Mechanisms of regulatory diversity within the p53 transcriptional network

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Abstract
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.