Anti-COX-3 (Cyclooxygenase-3, PGH Synthase)

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. The 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 arachiodonic acid to prostaglandin/prostanoid precursor PGH2. Two cyclooxygenase isozymes, COX1 (human, 576aa, 69-72kD, chromosome 9) and COX2 (human, 604aa, 74kD, chromosome 1) have been identified. COX1 is a constitutively expressed isoform. it produces physiologically relevant prostanoids such as those in stomach and platelets. COX2 isoform is inducible. it is rapidly upregulated at inflamation sites. It forms proinflamatory prostanoids. The overexpression of COX2 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. The nonsteroidal anti-inflammatory 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. COX3 and PCOX1a are made from the COX1 gene but retain intron 1 in their mRNAs. PCOX-1b (53kD) lacks the intron 1. This intron introduces an insertion of 30-34aa, depending on mammalian species, into hydrophobic signal peptide that directs COX1 into the lumen of endoplasmic reticulum and nucrear envelope. The signal peptide is cleaved in both COX1 and COX2 proteins. In COX3 and PCOX1a, this signal peptide is retained. Both proteins are glycosylated. The COX3 and PCOX mRNAs are expressed in canine cerebral cortex and in lesser amounts in other tissues analyzed. In humans, COX3 mRNA is most abundant in cerebral cortex and heart. COX3 and PCOX1A are expressed efficiently in insect cells as membrane-bound proteins. The nonsteroidal antiinflammatory drugs (NSAIDs) reduce the formation of prostaglandins by inhibiting the activity of cyclooxygenases (COX1, COX2 and COX3). COX3 activity is selectively inhibited by analgesic/antipyretic drugs such as acetaminophen, phenacetin, antipyrine and dipyrone. It is potently inhibited by some nonsteroidal anti-inflammatory drugs. Inhibition of COX3 could represent a primary central mechanism by which these drugs decrease pain and possibly fever. , Applications: , Suitable for use in ELISA. Western Blot, though not tested, may potentially be used as an application. Other applications not tested. Recommended Dilution: Western Blot: 1-10ug/ml (ECL). Recognizes ~65kD (COX3) and ~53kD PCOX1a of human aorta under reducing and non-reducing conditions., ELISA: 0.5-1ug/ml Control peptide can be used to coat ELISA plates at 1ug/ml., Optimal dilutions to be determined by the researcher. Control Peptide: C7904-88D: COX 3, Mouse (Cyclooxygenase 3, PGH Synthase), Storage and Stability: Storage and Stability:, May be stored at 4°C for short-term only. For long-term storage, store at -20°C. Aliquots are stable for at least 12 months at -20°C. For maximum recovery of product, centrifuge the original vial after thawing and prior to removing the cap. Further dilutions can be made in assay buffer.