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Cyclin C/cdk3 promotes Rb-dependent G0 exit.

G0 is a physiological state occupied by resting or terminally differentiated cells that have exited the cell cycle. In contrast to the well-characterized cyclin/cdk-mediated inactivation of pRb that controls the G1/S transition, little is known about regulation of the G0/G1 transition. However, pRb is likely to participate in this process because its acute somatic inactivation is sufficient for G0-arrested cells to re-enter the cell cycle. One physiological regulator of this event may be cyclin C because its highest mRNA levels occur during G0 exit. Here we show that a non-cdk8-associated cellular pool of cyclin C combines with cdk3 to stimulate pRb phosphorylation at S807/811 during the G0/G1 transition, and that this phosphorylation is required for cells to exit G0 efficiently. Thus, G1 entry is regulated in an analogous fashion to S phase entry, but involves a distinct cyclin/cdk combination.

Pubmed ID: 15084261


  • Ren S
  • Rollins BJ



Publication Data

April 16, 2004

Associated Grants

  • Agency: NCI NIH HHS, Id: CA72573

Mesh Terms

  • Cell Cycle
  • Cyclin C
  • Cyclin-Dependent Kinase 3
  • Cyclin-Dependent Kinases
  • Cyclins
  • G0 Phase
  • G1 Phase
  • Humans
  • Phosphorylation
  • RNA, Messenger
  • Retinoblastoma Protein
  • Serine
  • Tumor Cells, Cultured