ライフサイエンスコーパス: cyclooxygenase-1

1 genes (endothelial nitric oxide synthase and cyclooxygenase-1).

2 The activation of PKA is downstream of COX1 (cyclooxygenase-1).

3 eroidal anti-inflammatory drugs that inhibit cyclooxygenase 1.

4 here was no coexpression between mPGES-1 and cyclooxygenase-1.

5 activity of the molecular target of aspirin, cyclooxygenase-1.

6 ts newly discovered inhibition of the enzyme cyclooxygenase-1.

7 tion of proangiogenic 15(S)-HETE by platelet cyclooxygenase-1.

8 Similar to MSCs, ICC-SCs strongly expressed cyclooxygenase 1/2 and basally secreted prostaglandin E2

9 blockade of each of the downstream enzymes, cyclooxygenase-1/2 and 5-lipooxygenase.

10 Mice deficient in cyclooxygenase-1, a critical enzyme in prostaglandin bio

11 Aspirin, which inhibits cyclooxygenase-1 activity and thromboxane generation in

12 Measurement of platelet cyclooxygenase-1 activity following immunoprecipitation

13 Serum thromboxane B(2) levels (an index of cyclooxygenase-1 activity in platelets) and platelet agg

14 Renal cyclooxygenase 1 and 2 activity produces five primary pr

15 nstrictor and platelet agonist, whereas both cyclooxygenase 1 and 2 contribute to production of endot

16 which is converted primarily to PGs via the cyclooxygenase 1 and 2 pathways and to leukotrienes via

17 otal prostaglandin concentration and to show cyclooxygenase-1 and -2 (COX-1 and -2) immunoreactivitie

18 prostaglandin (PG) synthesis is mediated by cyclooxygenase-1 and -2 (COX1 and COX2).

19 nflammatory drugs (NSAIDs) are inhibitors of cyclooxygenase-1 and -2 and are useful for prevention an

20 oth compounds were shown to inhibit purified cyclooxygenase-1 and -2 by a reversible mechanism.

21 Cyclooxygenase-1 and -2 did not oxidize alkynyl linoleic

22 141.6 and 138.8 muM, respectively) inhibited cyclooxygenase-1 and -2 enzymes by 50%.

23 eries of uni-x sheep, accompanied by reduced cyclooxygenase-1 and -2 gene expression (P<0.05).

24 ize the current understanding of the role of cyclooxygenase-1 and -2 in different physiological situa

25 release of isoprostanes was inhibited by the cyclooxygenase-1 and -2 inhibitor indomethacin as well b

26 rine signaling molecules synthesized via the cyclooxygenase-1 and -2 pathways.

27 . canina hips showed some anti-inflammatory (cyclooxygenase-1 and 12-lipooxygense inhibition potency)

28 production of some monitored eicosanoids in cyclooxygenase-1 and 12-lipoxygenase pathways.

29 The enzymes cyclooxygenase-1 and cyclooxygenase-2 (COX-1 and COX-2)

30 nd nitric oxide production, increased aortic cyclooxygenase-1 and cyclooxygenase-2 expression, and in

31 tric mucosal integrity, the precise roles of cyclooxygenase-1 and cyclooxygenase-2 in these processes

32 (2) in the remaining patients, occurs via a cyclooxygenase-1 and cyclooxygenase-2 independent pathwa

33 The two cyclooxygenase isoforms, cyclooxygenase-1 and cyclooxygenase-2, both metabolize a

34 ost mouse with indomethacin, an inhibitor of cyclooxygenase-1 and cyclooxygenase-2, or with NS-398, a

35 l NSAIDs and aspirin inhibit active sites of cyclooxygenase-1 and cyclooxygenase-2.

36 e-2, and >100-fold selectivity against ovine cyclooxygenase-1 and human cyclooxygnease-2.

37 ilization [Ca(t)]i controls granule release, cyclooxygenase-1 and integrin activation, and phosphatid

38 occurrence of events despite treatment with cyclooxygenase-1 and P2Y12 inhibitors.

