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. 2003 Oct;23(19):6836–6848. doi: 10.1128/MCB.23.19.6836-6848.2003

FIG. 1.

FIG. 1.

Upregulation of p38 activity and downregulation of Akt activity by E1A correlated with E1A-mediated sensitization to paclitaxel-induced apoptosis. (A) Phospho-p38 (p38-p) and phospho-Akt (Akt-p) levels in E1A-expressing cells versus those in vector-transfected MDA-MB-231 and MCF-7 cells are shown. Total p38 (p38) and Akt (Akt) were used as loading controls. Results of kinase assays of p38 (B) and Akt (C) and densitometric analysis of relative p38 activity with GST-ATF-2 as a substrate and Akt activity with GST-GSK-3-β as a substrate in E1A-expressing cells versus vector-transfected control cells. E, E1A-expressing cells; V, vector transfected control cells. (D) Expression of caspase 3, 7, 8, and 9 proenzymes in E1A stable cells established in human breast cancer cell lines MCF-7, MDA-MB-231, and MDA-MB-453 and ovarian cancer cell line 2774. V, vector control; E, E1A stable cells.