ArticleNucleic acids research2020
ATAD5 deficiency alters DNA damage metabolism and sensitizes cells to PARP inhibition.
Article in Nucleic acids research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed.
- Integrated genomic and transcriptomic analysis reveals candidate genes associated with reproductive performance in Hetian Black chickens.Poultry science · 2026Article
- A DLBCL Prognostic model superior to the IPI score: Mechanistic study and clinical validation based on RFC2- and RFC4-mediated DNA damage repair.Clinical and experimental medicine · 2026Article
- The role of HECT-type E3 ubiquitin ligases in DNA damage response and repair.Cell death discovery · 2025Review
- Multiple roles of replication factor C family in pan‑cancer (Review).Oncology reports · 2025Review
- Novel mechanism of tumor metastasis: DDX11-ATAD5 interaction mediates epithelial-mesenchymal transition to promote gallbladder cancer progression.CytoJournal · 2025Article
- Exploring Novel Genome Instability-associated lncRNAs and their Potential Function in Pan-Renal Cell Carcinoma.Combinatorial chemistry & high throughput screening · 2024Article
- Short-range end resection requires ATAD5-mediated PCNA unloading for faithful homologous recombination.Nucleic acids research · 2023Article
- Targeting DNA Damage Repair and Immune Checkpoint Proteins for Optimizing the Treatment of Endometrial Cancer.Pharmaceutics · 2023Review
- Kinome-wide screening uncovers a role for Bromodomain Protein 3 in DNA double-stranded break repair.DNA repair · 2023Article
- Colorectal cancer concurrent gene signature based on coherent patterns between genomic and transcriptional alterations.BMC cancer · 2022Article
- PARP inhibition impedes the maturation of nascent DNA strands during DNA replication.Nature structural & molecular biology · 2022Article
- MolData, a molecular benchmark for disease and target based machine learning.Journal of cheminformatics · 2022Article
- Timely termination of repair DNA synthesis by ATAD5 is important in oxidative DNA damage-induced single-strand break repair.Nucleic acids research · 2021Article
- Eukaryotic clamp loaders and unloaders in the maintenance of genome stability.Experimental & molecular medicine · 2020Review
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Replication factor C (RFC), a heteropentamer of RFC1-5, loads PCNA onto DNA during replication and repair. Once DNA synthesis has ceased, PCNA must be unloaded. Recent findings assign the uloader role primarily to an RFC-like (RLC) complex, in which the largest RFC subunit, RFC1, has been replaced with ATAD5 (ELG1 in Saccharomyces cerevisiae). ATAD5-RLC appears to be indispensable, given that Atad5 knock-out leads to embryonic lethality. In order to learn how the retention of PCNA on DNA might interfere with normal DNA metabolism, we studied the response of ATAD5-depleted cells to several genotoxic agents. We show that ATAD5 deficiency leads to hypersensitivity to methyl methanesulphonate (MMS), camptothecin (CPT) and mitomycin C (MMC), agents that hinder the progression of replication forks. We further show that ATAD5-depleted cells are sensitive to poly(ADP)ribose polymerase (PARP) inhibitors and that the processing of spontaneous oxidative DNA damage contributes towards this sensitivity. We posit that PCNA molecules trapped on DNA interfere with the correct metabolism of arrested replication forks, phenotype reminiscent of defective homologous recombination (HR). As Atad5 heterozygous mice are cancer-prone and as ATAD5 mutations have been identified in breast and endometrial cancers, our finding may open a path towards the therapy of these tumours.
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