39 However, cyclooxygenase-1 and prostanoid receptor 2-4 levels were

40 ytic cytochrome P450 epoxygenase, astrocytic cyclooxygenase-1 and smooth muscle cytochrome P450 omega

41 sident peritoneal macrophages contained only cyclooxygenase-1 and synthesized (from either endogenous

42 reatment of inflammatory diseases and target cyclooxygenases 1 and 2 (Cox-1, Cox-2) that are responsi

43 -Prostaglandin (PG) F2alpha may be formed by cyclooxygenases 1 and 2 or by a free radical catalyzed p

44 werful inhibitor of prostaglandin synthases (cyclooxygenases 1 and 2), did not inhibit the formation

45 broblasts, mediated by the induction of both cyclooxygenases 1 and 2.

46 Cyclooxygenases-1 and -2 (Cox-1 and Cox-2) are two disti

47 Prostaglandin synthesis by cyclooxygenases-1 and -2 (COX-1 and COX-2) involves an i

48 H synthases-1 and 2 (PGHS-1 and PGHS-2; also cyclooxygenases-1 and 2, COX-1 and COX-2) catalyze the c

49 In contrast, the expression of fibronectin, cyclooxygenase 1, and GAPDH was not affected.

50 Fasted wild-type, cyclooxygenase-1, and cyclooxygenase-2 knockout mice wer

51 platelet 12-hLO, epithelial 15-hLO-2, ovine cyclooxygenase-1, and human cyclooxygenase-2.

52 e aspirin through faster renewal of platelet cyclooxygenase-1, and impaired platelet inhibition can b

53 ignaling migration, constitutively expressed cyclooxygenase-1 appears to contribute approximately 25%

54 W-480 colorectal cancer cells, which express cyclooxygenase-1 but little cyclooxygenase-2.

55 s diminished in HCT-116 cells overexpressing cyclooxygenase-1 compared with normal HCT-116 cells sugg

56 ons to generate three-dimensional models for cyclooxygenase-1 complexes with a series of indomethacin

57 stigate the role of the two cyclooxygenases, cyclooxygenase 1 (COX-1) and cyclooxygenase 2 (COX-2), i

58 Sex differences in cyclooxygenase 1 (COX-1) direct and indirect platelet ac

59 step in the cyclooxygenase reaction cycle of cyclooxygenase 1 (COX-1) is abstraction of the pro-S hyd

60 loproteinase 1, MCP-1, IL-1beta, IL-6, IL-8, cyclooxygenase 1 (COX-1), COX-2, leukemia inhibitory fac

61 l-specific, alternatively spliced isoform of cyclooxygenase 1 (COX-1).

62 by aspirin in vitro or in vivo, implicating cyclooxygenase-1 (COX).

63 We developed a novel assay of cyclooxygenase-1 (COX-1) acetylation in platelets isolat

64 Cyclooxygenase-1 (Cox-1) and Cox-2 convert arachidonic a

65 dal anti-inflammatory drugs (NSAIDs) inhibit cyclooxygenase-1 (COX-1) and COX-2 enzymes.

66 ndins (PGs), generated through the action of cyclooxygenase-1 (COX-1) and COX-2 protect the intestina

67 ucible nitric oxide synthase (NOS) and NOS3, cyclooxygenase-1 (COX-1) and COX-2, and hypoxia-inducing

68 PGE2 biosynthesis is controlled by cyclooxygenase-1 (COX-1) and COX-2, whose induction invo

69 Cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2) ar

70 NSAIDs inhibit the enzymatic activity of cyclooxygenase-1 (COX-1) and inducible COX-2, which cata

71 esult from inadequate inhibition of platelet cyclooxygenase-1 (COX-1) by aspirin.

