HK-BCG in vivo express constitutive COX-1 and inducible COX-2 that are catalytically inactiv

72 t has no apparent effect on the constitutive COX-1 isoform.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

87 LPS) was investigated using COX-1 deficient (COX-1(-/-)) mice or wild-type (COX-1(+/+)) mice pretreat

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

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

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

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

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

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

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

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

96 he discovery of two isoforms of this enzyme, COX-1 and COX-2, and that the latter is inducible by inf

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

98 8%, 63%, 81% and 43%, cyclooxygenase enzymes COX-1 by 55%, 33%, 43% and 24% and COX-2 by 65%, 55%, 77

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

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

101 e mechanism involving Gbetagamma/calcium/ERK/COX-1/prostacyclin signaling, and (ii) this PKA activati

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

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

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

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

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

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

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

109 does not include enzyme preparation (3 h for COX-1 and 24 h for COX-2) or preparation of ELISA plates

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

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

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

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

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

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

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

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

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

119 However, COX-1 failed to substitute effectively for COX-2 in lipo

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

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

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

123 such as candidate polymorphisms detected in COX-1 and CYP2C9.

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

125 dues that manifest the enantioselectivity in COX-1.

126 r (FR122047) and reduced DCF fluorescence in COX-1-deficient mBMMC.

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

128 cytokines and other inflammatory markers in COX-1(-/-) mice was mediated by a reduced activation of

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

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

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

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

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

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

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

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

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

138 flammatory drug that preferentially inhibits COX-1, compromises PPARdelta function and cell growth by

139 rs after lipopolysaccharide (LPS) injection, COX-1(-/-) mice showed decreased protein oxidation and L

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

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

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

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

144 STC had lower COX-1 protein and mRNA levels and higher COX-2 protein a

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

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

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

148 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)

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

150 ba-closo-dodecaborane, showed effectively no COX-1 or COX-2 inhibition at a concentration more than a

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

168 In the present study, the contribution of COX-1 in the neuroinflammatory response to intracerebrov

169 nducible isoform, COX-2, the contribution of COX-1 to the inflammatory response is unclear.

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

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

172 he effects of histamine on the expression of COX-1 and COX-2 and determined their contribution to the

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

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

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

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

177 Inhibition of COX-1 activity was completely removed.

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

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

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

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

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

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

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

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

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

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

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

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

190 The isolation of COX-1 and COX-2 enzymes is also described.

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

192 Deletion or knockdown of COX-1, but not deletion of COX-2, decreased urinary tetr

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

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

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

196 ouse and human EOCs have increased levels of COX-1, but not COX-2, and a COX-1-selective inhibitor, S

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

213 ws that whereas PPARdelta can be a target of COX-1, extracellular signal-regulated kinase is a potent

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

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

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

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

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

219 contrast, the heptapeptide had no effect on COX-1 mRNA in xenograft tumors or A549 cells.

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

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

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

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

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

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

226 the functional studies, inhibition of PKA or COX-1 attenuated ET1-induced VSMC hypertrophy, suggestin

227 lack undesirable thyroid hormone receptor or COX-1 binding.

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

229 Selective inhibition of COX-2 over COX-1 results in preferential decrease in prostacyclin p

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

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

232 und to be a poor inhibitor of purified ovine COX-1 and a relatively weak inhibitor of purified human

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

251 Selective COX-1 inhibition with SC560 similarly increased gastric

252 +)) mice pretreated with SC-560, a selective COX-1 inhibitor.

253 3g, 3s, 3d were potent and selective COX-1 inhibitors that affected platelet aggregation in v

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

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

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

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

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

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

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

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

262 landin G/H synthase enzymes, commonly termed COX-1 and COX-2, differ markedly in their responses to r

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

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

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

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

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

268 in vivo by HK-BCG, the results indicate that COX-1 and COX-2 dissociated from the NE are catalyticall

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

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

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

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

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

274 These findings suggest that COX-1 plays a previously unrecognized role in neuroinfla

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

278 ts, (-)-oleocanthal (1), an inhibitor of the COX-1 and COX-2 enzymes, possesses similar potency as th

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

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

281 aling in promoting cell motility through the COX-1-Ptges-EP4 pathway, a previously unrecognized role

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

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

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

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

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

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

288 -1 deficient (COX-1(-/-)) mice or wild-type (COX-1(+/+)) mice pretreated with SC-560, a selective COX

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

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

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

292 opolysaccharide (LPS) was investigated using COX-1 deficient (COX-1(-/-)) mice or wild-type (COX-1(+/

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

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

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

296 it COX-2 with almost equal efficacy, whereas COX-1 is selectively inhibited by the S-enantiomers.

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 onal damage in the hippocampus compared with COX-1(+/+) mice.

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