Fig. P1.

Regulation of p53 isoforms in H. pylori-infected cells. The p53 gene has the main P1 and alternative P2 promoters. Interaction of H. pylori with gastric epithelial cells, mediated by the cag-PAI, activates transcription from the P2 promoter and induces synthesis of N-terminally truncated ∆133p53 and ∆160p53 isoforms. The p53 isoforms inhibit the activities of p53 and p73, induce NF-κB activity, and increase survival of infected cells. The expression of ∆133p53 in response to H. pylori infection is regulated by activation of AP-1–dependent transcription. The transactivation, DNA binding, and oligomerization domains of p53 protein are shown in blue, red, and yellow, respectively.