72 to discover structurally novel inhibitors of cyclooxygenase-1 (COX-1) by screening a selected number

73 r studied in monoamine oxidase B (MAO-B) and cyclooxygenase-1 (COX-1) enzyme through molecular dockin

74 Estrogen upregulates cyclooxygenase-1 (COX-1) expression in endothelial cells

75 Cyclooxygenase-1 (COX-1) has been implicated in the path

76 d evaluated for cyclooxygenase-2 (COX-2) and cyclooxygenase-1 (COX-1) inhibition in human whole blood

77 yl-4-phenylisoxazole (P6), a known selective cyclooxygenase-1 (COX-1) inhibitor, was used to design a

78 The ingestion of aspirin and other cyclooxygenase-1 (COX-1) inhibitors induces exacerbation

79 Cyclooxygenase-1 (COX-1) is the rate-limiting component

80 Vascular cyclooxygenase-1 (COX-1) is the rate-limiting step in pr

81 mboxane A(2) formed by platelets from AA via cyclooxygenase-1 (COX-1) mediates thrombosis.

82 Prostaglandins formed by cyclooxygenase-1 (COX-1) or COX-2 produce hyperalgesia i

83 achidonate by either of two cyclooxygenases, cyclooxygenase-1 (Cox-1) or cyclooxygenase-2 (Cox-2), wh

84 From this analysis, we found that cyclooxygenase-1 (COX-1), 5-lipoxygenase (5-LOX), and FL

85 The mechanism by which cyclooxygenase-1 (COX-1), a heme- and tyrosyl radical-co

86 Deletion of cyclooxygenase-1 (Cox-1), an enzyme involved in producti

87 ess the prostaglandin (PG) synthesis enzyme, cyclooxygenase-1 (COX-1), as well as both components of

88 directed ligand that simultaneously inhibits cyclooxygenase-1 (COX-1), COX-2, and fatty acid amide hy

89 cytes by examining its respective effects on cyclooxygenase-1 (COX-1), cyclooxygenase-2 (COX-2), and

90 ed and used to characterize their binding to cyclooxygenase-1 (COX-1), cyclooxygenase-2 (COX-2), seve

91 nti-inflammatory drugs (NSAIDs) inhibit both cyclooxygenase-1 (COX-1), whose inhibition is associated

92 -nociceptors; for example, inhibition of the cyclooxygenase-1 (COX-1)-prostaglandin system within the

93 anced expression of the rate-limiting enzyme cyclooxygenase-1 (COX-1).

94 of endothelial cell NO synthase (ecNOS) and cyclooxygenase-1 (COX-1).

95 e-2 (COX-2) expression, but has no effect on cyclooxygenase-1 (COX-1).

96 ction was also diminished in vessels lacking cyclooxygenase-1 [COX1 knockout (KO)] or the thromboxane

97 vels of proinflammatory effectors, including cyclooxygenase-1, cyclooxygenase-2, inducible nitric oxi

98 of infected macrophages with indomethacin, a cyclooxygenase-1/cyclooxygenase-2 inhibitor, blocked PGE

99 The antagonism of the thromboxane A(2), cyclooxygenase-1/cyclooxygenase-2, or phospholipase C pa

100 nontransformed cells derived from wild-type, cyclooxygenase 1-deficient (COX-1(-/-)) or cyclooxygenas

101 PGES3 and an arrestin-dependent increase in cyclooxygenase 1-dependent prostaglandin E(2) synthesis.

102 lso shown to be a high-affinity receptor for cyclooxygenase-1 derived 12(S)-hydroxyheptadeca-5Z, 8E,

103 ne loop in macrophages involving cPLA2alpha, cyclooxygenase 1-derived prostaglandins and increased cA

104 2, a unique receptor for 5-lipoxygenase- and cyclooxygenase-1-derived lipid mediators, represents a n

105 capacitative calcium influx, and inhibiting cyclooxygenase-1, endothelial NO limits platelet activat

106 panied by a compensatory increase in ovarian cyclooxygenase 1 expression and prostaglandin E(2) synth

107 Here the ability of recombinant human cyclooxygenase-1 (hCOX-1) and cyclooxygenase-2 (hCOX-2)

108 The constitutively expressed cyclooxygenase-1, however, was not affected by the sugar

109 thrombin, the thrombospondin-1/CD36 axis and cyclooxygenase 1 in subsequent platelet activation and s

110 spirin are consistent with the inhibition of cyclooxygenase-1 in platelets, we used liquid chromatogr

111 The detection of 12-lipoxygenase and cyclooxygenase-1 in single bovine coronary artery endoth

112 activity and endothelial NO production in a cyclooxygenase-1-independent fashion.

