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. 2015 Sep 16;148(2):443–459. doi: 10.1093/toxsci/kfv193

FIG. 3.

FIG. 3.

IκBαAA expression abrogates the inhibitory effect of TCDD on 3′IghRR activation. CH12.IκBαAA cells transiently transfected with the VH (variable Ig heavy chain promoter)-Luc-3′IghRR luciferase reporter plasmid (3′IghRR) were either cultured for 2 h in media alone or with IPTG to activate the IκBαAA superrepressor. The cells were then cultured in the absence or presence of increasing concentrations of TCDD with 1 μg/ml LPS (A) or increasing concentrations of LPS with 10 nM TCDD (B). Luciferase enzyme activity is represented on the y-axis as relative light units (mean ± SE, n = 4 per treatment group). For graph A, “NA” denotes the unstimulated control; “C”, the LPS control; and “0.0 nM TCDD”, the 0.01% DMSO control. For graph B, “0.0 μg/ml LPS” denotes the unstimulated control; gray bars are treated with 0.01% DMSO and increasing concentrations of LPS; and checkered bars are treated with 10 nM TCDD and increasing concentrations of LPS. Statistical significance was determined by a 2-way ANOVA followed by a Bonferroni’s post hoc test. “*”, “**”, “***” denote significance at P < .05, P < .01, and P < .001, respectively, from the appropriate vehicle control (0.0 nM TCDD for A or 0.01% DMSO for B). “‡”, “‡‡”, “‡‡‡” denote significance for a specific treatment at P < .05, P < .01, and P < .001, respectively, between the control cells (no IκBαAA) and the cells induced to express the IκBαAA superrepressor (+ IκBαAA). Results are representative of 3 separate experiments. IκBαAA, IκBα superrepressor.