BRD4-Regulated Transcription Programs and Cancer Pathways
The identification of BRD4 as a key transcription regulator in HPV and cellular gene transcription, DNA replication, DNA repair, cell cycle control, and stem cell renewal and differentiation has prompted my lab research in BRD4-centered gene regulation and chromatin dynamics over the past 15 years.
- transcription mechanisms
- phosphorylation-driven BRD4 gene control and factor recruitment
- loss and gain of p53 functions
- DNA replication
- mitotic chromosome progression and bookmarking
- DNA repair
- cancer etiology
- cellular systems
- genome editing
- in vivo cancer models
Our initial interest in HPV-driven cervical cancer and head-and-neck cancer has been further expanded to non-HPV-associated breast cancer and other human diseases. Recent studies have been focused primarily on how phosphorylation controls BRD4 protein conformation, factor recruitment, and pathway selectivity and also how BRD4 protein isoforms modulate cancer initiation and progression. The discoveries we have made over the years continuously shed new light on the roles of BRD4 in viral and cellular processes and disease implications.