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Cell. 2007 Jan 26;128(2):241-4.

Another piece of the p27Kip1 puzzle.

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  • 1Mouse Cancer Genetics Program, Center for Cancer Research, National Cancer Institute-Frederick, Building 560/22-56, 1050 Boyles Street, Frederick, MD 21702, USA.


How extracellular signals communicate with the cell cycle is poorly understood. In this issue, two papers 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.

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