COX 2, unactive, sheep placenta (Cyclooxygenase 2, PGHS 2, Prostaglandin Endoperoxide Synthase 2, PHS 2)

The prostanoid family includes PGD2, PGE2, PGF2alpha, PGI2, thromboxane A2 and prostaglandins. The prostaglandins (PGs) are implicated in various physiological and pathophysiological events, including male fertility, menstruation, ovulation, pregnancy, implantation and inflamatory and neoplastic diseases.\n\nThe biosynthesis of PGs and some other prostanoids, is catalyzed in a rate limiting step by PG-H synthase (also known as cyclooxygenase (COX), PG-endoperoxidase synthase (PTGS)) which converts arachidonic acid to prostaglandin/prostanoid precursor PGH2.\n\nTwo cyclooxygenase isozymes, COX1 (human, 576aa, 69-72kD; chromosome 9) and COX2 (human, 604aa, 74kD; chromosome 1) have been identified. COX1, a constitutively expressed isoform, produces physiologically relevant prostanoids such as those in stomach and platelets. COX2 isoform is inducible and rapidly upregulated at inflamation sites and forms proinflamatory prostanoids. The overexpression of COX-2 also leads to tumerogenesis. Recently, a third isoform COX3 (canine 633aa; ~65kD in human aorta) has been reported. Two smaller COX1-derived proteins (partial COX1) PCOX1a (canine 414aa, ~53kD in human aorta) and PCOX1b have also been characterized. The COX3, but not PCOX1a, possesses glycosylation dependent cyclooxygenase activity.\n\nThe nonsteroidal antiinflammatory drugs (NSAIDs) reduce the formation of prostaglandins by inhibiting the activity of cyclooxygenases (COX1, COX2 and COX3), This ability was associated with inhibition of COX, which converts arachidonic acid to the prostaglandin precursor prostaglandin H2.\n\nSource:\nOvine Placenta\n\nRecommended Use:\nMix with sample buffer, boil, and run on SDS gel. For best results, use 1ug per lane when developing with alkaline phosphatase.\n\nStorage and Stability:\nStable for several months at -20 degrees C and indefinitely at -70 degrees C.

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