ライフサイエンスコーパス: prostaglandin synthesis

1 ucts act downstream of PKC in TPA-stimulated prostaglandin synthesis.

2 ent with indomethacin, a potent inhibitor of prostaglandin synthesis.

3 aglandin synthase-1 present in 3T3 cells for prostaglandin synthesis.

4 males and appears to require intraganglionic prostaglandin synthesis.

5 ation of WNT ligand production and increased prostaglandin synthesis.

6 quired TLR4 signaling and was independent of prostaglandin synthesis.

7 without affecting related non-eCB lipids or prostaglandin synthesis.

8 an inflammatory component and/or increase in prostaglandin synthesis.

9 gs, such as aspirin or ibuprofen, that block prostaglandin synthesis.

10 trasynaptic NMDARs maximizes COX-2-dependent prostaglandin synthesis.

11 (COX), the rate-limiting step in vertebrate prostaglandin synthesis.

12 o induction of the cyclooxygenase 2 gene and prostaglandin synthesis.

13 gen atom from arachidonic acid, initializing prostaglandin synthesis.

14 during the LPS incubation without additional prostaglandin synthesis.

15 ) would be as effective as inhibiting global prostaglandin synthesis.

16 survival pathways, Abeta sequestration, and prostaglandin synthesis.

17 ession in Rb-/-PrE cell lines with increased prostaglandin synthesis.

18 sm of action of aspirin is the inhibition of prostaglandin synthesis.

19 ser to Group IV PLA2 and COX-2 for efficient prostaglandin synthesis.

20 e/burden is unrelated to their inhibition of prostaglandin synthesis.

21 ein expression with concomitant reduction of prostaglandin synthesis.

22 istry of the carbon-15 hydroxyl group during prostaglandin synthesis.

23 -1 and COX-2) catalyze the committed step in prostaglandin synthesis.

24 evels of COX-2 protein and mRNA and enhanced prostaglandin synthesis.

25 with indomethacin (40 microg/mL) to inhibit prostaglandin synthesis.

26 ry agents or NSAIDs are potent inhibitors of prostaglandin synthesis.

27 -+NO.) reacts directly with PGHS to activate prostaglandin synthesis.

28 ith an altered gingival lipid metabolism and prostaglandin synthesis.

29 ression, including an increased capacity for prostaglandin synthesis.

30 patent, state in fetal mice is dependent on prostaglandin synthesis.

31 nase (COX) inhibitors that inhibit mammalian prostaglandin synthesis affected the worm's motility but

32 Inhibition of prostaglandin synthesis alone had little affect on the r

33 which completely blocks the effect of CT on prostaglandin synthesis, also blocked that of PAF, sugge

34 results suggested that diclofenac inhibited prostaglandin synthesis and affected the carnitine shutt

35 role in the progression of colon cancer via prostaglandin synthesis and angiogenesis.

36 GHS-1 and -2) catalyze the committed step in prostaglandin synthesis and are targets for nonsteroidal

37 known to catalyze the rate-limiting step of prostaglandin synthesis and are the targets of nonsteroi

38 cible cyclooxygenase 2 spare gastric mucosal prostaglandin synthesis and do not damage the gastric mu

39 oidal anti-inflammatory drugs (NSAIDs) block prostaglandin synthesis and impair healing of gastrointe

40 of transcripts encoding enzymes involved in prostaglandin synthesis and metabolism.

41 The pathway involving prostaglandin synthesis and regulation was significantly

42 g and pentose phosphate pathways, as well as prostaglandin synthesis and regulatory proteins, compare

43 Prostaglandin synthesis and release by amnion cells in r

44 al application of diclofenac inhibited tumor prostaglandin synthesis and retarded angiogenesis and tu

45 ity, because specific fatty acids may affect prostaglandin synthesis and steroidogenesis.

46 y examined the relationship between enhanced prostaglandin synthesis and UVB-induced cataract formati

47 nto the intestinal lumen, where they promote prostaglandin synthesis and Wnt signaling.

