Fig. 9.

Delayed death in flavopiridol-treated, p53-deficient, or Bax-deficient mice is not accompanied by caspase-3-like activity. DNA damage-induced caspase activation in neurons is CDK-, p53-, and Bax-dependent. Cortical neurons were treated with camptothecin (campto; 10 μm) and assessed for survival (left column) or DEVD-AFC cleavage activity (right column). For survival experiments, eachpoint is the mean ± SEM of data from three cultures. Cleavage activity in camptothecin-treated wild-type or p53/Bax littermate cultures was assessed only at 0 and 24 hr because of low levels of total protein observed at later time points.A, Wild-type cortical neurons were cotreated with flavopiridol (1 μm). B, p53-Deficient neurons or littermate controls. C, Bax-deficient neurons or littermate controls.