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1 the common precursor to all prostanoids, by prostaglandin synthase.
3 te phases of PGD2 generation are mediated by prostaglandin synthase 1 (PGS1) and prostaglandin syntha
4 phases, an early phase that is dependent on prostaglandin synthase 1 and a delayed phase that is dep
6 released in these contexts is unavailable to prostaglandin synthase-1 constitutively present in fibro
7 zing enzymes cyclooxygenase-2 and microsomal prostaglandin synthase-1 in brain endothelial cells, kno
16 ligand stimulation is made available only to prostaglandin synthase-2, and (ii) a transcellular pathw
17 rophages require expression of the inducible prostaglandin synthase-2; arachidonate released in these
19 f AGM, exhibit lower levels of expression of prostaglandin synthases and reduced phosphorylation of t
28 ect on COX-2 in this model, but did suppress prostaglandin synthase E2 production, presumably by inhi
30 ygenase-2 (COX-2) gene encodes the inducible prostaglandin synthase enzyme implicated in inflammation
31 ooxygenase (COX)-2 gene encodes an inducible prostaglandin synthase enzyme that is overexpressed in a
36 also downregulated cell adhesion molecules, prostaglandin synthases, mast cell tryptases, MMP1, MMP1
38 results in cell-specific differential use by prostaglandin synthases of the accumulated prostaglandin
39 the common property of the NSAIDs to inhibit prostaglandin synthase (PHS) enzymes and thereby cause a
40 Further metabolism of PGH2-EA and PGH2-G by prostaglandin synthases produces a variety of prostaglan
41 factor (cornea-derived transcript 6), and a prostaglandin synthase (prostaglandin D(2) synthase).
42 y was to examine the role of cyclooxygenase (prostaglandin synthase [PTGS]) enzymes and prostaglandin
43 actions, thus combining features of both the prostaglandin synthase/squaline-hopine cyclase and the C
44 ynthase-2 (PGS-2) gene encodes an isoform of prostaglandin synthase that is transiently induced by pr