Cell Cycle / Checkpoint Control

Activity of the cyclin-dependent kinases CDK4 and CDK6 is regulated by T-loop phosphorylation, by the abundance of their cyclin partners (the D-type cyclins), and by association with CDK inhibitors of the Cip/Kip or INK family of proteins (1). The inactive ternary complex of cyclin D/CDK4 and p27 Kip1 requires extracellular mitogenic stimuli for the release and degradation of p27 concomitant with a rise in cyclin D levels to effect progression through the restriction point and pRb-dependent entry into S-phase (2). The active complex of cyclin D/CDK4 targets the retinoblastoma protein for phosphorylation, allowing the release of E2F transcription factors that activate G1/S-phase gene expression (3). Levels of cyclin D protein drop upon withdrawal of growth factors through downregulation of its protein expression and through phosphorylation-dependent degradation (4).

1. Hirai, H. et al. (1995) Mol. Cell. Biol. 15, 2672-2681.
2. Sherr, C.J. (1996) Science 274, 1672-1677.
3. Lukas, J. et al. (1996) Mol. Cell. Biol. 16, 6917-6925.
4. Diehl, J.A. et al. (1997) Genes Dev. 11, 957-972.

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Cyclin D1 Blocking Peptide

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