Fig. 4 | Nature Communications

Fig. 4

From: Ap4 is rate limiting for intestinal tumor formation by controlling the homeostasis of intestinal stem cells

Fig. 4

Ap4-dependent expression profiles in ApcMin/+ adenomas. a GSEA comparing gene expression profiles from ApcMin/+/Ap4fl/fl and ApcMin/+/Ap4∆IEC adenomas from 120 days old mice with Lgr5-positive stem cell signatures13, Wnt/β-catenin signaling (mSigDB: molecular Signatures Database), Notch target genes or c-Myc target genes (mSigDB). NES: normalized enrichment score, Nom. p-value: nominal p-value. b Heatmap of selected differentially expressed mRNAs (p-value < 0.05) from intestinal stem cell gene signatures, Wnt/β-catenin signaling and/or Notch signaling gene signatures analyzed in a. The heatmap displays relative fold changes in expression levels normalized to the mean expression in the control, ApcMin/+/Ap4fl/fl, samples for each indicated mRNA. Three biological replicates per genotype were analyzed. c qPCR analysis of the indicated mRNA derived from tumors from three female mice (five tumors per mouse) per genotype. d The murine CRC cells CT26 were subjected to qChIP analysis with Ap4 or IgG-specific antibodies for ChIP. The mouse acetylcholine receptor (AchR) promoter, which lacks Ap4-binding motifs, served as a negative control. E-boxes used for qChIP analysis are marked in Supplementary Fig. 3. c, d Results represent the mean ± SD. Results were subjected to an unpaired, two-tailed Student’s t-test with p-values * < 0.05, ** < 0.01, *** < 0.001, n.s.: not significant. See also Supplementary Fig. 3, Supplementary Data 1 and Supplementary Data 2

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