14-3-3σ is a p53-regulated inhibitor of G2/M progression

Heiko Hermeking, Christoph Lengauer, Kornelia Polyak, Tong Chuan He, Lin Zhang, Sam Thiagalingam, Kenneth W. Kinzler, Bert Vogelstein

Research output: Contribution to journalArticle

Abstract

Exposure of colorectal cancer (CRC) cells to ionizing radiation results in a cell-cycle arrest in G1 and G2. The G1 arrest is due to p53-mediated induction of the cyclin-dependent kinase inhibitor p21WAF1/CIP1/SDI1, but the basis for the G2 arrest is unknown. Through a quantitative analysis of gene expression patterns in CRC cell lines, we have discovered that 14-3-3σ is strongly induced by 7 irradiation and other DNA-damaging agents. The induction of 14-3-3σ is mediated by a p53-responsive element located 1.8 kb upstream of its transcription start site. Exogenous introduction of 14-3-3σ into cycling cells results in a G2 arrest. As the fission yeast 14-3-3 homologs rad24 and rad25 mediate similar checkpoint effects, these results document a molecular mechanism for G2/M control that is conserved throughout eukaryotic evolution and regulated in human cells by p53.

Original languageEnglish (US)
Pages (from-to)3-11
Number of pages9
JournalMolecular cell
Volume1
Issue number1
DOIs
StatePublished - Dec 1997

ASJC Scopus subject areas

  • Molecular Biology
  • Cell Biology

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    Hermeking, H., Lengauer, C., Polyak, K., He, T. C., Zhang, L., Thiagalingam, S., Kinzler, K. W., & Vogelstein, B. (1997). 14-3-3σ is a p53-regulated inhibitor of G2/M progression. Molecular cell, 1(1), 3-11. https://doi.org/10.1016/S1097-2765(00)80002-7