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

Fig. 5. CagA is essential for H. pylori-induced BIRC3 expression and apoptosis resistance.

Fig. 5

a, b AGS cells were infected with wild-type H. pylori G27 or the cagA-deficient isogenic mutant for 1 or 2 h for the expression of BIRC3 eRNA (a) or mRNA (b), respectively. Levels of BIRC3 eRNA and mRNA were analyzed by qRT-PCR. c AGS cells were infected with H. pylori G27 or cagA-deficient isogenic mutant for the indicated time points. Cell lysates were analyzed by immunoblotting for indicated proteins. d AGS cells were infected with WT 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 the indicated proteins. e AGS cells infected with WT H. pylori G27 or cagA-deficient isogenic mutant for 1 h followed by the treatment with Raptinal (10 µM) for 2 h. Apoptotic cells was analyzed by FACS with Annexin V-FITC/PI staining. f The percentage of apoptotic cells from (e) for Raptinal-treated samples. All data are shown as the mean ± SD from three independent experiments. *p < 0.05, ***p < 0.001, n.s.: not significant.