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. 2018 Aug 24;29(10):2529–2545. doi: 10.1681/ASN.2018030324

Figure 5.

Figure 5.

Wilms Tumor 1 (WT1) mediates the Krüppel-like factor 15 (KLF15) transcriptome. (A) Chromatin immunoprecipitation (ChIP) enrichment analysis of the differentially upregulated genes in glomerular extracts from the Tg26;Podocin-rtTA (PODTA);TRE-KLF15 mice compared with the Tg26;PODTA mice. We subsequently crossmatched with the previously experimentally validated WT1 ChIP-seq data70 with predicted KLF15 binding sites (TRANSFAC promoter analysis). (B) The Venn diagram shows the overlap in KLF15 and WT1 binding sites (BSs) in the differentially upregulated genes. In addition, the heat map shows the differentially upregulated genes (with a minimum of a 1.2-fold change) in the Tg26;PODTA;TRE-KLF15 mice compared with the Tg26;PODTA mice (C) with KLF15 binding sites and (D) without KLF15 binding sites. Genes shown in green are WT1 binding class 2 (WT1 binding sites in the promoter region). Genes shown in yellow are WT1 binding class 1 (WT1 binding sites at any location). Genes shown in black are WT1 binding class 0 (no WT1 binding sites).