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 and Chu et al., 2007) address this problem by reporting phosphorylation of the cyclin-dependent kinase inhibitor p27Kip1 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.