ArticleDNA repair2008
Fanconi anemia proteins stabilize replication forks.
Article in DNA repair, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
47 citing papers in PubMed, 67 citations in OpenAlex.
- The FANCD2-FANCI heterodimer coordinates chromatin openness and cell cycle progression throughout DNA double-strand break repair.Cell reports · 2026Article
- MCM8/9 and FANCD2 interact within a shared pathway in response to replication stress caused by DNA crosslinks.DNA repair · 2025Article
- Review
- Article
- The RPA inhibitor HAMNO sensitizes Fanconi anemia pathway-deficient cells.Cell cycle (Georgetown, Tex.) · 2022Article
- Review
- Phosphorylation of FANCD2 Inhibits the FANCD2/FANCI Complex and Suppresses the Fanconi Anemia Pathway in the Absence of DNA Damage.Cell reports · 2019Article
- Stat3 and CCAAT enhancer-binding protein β (C/ebpβ) activate Fanconi C gene transcription during emergency granulopoiesis.The Journal of biological chemistry · 2018Article
- Article
- Maintenance of genome stability by Fanconi anemia proteins.Cell & bioscience · 2017Review
- FANCD2 functions as a critical factor downstream of MiTF to maintain the proliferation and survival of melanoma cells.Scientific reports · 2016Article
- Cell resistance to the Cytolethal Distending Toxin involves an association of DNA repair mechanisms.Scientific reports · 2016Article
- Replication Protein A (RPA) deficiency activates the Fanconi anemia DNA repair pathway.Cell cycle (Georgetown, Tex.) · 2016Article
- The Interferon Consensus Sequence Binding Protein (Icsbp/Irf8) Is Required for Termination of Emergency Granulopoiesis.The Journal of biological chemistry · 2016Article
- Cell-free Xenopus egg extracts for studying DNA damage response pathways.The International journal of developmental biology · 2016Review
- The human oncoprotein and chromatin architectural factor DEK counteracts DNA replication stress.Oncogene · 2015Article
- Review
- Fanconi anemia signaling and Mus81 cooperate to safeguard development and crosslink repair.Nucleic acids research · 2014Article
- Hypoxic stress facilitates acute activation and chronic downregulation of fanconi anemia proteins.Molecular cancer research : MCR · 2014Article
- DNA double-strand break repair pathway choice and cancer.DNA repair · 2014Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
Fanconi anemia (FA) is a recessive genetic disorder characterized by hypersensitivity to crosslinking agents that has been attributed to defects in DNA repair and/or replication. FANCD2 and the FA core complex bind to chromatin during DNA replication; however, the role of FA proteins during replication is unknown. Using Xenopus cell-free extracts, we show that FANCL depletion results in defective DNA replication restart following treatment with camptothecin, a drug that results in DSBs during DNA replication. This defect is more pronounced following treatment with mitomycin C, presumably because of an additional role of the FA pathway in DNA crosslink repair. Moreover, we show that chromatin binding of FA core complex proteins during DNA replication follows origin assembly and origin firing and is dependent on the binding of RPA to ssDNA while FANCD2 additionally requires ATR, consistent with FA proteins acting at replication forks. Together, our data suggest that FA proteins play a role in replication restart at collapsed replication forks.
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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.