| First Author | Morham SG | Year | 1995 |
| Journal | Cell | Volume | 83 |
| Issue | 3 | Pages | 473-82 |
| PubMed ID | 8521477 | Mgi Jnum | J:29510 |
| Mgi Id | MGI:77042 | Doi | 10.1016/0092-8674(95)90125-6 |
| Citation | Morham SG, et al. (1995) Prostaglandin synthase 2 gene disruption causes severe renal pathology in the mouse. Cell 83(3):473-82 |
| abstractText | The prostaglandin endoperoxide H synthase isoform 2, cyclooxygenase 2 (COX-2), is induced at high levels in migratory and other responding cells by pro-inflammatory stimuli. COX-2 is generally considered to be a mediator of inflammation. Its isoform, COX-1, is constitutively expressed in most tissues and is thought to mediate housekeeping functions. These two enzymes are therapeutic targets of the widely used nonsteroidal anti-inflammatory drugs (NSAIDs). To investigate further the different physiologic roles of these isoforms, we have used homologous recombination to disrupt the mouse gene encoding COX-2 (Ptgs2). Mice lacking COX-2 have normal inflammatory responses to treatments with tetradecanoyl phorbol acetate or with arachidonic acid. However, they develop severe nephropathy and are susceptible to peritonitis. |
