ATAD5 functions as a regulatory platform for Ub-PCNA deubiquitination

• 成果类型: Article
• 署名作者: Ryu, Eunjin; Yoo, Juyeong; Kang, Mi-Sun; Ha, Na Young; Jang, Yewon; Kim, Jinwoo; Kim, Yeongjae; Kim, Byung-Gyu; Kim, Shinseog; Myung, Kyungjae; Kang, Sukhyun
• 署名单位: Institute for Basic Science - Korea (IBS); Ulsan National Institute of Science & Technology (UNIST); Ulsan National Institute of Science & Technology (UNIST); Harvard University; Harvard Medical School
• 刊物名称: PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
• ISSN/ISSBN: 0027-15358
• DOI: 10.1073/pnas.2315759121
• 发表日期: 2024-08-20
• 关键词: nuclear antigen pcna; genomic instability; ubiquitin ligase; dna-replication; human shprh; protein; recruits; complex; zranb3; bypass

摘要

Ubiquitination status of proliferating cell nuclear antigen (PCNA) is crucial for regulating DNA lesion bypass. After the resolution of fork stalling, PCNA is subsequently deubiquitinated, but the underlying mechanism remains undefined. We found that the DNA- loaded Ub-PCNA through distinct DNA- binding and PCNA- binding motifs. facilitating the deubiquitination of DNA- loaded Ub-PCNA. ATAD5 also enhances the Ub-PCNA deubiquitination by USP7 and USP11 through specific interactions. had increased sensitivity to DNA- damaging agents. Our results ultimately reveal that from the DNA in order to safely deactivate the DNA repair process.