113 ailable vascular NO in an eNOS-dependent and cyclooxygenase-1-independent manner.

114 y supplied by PGE2, are removed secondary to cyclooxygenase-1 inhibition.

115 effect of aspirin is attributed to platelet cyclooxygenase-1 inhibition.

116 of only 1-2 s, and both indomethacin and the cyclooxygenase-1 inhibitor SC-560 blocked the photolysis

117 asal polyposis, and respiratory reactions to cyclooxygenase-1 inhibitors (nonsteroidal anti-inflammat

118 e studies provide insight into the nature of cyclooxygenase-1 interactions with a series of novel inh

119 The gastric injury induced by aspirin/HCl in cyclooxygenase-1 knockout mice could be prevented if the

120 ed increase in gastric prostaglandin E(2) in cyclooxygenase-1 knockout mice seemed to correspond to a

121 ofound decrease in surface hydrophobicity in cyclooxygenase-1 knockout mice than in wild-type mice, w

122 The gastric mucosa of cyclooxygenase-1 knockout mice was more severely injured

123 mucosal prostaglandin E(2) concentration in cyclooxygenase-1 knockout mice, possibly by the inductio

124 osal prostaglandin E(2) concentration in the cyclooxygenase-1 knockout mice, whereas it decreased pro

125 However, prostaglandins generated by cyclooxygenase-1 may play an important permissive role i

126 Cyclooxygenase-1 mediates production of platelet thrombo

127 okines, inducible nitric oxide synthase, and cyclooxygenase-1 mRNA expression (P< or =0.013 for each)

128 E-7869 does not inhibit either cyclooxygenase-1 or cyclooxygenase-2.

129 ay exert antiplatelet properties through non-cyclooxygenase-1 pathways and deserves further investiga

130 OS-1 cells that overexpress iPLA(2)gamma and cyclooxygenase-1, PGE(2) production was induced by co-ex

131 aces (h2=0.266 to 0.762; P<0.01), but direct cyclooxygenase-1 phenotypes were not.

132 itric oxide (NO)-releasing derivative of the cyclooxygenase-1-preferring nonsteroidal anti-inflammato

133 esults reveal 15(S)-HETE as a major platelet cyclooxygenase-1 product with strong proangiogenic effec

134 teins including the monotopic lumenal enzyme cyclooxygenase 1 (prostaglandin H synthase 1) that share

135 in the spinal cord of diabetic rats, whereas cyclooxygenase-1 protein was reduced.

136 aggregation, indicative of aspirin-mediated cyclooxygenase-1 suppression, occurred in 95% and >99% o

137 transcripts of 5000 were induced >2.5-fold: cyclooxygenase-1, tenascin-C, and plasminogen activator

138 pathways directly and indirectly related to cyclooxygenase-1, the enzyme inhibited by ASA.

139 stanoids with diverse effects as mediated by cyclooxygenase-1 to the preferential synthesis of two pr

140 activation in pathways indirectly related to cyclooxygenase-1 was less pronounced and more variable (

141 shift in product profile was accentuated if cyclooxygenase-1 was permanently inactivated with aspiri

142 Conversely, cyclooxygenase-1 was significantly up-regulated.

143 Phenotypes indirectly related to cyclooxygenase-1 were strongly and consistently heritabl

144 t effects through irreversible inhibition of cyclooxygenase-1, whereas its anticancer effects may be

145 cyclooxygenase have been characterized: (i) cyclooxygenase-1, which is found in many tissues and is