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. 2021 Jun 15;183(1):154–169. doi: 10.1093/toxsci/kfab075

Figure 10.

Figure 10.

Pharmacological inhibition of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-inducible poly- adenosine diphosphate-ribose polymerase (TIPARP) increases aryl hydrocarbon receptor (AHR) signaling in mouse embryonic fibroblasts (MEFs) isolated from Tiparp+/+ but not TiparpH532A mice. Increased TCDD-induced mRNA expression levels of (A) Cyp1a1, and (B) Cyp1b1 in MEFs isolated from TiparpH532A and Tiparp+/+ mice treated with TCDD alone or in combination with increasing concentrations of RBN-2397. Real time-quantitative PCR data are shown relative to the gene-specific expression level observed for TiparpH532A MEFs exposed to 1 nM TCDD. *p <.05 by 1-way analysis of variance followed by Tukey’s post hoc test compared with genotype-matched TCDD-treated MEFs. Figure depicts the mean ± SEM (n =3).