Genome-wide profiling of histone modification H3K27ac and CTCF transcription factor binding following VPA treatment in HEK293 cells
Valproic acid (VPA), a histone deacetylase (HDAC) inhibitor induces epigenetic changes through histone hyperacetylation which lead to alteration to H3K27ac and CTCF binding in the genome. To determine the effects of VPA on 3D chromatin organization, we performed ChIP-seq  on untreated and VPA-treated HEK293T cells. VPA treatment results in elevated H3K27ac marks and slightly reduced CTCF binding, which supports the evidence of active transcription triggered upon histone hyperacetylation induced by VPA. Overall design: We performed chromatin immunoprecipitation DNA-sequencing (ChIP-seq) for histone modification H3K27ac and transcription factor CCCTC-binding factor (CTCF) in both untreated and VPA-treated HEK293T cells. The experiments were performed in triplicates. Peak calling and differential ChIP-seq peak analysis was performed to elucidate the genomic changes triggered by VPA.