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Fig. 1 | Cell Communication and Signaling

Fig. 1

From: Helicobacter pylori-controlled c-Abl localization promotes cell migration and limits apoptosis

Fig. 1

Hp-induced threonine phosphorylation and kinase activity of c-Abl. pSGT-Ablwt-transfected AGS cell were infected with Hp as indicated. (a) Phosphorylation of pAblT735, pAblY245 and pAblY412 was analyzed by using phospho-specific antibodies. Abl and GAPDH were shown as loading controls. (b) To analyze the kinase activity, c-Abl was immunoprecipitated and incubated with recombinant GST-Crk as a substrate. Crk phosphorylation was demonstrated using an anti-phospho-CrkY221 antibody. In whole cell lysates, pCagA, Abl and total CagA were detected as controls. (c) AGS cells were infected with Hp wt or ΔPAI, ΔCagA, or ΔVacA mutants to investigate pAblT735, pAblY245, pAblY412 and Abl. Where indicated, cells were treated with PMA or H2O2/sodium vanadate (H/V). Translocated pCagA, CagA and β-actin were shown as controls (left panel). The relative amounts of pAblT735, pAblY245 and pAblY412 signals were quantified by blot densitometry and normalized to the loading control (right panel). (d) Cells were infected with Hp wt, ΔRfaE or treated with PMA. pAblT735, Abl and GAPDH were detected using specific antibodies (left panel). The relative amounts of pAblT735, pAblY245 and pAblY412 signals were quantified by blot densitometry and normalized to the loading control. These results are presented as relative phosphorylation with the levels induced by Hp (wt) set to 1.0 (right panel)

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