Another piece of the p27Kip1 puzzle

How extracellular signals communicate with the cell cycle is poorly understood. In this issue, two papers (Grimmler et al., 2007; Chu et al., 2007) address this problem by reporting phosphorylation of the cyclin-dependent kinase inhibitor p27(Kip1) on a tyrosine residue by nonreceptor tyrosine kinases, which decreases p27 stability. This new mechanism could explain how cells enter the cell cycle from a quiescent state.