| First Author | Li P | Year | 1997 |
| Journal | J Cell Biochem | Volume | 64 |
| Issue | 1 | Pages | 27-32 |
| PubMed ID | 9015751 | Mgi Jnum | J:40691 |
| Mgi Id | MGI:708069 | Doi | 10.1002/(sici)1097-4644(199701)64:1<27::aid-jcb5>3.0.co;2-1 |
| Citation | Li P, et al. (1997) Characterization of mice deficient in interleukin-1 beta converting enzyme. J Cell Biochem 64(1):27-32 |
| abstractText | Interleukin-1 beta converting enzyme (ICE) processes the inactive prolL-1 beta to the proinflammatory mature IL-1 beta. ICE belongs to a family of cysteine proteases that have been implicated in apoptosis. To address the biological functions of ICE, we generated ICE-deficient mice through gene targeting technology. ICE-deficient mice developed normally, appeared healthy, and were fertile. Peritoneal macrophages from ICE-deficient mice underwent apoptosis normally upon ATP treatment. Thymocytes from young ICE-deficient mice also underwent apoptosis when triggered by dexamethasone, gamma irradiation, or aging. ICE-deficient mice had a major defect in the production of mature IL-1 beta and had impaired IL-1 alpha production on LPS stimulation in vitro and in vivo. ICE-deficient mice were resistant to LPS-induced endotoxic shock. |
