ArticleNucleic acids research2017
FANCI and FANCD2 have common as well as independent functions during the cellular replication stress response.
Article in Nucleic acids research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 40 citations in OpenAlex.
- Insights and modulation of RNA polymerase-dependent R-loop and dsRNA in Fanconi anemia hematopoietic stem cells.JCI insight · 2026Article
- Critical roles of Hedgehog signaling pathway in regulating the multidrug resistance of ovarian cancer.Journal of ovarian research · 2026Review
- FANCD2 restrains fork progression and prevents fragility at early origins upon re-replication.Nature communications · 2026Article
- FANCI: from genome guardian to translational therapeutic target.Frontiers in oncology · 2026Review
- MCM8/9 and FANCD2 interact within a shared pathway in response to replication stress caused by DNA crosslinks.DNA repair · 2025Article
- Knockdown of FANCI suppresses hepatocellular carcinoma development via the PI3K/Akt/GSK-3β pathway.Heliyon · 2025Article
- Cell Type Specific Suppression of Hyper-Recombination by Human RAD18 Is Linked to Proliferating Cell Nuclear Antigen K164 Ubiquitination.Biomolecules · 2025Article
- Deregulated protein homeostasis constrains fetal hematopoietic stem cell pool expansion in Fanconi anemia.Nature communications · 2024Article
- Mitotic DNA Synthesis in Untransformed Human Cells Preserves Common Fragile Site Stability via a FANCD2-Driven Mechanism That Requires HELQ.Journal of molecular biology · 2023Article
- 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
- FANCI is Associated with Poor Prognosis and Immune Infiltration in Liver Hepatocellular Carcinoma.International journal of medical sciences · 2023Article
- SIK2 inhibition enhances PARP inhibitor activity synergistically in ovarian and triple-negative breast cancers.The Journal of clinical investigation · 2022Article
- 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
- FANCI plays an essential role in spermatogenesis and regulates meiotic histone methylation.Cell death & disease · 2021Article
- FANCI functions as a repair/apoptosis switch in response to DNA crosslinks.Developmental cell · 2021Article
- SLFN11 promotes stalled fork degradation that underlies the phenotype in Fanconi anemia cells.Blood · 2021Article
- Functional cross talk between the Fanconi anemia and ATRX/DAXX histone chaperone pathways promotes replication fork recovery.Human molecular genetics · 2020Article
- Article
- FANCD2-FANCI is a clamp stabilized on DNA by monoubiquitination of FANCD2 during DNA repair.Nature structural & molecular biology · 2020Article
- A Fanci knockout mouse model reveals common and distinct functions for FANCI and FANCD2.Nucleic acids research · 2019Article
Corrections and comments
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Authors and funding
10 authors at 6 institutions in 3 countries.
Funding
Abstract
Fanconi anemia (FA) is an inherited cancer predisposition syndrome characterized by cellular hypersensitivity to DNA interstrand crosslinks (ICLs). To repair these lesions, the FA proteins act in a linear hierarchy: following ICL detection on chromatin, the FA core complex monoubiquitinates and recruits the central FANCI and FANCD2 proteins that subsequently coordinate ICL removal and repair of the ensuing DNA double-stranded break by homology-dependent repair (HDR). FANCD2 also functions during the replication stress response by mediating the restart of temporarily stalled replication forks thereby suppressing the firing of new replication origins. To address if FANCI is also involved in these FANCD2-dependent mechanisms, we generated isogenic FANCI-, FANCD2- and FANCI:FANCD2 double-null cells. We show that FANCI and FANCD2 are partially independent regarding their protein stability, nuclear localization and chromatin recruitment and contribute independently to cellular proliferation. Simultaneously, FANCD2-but not FANCI-plays a major role in HDR-mediated replication restart and in suppressing new origin firing. Consistent with this observation, deficiencies in HDR-mediated DNA DSB repair can be overcome by stabilizing RAD51 filament formation in cells lacking functional FANCD2. We propose that FANCI and FANCD2 have partially non-overlapping and possibly even opposing roles during the replication stress response.
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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.