ArticleCell reports2013
Two distinct modes of ATR activation orchestrated by Rad17 and Nbs1.
Article in Cell reports, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 98 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
98 citing papers in PubMed, 138 citations in OpenAlex.
- Replication stress in cancer: origins, consequences and therapeutic opportunities.Nature reviews. Cancer · 2026Review
- Lipid Conjugation of a Photoprotective Meadowfoam (Biomolecules · 2026Article
- Review
- Reciprocal compensation of caspase-2 and p53 regulates the DNA damage response in HCT116 colon cancer cells.The Journal of biological chemistry · 2026Article
- Microhomology-mediated end joining acts directly on replication forks to repair single-ended double-strand breaks.Molecular cell · 2026Article
- Mechanism of RPA phosphocode priming and tuning by CDK1/WEE1 signaling circuit.Nature communications · 2025Article
- Medicinal chemistry breakthroughs on ATM, ATR, and DNA-PK inhibitors as prospective cancer therapeutics.Journal of enzyme inhibition and medicinal chemistry · 2025Review
- How DNA secondary structures drive replication fork instability.DNA repair · 2025Review
- XPO1 R749Q Mutations Co-occur with POLE Mutations in Cancer and Can Be Targeted to Overcome Chemoresistance.Cancer research · 2025Article
- TTK activates ATR through RPA2 phosphorylation to promote olaparib resistance in ovarian cancer.Communications biology · 2025Article
- ATM priming and end resection-coupled phosphorylation of MRE11 is important for fork protection and replication restart.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Non-homologous end joining shapes the genomic rearrangement landscape of chromothripsis from mitotic errors.Nature communications · 2024Article
- Resection of DNA double-strand breaks activates Mre11-Rad50-Nbs1- and Rad9-Hus1-Rad1-dependent mechanisms that redundantly promote ATR checkpoint activation and end processing in Xenopus egg extracts.Nucleic acids research · 2024Article
- ATR signaling controls the bystander responses of human chondrosarcoma cells by promoting RAD51-dependent DNA repair.International journal of radiation biology · 2024Article
- Article
- An ATR-PrimPol pathway confers tolerance to oncogenic KRAS-induced and heterochromatin-associated replication stress.Nature communications · 2023Article
- Emerging strategies for cancer therapy by ATR inhibitors.Cancer science · 2023Review
- Maintaining Genome Integrity: Protein Kinases and Phosphatases Orchestrate the Balancing Act of DNA Double-Strand Breaks Repair in Cancer.International journal of molecular sciences · 2023Review
- Comprehensive mutational analysis of the checkpoint signaling function of Rpa1/Ssb1 in fission yeast.PLoS genetics · 2023Article
- Comprehensive mutational analysis of the checkpoint signaling function of Rpa1/Ssb1 in fission yeast.bioRxiv : the preprint server for biology · 2023Article
38 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
The ATM- and Rad3-related (ATR) kinase is a master regulator of the DNA damage response, yet how ATR is activated toward different substrates is still poorly understood. Here, we show that ATR phosphorylates Chk1 and RPA32 through distinct mechanisms at replication-associated DNA double-stranded breaks (DSBs). In contrast to the rapid phosphorylation of Chk1, RPA32 is progressively phosphorylated by ATR at Ser33 during DSB resection prior to the phosphorylation of Ser4/Ser8 by DNA-PKcs. Surprisingly, despite its reliance on ATR and TopBP1, substantial RPA32 Ser33 phosphorylation occurs in a Rad17-independent but Nbs1-dependent manner in vivo and in vitro. Importantly, the role of Nbs1 in RPA32 phosphorylation can be separated from ATM activation and DSB resection, and it is dependent upon the interaction of Nbs1 with RPA. An Nbs1 mutant that is unable to bind RPA fails to support proper recovery of collapsed replication forks, suggesting that the Nbs1-mediated mode of ATR activation is important for the repair of replication-associated DSBs.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.