Mono-ubiquitinated PCNA (mono-Ub-PCNA) is generated when replication forks stall and facilitates the DNA lesion bypass process. After resolving a replication stall, Ub-PCNA needs to be de-ubiquitinated to resume high-fidelity DNA synthesis. ATAD5 cooperates with UAF1-USP1 to de-ubiquitinate mono-Ub-PCNA. However, it remains unclear how Ub-PCNA de-ubiquitination is regulated in a timely manner. We found that BAZ1B, a regulatory subunit of the chromatin-remodeling complex, fine-tunes de-ubiquitination of Ub-PCNA. The BAZ1B binding region of ATAD5 surrounds the ATAD5 UAF1-binding domain. Abrogation of the ATAD5-BAZ1B interaction leads to premature de-ubiquitination of Ub-PCNA after hydrogen peroxide treatment. BAZ1B-binding defective ATAD5 cells are more sensitive to oxidative stress compared to wild-type cells. These results suggest that BAZ1B inhibits premature Ub-PCNA de-ubiquitination to maintain genome integrity.