FIGURE 6.

Schematic depiction of how NPM blocks stress-induced apoptosis. TPA activates NF-κB and p53. The interplay between p53 and NPM leading to apoptosis or survival is dependent on the presence of p53 in mitochondria. NPM enhances p53 stabilization in the nucleus and activates p53 target genes, including bax; NPM as an NF-κB co-activator also induces NF-κB target genes, including bcl2. In normal cells, stress activates p53 and Bax translocation to mitochondria, leading to apoptosis. In cells expressing high levels of NPM, NPM blocks p53 localization to mitochondria, leading to protection from apoptosis despite the increase in Bax level.