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 quired TLR4 signaling and was independent of prostaglandin synthesis.

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

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

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

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

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

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

11 gen atom from arachidonic acid, initializing prostaglandin synthesis.

12 during the LPS incubation without additional prostaglandin synthesis.

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

14 survival pathways, Abeta sequestration, and prostaglandin synthesis.

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

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

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

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

19 ein expression with concomitant reduction of prostaglandin synthesis.

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

21 -1 and COX-2) catalyze the committed step in prostaglandin synthesis.

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

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

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

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

26 ith an altered gingival lipid metabolism and prostaglandin synthesis.

27 ression, including an increased capacity for prostaglandin synthesis.

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

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

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

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

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

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

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

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

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

37 Prostaglandin synthesis and release by amnion cells in r

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

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

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

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

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

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

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

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

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

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

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

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

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

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

52 Perturbation of prostaglandin synthesis by manipulating Cox1 or Cox2 act

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

79 6Ralpha on brain endothelial cells to induce prostaglandin synthesis in these cells, probably in conc

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

99 By inhibiting prostaglandin synthesis, nonsteroidal anti-inflammatory

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

115 To determine whether prostaglandin synthesis was required for progesterone pr

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

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

118 Blockade of prostaglandin synthesis with ibuprofen did not alter the