Fig. 5: Homeostatic control of NK-cells by PRDM1 may be counteracted by AP-1 factors when stimulated with feeder cells.
From: Key regulatory roles of PRDM1 in human NK-cell differentiation and activation
A Volcano plots showing significantly enriched TF footprints in ATAC-seq comparing NK-F-D13 with NK-IL2-D6. B Number and percentage (left) and pathway analysis (right) of all differential ATAC-seq peaks and AP-1 footprint-containing differential ATAC-seq peaks comparing NK-F-D13 and NK-IL2-D6. P value on the bar graph indicates significance in Chi-squared test of the proportion. C Number (top) and pathway analysis (bottom) of genes with both AP-1 and PRDM1 footprint that showed higher ATAC-seq signal in NK-F-D13 compared to NK-IL2-D6. D Distance between AP-1 and PRDM1 footprints or any footprints within differential ATAC-seq peaks between NK-F-D13 and NK-IL2-D6. P-value indicates the significance of Kolmogorov–Smirnov test of the two distributions. E Number and percentage of DEGs between NK-F-D13 and NK-IL2-D6 among genes with differential ATAC-seq signals between NK-F-D13 and NK-IL2-D6 containing PRDM1 footprint only or both PRDM1 and AP-1 footprints. P value indicates significance in Chi-squared test of the proportion. F Cell counting of primary human NK-cells transduced with A-FOS or treated with 5 μM AP-1 inhibitor T5224 after feeder cell stimulation in two independent experiments with 3 replicates. Comparison with control group as reference were performed by one-way ANOVA following Tukey ad-hoc test at each time point. *, p < 0.05; **, p < 0.01; ***, p < 0.001.
