ArticleNature communications2024
ATAD5-BAZ1B interaction modulates PCNA ubiquitination during DNA repair.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Dietary Chlorogenic Acid-Rich Green Coffee Bean Extract Improves Laying Performance and Antioxidant Status in Heat-Stressed Laying Hens.Animals : an open access journal from MDPI · 2026Article
- TONSL promotes hepatocellular carcinoma progression and radioresistance by orchestrating DNA damage repair and cell cycle dynamics.Discover oncology · 2026Article
- Disrupting the USP1-UAF1 deubiquitinase complex: a master regulator of replication stress and frontier target in cancer therapy.Medical oncology (Northwood, London, England) · 2026Review
- HSP72-AMPK axis mitigates hypoxia-induced cellular senescence to promote colorectal cancer development.Molecular and cellular biochemistry · 2026Article
- WSTF-associated regulation of GLYCTK and metabolic adaptation in colorectal cancer.Frontiers in immunology · 2026Article
- Professor Emma Whitelaw, a pioneer of epigenetic inheritance.Frontiers in epigenetics and epigenomics · 2025Article
- Novel mechanism of tumor metastasis: DDX11-ATAD5 interaction mediates epithelial-mesenchymal transition to promote gallbladder cancer progression.CytoJournal · 2025Article
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
Mono-ubiquitinated PCNA (mono-Ub-PCNA) is generated when replication forks encounter obstacles, enabling the bypass of DNA lesions. After resolving stalled forks, Ub-PCNA must be de-ubiquitinated to resume high-fidelity DNA synthesis. ATAD5, in cooperation with the UAF1-USP1 complex, is responsible for this de-ubiquitination. However, the precise regulation of timely Ub-PCNA de-ubiquitination remains unclear. Our research reveals that BAZ1B, a regulatory subunit of the BAZ1B-SMARCA5 chromatin-remodeling complex (also known as the WICH complex), plays a crucial role in fine-tuning the de-ubiquitination process of Ub-PCNA. The BAZ1B binding region of ATAD5 encompasses the UAF1-binding domain of ATAD5. Disruption of the ATAD5-BAZ1B interaction results in premature de-ubiquitination of Ub-PCNA following treatment with hydrogen peroxide. Cells with impaired BAZ1B binding to ATAD5 display increased sensitivity to oxidative stress compared to wild-type cells. These findings suggest that BAZ1B prevents premature Ub-PCNA de-ubiquitination, thereby safeguarding genome integrity.
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