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. Author manuscript; available in PMC: 2020 Apr 19.
Published in final edited form as: ACS Chem Biol. 2019 Mar 13;14(4):784–795. doi: 10.1021/acschembio.9b00134

Figure 4. Targeted RNASeq profiling defines activation of stress-responsive signaling pathways induced by diverse environmental toxins.

Figure 4.

A. Plot showing residuals calculated by comparing the expression of our stress-responsive gene panel between HEK293T cells following treatment with tunicamycin (Tm; 10 μM, 4 h) or vehicle. Calculation of residuals was performed as described in Fig. 2A. Genes are grouped by target stress-responsive signaling pathway. Statistics were calculated using one-way ANOVA, Significance shown reflects comparison to “Other” target transcript set. ***p<0.001, ****p<0.0001. See Table S3 for full ANOVA table.

B. Plot showing residuals calculated by comparing the expression of our stress-responsive gene panel between HEK293T cells following treatment with arsenite (As(III); 25 μM, 16 h) or vehicle. Calculation of residuals was performed as described in Fig. 2A. Genes are grouped by target stress-responsive signaling pathway. Statistics were calculated using one-way ANOVA, Significance shown reflects comparison to “Other” target transcript set. **p<0.01, ***p<0.001. See Table S3 for full ANOVA table.

C. Plot showing residuals calculated by comparing the expression of our stress-responsive gene panel between HEK293T cells following treatment with oligomycin A (Oligo; 100 nM, 24 h) or vehicle. Calculation of residuals was performed as described in Fig. 2A. Genes are grouped by target stress-responsive signaling pathway. Statistics were calculated using one-way ANOVA, Significance shown reflects comparison to “Other” target transcript set. **p<0.01. See Table S3 for full ANOVA table.