Fig. 3: HNF4A chromatin dissociation is associated with de-repression of acute-phase genes.
From: Downregulation of HNF4A enables transcriptomic reprogramming during the hepatic acute-phase response
a Subcellular fractionation of HepG2 cells treated with IL6/IL1β for 1 h, (b) displays densitometric quantification of HNF4A for treated conditions relative to reference protein of each fraction for 3 independent biological replicates: whole cell extract/cytosol-GAPDH, nuclear soluble-PARP, chromatin-H3 (n = 3, one-way ANOVA, Post-Hoc: Dunnett’s test). c Expression of HNF4A (pre-mRNA P1), G6PC1, HP and SAA1/2 in HepG2 WT treated for 6 h or 24 h with IL6/IL1β (10 ng/mL), n = 3. d HNF4A ChIP-Seq peaks (GSE96176)38 and HNF4A DNA binding motifs at target regions, amplicons for ChIP- and FAIRE-qPCR are highlighted in red. e, f HNF4A ChIP and FAIRE in HepG2 WT after 6 h of cytokine treatment (10 ng/mL IL6/IL1β), qPCR was performed at SAA, HP and G6PC1 regulatory regions, C2 gene desert served as a negative control (n = 3 (SAA2 promoter, G6PC1 promoter, C2 desert and FAIRE), n = 4 (SAA enhancer, HP promoter, G6PC1 enhancer), two-tailed unpaired Student’s t-test). Data are expressed as mean ± SEM, significance levels *< 0.05; **< 0.01; ***< 0.001; ****< 0.0001.
