OBF1 stabilizes the binding of OCT1 to chromatin. (A) Normalized number of OBF1 and OCT1 Bio-ChIP-seq reads in overlapping peaks from LPS-stimulated CD19⁺ mouse splenic B cells. (B) Violin plots showing enrichment of OCT1 Bio-ChIP-seq samples according to their overlap with OBF1. (C) Violin plots showing enrichment of OCT2 Bio-ChIP-seq samples according to their overlap with OBF1. (D) Violin plots showing enrichment of OCT1 Bio-ChIP-seq samples according to their overlap with OBF1, PU.1, or both. (B-D) Mean ± standard deviation; *P < .05; **P < .01; ***P < .001; ****P < .0001 (2-tailed Student t test). (E) Immunoblot showing OBF1 levels in LPS-treated splenic B cells in WT and Pou2af1 knockout mice. The membrane was probed with an antibody against OBF1; actin is shown as loading control. (F) Differential OCT1 binding regions in WT and Pou2af1^KO/KO CD19⁺ splenic B cells stimulated by LPS (red dots, OCT1 binding regions showing significantly weaker binding in Pou2af1 knockout samples than in WT; green dots, OCT1 binding regions showing significantly stronger binding in Pou2af1 knockout samples than in WT). (G) Heatmap showing the OCT1 Bio-ChIP-seq signal of WT and Pou2af1^KO/KO CD19⁺ splenic B cells on differentially bound regions. A total of 739 peaks regions show significantly decreased OCT1 Bio-ChIP-seq signal in Pou2af1 knockout samples. Gene ontology analysis was performed using genes nearest to the peak’s regions. (H) Mean of alignments of H3K27ac ChIP-seq signals centered on OCT1 peak summits within 6-kb genomic window in WT and Pou2af1^KO/KO CD19⁺ splenic B cells stimulated by LPS. (P value was calculated by Mann-Whitney U test). (I) OCT1 ChIP-seq read densities between Pou2af1^KO/KO and WT CD19⁺ splenic B treated with LPS for 72 hours.