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1 n G2 by the cyclooxygenase (COX) activity of prostaglandin endoperoxide synthases.
2 nic acid substrate was also not available to prostaglandin endoperoxide synthase 1 in the immediate p
3 chanisms of damage involve the activities of prostaglandin-endoperoxide synthase 1 (PTGS1 or cyclooxy
4 se domain mutations, but only a single gene, prostaglandin-endoperoxide synthase 1/cyclooxgenase 1 (P
5 r F2-isoprostanes, is a minor product of the prostaglandin endoperoxide synthase-1 (PG G/H S-1) expre
6 m of action of this drug, we expressed human prostaglandin endoperoxide synthase-1 (PGHS-1) and PGHS-
7 nation of the crystal structure of the ovine prostaglandin endoperoxide synthase-1 (PGHS-1)/S- flurbi
8 orted to inhibit arachidonate oxygenation by prostaglandin endoperoxide synthase-1 and -2 (PGHS-1 and
9 enhanced ovarian expression of PLA(2)G4A and prostaglandin endoperoxide synthase 2 (PTGS2) in wild-ty
10 volves the activation-dependent induction of prostaglandin endoperoxide synthase 2 and the supply of
11 imental evidence suggests that inhibition of prostaglandin-endoperoxide synthase 2 (PTGS2) (also know
12 teraction) = 0.02) with a genetic variant in prostaglandin-endoperoxide synthase 2 (PTGS2) (rs1204276
14 s that constitutively express high levels of prostaglandin-endoperoxide synthase 2 (Ptgs2, also known
15 es a role of RAF kinases in up-regulation of prostaglandin-endoperoxide synthase 2 (PTGS2, cyclooxyge
16 ionship between levels of MIC1 and levels of prostaglandin-endoperoxide synthase 2 expression (PTGS2
17 ted Myd88(-/-) (TLR signaling-deficient) and prostaglandin-endoperoxide synthase 2(-/-) (Ptgs2(-/-))
18 of transfected A549 cells showed that PTGS2 (prostaglandin-endoperoxide synthase 2) was one of the hi
19 TGS2 (also known as COX2), the gene encoding prostaglandin-endoperoxide synthase 2, allowing activate
20 Alternatively, celecoxib, an inhibitor of prostaglandin-endoperoxide synthase 2, reduced polyp num
22 al hypoperfusion increases the expression of prostaglandin endoperoxide synthase-2 (PGHS-2) in ovine
24 sly, we have shown that forced expression of prostaglandin endoperoxide synthase-2 [also called cyclo
25 t the cyclooxygenase-2 (COX-2, also known as prostaglandin endoperoxide synthase-2) signaling cascade
28 rleukin-8, toll-like receptor 4, cryropyrin, prostaglandin-endoperoxide synthase-2, and heparinase ge
29 din E(2) (PGE(2)) and its processing enzyme, prostaglandin-endoperoxide-synthase-2/ cyclooxygenase-2
31 with its primary mode of action in mammals (prostaglandin-endoperoxide synthases) but modulated gene
32 ase activities of constitutive and inducible prostaglandin endoperoxide synthases by serving as a sub
33 s as a neuroendocrine factor that stimulates prostaglandin-endoperoxide synthase [cyclooxygenase (Cox
34 duction of prostaglandin G/H synthase (PGHS; prostaglandin endoperoxide synthase, cyclooxygenase) by
35 repressed the mRNA and protein expression of prostaglandin endoperoxide synthase/cyclooxygenase-2 (CO
36 Cyclooxygenase (COX), also referred to as prostaglandin endoperoxide synthase, is the rate-limitin
38 thout affecting the levels of NO synthase or prostaglandin endoperoxide synthase or by inhibiting the
39 (PG) D2 through utilization of constitutive prostaglandin endoperoxide synthase (PGHS) -1 and induce
40 dal antiinflammatory agents (NSAIDs) bind to prostaglandin endoperoxide synthase (PGHS) and induce a
46 Ca2+]i) elevation in regulating ET-1-induced prostaglandin endoperoxide synthase, prostaglandin G/H s
49 p-regulation of the constitutively expressed prostaglandin endoperoxide synthase, Ptgs1 (Cox-1), a nu
50 umatoid arthritis to inhibit cyclooxygenase (prostaglandin-endoperoxide synthase), thereby decreasing
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