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Role for the p53 homologue p73 in E2F-1-induced apoptosis

Author

Listed:
  • Meredith Irwin

    (Dana-Farber Cancer Institute and Brigham and Womens Hospital, Harvard Medical School)

  • Maria Carmen Marin

    (Dana-Farber Cancer Institute and Brigham and Womens Hospital, Harvard Medical School)

  • Andrew C. Phillips

    (Regulation of Cell Growth Laboratory, NCI-FCRDC)

  • Ratnam S. Seelan

    (Mayo Clinic/ Mayo Medical School)

  • David I. Smith

    (Mayo Clinic/ Mayo Medical School)

  • Wanguo Liu

    (Mayo Clinic/ Mayo Medical School)

  • Elsa R. Flores

    (Massachusetts Institute of Technology
    Howard Hughes Medical Institute)

  • Kenneth Y. Tsai

    (Massachusetts Institute of Technology)

  • Tyler Jacks

    (Massachusetts Institute of Technology
    Howard Hughes Medical Institute)

  • Karen H. Vousden

    (Regulation of Cell Growth Laboratory, NCI-FCRDC)

  • William G. Kaelin Jr

    (Dana-Farber Cancer Institute and Brigham and Womens Hospital, Harvard Medical School
    Howard Hughes Medical Institute)

Abstract

The transcription factor E2F-1 induces both cell-cycle progression and, in certain settings, apoptosis. E2F-1 uses both p53-dependent and p53-independent pathways to kill cells1,2,3,4,5,6,7,8. The p53-dependent pathway involves the induction by E2F-1 of the human tumour-suppressor protein p14ARF, which neutralizes HDM2 (human homologue of MDM2) and thereby stabilizes the p53 protein9. Here we show that E2F-1 induces the transcription of the p53 homologue p73. Disruption of p73 function inhibited E2F-1-induced apoptosis in p53-defective tumour cells and in p53-/- mouse embryo fibroblasts. We conclude that activation of p73 provides a means for E2F-1 to induce death in the absence of p53.

Suggested Citation

  • Meredith Irwin & Maria Carmen Marin & Andrew C. Phillips & Ratnam S. Seelan & David I. Smith & Wanguo Liu & Elsa R. Flores & Kenneth Y. Tsai & Tyler Jacks & Karen H. Vousden & William G. Kaelin Jr, 2000. "Role for the p53 homologue p73 in E2F-1-induced apoptosis," Nature, Nature, vol. 407(6804), pages 645-648, October.
    • Handle: RePEc:nat:nature:v:407:y:2000:i:6804:d:10.1038_35036614
    DOI: 10.1038/35036614
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