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Fig. 3 | Clinical Epigenetics

Fig. 3

From: DNA hypomethylation of a transcription factor binding site within the promoter of a gout risk gene NRBP1 upregulates its expression by inhibition of TFAP2A binding

Fig. 3

Increased DNA-binding of TFAP2A to methylated B1 inhibits gene transcription in vitro. a TFAP2A exhibited methylation-dependent inhibition of luciferase activity on B1. Dual-luciferase reporter assays were performed to evaluate the transcriptional activity of the methylated or unmethylated B1 by TFAP2A in 293T cells, with firefly luciferase activity normalized to renilla activity. Data are represented as mean ± SEM (**P value < 0.001, ****P value < 0.00001, Student’s t test, unpaired, two-sided). b DNA methylation on B1 can increase its direct interaction with TFAP2A. Purified TFAP2A was incubated with streptavidin bead-bound, biotinylated B1 with or without DNA methylation modification. Bead-bound proteins were fractionated by SDS-PAGE, and TFAP2A was detected by immunoblotting. Portions (10%) of the purified TFAP2A (input) or unbound fractions were assayed in parallel

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Clinical Epigenetics

ISSN: 1868-7083

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