ArticleNucleic acids research2013
A novel interplay between the Fanconi anemia core complex and ATR-ATRIP kinase during DNA cross-link repair.
Article in Nucleic acids research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 58 citations in OpenAlex.
- β-tubulin phosphorylation by Chk1 is required for normal spindle formation during cell division.Communications biology · 2026Article
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- REV7 associates with ATRIP and inhibits ATR kinase activity.Nucleic acids research · 2026Article
- A NovelCurrent oncology (Toronto, Ont.) · 2025Article
- PRMT5-regulated splicing of DNA repair genes drives chemoresistance in breast cancer stem cells.Oncogene · 2025Article
- Deciphering the role of post-translational modifications in fanconi anemia proteins and their influence on tumorigenesis.Cancer gene therapy · 2024Review
- Phosphorylation by ATR triggers FANCD2 chromatin loading and activates the Fanconi anemia pathway.Cell reports · 2023Article
- Variants in ATRIP are associated with breast cancer susceptibility in the Polish population and UK Biobank.American journal of human genetics · 2023Article
- Fanconi anemia: current insights regarding epidemiology, cancer, and DNA repair.Human genetics · 2022Review
- Regulation of the Fanconi Anemia DNA Repair Pathway by Phosphorylation and Monoubiquitination.Genes · 2021Review
- RNF168 E3 ligase participates in ubiquitin signaling and recruitment of SLX4 during DNA crosslink repair.Cell reports · 2021Article
- Article
- The Role of Ataxia Telangiectasia Mutant and Rad3-Related DNA Damage Response in Pathogenesis of Human Papillomavirus.Pathogens (Basel, Switzerland) · 2020Review
- Review
- SMC5/6 acts jointly with Fanconi anemia factors to support DNA repair and genome stability.EMBO reports · 2020Article
- Detours to Replication: Functions of Specialized DNA Polymerases during Oncogene-induced Replication Stress.International journal of molecular sciences · 2018Review
- Warsaw breakage syndrome DDX11 helicase acts jointly with RAD17 in the repair of bulky lesions and replication through abasic sites.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- FAM35A associates with REV7 and modulates DNA damage responses of normal and BRCA1-defective cells.The EMBO journal · 2018Article
- Replication stress induces accumulation of FANCD2 at central region of large fragile genes.Nucleic acids research · 2018Article
- PathCORE-T: identifying and visualizing globally co-occurring pathways in large transcriptomic compendia.BioData mining · 2018Article
Corrections and comments
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Authors and funding
19 authors at 10 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
When DNA replication is stalled at sites of DNA damage, a cascade of responses is activated in the cell to halt cell cycle progression and promote DNA repair. A pathway initiated by the kinase Ataxia teleangiectasia and Rad3 related (ATR) and its partner ATR interacting protein (ATRIP) plays an important role in this response. The Fanconi anemia (FA) pathway is also activated following genomic stress, and defects in this pathway cause a cancer-prone hematologic disorder in humans. Little is known about how these two pathways are coordinated. We report here that following cellular exposure to DNA cross-linking damage, the FA core complex enhances binding and localization of ATRIP within damaged chromatin. In cells lacking the core complex, ATR-mediated phosphorylation of two functional response targets, ATRIP and FANCI, is defective. We also provide evidence that the canonical ATR activation pathway involving RAD17 and TOPBP1 is largely dispensable for the FA pathway activation. Indeed DT40 mutant cells lacking both RAD17 and FANCD2 were synergistically more sensitive to cisplatin compared with either single mutant. Collectively, these data reveal new aspects of the interplay between regulation of ATR-ATRIP kinase and activation of the FA pathway.
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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.