ICE/CED3-like proteases as therapeutic targets for the control of inappropriate apoptosis.
Excessive or failed apoptosis is a prominent morphological feature of several human diseases. Many of the key biochemical players that contribute to the highly ordered process of apoptotic cell death have recently been identified. These include members of the emerging family of cysteine proteases related to mammalian interleukin-1 beta converting enzyme (ICE) and to CED-3, the product of a gene that is necessary for programmed cell death in the nematode C. elegans. Among a growing number of potential molecular targets for the control of human diseases where inappropriate apoptosis is prominent, ICE/CED-3-like proteases may be an attractive and tangible point for therapeutic intervention.
Nicholson
D W
DW
Department of Biochemistry and Molecular Biology, Merck Frosst Centre for Therapeutic Research, Pointe Claire-Dorval, Quebec, Canada. donald_nicholson@merck.com
D000595:Amino Acid Sequence; D000818:Animals; D017209:Apoptosis / Q000187:drug effects / Q000235:genetics / Q000502:physiology*; D001709:Biotechnology; D017173:Caenorhabditis elegans; D029742:Caenorhabditis elegans Proteins; D020169:Caspases; D002384:Catalysis; D003546:Cysteine Endopeptidases / Q000235:genetics / Q000502:physiology*; D015853:Cysteine Proteinase Inhibitors / Q000737:chemistry / Q000494:pharmacology; D015195:Drug Design; D006801:Humans; D009842:Oligopeptides / Q000737:chemistry / Q000494:pharmacology; D011487:Protein Conformation
D029742:Caenorhabditis elegans Proteins; D015853:Cysteine Proteinase Inhibitors; D009842:Oligopeptides; D020169:Caspases; D003546:Cysteine Endopeptidases; C089223:ced-3 protein, C elegans