TRABID deubiquitinase overexpression enables synthetic lethality to PARP inhibitor via prolonged retention of 53BP1 at DSB sites

Here, we demonstrate that TRABID deubiquitinase (DUB) binds to 53BP1 at endogenous level and regulates 53BP1 retention at DSB sites. TRABID deubiquitinates K29-linked polyubiquitination of 53BP1 mediated by E3 ubiquitin ligase SPOP and prevents 53BP1 dissociation from DSBs, consequently inducing HR defects and chromosomal instability. Prostate cancer cells with TRABID overexpression exhibit a high sensitivity to poly (ADP-ribose) polymerase (PARP) inhibitors. This dataset include all the raw data of western blot from this project.