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the algal PGHS lacks structural elements identified in all known animal PGHSs, such as epidermal growth factor-like domain and helix B in the membrane binding domain. The key residues of animal PGHS, like catalytic Tyr385 and heme liganding His388 are conserved in the algal enzyme, but the amino acid residues shown to be important for substrate binding and coordination, and the target residues for nonsteroidal anti-inflammatory drugs, Arg120, Tyr355, and Ser530, are not found at the appropriate positions in the algal sequences. The preferred substrate for the algal PGHS is arachidonic acid with cyclooxygenase reaction rate remarkably higher than values reported for mammalian PGHS isoforms
cervical distensibility is decreased in enzyme knockout mice on the day of expected delivery. Delayed parturition in enzyme knockout mice is the result of impaired luteolysis and cervical dilation
PGHS-1 inhibition in activated human plateletts significantly decreases PGHS-1-dependent thromboxane B2 formation in parallel with a decrease in platelet aggregation
prostaglandin H synthase-1 catalyzes the first two steps in prostaglandin synthesis; prostaglandin H synthase-2 catalyzes the first two steps in prostaglandin synthesis
the enzyme catalyzes the committed step in prostaglandin biosynthesis
aqueous extracts of Chromoleana odorata, commonly used in traditional medicine as antiinflammatory drug against pains or as cataplasm to stop hemorrhage in Ivory Coast, the essential oil extracted from the fresh leaves activates the cyclooxygenase activity of the PGHS, overview
neurotoxicity of the amphetamine analogues methamphetamine and 3,4-methylenedioxyamphetamine, the active metabolite of ecstasy, may involve their prostaglandin H synthase-dependent bioactivation to free radical intermediates that generate reactive oxygen species and oxidatively damage cellular macromolecules. The activation effect is blocked by irreversible enzyme inhibitor acetylsalicylic acid, overview
PHS is involved in the mechanism of thalidomide to cause increased embryonic DNA oxidation measured as 8-oxoguanine leading to embryopathies, phenotype, overview. A prostaglandin H synthase-dependent, reactive oxygen species-mediated mechanism. Thalidomide teratogenicity was blocked by maternal pretreatment with acetylsalicylic acid, an irreversible inhibitor of prostaglandin H synthase
seminal plasma-induced PTGS2 expression is mediated by intracellular signaling pathways involving MAPKs and NF-kappaB. Depending on cell type and stimulus, different intracellular signaling pathways are involved in inflammation and PTGS2 expression
physiological function
periovulatory expression of the Ptgs2 gene is essential for ovulation
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