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

Nature | Oct 5, 2000

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.

Pubmed ID: 11034215 RIS Download

Mesh terms: Animals | Apoptosis | Carrier Proteins | Cell Cycle Proteins | Cell Line | DNA | DNA-Binding Proteins | E2F Transcription Factors | E2F1 Transcription Factor | Gene Expression Regulation | Genes, Tumor Suppressor | Mice | Mutation | Nuclear Proteins | Protein Binding | Retinoblastoma-Binding Protein 1 | Transcription Factor DP1 | Transcription Factors | Transcription, Genetic | Tumor Protein p73 | Tumor Suppressor Protein p53 | Tumor Suppressor Proteins

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