5.3.99.4: prostaglandin-I synthase
This is an abbreviated version!
For detailed information about prostaglandin-I synthase, go to the full flat file.
Word Map on EC 5.3.99.4
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5.3.99.4
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thromboxane
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cyclooxygenase
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endothelial
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arachidonic
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artery
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platelet
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cox-2
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vasodilator
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hypertension
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prostanoids
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endoperoxide
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eicosanoids
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pulmonary
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vessel
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indomethacin
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aorta
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6-keto-pgf1
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tranylcypromine
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peroxynitrite
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vasoconstriction
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endothelium-dependent
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6-keto-prostaglandin
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6-keto-pgf1alpha
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phosphoglucose
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iloprost
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tx
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mpges-1
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medicine
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6-keto
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antithrombotic
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5-lipoxygenase
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dazoxiben
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heme-thiolate
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ptges
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f1alpha
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synthase-1
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beraprost
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15-hpete
- 5.3.99.4
-
thromboxane
-
cyclooxygenase
- endothelial
-
arachidonic
- artery
- platelet
- cox-2
-
vasodilator
- hypertension
-
prostanoids
-
endoperoxide
-
eicosanoids
- pulmonary
- vessel
- indomethacin
- aorta
-
6-keto-pgf1
- tranylcypromine
- peroxynitrite
-
vasoconstriction
-
endothelium-dependent
-
6-keto-prostaglandin
-
6-keto-pgf1alpha
-
phosphoglucose
-
iloprost
- tx
- mpges-1
- medicine
-
6-keto
-
antithrombotic
-
5-lipoxygenase
- dazoxiben
-
heme-thiolate
- ptges
- f1alpha
- synthase-1
-
beraprost
- 15-hpete
Reaction
Synonyms
Aortic cytochrom P450, CYP8A1, PGI synthase, PGI2 synthase, PGI2 synthetase, PGI2-S, PGIS, prostacyclin synthase, Prostacyclin synthetase, prostacyclin-synthase, prostacyclin/PGI2 synthase, Prostacycline synthetase, prostaglandin I synthase, Prostaglandin I2 synthase, Prostaglandin I2 synthetase, Ptgis, Synthetase, prostacyclin
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medicine
medicine
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manipulation of prostaglandin production distal to cyclooxygenase significantly reduces lung carcinogenesis in a tobacco smoke exposure model
medicine
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overexpression of PGIS is highly effective in controlling vascular diseases and ischemia-reperfusion tissue injury, gene transfer of bicistronic COX-1/PGIS has the potential for treatment of diverse clinical disorders including vascular diseases, pulmonary hypertension, and ischemia-reperfusion cerebral and cardiac injury
medicine
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prostaglandin-I synthase protects the brain by enhancing prostaglandin I2 synthesis and creating a favorable prostaglandin I2/thromboxane A2 ratio, prostaglandin-I synthase expression after ischemic insult is important in promoting neuronal cell survival
medicine
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the enzyme acts as a regulator of thyroid papillary carcinoma proliferation, increased expression levels may play a role in the pathogenesis of these tumors
medicine
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exposure of isolated coronary arteries to high glucose switches angiotensin II-stimulated prostacyclin-dependent relaxation into a persitent vascoconstriction. High glucose, but not mannitol, significantly increases superoxide and nitration of tyrosine in prostacyclin synthase. Concurrent administration of polyethylene-coated superoxide dismutase, L-nitroarginine methyl ester, or sepiapterin abolishes enzyme nitration, as well as its association with endothelial nitric oxide synthase
medicine
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significant suppression of enzyme activity in parallel with increased superoxide and enzyme nitration in the aortas of diabetic C57BL6 mice, but less effect in diabetic mice either lacking endothelial nitric oxide synthase or overexpressing human superoxide dismutase
medicine
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study on involvement of enzyme polymorphism in adenomatous or hyperplastic colorectal polyps. The enzyme promoter polymorphism may affect risk of colorectal polyps and modify the effects of nonsteroidal anti-inflammatory drug use on polyp risk
medicine
synthesis of prostaglandin by enzyme contributes to renal protection against endotoxemia-related acute kidney injury
medicine
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upregulation of prostaglandin I2 synthesis by expression of a fusion protein linking cyclooxygenase COX-2 and prostacyclin synthase shows strong activity in inhibiting platelet aggregation induced by arachidonic acid in vitro and may be used for therapeutic inventions for strokes and heart attacks
medicine
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after culture of embryos in presence of the selective cyclooxygenase-1 inhibitor SC560, the selective cyclooxygenase-2 inhibitor NS398, or the selective prostacyclin synthase inhibitor U51605 in a 48-h culture, the implantation rate decreases with exposure to either the cyclooxygenase-2 inhibitor of the prostaglandin-I synthase inhibitor, which is increased further after supplementation with prostaglandin I2. The level of prostaglandin I2 is also higher at the 8-16 cell stage, compaction and blastocyst stage than prostaglandin E2
medicine
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by impairing prostacyclin synthase function, and thus PGI2 release, C-reactive protein, CRP, could promote endothelial dysfunction and participate in the development of coronary artery disease
medicine
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it is hypothesized that the combination of prostacyclin synthase overexpression and epidermal growth factor receptor tyrosine kinase inhibitor, EGFR TKI, would lead to augmented chemoprevention for lung cancer
medicine
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prostacyclin synthase overexpression apparently protects insulin-producing cells against cytokine toxicity via suppression of endoplasmic reticulum and mitochondrial stress-mediated cell death pathways
medicine
sustained release of prostaglandin I2 enhances the proangiogenic function of mesenchymal stem cells and subsequent muscle cell regrowth in the ischemic tissue suggesting potential therapeutic benefits of cell-based gene therapy for critical limb ischemia
medicine
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tyrosine nitration of prostacyclin synthase is correlated with an excessive inflammatory response in atherosclerotic carotid arteries from patients with type 2 diabetes
medicine
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co-adjuvant therapy with enzyme enhancers, such as retinoids, has therapeutic value for head and neck squamous cell carcinoma treatment