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. Author manuscript; available in PMC: 2018 Nov 30.
Published in final edited form as: Oncogene. 2018 May 30;37(37):5054–5065. doi: 10.1038/s41388-018-0343-8

Figure 6. Bacterial virulence factor CagA regulates TRIP12 and degradation of p14ARF protein.

Figure 6

(A) SNU1 cells were co-cultured with cagA-positive H. pylori strain 7.1314 or its isogenic cagA- or cagE- mutants for 2 hours, p14ARF protein was then assessed by Western blotting.

(B) SNU1 or AGS cells were transfected with CagA-expressing plasmid (+) or empty vector (−) for 24 hours. TRIP12 protein was analyzed in AGS cells (upper panel). Given that SNU1 cells express higher levels of ARF protein than AGS, ARF was assessed in SNU1 cells (lower panel). (C) AGS cells transfected with ARF and GFP plasmids were co-transfected with either empty vector or CagA expressing plasmid and siRNA against TRIP12 as indicated in the panel. TRIP12 and p14ARF proteins were analyzed using Western blotting. β-actin and GFP were used for normalization of protein loading and transfection efficiency, respectively.