Fig. 4From: Helicobacter pylori CagA promotes epithelial mesenchymal transition in gastric carcinogenesis via triggering oncogenic YAP pathwayInactivation of cagA decreased expression and nuclear localization of YAP and also downregulated transcription of YAP downstream target genes. Construction and characterization of isogenic PMSS1 ΔcagA mutants. a schematic depiction of generation of PMSS1 ΔcagA mutants. b, c Complete deletion of cagA from the genomes of the representive transformants was completely verified using primer sets F1/R1 and F2/R2 for targeting cagA (b), and Fup/54 and Fup/55 for targeting the locus containing the sequence upstream of cagA and the cat cassette (c). d Western blotting to characterize CagA expression in H. pylori cell lysates. UreB was used as a positive control. Total CagA and phosphorylated CagA in AGS cells infected with CagA+ H. pylori strains PMSS1 and 7.13 as well as their CagA− mutant strains at MOI of 200 for 24 h were detected using Western blotting. e Cell elongation assay (Hummingbird phenotype) was performed on AGS cells infected with CagA+ H. pylori strains PMSS1 and 7.13 as well as their CagA− mutants at MOI of 200 for 24 h. All pictures were obtained under 100× magnification. Degrees of cell elongation (lower right image) was calculated as the ratio of length to breath of a AGS cellBack to article page