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Another piece of the p27(Kip1) puzzle

  1. Author:
    Kaldis, P.

  2. Author Address

    NCI, Mouse Canc Genet Program, Canc Res Ctr, Frederick, MD 21702 USA.;Kaldis, P, NCI, Mouse Canc Genet Program, Canc Res Ctr, Bldg 560-22-56,1050 Boyles St, Frederick, MD 21702 USA.;kaldis@ncifcrf.gov
    1. Year: 2007
    2. Date: Jan
  2. Journal: Cell
    1. 128
    2. 2
    3. Pages: 241-244
  4. Type of Article: Review
  5. ISSN: 0092-8674
  1. Abstract:

    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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External Sources

  1. View Full Text
  2. DOI: 10.1016/j.cell.2007.01.006
  3. View record in Web of Science®
  4. WOS: 000244420500010

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