Abstract
The p53 protein is one of the most important tumor suppressor proteins. Normally, the p53 protein is in a latent state. However, when its activity is required, e.g. upon DNA damage, nucleotide depletion or hypoxia, p53 becomes rapidly activated and initiates transcription of pro-apoptotic and cell cycle arrest-inducing target genes. The activity of p53 is regulated both by protein abundance and by post-translational modifications of pre-existing p53 molecules. In the 30 years of p53 research, a plethora of modifications and interaction partners that modulate p53’s abundance and activity have been identified and new ones are continuously discovered. This review will summarize our current knowledge on the regulation of p53 abundance and activity.
Acknowledgements
We apologize for the omission of several references due to space limitations. C.B. is supported by the BMBF grant 02S8223.
Declaration of interest: The authors declare to have no conflict of interest. The authors alone are responsible for the content and the writing of the manuscript.
Editor: Michael M. Cox