ArticleCell reports2024
PP2A licenses the FANCD2/FANCI complex for chromosome loading.
Article in Cell reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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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
4 citing papers in PubMed.
- FANCI: from genome guardian to translational therapeutic target.Frontiers in oncology · 2026Review
- Revisiting an old therapy for new, promising combinations: Biology and perspectives of lomustine in glioma treatment.Neuro-oncology · 2025Review
- Piperine Targets the FANCL/UBE2T Complex to Inhibit the FA Pathway and Sensitize Bladder Cancer to Cisplatin.Dose-response : a publication of International Hormesis SocietyArticle
- Ubiquitin and SUMO pathways in DNA replication and replication-coupled repair.Critical reviews in biochemistry and molecular biologyReview
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
The Fanconi anemia (FA) pathway removes interstrand crosslinks (ICLs) between the Watson-Crick strands of the DNA double helix in humans. Central to the pathway is the FANCD2/FANCI complex, which must be loaded onto chromosomes. Here, we report the identification of a PP2A phosphatase complex, which specifically dephosphorylates an inhibitory cluster in FANCD2, thereby licensing its loading in response to DNA damage. We show that PP2A is required for normal monoubiquitination of the FANCD2/FANCI complex and for its loading onto chromosomes. We have fully reconstituted a coupled dephosphorylation-ubiquitination reaction in vitro using a highly purified PP2A complex. Using super-resolution live-cell single-molecule tracking, we show how PP2A switches on the FA pathway in response to ICLs and that cells are sensitive to ICL-forming drugs in the absence of PP2A. Our work uncovers a mechanism where PP2A facilitates the activation of the FA pathway by licensing chromosome loading of the FANCD2/FANCI complex.
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Registered trials
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