Nature genetics, 2000-12, Vol.26 (4), p.464-469
2000
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- Autor(en) / Beteiligte
- Titel
- Role of the p53-homologue p73 in E2F1-induced apoptosis
- Ist Teil von
- Nature genetics, 2000-12, Vol.26 (4), p.464-469
- Ort / Verlag
- London: Nature Publishing Group
- Erscheinungsjahr
- 2000
- Quelle
- MEDLINE
- Beschreibungen/Notizen
- Most human cancers harbour aberrations of cell-cycle control, which result in deregulated activity of the E2F transcription factors with concomitant enhanced cell-cycle progression. Oncogenic signalling by E2F1 has recently been linked to stabilization and activation of the tumour suppressor p53 (refs 1,3,4). The p73 protein shares substantial sequence homology and functional similarity with p53 (refs 5-7 ). Hence, several previously considered p53-independent cellular activities may be attributable to p73. Here we provide evidence that E2F1 directly activates transcription of TP73, leading to activation of p53-responsive target genes and apoptosis. Disruption of p73 function by a tumour-derived p53 mutant reduced E2F1-mediated apoptosis. Thus, p73 activation by deregulated E2F1 activity might constitute a p53-independent, anti-tumorigenic safeguard mechanism.
- Sprache
- Englisch
- Identifikatoren
- ISSN: 1061-4036eISSN: 1546-1718DOI: 10.1038/82617Titel-ID: cdi_proquest_miscellaneous_807268285
- Format
- –
- Schlagworte
- Ageing, cell death, Animals, Apoptosis, Apoptosis - drug effects, Apoptosis - genetics, Apoptosis - physiology, Base Sequence, Binding sites, Binding Sites - genetics, Biological and medical sciences, Carrier Proteins, Causes of, Cell Cycle Proteins, Cell Line, Cell physiology, COS Cells, DNA microarrays, DNA Primers - genetics, DNA-Binding Proteins - genetics, DNA-Binding Proteins - physiology, E2F Transcription Factors, E2F1 Transcription Factor, Fundamental and applied biological sciences. Psychology, Gene Expression Regulation - drug effects, Genes, Tumor Suppressor, Humans, Identification and classification, Mice, Molecular and cellular biology, Molecular Sequence Data, Mutation, Nuclear Proteins - genetics, Nuclear Proteins - physiology, Physiological aspects, Plasmids, Promoter Regions, Genetic, Proteins, Publishing, Retinoblastoma-Binding Protein 1, Transcription Factor DP1, Transcription Factors - metabolism, Transcription Factors - pharmacology, Transcriptional Activation, Transfection, Tumor Protein p73, Tumor suppressor genes, Tumor Suppressor Protein p53 - genetics, Tumor Suppressor Protein p53 - physiology, Tumor Suppressor Proteins, U937 Cells