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. 2025 Dec 11;17:696. doi: 10.1038/s41467-025-67304-4

Fig. 6. H₂O₂-dependent regulation of the ATF2-KAP1-ZNF354A epigenetic complex.

Fig. 6

a, b Western blots of U2OS cells treated with H₂O₂ (50 μM, 4 h) in presence of indicated kinase inhibitors. Blots show ZDHHC20 (Short-S, 20 L isoforms), phospho-KAP1 (S473), phospho-ATF2 (T69), total KAP1 and ATF2, GAPDH (loading control) (a), and phospho-Ser/Thr proteins with total ZNF354A (b). Quantification of phospho-ATF2, phospho-KAP1, ZDHHC20L (a), and phospho-Ser/Thr/ZNF354A (b) bands. Mean ± SEM; each dot represents an independent experiment (n = 4). Statistical analysis by two-way ANOVA, Dunnett’s test; p values compare treated conditions to untreated control (Ctrl). c Western blots as in (a), in KAP1 or ZNF354A immunoprecipitates from H₂O₂-treated cells as in (a). d Heat maps of ChIP-seq profiles centered on ZNF354A-HA peaks ( ± 1 kb) showing enrichment in HEK293T and K562 cells under untreated and H₂O₂-treated conditions (50 μM, 4 h). e, IGV browser screenshots illustrating selected ZNF354A ChIP-seq peaks (arrows) within MAT1A, and ZDHHC20 loci from cells treated as described in (d). f ChIP–qPCR quantification of ZNF354A-HA peaks at indicated gene regions (two peaks for ZDHHC20; EVX1 used as control). Results mean ± SEM; dots represent independent experiments (n  =  3). p values vs untreated ( − H₂O₂), two-way ANOVA, Tukey’s correction. Source data and entire blots provided as a Source Data file and supplementary information.