ChIP-seq of TP53 R175H/G mutations in cancer cells.

p53 is a pivotal transcription factor that suppresses tumor proliferation by inducing mechanisms such as cell cycle arrest, senescence, and apoptosis. Mutant p53 loses the canonical DNA-binding capability of wild-type p53 but can form complex regulatory networks by interacting with other transcription factors or altering its DNA-binding properties, thereby participating in various molecular pathways that promote tumor progression. This chapter delves into the transcriptional regulatory roles of p53R175H and p53R175G through chromatin immunoprecipitation coupled with high-throughput sequencing (ChIP-seq).