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

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

Research output: Contribution to journalArticlepeer-review

513 Scopus citations


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. 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. 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.

Original languageEnglish (US)
Pages (from-to)645-648
Number of pages4
Issue number6804
StatePublished - Oct 5 2000

ASJC Scopus subject areas

  • General


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