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. 2013 Sep 12;8(9):e73693. doi: 10.1371/journal.pone.0073693

Figure 1. E2F7/8 directly regulate CCBE1 and FLT4 expression.

Figure 1

A, Genes associated with the gene ontology (GO) term angiogenesis were extracted from the Sox2-cre;E2f7loxP/−E2f8loxP/− vs. wild-type E10.5 mouse embryos (P<0.05) database (GEO: GSE30488) and additionally analyzed for E2F binding sites and their presence in GO lymphangiogenesis (GO:0001946). B, E2F binding elements within the CCBE1 and FLT4 promoter. Average and canonical E2F binding consensus. C, E2F7 and E2F8 ChIP performed on CCBE1 and FLT4 promoters in HeLa cells, arrows in (B) indicate primers used for ChIP. A previous reported E2F site within the E2F1 promoter and a non-specific site upstream (+700 bp) served as controls. D, mRNA and protein levels of E2f7-EGFP inducible HeLa cells treated with doxycyclin (0.2 µg /ml) for 24 hours. E, mRNA and protein levels of HeLa cells treated with scrambled or E2f7/8 siRNAs. Fold change in protein were calculated using TUBULIN as reference. Data presented as the average (±s.e.m.) compared to the control condition in three independent experiments.