Skip to main content
. 2013 Apr;33(7):1285–1302. doi: 10.1128/MCB.06798-11

Fig 6.

Fig 6

(A) The role of SCO2 in inducing the activation of ASK-1 downstream kinases was studied in HCT p53+/+ cells. The ratio of the phosphorylated and total cellular levels of MAP2Ks, JNK, and p38 in SCO2-overexpressing HCT p53+/+ cells was obtained by an in vivo ELISA. Untreated control cells showed low-level expression of total MAP2Ks and phosphorylated MAP2Ks (bar 1). Ectopic expression of SCO2 cDNA resulted in significant increases in the expression levels of total MAP2Ks and their phosphorylated forms (bar 2). ROS quenching by NAC resulted in significant decreases in the expression levels of both forms in SCO2-transfected cells (bar 3). Tamoxifen treatment was used as a positive control (bar 4) (error bars represent standard deviations determined by analysis of variance; n = 7). (B) The ratio of the phosphorylated and total cellular levels of MAP2Ks, JNK, and p38 in SCO2-transfected HCT p53+/+ tumor xenografts was determined by an in vivo ELISA. Untreated control cells showed low-level expression of total MAP2Ks and phosphorylated MAP2Ks (bar 1). Ectopic expression of SCO2 cDNA resulted in significant increases in the expression levels of total MAP2Ks and their phosphorylated forms (bar 2). ROS quenching via NAC resulted in significant decreases in the expression levels of both forms in SCO2-transfected cells (bar 3). Tamoxifen treatment was used as a positive control (bar 4) (error bars represent standard deviations determined by analysis of variance; n = 5). O.D, optical density.