Fig. 3: ZNF263 recruits chromatin modifiers to SIX3 promoter through protein–protein interactions.
From: The EGFR-ZNF263 signaling axis silences SIX3 in glioblastoma epigenetically
a ChIP-qPCR analysis showing that knockdown of ZNF263 enhances H3K9 acetylation and attenuates H3K9me3, H3K27me3 in SIX3 promoter. b ChIP-qPCR analysis showing that overexpression of ZNF263 promotes the enrichment of H3K9me3 and H3K27me3 in SIX3 promoter. c Experiments with TCGA showing that ZNF263 expression positively correlates with the DNA methylation level of SIX3 promotor. d MSP analysis showing that overexpression of ZNF263 elevates DNA methylation of SIX3 promoter, while knockdown of ZNF263 reduces DNA methylation level. Numbers represent the relative ratio of methylated DNA and unmethylated DNA. e IP analysis showing the interactions between ZNF263 and candidate proteins. HEK293 cells were transfected with ZNF63-FLAG and DNMT3A vectors. *p < 0.05; **p < 0.01; ***p < 0.001.
