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. Author manuscript; available in PMC: 2011 Apr 4.
Published in final edited form as: Cell Res. 2010 Apr 20;20(6):614–621. doi: 10.1038/cr.2010.53

Figure 1.

Figure 1

A model for p53 activation. (A) Classical model of p53 activation. DNA damage and oxidative stress signals lead to the rapid stabilization of p53 by blocking Mdm2 through various mechanisms described in the text. Once stabilized, p53 is activated through posttranslational modifications and binds to DNA, where it can interact with other transcriptional regulators for the induction of p53-responsive target genes. (B) A refined model of p53 activation. In addition to p53 stabilization, an additional step of antirepression may occur in vivo for full p53 activation. Mdm2 and MdmX repress p53 function and activation in vivo. Removal of this repression (i.e., antirepression) may be required for subsequent steps of p53 activation such as post-translational modifications, DNA binding, and induction of p53-responsive target genes.