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

Molecular cell | Dec 24, 1997

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 14-3-3sigma is strongly induced by gamma irradiation and other DNA-damaging agents. The induction of 14-3-3sigma is mediated by a p53-responsive element located 1.8 kb upstream of its transcription start site. Exogenous introduction of 14-3-3sigma 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.

Pubmed ID: 9659898 RIS Download

Mesh terms: 14-3-3 Proteins | Biomarkers, Tumor | Colorectal Neoplasms | Cyclin-Dependent Kinase Inhibitor p21 | Cyclins | DNA Damage | Enzyme Inhibitors | Eukaryotic Cells | Evolution, Molecular | Exonucleases | Exoribonucleases | G2 Phase | Gene Expression Regulation, Neoplastic | Growth Inhibitors | Humans | In Situ Hybridization, Fluorescence | Isoenzymes | Mitosis | Molecular Sequence Data | Neoplasm Proteins | Polyploidy | Proteins | RNA, Messenger | Tumor Cells, Cultured | Tumor Suppressor Protein p53 | Tyrosine 3-Monooxygenase

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Associated grants

  • Agency: NCI NIH HHS, Id: CA 43460
  • Agency: NCI NIH HHS, Id: CA 57345

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