Genome-wide studies identify genes directly regulated by PML_RARα fusion protein and co-activator BRD4 [ChIP-Seq]

Acute promyelocytic leukemia (APL) is characterized by a specific t(15;17) chromosome translocation that generates the promyelocytic leukemia/retinoic acid receptor-α (PML_RARα) fusion gene. However, the global association between PML_RARα and transcriptional co-regulators, and the rules of their association in governing the key processes during the leukemogenesis remain unclear. Here, we performed the genome-wide binding profiling of BRD4 in NB4, an APL patient-derived cell line. Moreover, we also performed ChIP-seq of PML_RARα and BRD4 upon genetic or pharmacological pertubation of PML_RARα or BRD4 to determine how they target regulatory elements. Genome-wide binding profiling of PML_RARa and BRD4 in NB4 cells as well as PML_RARa in K562 cells using ChIP-seq.