Expression of p16Ink4a compensates for p18Ink4c loss in cyclin-dependent kinase 4/6-dependent tumors and tissues.

@article{Ramsey2007ExpressionOP,
  title={Expression of p16Ink4a compensates for p18Ink4c loss in cyclin-dependent kinase 4/6-dependent tumors and tissues.},
  author={Matthew R. Ramsey and Janakiraman Krishnamurthy and Xin-Hai Pei and Chad D Torrice and Weili Lin and Daniel Ruben Carrasco and Keith L Ligon and Yue Xiong and Norman E Sharpless},
  journal={Cancer research},
  year={2007},
  volume={67 10},
  pages={4732-41}
}
Cell cycle progression from G(1) to S phase depends on phosphorylation of pRb by complexes containing a cyclin (D type or E type) and cyclin-dependent kinase (e.g., cdk2, cdk4, or cdk6). Ink4 proteins function to oppose the action of cdk4/6-cyclin D complexes by inhibiting cdk4/6. We employed genetic and pharmacologic approaches to study the interplay among Ink4 proteins and cdk4/6 activity in vivo. Mouse embryo fibroblasts (MEF) lacking p16(Ink4a) and p18(Ink4c) showed similar growth kinetics… CONTINUE READING