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Characterization of mice deficient in interleukin‐1β converting enzyme
Author(s) -
Li Ping,
Allen Hamish,
Banerjee Subhashis,
Seshadri Tara
Publication year - 1997
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/(sici)1097-4644(199701)64:1<27::aid-jcb5>3.0.co;2-1
Subject(s) - apoptosis , proteases , proinflammatory cytokine , in vivo , microbiology and biotechnology , interleukin , biology , enzyme , chemistry , immunology , inflammation , biochemistry , cytokine , genetics
Interleukin‐1β converting enzyme (ICE) processes the inactive proIL‐1β to the proinflammatory mature IL‐1β. 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‐1β and had impaired IL‐1α production on LPS stimulation in vitro and in vivo . ICE‐deficient mice were resistant to LPS‐induced endotoxic shock. J. Cell. Biochem. 64:27–32. © 1997 Wiley‐Liss, Inc.