ライフサイエンスコーパス: prostaglandin synthase

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1 the common precursor to all prostanoids, by prostaglandin synthase.

2 ollowed by sustained elevation in microsomal prostaglandin synthase 1 (mPGES-1) expression.

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

5 Expression of prostaglandin synthase-1 (PGHS1), prostaglandin D syntha

6 released in these contexts is unavailable to prostaglandin synthase-1 constitutively present in fibro

7 This arachidonate is then used by prostaglandin synthase-1 present in 3T3 cells for prosta

8 hesis by activated mast cells is mediated by prostaglandin synthase-1.

9 , in distal cells, arachidonate available to prostaglandin synthase-1.

10 Prostaglandin synthase 2 (PGS2) is an immediate-early ge

11 iated by prostaglandin synthase 1 (PGS1) and prostaglandin synthase 2 (PGS2), respectively.

12 eceptor (PR) signaling, and the induction of prostaglandin synthase 2 (Ptgs2).

13 hase that is dependent on activation-induced prostaglandin synthase 2 gene expression.

14 ligand stimulation is made available only to prostaglandin synthase-2, and (ii) a transcellular pathw

15 rophages require expression of the inducible prostaglandin synthase-2; arachidonate released in these

16 Both the prostaglandin synthase and the constitutive nitric oxide

17 f AGM, exhibit lower levels of expression of prostaglandin synthases and reduced phosphorylation of t

18 Bioactive prostaglandins produced by prostaglandin synthases and secreted by the prostate int

19 The inducible prostaglandin synthase cyclooxygenase-2 (COX-2) is aberr

20 Elevated expression of the prostaglandin synthase cyclooxygenase-2 (COX-2) is commo

21 The inducible prostaglandin synthase cyclooxygenase-2 (Cox-2) is overe

22 The prostaglandin synthase cyclooxygenase-2 (COX-2) is produ

23 Expression of the inducible prostaglandin synthase cyclooxygenase-2 appears critical

24 regulation in brain of an inducible form of prostaglandin synthase/cyclooxygenase, termed COX-2.

25 INDO, a powerful inhibitor of prostaglandin synthases (cyclooxygenases 1 and 2), did n

26 ect on COX-2 in this model, but did suppress prostaglandin synthase E2 production, presumably by inhi

27 expression, which resulted in a decrease in prostaglandin synthase E2 production.

28 ygenase-2 (COX-2) gene encodes the inducible prostaglandin synthase enzyme implicated in inflammation

29 ooxygenase (COX)-2 gene encodes an inducible prostaglandin synthase enzyme that is overexpressed in a

30 erence for coupling with distinct downstream prostaglandin synthases in vivo.

31 Clinical use of prostaglandin synthase-inhibiting NSAIDs is associated w

32 Cyclooxygenase (COX)-2, the inducible prostaglandin synthase, is overexpressed in cancer and c

33 The expression of none of the three prostaglandin synthases (microsomal PGES1, PGES2 and cys

34 results in cell-specific differential use by prostaglandin synthases of the accumulated prostaglandin

35 the common property of the NSAIDs to inhibit prostaglandin synthase (PHS) enzymes and thereby cause a

36 Further metabolism of PGH2-EA and PGH2-G by prostaglandin synthases produces a variety of prostaglan

37 factor (cornea-derived transcript 6), and a prostaglandin synthase (prostaglandin D(2) synthase).

38 y was to examine the role of cyclooxygenase (prostaglandin synthase [PTGS]) enzymes and prostaglandin

39 actions, thus combining features of both the prostaglandin synthase/squaline-hopine cyclase and the C

40 ynthase-2 (PGS-2) gene encodes an isoform of prostaglandin synthase that is transiently induced by pr

41 es similar in sequence to specific mammalian prostaglandin synthases, the cyclooxygenases.

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