48 B, IL10, STAT3 (inflammation), PTGS2, PTGES (prostaglandin synthesis), and PLA2G4A and ALOX5AP (eicos

49 ssion of genes related to hexose metabolism, prostaglandin synthesis, and glycosphingolipid biology t

50 latter response was blocked by inhibition of prostaglandin synthesis, and restored by addition of bot

51 of the C-13 pro-S hydrogen, the blocking of prostaglandin synthesis, and the formation of 15R-HETE a

52 c administration of a COX-2 inhibitor blocks prostaglandin synthesis at multiple sites, and may have

53 at this response does not require endogenous prostaglandin synthesis but may involve processes whereb

54 upting chemicals have been found to suppress prostaglandin synthesis, but to our knowledge, pesticide

55 the results for fibroblasts and macrophages, prostaglandin synthesis by activated mast cells is media

56 oid adenosine independently of inhibition of prostaglandin synthesis by COX-1 or COX-2 or of the pres

57 Prostaglandin synthesis by cyclooxygenases-1 and -2 (COX

58 at least in part to its ability to decrease prostaglandin synthesis by inhibiting the activity of cy

59 Perturbation of prostaglandin synthesis by manipulating Cox1 or Cox2 act

60 progressive microglial COX-1 expression and prostaglandin synthesis can underpin susceptibility to c

61 A study of oxytocin-stimulated prostaglandin synthesis capacity was performed in an adv

62 that, in addition to peripheral blockade of prostaglandin synthesis, central inhibition of cyclooxyg

63 increased HSC numbers, and those that block prostaglandin synthesis decreased stem cell numbers.

64 e studied to determine if these effects were prostaglandin synthesis dependent.

65 of prostaglandin H synthase, which mediates prostaglandin synthesis during inflammation, and which i

66 and significant upregulation (p < 0.0001) of prostaglandin-synthesising enzymes on brain tissue.

67 Cyclooxygenase-2 (COX-2) catalyzes prostaglandin synthesis from arachidonic acid and is exp

68 d COX-2 catalyze the first committed step of prostaglandin synthesis from arachidonic acid.

69 delay ulcer healing, presumably by blocking prostaglandin synthesis from cyclooxygenase (COX)-1 and

70 Cyclooxygenase-2 (COX-2)-mediated prostaglandin synthesis has recently been implicated in

71 gc1a), which acts upstream of Ptgs1-mediated prostaglandin synthesis, has a synergistic relationship

72 enase-2 (COX-2), the rate-limiting enzyme in prostaglandin synthesis, has been associated with growth

73 gs (NSAIDs) reduce nociception by inhibiting prostaglandin synthesis, however, the disruption of upst

74 We thus distinguish two pathways for prostaglandin synthesis: (i) an intracellular pathway by

75 play a significant role in murine mast cell prostaglandin synthesis, (ii) group V PLA2 mediates earl

76 periments did not support a role for IL-2 or prostaglandin synthesis in activating the HPA axis.

77 opolysaccharide and that selective rescue of prostaglandin synthesis in brain endothelial cells reins

78 We show in mice that selective deletion of prostaglandin synthesis in brain endothelial cells, but

79 ENT By using mice with selective deletion of prostaglandin synthesis in brain endothelial cells, we d

80 d polycyclic aromatic hydrocarbons (PAHs) on prostaglandin synthesis in endotoxin-activated murine ma

81 pecific matrix metalloproteinases (MMPs) and prostaglandin synthesis in fetal membranes.

82 Both mitogen-induced prostaglandin synthesis in fibroblasts and endotoxin-ind

83 rnesyltransferase inhibitor BZA-5B inhibited prostaglandin synthesis in H2122 cells by decreasing exp

84 ot inhibit endogenous expression of COX-2 or prostaglandin synthesis in lung carcinoma cells.

85 nthesis in fibroblasts and endotoxin-induced prostaglandin synthesis in macrophages require expressio

86 ding roles in olfaction, transportation, and prostaglandin synthesis in mammals.

87 Briefly preventing prostaglandin synthesis in newborn males with the COX in

88 signaling to sperm at a step after F-series prostaglandin synthesis in oocytes.

89 long-term objective of specific targeting of prostaglandin synthesis in prevention of preterm birth.

90 induced a threefold increase in LPS-mediated prostaglandin synthesis in the absence of significant ch

91 PAF may enhance prostaglandin synthesis in the corneal epithelium by inc

92 in-6 signaling and cyclooxygenase-1 mediated prostaglandin synthesis in the microglia were critical f

93 synthase [cyclooxygenase (Cox)]-independent prostaglandin synthesis in the ovary.

