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1 zymes, endothelial nitric oxide synthase and prostacyclin synthase.
2 uced insulin-resistant mice--inactivation of prostacyclin synthase and eNOS was prevented by inhibiti
3 tivated 2 important antiatherogenic enzymes, prostacyclin synthase and eNOS.
4 d ELPCs (expressing cyclooxygenase isoform 1-prostacyclin synthase and nuRFP) were tested in rats wit
5 y, we observed that COX-2 deletion decreased prostacyclin synthase and production and peroxisome prol
6 ric oxide synthase-3) nitric oxide synthase, prostacyclin synthase, and constitutive cyclooxygenase (
7                       Nitric oxide synthase, prostacyclin synthase, and tissue inhibitors of metallop
8 NA and protein levels of cPLA(2), COX-2, and prostacyclin synthase, as well as the promoter and enzym
9                            Similarly, bovine prostacyclin synthase catalyzed the isomerization of the
10 und II in analogy with plant AOS (CYP74) and prostacyclin synthase (CYP8A1).
11 tacyclin) by lung-specific overexpression of prostacyclin synthase decreases lung tumor incidence and
12 HIF-responsive genes (VEGF-A, PPARgamma, and prostacyclin synthase) due to an insufficient increase i
13                     Cyclooxygenase isoform 1-prostacyclin synthase-expressing ELPCs reversed MCT-indu
14 ressing a human cyclooxygenase isoform 1 and prostacyclin synthase fusion protein that produces prost
15  activation suppressed tyrosine nitration of prostacyclin synthase in diabetes.
16 ypothesized that pulmonary overexpression of prostacyclin synthase may prevent the development of mur
17  addition of AICAR reduced both O(2).(-) and prostacyclin synthase nitration caused by high glucose,
18 lting in the inhibition of both O(2).(-) and prostacyclin synthase nitration in diabetes.
19 P-2 expression and reduced both O(2).(-) and prostacyclin synthase nitration in diabetic wild-type mi
20 CP-2 significantly ablated both O(2).(-) and prostacyclin synthase nitration triggered by high glucos
21 ) increased superoxide anions (O(2).(-)) and prostacyclin synthase nitration.
22     Transgenic FVB/N mice with lung-specific prostacyclin synthase overexpression were exposed to mai
23     Transgenic mice with selective pulmonary prostacyclin synthase overexpression were exposed to two
24               We hypothesized that pulmonary prostacyclin synthase overexpression would prevent lung
25 nes (angiotensin-converting enzyme [ACE] and prostacyclin synthase [PGI2S]) were measured in samples
26 ived from adenoviral cyclo-oxygenase (COX)-1/prostacyclin synthase (PGIS) (Adv-COPI) gene transfer in
27               The eicosanoid pathway enzymes prostacyclin synthase (PGIS) and inducible prostaglandin
28 s to determine whether tyrosine nitration of prostacyclin synthase (PGIS) contributes to retinal cell
29                                              Prostacyclin synthase (PGIS) is a membrane-bound class I
30                                              Prostacyclin synthase (PGIS) is the final committed enzy
31                                              Prostacyclin synthase (PGIS) is tyrosine nitrated in dis
32      The most significant interaction was at prostacyclin synthase (PGIS) rs5602 (OR = 0.34, 95% CI 0
33                                              Prostacyclin synthase (PGIS), a cytochrome P450 enzyme,
34 sis via tyrosine nitration and inhibition of prostacyclin synthase (PGIS), an enzyme with antithrombo
35 rdinate up-regulation of cPLA(2), COX-2, and prostacyclin synthase (PGIS).
36 ransfected with the cyclooxygenase isoform 1-prostacyclin synthase plasmid and labeled with lentiviru
37               We demonstrated differences of prostacyclin synthase promoter activities dependent on t
38                                              Prostacyclin synthase promoter haplotypes' transcription
39 g prostacyclin analogs, we hypothesized that prostacyclin synthase promoter sequence variants associa
40                                              Prostacyclin synthase promoter sequence variants exhibit
41         We identified a comprehensive set of prostacyclin synthase promoter variants and tested their
42 in reaction approaches were used to genotype prostacyclin synthase promoter variants in more than 300
43             To determine the distribution of prostacyclin synthase promoter variants in PAH, unaffect
44 iscovered a significant bias for more active prostacyclin synthase promoter variants in unaffected ca
45 86-fold), cyclooxygenase I (COX1, 4.5-fold), prostacyclin synthase (PTGIS, 5.66-fold), thromboxane A2
46 tion factor Gata6 controls the expression of prostacyclin synthase, which is required for prostacycli
47 try analysis showed that CBP/p300 acetylates prostacyclin synthase, which regulates Treg differentiat