EC Number   |
Activating Compound |
Reference |
|---|
    5.3.99.4 | 13-cis-retinoic acid |
induces prostaglandin-I synthase activity and expression of mRNA and protein, mediated by retinoic acid receptor. Actinomycin and cycloheximide both inhibit the retinoic acid-induced expression. 13-cis-Retinoic acid additionally increases the release of prostaglandin I2, both spontaneous and thrombin-induced. Co-incubation with 13-cis-retinoic acid and interleukin-1beta results in a synergic increase in the release of prostaglandin I2 |
693514 |
| 5.3.99.4 | dithiothreitol |
increase in activity with increasing glutathione concentration from 0.1 mM up to 5 mM |
3127 |
| 5.3.99.4 | High density lipoprotein cholesterol |
1.0 mg/ml stimulates 21%. Lower concentrations inhibit, 16% inhibition by 0.25 mg/ml |
37462 |
| 5.3.99.4 | interleukin-1 |
- |
702474 |
| 5.3.99.4 | interleukin-6 |
- |
702474 |
| 5.3.99.4 | Low density lipoprotein cholesterol |
0.5 mg/ml stimulates 27%. Inhibition at higher concentrations |
37462 |
| 5.3.99.4 | more |
constitutive expression of prostaglandin-I synthase and cyclooxygenase-1 in HK cells, while expression of cyclooxygenase-2 and prostaglandin-E synthase are up-regulated in response to tumor necrosis factor-alpha, tumor growth factor-beta, and lipopolysaccharide |
693452 |
| 5.3.99.4 | more |
the extent of prostaglandin I2 production is determined by an appropriate ratio of COX-1/COX-2 to PGIS. Human vascular endothelial cells transfected with a construct that contains COX-1 and prostaglandin-I synthase cDNAs have an equivalent increase in COX-1 and PGIS, and produce a large quantity of prostaglandin-I synthase which is more than 200fold over that produced by untransfected cells |
660924 |
| 5.3.99.4 | NO |
activation at moderate concentration, inhibition at high concentrations. Hemoglobin prevents both, activation and inhibition |
37485 |
| 5.3.99.4 | reduced glutathione |
increase in activity with increasing glutathione concentration from 0.1 mM up to 5 mM |
3127 |
