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Identification and characterization of Ich-3, a member of the interleukin-1beta converting enzyme (ICE)/Ced-3 family and an upstream regulator of ICE.

Author information

Affiliations

  • 1. Cardiovascular Research Center, Massachusetts General Hospital-East, Charlestown, Massachusetts 02129, USA.
      Authors
    • Wang S 1
    (1 author)

ORCIDs linked to this article

The Journal of Biological Chemistry, 01 Aug 1996, 271(34):20580-20587
https://doi.org/10.1074/jbc.271.34.20580 PMID: 8702803 

Abstract 

We report here the isolation and characterization of a new member of the ice/ced-3 family of cell death genes, named ich-3. The predicted amino acid sequence of Ich-3 protein shares 54% identity with murine interleukin-1beta converting enzyme (ICE). Overexpression of ich-3 in Rat-1 and HeLa cells induces apoptosis, which can be inhibited by CrmA and Bcl-2. The mRNA and proteins of ich-3 are dramatically induced in vivo upon stimulation with lipopolysaccharide, an inducer of septic shock. The ich-3 gene product can be cleaved by cytotoxic T cells granule serine protease granzyme B, suggesting that Ich-3 may mediate apoptosis induced by granzyme B. Ich-3 does not process proIL-1beta directly but does promote proIL-1beta processing by ICE. These results suggest that Ich-3 may play a very important role in apoptosis and inflammatory responses and may be an upstream regulator of ICE.

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Read article at publisher's site: https://doi.org/10.1074/jbc.271.34.20580

Read article for free, from open access legal sources, via Unpaywall: http://www.jbc.org/article/S002192581973871X/pdfUnpaywall

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