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1 ed by measuring rates of MDA production from prostaglandin endoperoxide.
2 alyze the oxygenation of arachidonic acid to prostaglandin endoperoxides.
3 to chemically unstable products, such as the prostaglandin endoperoxides and leukotriene A(4) epoxide
7 dicals have been detected during turnover of prostaglandin endoperoxide H synthase (PGHS), and they a
10 e substrate channel leads to inactivation of prostaglandin endoperoxide H synthase, the three serine
11 inhibit the cyclooxygenase (COX) activity of prostaglandin endoperoxide H synthase, which ultimately
12 s formed by native and mutant forms of ovine prostaglandin endoperoxide H synthase-1 (oPGHS-1) have s
14 tudies of the crystal structure of the ovine prostaglandin endoperoxide H synthase-1 (PGHS-1)/S-flurb
19 ed with dexamethasone but not by SC 58125, a prostaglandin endoperoxide H synthase-2 (PGHS-2)-selecti
23 (PGG(2)) by the cyclooxygenase activities of prostaglandin endoperoxide H synthases (PGHSs) 1 and 2.
28 that forms the cyclooxygenase active site of prostaglandin endoperoxide H synthases (PGHSs)-1 and -2.
39 induces conformational changes in the human prostaglandin endoperoxide H(2) synthase enzyme (PGHS-2)
42 unctional pairs with specific members of the prostaglandin-endoperoxide H synthase (PGHS) family.
43 ramatically induces hyaluronan synthesis and prostaglandin-endoperoxide H synthase 2 in human orbital
44 erone, p23, and associates functionally with prostaglandin-endoperoxide H synthase-1 (PGHS-1), the co
45 gulation is mediated through an induction of prostaglandin-endoperoxide H synthase-2 (PGHS-2), the in
51 (COX) which converts arachidonic acid to the prostaglandin endoperoxide PGH2, from which all other pr
52 (CYP450) enzyme catalyzing the conversion of prostaglandin endoperoxide (PGH2) into thromboxane A2 (T
54 (PG) D2 through utilization of constitutive prostaglandin endoperoxide synthase (PGHS) -1 and induce
55 dal antiinflammatory agents (NSAIDs) bind to prostaglandin endoperoxide synthase (PGHS) and induce a
61 nic acid substrate was also not available to prostaglandin endoperoxide synthase 1 in the immediate p
62 enhanced ovarian expression of PLA(2)G4A and prostaglandin endoperoxide synthase 2 (PTGS2) in wild-ty
63 volves the activation-dependent induction of prostaglandin endoperoxide synthase 2 and the supply of
64 thout affecting the levels of NO synthase or prostaglandin endoperoxide synthase or by inhibiting the
66 duction of prostaglandin G/H synthase (PGHS; prostaglandin endoperoxide synthase, cyclooxygenase) by
67 Cyclooxygenase (COX), also referred to as prostaglandin endoperoxide synthase, is the rate-limitin
68 Ca2+]i) elevation in regulating ET-1-induced prostaglandin endoperoxide synthase, prostaglandin G/H s
69 p-regulation of the constitutively expressed prostaglandin endoperoxide synthase, Ptgs1 (Cox-1), a nu
70 r F2-isoprostanes, is a minor product of the prostaglandin endoperoxide synthase-1 (PG G/H S-1) expre
71 m of action of this drug, we expressed human prostaglandin endoperoxide synthase-1 (PGHS-1) and PGHS-
72 nation of the crystal structure of the ovine prostaglandin endoperoxide synthase-1 (PGHS-1)/S- flurbi
73 orted to inhibit arachidonate oxygenation by prostaglandin endoperoxide synthase-1 and -2 (PGHS-1 and
74 al hypoperfusion increases the expression of prostaglandin endoperoxide synthase-2 (PGHS-2) in ovine
76 sly, we have shown that forced expression of prostaglandin endoperoxide synthase-2 [also called cyclo
77 t the cyclooxygenase-2 (COX-2, also known as prostaglandin endoperoxide synthase-2) signaling cascade
78 repressed the mRNA and protein expression of prostaglandin endoperoxide synthase/cyclooxygenase-2 (CO
80 chanisms of damage involve the activities of prostaglandin-endoperoxide synthase 1 (PTGS1 or cyclooxy
81 se domain mutations, but only a single gene, prostaglandin-endoperoxide synthase 1/cyclooxgenase 1 (P
82 imental evidence suggests that inhibition of prostaglandin-endoperoxide synthase 2 (PTGS2) (also know
83 teraction) = 0.02) with a genetic variant in prostaglandin-endoperoxide synthase 2 (PTGS2) (rs1204276
85 s that constitutively express high levels of prostaglandin-endoperoxide synthase 2 (Ptgs2, also known
86 es a role of RAF kinases in up-regulation of prostaglandin-endoperoxide synthase 2 (PTGS2, cyclooxyge
87 ionship between levels of MIC1 and levels of prostaglandin-endoperoxide synthase 2 expression (PTGS2
88 ted Myd88(-/-) (TLR signaling-deficient) and prostaglandin-endoperoxide synthase 2(-/-) (Ptgs2(-/-))
89 of transfected A549 cells showed that PTGS2 (prostaglandin-endoperoxide synthase 2) was one of the hi
90 TGS2 (also known as COX2), the gene encoding prostaglandin-endoperoxide synthase 2, allowing activate
91 Alternatively, celecoxib, an inhibitor of prostaglandin-endoperoxide synthase 2, reduced polyp num
93 s as a neuroendocrine factor that stimulates prostaglandin-endoperoxide synthase [cyclooxygenase (Cox
94 umatoid arthritis to inhibit cyclooxygenase (prostaglandin-endoperoxide synthase), thereby decreasing
97 rleukin-8, toll-like receptor 4, cryropyrin, prostaglandin-endoperoxide synthase-2, and heparinase ge
98 din E(2) (PGE(2)) and its processing enzyme, prostaglandin-endoperoxide-synthase-2/ cyclooxygenase-2
100 ase activities of constitutive and inducible prostaglandin endoperoxide synthases by serving as a sub
102 with its primary mode of action in mammals (prostaglandin-endoperoxide synthases) but modulated gene
103 receptor (AR) agonist and a thromboxane A(2)/prostaglandin endoperoxide (TP) receptor antagonist, whi
104 o most extensively characterized thromboxane/prostaglandin endoperoxide (TP) receptors, from human pl
107 alyze the oxygenation of arachidonic acid to prostaglandin endoperoxides, which are the common interm
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