ArticleCell cycle (Georgetown, Tex.)2015
FANCD2, FANCJ and BRCA2 cooperate to promote replication fork recovery independently of the Fanconi Anemia core complex.
Article in Cell cycle (Georgetown, Tex.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
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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
52 citing papers in PubMed, 73 citations in OpenAlex.
- Molecular architecture of meiotic pro-crossover factor HEI10 reveals coupling of higher-order assembly and ubiquitin chain formation.bioRxiv : the preprint server for biology · 2026Article
- FANCD2 restrains fork progression and prevents fragility at early origins upon re-replication.Nature communications · 2026Article
- The NuRD chromatin remodeling complex contributes to repairing exogenous double-strand breaks in the Caenorhabditis elegans germline.Genetics · 2026Article
- NuRD chromatin remodeling is required to repair exogenous DSBs in thebioRxiv : the preprint server for biology · 2025Article
- Critical role of alpha spectrin in DNA repair: the importance of μ-calpain and Fanconi anemia proteins.Experimental biology and medicine (Maywood, N.J.) · 2025Review
- UFL1 triggers replication fork degradation by MRE11 in BRCA1/2-deficient cells.Nature chemical biology · 2024Article
- FANCD2 and RAD51 recombinase directly inhibit DNA2 nuclease at stalled replication forks and FANCD2 acts as a novel RAD51 mediator in strand exchange to promote genome stability.Nucleic acids research · 2023Article
- Simulating Space Conditions Evokes Different DNA Damage Responses in Immature and Mature Cells of the Human Hematopoietic System.International journal of molecular sciences · 2023Article
- A clickable melphalan for monitoring DNA interstrand crosslink accumulation and detecting ICL repair defects in Fanconi anemia patient cells.Nucleic acids research · 2023Article
- The RPA inhibitor HAMNO sensitizes Fanconi anemia pathway-deficient cells.Cell cycle (Georgetown, Tex.) · 2022Article
- TheInternational journal of molecular sciences · 2022Article
- BRCA2 associates with MCM10 to suppress PRIMPOL-mediated repriming and single-stranded gap formation after DNA damage.Nature communications · 2021Article
- Hedgehog/GLI1 Transcriptionally Regulates FANCD2 in Ovarian Tumor Cells: Its Inhibition Induces HR-Deficiency and Synergistic Lethality with PARP Inhibition.Neoplasia (New York, N.Y.) · 2021Article
- Guardians of the Genome: BRCA2 and Its Partners.Genes · 2021Review
- PRMT1-dependent regulation of RNA metabolism and DNA damage response sustains pancreatic ductal adenocarcinoma.Nature communications · 2021Article
- Fanconi anemia and mTOR pathways functionally interact during stalled replication fork recovery.FEBS letters · 2021Article
- Evolving insights: how DNA repair pathways impact cancer evolution.Cancer biology & medicine · 2020Review
- A distinct role for recombination repair factors in an early cellular response to transcription-replication conflicts.Nucleic acids research · 2020Article
- Inhibition of the translesion synthesis polymerase REV1 exploits replication gaps as a cancer vulnerability.Science advances · 2020Article
- Functional cross talk between the Fanconi anemia and ATRX/DAXX histone chaperone pathways promotes replication fork recovery.Human molecular genetics · 2020Article
Corrections and comments
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Authors and funding
5 authors at 5 institutions in 3 countries.
Funding
Abstract
Fanconi Anemia (FA) is an inherited multi-gene cancer predisposition syndrome that is characterized on the cellular level by a hypersensitivity to DNA interstrand crosslinks (ICLs). To repair these lesions, the FA pathway proteins are thought to act in a linear hierarchy: Following ICL detection, an upstream FA core complex monoubiquitinates the central FA pathway members FANCD2 and FANCI, followed by their recruitment to chromatin. Chromatin-bound monoubiquitinated FANCD2 and FANCI subsequently coordinate DNA repair factors including the downstream FA pathway members FANCJ and FANCD1/BRCA2 to repair the DNA ICL. Importantly, we recently showed that FANCD2 has additional independent roles: it binds chromatin and acts in concert with the BLM helicase complex to promote the restart of aphidicolin (APH)-stalled replication forks, while suppressing the firing of new replication origins. Here, we show that FANCD2 fulfills these roles independently of the FA core complex-mediated monoubiquitination step. Following APH treatment, nonubiquitinated FANCD2 accumulates on chromatin, recruits the BLM complex, and promotes robust replication fork recovery regardless of the absence or presence of a functional FA core complex. In contrast, the downstream FA pathway members FANCJ and BRCA2 share FANCD2's role in replication fork restart and the suppression of new origin firing. Our results support a non-linear FA pathway model at stalled replication forks, where the nonubiquitinated FANCD2 isoform - in concert with FANCJ and BRCA2 - fulfills a specific function in promoting efficient replication fork recovery independently of the FA core complex.
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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.