Prostaglandin endoperoxide H synthase-2 (COX-2) catalyzes the first rate-limiting step in prostaglandin biosynthesis and is the target of non-steroidal anti-inflammatory drugs.  These mice carry a knock-out allele of the <i>Ptgs2</i> gene containing a deletion of the 18 amino acids required for N-glycosylation of Asn 594. This region is required for entry of the COX2 protein into the endoplasmic reticulum-associated protein degradation (ERAD) system. 
Homozygous mice develop a more pronounced and prolonged bacterial endotoxin-induced febrile response than wildtype controls.  12 week old homozygous male mice exhibit approximately 50% higher levels of prostaglandin E2 in urine.  Western blot analysis of serum-stimulated fibroblasts isolated from homozygotes does not detect any full length gene product (protein) and mutant &Delta;18 COX-2 protein levels are higher than wildtype COX-2 protein levels.  &Delta;18 COX-2 protein levels are also higher in brain tissue from homozygotes, as determined by Western blot analysis.  The catalytic activity of the &Delta;18 COX-2 protein is similar to that of the wildtype prostaglandin endoperoxide H synthase-2 enzyme.  LPS challenge does not increase &Delta;18 COX-2 protein in brain, kidney or spleen.  Mice that are homozygous for the targeted mutation are viable and fertile.  

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These &Delta;18 COX-2 mice express a mutant prostaglandin endoperoxide H synthase-2 with an 18-amino acid deletion in exon 10 that prevents the protein's entry into the endoplasmic reticulum-associated protein degradation (ERAD) system.


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