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Abstract
Cell division relies on the activation of cyclins, which bind to cyclin-dependent
kinases (CDKs) to induce cell-cycle progression towards S phase and later to initiate
mitosis. Since uncontrolled cyclin-dependent kinase activity is often the cause of
human cancer, their function is tightly regulated by cell-cycle inhibitors such as
the p21 and p27 Cip/Kip proteins. Following anti-mitogenic signals or DNA damage,
p21 and p27 bind to cyclin-CDK complexes to inhibit their catalytic activity and induce
cell-cycle arrest. Interestingly, recent discoveries suggest that p21 and p27 might
have new activities that are unrelated to their function as CDK inhibitors. The identification
of new targets of Cip/Kip proteins as well as evidence of Cip/Kip cytoplasmic relocalization
have revealed unexpected functions for these proteins in the control of CDK activation,
in the regulation of apoptosis and in transcriptional activation. This article discusses
recent insights into these possible additional functions of p21 and p27.