The targets of p-KDM3A in the human genome.

<p>(<b>A</b>) <i>Right</i>, Meta Gene profiles of KDM3A binding to gene loci from the TSS to the TTS. <i>Left</i>, The color intensity represents the tag count, which is standardized across the gene groups for each ChIP-seq dataset. (<b>B</b>) Pie chart of KDM3A HS(-), p-KDM3A HS(-), p-KDM3A HS(+), and random occupancies across the genome. (<b>C</b>) The Venn diagram shows the binding regions of KDM3A, p-KDM3A HS(-), and p-KDM3A HS(+) for the Jurkat cells. (<b>D</b>) GO analysis of HS-induced p-KDM3A targets using GREAT. The control analyses of KDM3A and p-KDM3A without HS treatment are shown in <a href="http://www.plosbiology.org/article/info:doi/10.1371/journal.pbio.1002026#pbio.1002026.s006" target="_blank">S5 Figure</a>. (<b>E</b>) Motif analysis of the p-KDM3A-enriched regions using MEME. The three most distinct identified motifs are shown. (<b>F</b>) Representative ChIP-seq tracks for KDM3A and p-KDM3A on <i>DNAJB1, SERPIH1, SMIM20</i>, and <i>RNASEK</i> in Jurkat cells with or without HS treatment. The <i>x</i>-axis indicates the genomic location, and the <i>y</i>-axis represents the normalized ChIP-seq signal density. The binding peaks of Stat1 induced in HeLa S3 cells that were treated with (+) or without (-) IFN-γ were taken from Robert et al. <a href="http://www.plosbiology.org/article/info:doi/10.1371/journal.pbio.1002026#pbio.1002026-Robertson1" target="_blank">[27]</a> and are shown on the top two rows. (<b>G</b>) ChIP-qPCR for changes in the percentage relative to the input (top) and the fold-change in mRNA expression of the indicated genes that were induced by HS treatment. Data are mean ± SD (**<i>p</i><0.01).