DISCORDANCE BETWEEN THE EFFECT OF MODULATORS OF CALCIUM ON STAUROSPORINE-INDUCED APOPTOSIS AND STAUROSPORINE-INDUCED ACTIN DEGRADATION

Authors

  • Simon W. Rabkin,

    Corresponding author
    1. Faculty of Medicine, University of British Columbia, Vancouver, BC, Canada
      To whom correspondence should be addressed: Dr Simon Rabkin, University of British Columbia, 2733 Heather St., Room D404, Vancouver, B.C., Canada V5Z 3J5. Tel.: (604) 875-5847; Fax: (604) 875-5849; E-mail: rabkin@interchange.ubc.ca
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  • Jennifer Y. Kong

    1. Faculty of Medicine, University of British Columbia, Vancouver, BC, Canada
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To whom correspondence should be addressed: Dr Simon Rabkin, University of British Columbia, 2733 Heather St., Room D404, Vancouver, B.C., Canada V5Z 3J5. Tel.: (604) 875-5847; Fax: (604) 875-5849; E-mail: rabkin@interchange.ubc.ca

Abstract

Staurosporine produced DNA fragmentation characteristic of apoptosis and a dramatic alteration of cell structure that include alterations of cytoskeletal actin and cytoplasmic condensation with vacuolization. These changes were not induced by chelerythrine, a more specific PKC inhibitor than staurosporine. The calcium chelator, BAPTA, significantly reduced staurosporine-induced DNA fragmentation but did not affect staurosporine-induced changes in cytoskeletal actin. These data suggest that DNA fragmentation and actin degradation in apoptosis, induced by staurosporine, are under different regulatory control by calcium.

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