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Mice deficient in IL-1 beta-converting enzyme are defective in production of mature IL-1 beta and resistant to endotoxic shock.

IL-1 beta-converting enzyme (ICE) cleaves pro-IL-1 beta to generate mature IL-1 beta. ICE is homologous to other proteins that have been implicated in apoptosis, including CED-3 and Nedd-2/lch-1. We generated ICE-deficient mice and observed that they are overtly normal but have a major defect in the production of mature IL-1 beta after stimulation with lipopolysaccharide. IL-1 alpha production is also impaired. ICE-deficient mice are resistant to endotoxic shock. Thymocytes and macrophages from the ICE-deficient animals undergo apoptosis normally. ICE therefore plays a dominant role in the generation of mature IL-1 beta, a previously unsuspected role in production of IL-1 alpha, but has no autonomous function in apoptosis.

Pubmed ID: 7859282

Authors

  • Li P
  • Allen H
  • Banerjee S
  • Franklin S
  • Herzog L
  • Johnston C
  • McDowell J
  • Paskind M
  • Rodman L
  • Salfeld J

Journal

Cell

Publication Data

February 10, 1995

Associated Grants

None

Mesh Terms

  • Animals
  • Apoptosis
  • Base Sequence
  • Caspase 1
  • Chimera
  • Cysteine Endopeptidases
  • Cytokines
  • Female
  • Interleukin-1
  • Lipopolysaccharides
  • Macrophage Activation
  • Macrophages, Peritoneal
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Molecular Sequence Data
  • RNA, Messenger
  • Sequence Deletion
  • Shock, Septic
  • Thymus Gland