Mechanisms of regulatory diversity within the p53 transcriptional network

• Published in: Oncogene Vol. 27; no. 29; pp. 4013 - 4023
• Main Author: Espinosa, J M
• Format: Journal Article
• Language: English
• Published: London Nature Publishing Group UK 03-07-2008; Nature Publishing; Nature Publishing Group
• Subjects: Animals; Apoptosis; Apoptosis - physiology; Biological and medical sciences; Cancer; Cell activation; Cell Biology; Cell cycle; Cell Cycle - physiology; Cell physiology; Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes; Fundamental and applied biological sciences. Psychology; Genetic aspects; Genetic regulation; Genetic transcription; Genetics; Human Genetics; Humans; Internal Medicine; Medicine; Medicine & Public Health; Models, Biological; Molecular and cellular biology; Molecular genetics; Oncology; p53 Protein; Physiological aspects; Proteins; review; Transcription, Genetic - physiology; Transcription. Transcription factor. Splicing. Rna processing; Tumor suppressor genes; Tumor Suppressor Protein p53 - genetics; Tumor Suppressor Protein p53 - metabolism; United States; lysine 120; ASPP; HZF; hCAS; serine 46; p21; Transcription; Serine; CDKN1A Gene; Carcinogenesis; Mechanism; TP53 Gene; Lysine; Tumor suppressor gene
• ISSN: 0950-9232; 1476-5594
• DOI: 10.1038/onc.2008.37

p53 is arguably the most intensively studied protein to date, yet there is much that we ignore about its function as a transcription factor. The p53-dependent transcriptional program is remarkably flexible, as it varies with the nature of p53-activating stimuli, the cell type and the duration of the activation signal. This flexibility may allow cells to mount alternative responses to p53 activation, such as cell cycle arrest or apoptosis. Here, I organize the available data into two alternative models to explain how this regulatory diversity is achieved.