Figure 8.

Proposed schema showing coordination of cell-cycle events by the CDK inhibitor p27. When grown in the presence of growth factors, reduced or absent p27 levels are associated with a coordinated and synchronous increase in cyclin E–CDK2 and cyclin A–CDK2 activity. This favors cell-cycle progression and proliferation. Under stress states such as growth factor deprivation, the loss of p27 is associated with an unconstrained increase in cyclin A–CDK2 activity, but not cyclin E–CDK2 activity. This unscheduled increase in CDK2 activity causes cell-cycle exit by apoptosis.