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. 2022 Oct 20;13:6234. doi: 10.1038/s41467-022-33858-w

Fig. 5. Analysis of the dAHR:mARNT PAS-B heterodimer interface.

Fig. 5

a The binding affinities of dAHR PAS-B mutants to mARNT PAS-B measured by ELISA. b DRE luciferase reporter assay examining the effect of AHR mutation on the transactivation of mAHR in HEK293T cells in the presence or absence of agonists. FICZ, βNF and BaP were supplied at 200 nM, 500 nM and 200 nM, respectively. The lower panel shows the fold of induction in luciferase activity due to ligand treatment (luciferase activity in the presence of ligand divided by that in the presence of DMSO). c Superimposition of the dAHR PAS-B:αNF and dAHR PAS-B:mARNT complex structures. d Analysis of the impact of αNF on the interaction between dAHR PAS-B and ARNT. Data for d are the mean of two independent experiments, and data for (a, b) are the mean ± standard deviation of n = 3 independent replicates. p values were calculated using two-way ANOVA with Tukey’s multiple comparisons test with the WT mAHR group treated by the same ligand as a control and presented in the Source Data file. *p < 0.05, ***p < 0.001, ****p < 0.0001, ns: not statistically significant (p > 0.05). Source data are provided as a Source Data file.