94 6Ralpha on brain endothelial cells to induce prostaglandin synthesis in these cells, probably in conc

95 hieved through pharmacological inhibition of prostaglandin synthesis in wild-type mice using a cycloo

96 (PLA2), the key enzyme in the regulation of prostaglandin synthesis, in kidney and vascular tissue o

97 Inhibiting NO and prostaglandin synthesis increased CGRP EC50 in Young and

98 protein that was suppressed by inhibitors of prostaglandin synthesis (indomethacin), adenylyl cyclase

99 However, with superimposition of acute prostaglandin synthesis inhibition (meclofenamate, 10 mg

100 ts of chronic NO synthase blockade and acute prostaglandin synthesis inhibition led to the equalizati

101 ought to derive from mechanisms unrelated to prostaglandin synthesis inhibition.

102 ctivate PPARs induced COX-2 independently of prostaglandin synthesis inhibition.

103 Injection of a prostaglandin synthesis inhibitor abolishes this attract

104 , the neuronal blocker tetrodotoxin, and the prostaglandin synthesis inhibitor indomethacin.

105 cts of LPS were inhibited by indomethacin, a prostaglandin synthesis inhibitor, and replicated by int

106 e not related because indomethacin, a potent prostaglandin synthesis inhibitor, does not prevent IL-1

107 Impairment of prostaglandin synthesis is a crucial step by which aspir

108 ehyde, a byproduct of lipid peroxidation and prostaglandin synthesis, is 3-(2'-deoxy-beta-D-erythro-p

109 the enzyme primarily responsible for induced prostaglandin synthesis, is an immediate early gene indu

110 ducible form of the rate-limiting enzyme for prostaglandin synthesis, is up-regulated in gastrointest

111 ts signals an arrest in the normal course of prostaglandin synthesis just prior to closing of the 5-m

112 of genes involved in water and salt balance, prostaglandin synthesis, keratinocyte differentiation as

113 mal experiments indicates that inhibitors of prostaglandin synthesis lower the risk of colon cancer.

114 Inhibition of prostaglandin synthesis may provide a novel treatment fo

115 e NSAIDs also cause dyspepsia, inhibition of prostaglandin synthesis may reduce this from even higher

116 looxygenase-2 (COX-2), an enzyme involved in prostaglandin synthesis, may be involved in the pathogen

117 By inhibiting prostaglandin synthesis, nonsteroidal anti-inflammatory

118 gned to determine the involvement of central prostaglandin synthesis on the pressor and bradycardic e

119 To determine the effect of inhibition of prostaglandin synthesis on UVB-induced cataract formatio

120 Blockade of ENaC, prostaglandin synthesis, or PGE2 receptors all reduce ma

121 ither erbB-1 receptor signal transduction or prostaglandin synthesis prevented the stimulatory effect

122 us treatment with an inhibitor of additional prostaglandin synthesis prevents this masculinization, i

123 dation of 2-AG in astrocytes provides AA for prostaglandin synthesis promoting LPS-induced neuroinfla

124 t cyclooxygenase activity and thereby reduce prostaglandin synthesis; prostaglandins stimulate aromat

125 upregulation of toll-like receptors (TLR4), prostaglandin synthesis (PTGS2 and PTGES), apoptosis (MM

126 chidonic acid, phospholipases (PLA2G10), and prostaglandin synthesis-related enzymes (PTGD/PTGS2S).

127 hat the sulfone lacks inhibitory activity on prostaglandin synthesis suggest a mechanism(s) of chemop

128 mmatory effects are rather caused by reduced prostaglandin synthesis than by activation of cannabinoi

129 s of COX-2 messenger RNA, COX-2 protein, and prostaglandin synthesis than conjugated bile acids.

130 gulate cyclooxygenase (COX-2), a mediator of prostaglandin synthesis that increases in the colon tumo

131 sults suggest that CDP-choline may stimulate prostaglandin synthesis through the activation of PLA2,

132 nctional roles, including nuclear transport, prostaglandin synthesis, ubiquitination, and transcripti

133 The demonstration that inhibition of prostaglandin synthesis via a cyclo-oxygenase (COX) enzy

134 To determine whether prostaglandin synthesis was required for progesterone pr

135 minophen, an analgesic that does not inhibit prostaglandin synthesis, was not associated with a reduc

136 All enzymes involved in prostaglandin synthesis were expressed in both adipose t

137 Blockade of prostaglandin synthesis with ibuprofen did not alter the

138 RG of males but not females, suggesting that prostaglandin synthesis within the DRG mediates the phos