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. 2020 Aug 21;11(8):667. doi: 10.1038/s41419-020-02894-z

Fig. 6. H. pylori induces cIAP2 expression and inhibits apoptosis in primary human gastric epithelial cells.

Fig. 6

a Representative images of primary human gastric epithelial cells with or without infection by wild-type H. pylori G27 or the cagA-deficient isogenic mutant for 1 h, followed by Raptinal treatment for 2 h. Scale bar = 50 μm. b, c Primary human gastric epithelial cells were infected with H. pylori G27 or cagA-deficient isogenic mutant for 1 h. Levels of BIRC3 eRNA (b) or mRNA (c) were analyzed by qRT-PCR. d Primary human gastric epithelial cells were infected with H. pylori G27 or cagA-deficient isogenic mutant for 8 h. Cell lysates were immunoblotted for indicated proteins. (e). Primary human gastric epithelial cells were infected with H. pylori G27 or cagA-deficient isogenic mutant for 1 h followed by the treatment with Raptinal (10 µM) for 2 h. Cell lysates were immunoblotted for indicated proteins. f Schematic model for the H. pylori infection-mediated cIAP2 induction and apoptosis resistance. H. pylori stimulates the recruitment of Brd4 to the enhancer of BIRC3 in a CagA-dependent manner. This recruitment facilitates RNAPII-mediated eRNA and mRNA synthesis and the induction of cIAP2, resulting in the inhibition of apoptosis. All data are shown as the mean ± SD from three independent experiments. *p < 0.05.