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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.
41 thesis-the conversion of arachidonic acid to prostaglandin endoperoxide H(2) Both COX isoforms are se
42 induces conformational changes in the human prostaglandin endoperoxide H(2) synthase enzyme (PGHS-2)
46 unctional pairs with specific members of the prostaglandin-endoperoxide H synthase (PGHS) family.
47 ramatically induces hyaluronan synthesis and prostaglandin-endoperoxide H synthase 2 in human orbital
48 erone, p23, and associates functionally with prostaglandin-endoperoxide H synthase-1 (PGHS-1), the co
49 gulation is mediated through an induction of prostaglandin-endoperoxide H synthase-2 (PGHS-2), the in
55 (COX) which converts arachidonic acid to the prostaglandin endoperoxide PGH2, from which all other pr
56 (CYP450) enzyme catalyzing the conversion of prostaglandin endoperoxide (PGH2) into thromboxane A2 (T
58 (PG) D2 through utilization of constitutive prostaglandin endoperoxide synthase (PGHS) -1 and induce
59 dal antiinflammatory agents (NSAIDs) bind to prostaglandin endoperoxide synthase (PGHS) and induce a
65 nic acid substrate was also not available to prostaglandin endoperoxide synthase 1 in the immediate p
66 nase, ephrin-A receptor 2 (EPHA2), regulates prostaglandin endoperoxide synthase 2 (PTGS2) (encodes C
67 enhanced ovarian expression of PLA(2)G4A and prostaglandin endoperoxide synthase 2 (PTGS2) in wild-ty
68 volves the activation-dependent induction of prostaglandin endoperoxide synthase 2 and the supply of
69 thout affecting the levels of NO synthase or prostaglandin endoperoxide synthase or by inhibiting the
71 duction of prostaglandin G/H synthase (PGHS; prostaglandin endoperoxide synthase, cyclooxygenase) by
72 Cyclooxygenase (COX), also referred to as prostaglandin endoperoxide synthase, is the rate-limitin
73 Ca2+]i) elevation in regulating ET-1-induced prostaglandin endoperoxide synthase, prostaglandin G/H s
74 p-regulation of the constitutively expressed prostaglandin endoperoxide synthase, Ptgs1 (Cox-1), a nu
75 r F2-isoprostanes, is a minor product of the prostaglandin endoperoxide synthase-1 (PG G/H S-1) expre
76 m of action of this drug, we expressed human prostaglandin endoperoxide synthase-1 (PGHS-1) and PGHS-
77 nation of the crystal structure of the ovine prostaglandin endoperoxide synthase-1 (PGHS-1)/S- flurbi
78 orted to inhibit arachidonate oxygenation by prostaglandin endoperoxide synthase-1 and -2 (PGHS-1 and
79 al hypoperfusion increases the expression of prostaglandin endoperoxide synthase-2 (PGHS-2) in ovine
81 sly, we have shown that forced expression of prostaglandin endoperoxide synthase-2 [also called cyclo
82 t the cyclooxygenase-2 (COX-2, also known as prostaglandin endoperoxide synthase-2) signaling cascade
83 repressed the mRNA and protein expression of prostaglandin endoperoxide synthase/cyclooxygenase-2 (CO
85 chanisms of damage involve the activities of prostaglandin-endoperoxide synthase 1 (PTGS1 or cyclooxy
86 pithelium and included IL-1 receptor like 1, prostaglandin-endoperoxide synthase 1, CCL26, and perios
87 se domain mutations, but only a single gene, prostaglandin-endoperoxide synthase 1/cyclooxgenase 1 (P
88 cyclooxygenase 2 (COX-2) gene, also known as prostaglandin-endoperoxide synthase 2 ( PTGS2), occurs i
89 s, such as histamine and proteases, activate prostaglandin-endoperoxide synthase 2 (also called COX2)
90 imental evidence suggests that inhibition of prostaglandin-endoperoxide synthase 2 (PTGS2) (also know
91 teraction) = 0.02) with a genetic variant in prostaglandin-endoperoxide synthase 2 (PTGS2) (rs1204276
92 into the nucleus.Notably, after OT challenge prostaglandin-endoperoxide synthase 2 (PTGS2) expression
93 rowth/differentiation factor 15 (GDF15), and Prostaglandin-endoperoxide synthase 2 (PTGS2) genes, pre
95 s that constitutively express high levels of prostaglandin-endoperoxide synthase 2 (Ptgs2, also known
96 es a role of RAF kinases in up-regulation of prostaglandin-endoperoxide synthase 2 (PTGS2, cyclooxyge
98 ionship between levels of MIC1 and levels of prostaglandin-endoperoxide synthase 2 expression (PTGS2
99 ted Myd88(-/-) (TLR signaling-deficient) and prostaglandin-endoperoxide synthase 2(-/-) (Ptgs2(-/-))
100 of transfected A549 cells showed that PTGS2 (prostaglandin-endoperoxide synthase 2) was one of the hi
101 TGS2 (also known as COX2), the gene encoding prostaglandin-endoperoxide synthase 2, allowing activate
102 Alternatively, celecoxib, an inhibitor of prostaglandin-endoperoxide synthase 2, reduced polyp num
104 s as a neuroendocrine factor that stimulates prostaglandin-endoperoxide synthase [cyclooxygenase (Cox
105 umatoid arthritis to inhibit cyclooxygenase (prostaglandin-endoperoxide synthase), thereby decreasing
109 rleukin-8, toll-like receptor 4, cryropyrin, prostaglandin-endoperoxide synthase-2, and heparinase ge
110 din E(2) (PGE(2)) and its processing enzyme, prostaglandin-endoperoxide-synthase-2/ cyclooxygenase-2
112 ase activities of constitutive and inducible prostaglandin endoperoxide synthases by serving as a sub
114 with its primary mode of action in mammals (prostaglandin-endoperoxide synthases) but modulated gene
115 rved in carcinogenesis, prostaglandins (PG), prostaglandin-endoperoxide synthases, and PG receptors a
116 receptor (AR) agonist and a thromboxane A(2)/prostaglandin endoperoxide (TP) receptor antagonist, whi
117 o most extensively characterized thromboxane/prostaglandin endoperoxide (TP) receptors, from human pl
120 alyze the oxygenation of arachidonic acid to prostaglandin endoperoxides, which are the common interm