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

  1. Author:
    Irwin, M.
    Marin, M. C.
    Phillips, A. C.
    Seelan, R. S.
    Smith, D. I.
    Liu, W. G.
    Flores, E. R.
    Tsai, K. Y.
    Jacks, T.
    Vousden, K. H.
    Kaelin, W. G.

  2. Author Address

    Harvard Univ, Sch Med, Dana Farber Canc Inst, 44 Binney St, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA. Harvard Univ, Sch Med, Brigham & Womens Hosp, Boston, MA 02115 USA. NCI, Regulat Cell Growth Lab, FCRDC, Frederick, MD 21702 USA. Mayo Clin & Mayo Fdn, Mayo Med Sch, Dept Lab Med & Pathol, Rochester, MN 55905 USA. MIT, Dept Biol, Cambridge, MA 02139 USA. MIT, Ctr Canc Res, Cambridge, MA 02139 USA. Howard Hughes Med Inst, Chevy Chase, MD 20185 USA.
    1. Year: 2000
  2. Journal: Nature
    1. 407
    2. 6804
    3. Pages: 645-648
  4. Type of Article: Article
  1. 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 cells(1-8). 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 protein(9). 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.

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