Global re-wiring of p53 transcription regulation by the hepatitis B virus X (HBx) protein [ChIP-Seq]. Homo sapiens

As HBx has been reported to interact with p53 and alter the recruitment of p53 to its binding sites, we obtained a comprehensive genome-wide profile of deregulated p53 transcription complex-DNA binding by the HBx protein using massively parallel deep sequencing coupled to p53 chromatin immunoprecipitation (ChIP-Seq) on HBx-expressing and control HepG2 liver cell culture model system. Overall design: HepG2 cells were transduced with recombinant HBx and control adenoviruses 24 hours post seeding. HepG2 cells were treated with UVC (254 nm) irradiation 48 hours postransduction and harvested 24 hours after UV irradiation. 30 µg of control and HBx-expressing UV-treated HepG2 cell lysates were immunoprecipitated using 4 µg of p53 FL-393 antibody (Santa Cruz Biotechnology). The subsequent yield and size of the ChIP library generated was quantified, followed by sequencing using HiSeq (Illumina, CA, USA) to read counts of 7.7 M total reads.