Premature p34 <sup>cdc2</sup> Activation Required for Apoptosis

DOI Web Site 3 Citations
  • Lianfa Shi
    Manitoba Institute of Cell Biology, University of Manitoba, Winnipeg, Canada.
  • Walter K. Nishioka
    La Jolla Institute of Allergy and Immunology, La Jolla, CA 92037, USA.
  • John Th'ng
    Department of Biological Chemistry, University of California, Davis, CA 95616, USA.
  • E. Morton Bradbury
    Department of Biological Chemistry, University of California, Davis, CA 95616, USA.
  • David W. Litchfield
    Manitoba Institute of Cell Biology, University of Manitoba, Winnipeg, Canada.
  • Arnold H. Greenberg
    Manitoba Institute of Cell Biology, University of Manitoba, Winnipeg, Canada.

Description

<jats:p> Activation of the serine-threonine kinase p34 <jats:sup>cdc2</jats:sup> at an inappropriate time during the cell cycle leads to cell death that resembles apoptosis. Premature activation of p34 <jats:sup>cdc2</jats:sup> was shown to be required for apoptosis induced by a lymphocyte granule protease. The kinase was rapidly activated and tyrosine dephosphorylated at the initiation of apoptosis. DNA fragmentation and nuclear collapse could be prevented by blocking p34 <jats:sup>cdc2</jats:sup> activity with excess peptide substrate, or by inactivating p34 <jats:sup>cdc2</jats:sup> in a temperature-sensitive mutant. Premature p34 <jats:sup>cdc2</jats:sup> activation may be a general mechanism by which cells induced to undergo apoptosis initiate the disruption of the nucleus. </jats:p>

Journal

  • Science

    Science 263 (5150), 1143-1145, 1994-02-25

    American Association for the Advancement of Science (AAAS)

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