Skip to main content
. 2014 Dec;34(23):4216–4231. doi: 10.1128/MCB.00611-14

FIG 3.

FIG 3

The binding sites of miR-424(322)/503 within the CDC25A 3′ UTR contribute to the reduction of the CDC25A level upon TGF-β exposure. (A) Cloning of the wild-type CDC25A promoter into the pGL3-Basic vector (WT-PROM) and mutagenesis of the repressive E2F-A binding site (MUT-PROM). (B) Addition of a wild-type and mutated CDC25A 3′ UTR tail to the WT-PROM and MUT-PROM constructs. (C) Luciferase assays show that addition of the extra wild-type 3′ UTR tail is necessary to achieve maximum CDC25A repression by TGF-β. The data represent five independent experiments. The TGF-β-mediated transcriptional repression values are calculated relative to no-TGF-β treatment for each construct.