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. 2016 Mar 19;7(17):24005–24017. doi: 10.18632/oncotarget.8209

Figure 4.

Figure 4

(A) Pathway analysis of C-terminal truncated HBx mutants regulated genes by IPA. The p value was calculated using Fisher exact test to show the likelihood of association between our dataset of deregulated genes and canonical pathways. (B) FXR/RXR interaction and functional network identified by IPA. Genes in red and green indicate up- and down-regulated genes found in C-terminal truncated HBx mutants, respectively. Genes in white are not included in our dataset, but added by IPA to complete the network connections. Molecules predicted to be activated and inhibited by the IPA molecule activity predictor are labeled in orange and blue, respectively. (C) Heatmap showing fold change of individual genes involved in FXR/RXR pathway and drug metabolism. A total of 22 and 5 genes were found commonly up- and down-regulated, respectively. Each cell in the matrix represents a particular expression level of genes, where red and green cells indicate high and low gene expression, respectively. (D) Drug metabolism interaction and functional network identified by IPA. Genes in red and green indicate up- and down-regulated genes found in C-terminal truncated HBx mutants, respectively. Genes in pink are related to drug metabolism. Genes in white are not included in our dataset, but added by IPA to complete the network connections. Molecules predicted to be activated and inhibited by the IPA molecule activity predictor are labeled in orange and blue, respectively. (E) qRT-PCR validation of identified differentially expressed genes relating to FXR/RXR pathway and drug metabolism in MIHA cells with or without HBx-Δ14 and HBx-Δ35 stably overexpressed.