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Fig. 2 | Journal of Experimental & Clinical Cancer Research

Fig. 2

From: HBV-driven host chromatin accessibility changes affect liver metabolic pathways, iron homeostasis and promote a preneoplastic phenotype

Fig. 2

Chromatin remodeling in productively HBV-infected PHHs. a Chromatin accessibility in HBV-infected PHHs. Left panel: Differentially accessible regions (DARs) common to the biological (N = 2) and technical replicates (N = 2) at 2 h and 72 h post-infection (p.i.). The number of common DARs increases from 2 to 72 h p.i. (670 and 1804 respectively; N = 4 at each time point), with a small proportion of regions (n = 140) showing differential accessibility at both time points. Right panels: ATAC-seq density profiles of the 1804 DARs at 72 h p.i. in MOCK- and HBV-infected PHHs. S1 = donor 1; S2 donor 2. Intensities are represented with a color scale from blue (more accessible chromatin) to red (less accessible chromatin). b ATAC-seq density profiles at 72 h p.i. in MOCK, HBV-infected and IFN-treated HBV-infected PHHs (2 replicates from a third donor). Intensities values are represented as in a). c Violin plot depicting the ranking index (RI) distribution for the 1285 detected ATAC-seq peaks across MOCK, HBV, and IFN conditions, with two biological replicates per group. The RI values were generated as described in the supplementary data. A Kruskal–Wallis test was conducted to assess significant differences in RI distributions between the three groups. d VENN Diagram showing the intersection of the 773 ATAC-seq DARs down-regulated (i.e., displaying a reduced accessibility) in response to HBV infection with the 486 ATAC-seq DARs up-regulated by IFN treatment in HBV infected cells

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