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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. kaldis@ncifcrf.gov

Abstract

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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