Exposure of esophageal cells to BA/A leads to activation of c-Abl kinase and upregulation of ΔNp73 protein.

<p><b>A.</b> Dynamics of c-Abl phosphorylation in BA/A-treated cells. SK-GT-4 cells were treated with 100 µM BA cocktail, pH 4.0. Extracts were collected at the indicated time and analyzed by Western blotting. Early (5–30 minutes) and late (4–24 hours) time points are shown. <b>B.</b> Western blot analysis for phospho-ΔNp73(Y50) in SK-GT-4 cells stably transfected with ΔNp73α. Cells were collected at indicated time after treatment with BA/A (100 µM, 30 min). <b>C.</b> c-Abl chemical inhibitor Imatinib downregulates the ΔNp73 protein. SK-GT-4 cells were pretreated with Imatinib (30 µM) for 1 hour, treated with BA/A (100 µM) for 30 minutes and then incubated for an additional 7 hours in the presence of the indicated inhibitor. Total cell extracts were analyzed by Western blotting. <b>D.</b> Inhibition of c-Abl by siRNA leads to downregulation of the ΔNp73 protein in BA/A-treated cells. SK-GT-4 cells were transfected with c-Abl-specific siRNA for 48 hours, treated with BA/A (100 µM) for 30 minutes, and then collected 7 hours after treatment. Levels of ΔNp73 were analyzed by Western blotting. <b>E.</b> Transfection of constitutively active c-Abl leads to upregulation of the ΔNp73 protein. SK-GT-4 cells were transfected with the c-Abl (P242E/P249E)-pcDNA3 vector for 24 hours and analyzed by Western blotting.