Figure 3.

Dysregulation of the adherens junction by H. pylori. H. pylori-translocated CagA interacts with E-cadherin and p120. This destabilizes the adherens junction and results in nuclear translocation of β-catenin and p120 and alterations in transcriptional activity. The H. pylori outer membrane protein OipA disrupts adherens junctions through redistribution of β-catenin, and H. pylori-secreted high-temperature requirement A (HtrA) cleaves E-cadherin, disrupting the adherens junction. Hypermethylation of the E-cadherin promoter also occurs in response to H. pylori infection and epithelial protein lost in neoplasm (EPLIN) binds α-catenin and links the cadherin-catenin complex with actin.