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Inhibition of CBF/NF-Y mediated transcription activation arrests cells at G2/M phase and suppresses expression of genes activated at G2/M phase of the cell cycle.

Previous studies showed that binding of the CBF/NF-Y (CBF) transcription factor to cellular promoters is essential for cell proliferation. This observation prompted us to investigate the function of CBF in relation to cell cycle progression and in cell-cycle-regulated transcription. In this study, we used a tetracycline-inducible adenoviral vector to express a truncated CBF-B subunit, Bdbd, lacking a transcription activation domain in various mammalian cell lines. The Bdbd polypeptide interacts with cellular CBF-A/CBF-C and binds to promoters containing CBF-binding sites. Interestingly, expression of Bdbd in various mammalian cells resulted in the inhibition of cell proliferation and specific cell cycle arrest at G2/M phase. Gene expression analysis demonstrated that the expression of Bdbd strongly suppressed cell cycle-dependent transcription activation of Cyclin B1, Aurora A and CDK1 genes, key regulators for cell cycle progression at G2/M phase. Chromatin immunoprecipitation analysis showed that Bdbd significantly inhibited binding of TATA-binding protein, TBP to both Cyclin B1 and Aurora A promoters, but did not inhibit binding of E2F3 activator to Cyclin B1 promoter. This study suggested that the activation domain of CBF-B plays an essential role in the transcription activation of Cyclin B1 and Aurora A genes at G2/M phase, thus regulating cell cycle progression at G2/M phase.

Pubmed ID: 17098936


  • Hu Q
  • Lu JF
  • Luo R
  • Sen S
  • Maity SN


Nucleic acids research

Publication Data

December 6, 2006

Associated Grants

  • Agency: NCI NIH HHS, Id: CA 16672
  • Agency: NIAMS NIH HHS, Id: R01 AR46264
  • Agency: NCI NIH HHS, Id: R01 CA89716

Mesh Terms

  • Adenoviridae
  • Aurora Kinases
  • CCAAT-Binding Factor
  • Cell Division
  • Cyclin B
  • Cyclin B1
  • G2 Phase
  • Genetic Vectors
  • HeLa Cells
  • Humans
  • Promoter Regions, Genetic
  • Protein Structure, Tertiary
  • Protein-Serine-Threonine Kinases
  • Sequence Deletion
  • TATA-Box Binding Protein
  • Tetracycline
  • Transcriptional Activation