期刊
CELL
卷 128, 期 2, 页码 241-244出版社
CELL PRESS
DOI: 10.1016/j.cell.2007.01.006
关键词
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资金
- Intramural NIH HHS Funding Source: Medline
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.
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