ArticleCell cycle (Georgetown, Tex.)2015
FANCD2 influences replication fork processes and genome stability in response to clustered DSBs.
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. An erratum has been issued. Cited by 17 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
17 citing papers in PubMed, 26 citations in OpenAlex.
- Immunological Reprogramming by Radiation Therapy: Implications for Precision Cancer Treatment.Immunology · 2026Review
- Decoding the ubiquitin network: molecular mechanisms and therapeutic vulnerabilities for precision radio-sensitization in cancer.Molecular cancer · 2025Review
- Deep visual proteomics reveals DNA replication stress as a hallmark of signet ring cell carcinoma.NPJ precision oncology · 2025Article
- Therapeutic implications of germline vulnerabilities in DNA repair for precision oncology.Cancer treatment reviews · 2022Review
- 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
- Role of HP1β during spermatogenesis and DNA replication.Chromosoma · 2020Article
- Immunomodulatory Effects of Radiotherapy.International journal of molecular sciences · 2020Review
- Testis transcriptome profiling identified genes involved in spermatogenic arrest of cattleyak.PloS one · 2020Article
- The BRUCE-ATR Signaling Axis Is Required for Accurate DNA Replication and Suppression of Liver Cancer Development.Hepatology (Baltimore, Md.) · 2019Article
- Expression and prognostic significance of Fanconi anemia group D2 protein and breast cancer type 1 susceptibility protein in familial and sporadic breast cancer.Oncology letters · 2019Article
- Mechanistic link between DNA damage sensing, repairing and signaling factors and immune signaling.Advances in protein chemistry and structural biology · 2019Review
- Thymineless Death by the Fluoropyrimidine Polymer F10 Involves Replication Fork Collapse and Is Enhanced by Chk1 Inhibition.Neoplasia (New York, N.Y.) · 2018Article
- Three-dimensional Culture of Human Airway Epithelium in Matrigel for Evaluation of Human Rhinovirus C and Bocavirus Infections.Biomedical and environmental sciences : BES · 2018Article
- Fanconi Anemia Signaling and Cancer.Trends in cancer · 2017Review
- FANCD2 and DNA Damage.International journal of molecular sciences · 2017Review
- RAD51 interconnects between DNA replication, DNA repair and immunity.Nucleic acids research · 2017Article
- Replication stress induced site-specific phosphorylation targets WRN to the ubiquitin-proteasome pathway.Oncotarget · 2016Article
Corrections and comments
- Erratum issuedCorrigendum.2016
Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fanconi Anemia (FA) is a cancer predisposition syndrome and the factors defective in FA are involved in DNA replication, DNA damage repair and tumor suppression. Here, we show that FANCD2 is critical for genome stability maintenance in response to high-linear energy transfer (LET) radiation. We found that FANCD2 is monoubiquitinated and recruited to the sites of clustered DNA double-stranded breaks (DSBs) specifically in S/G2 cells after high-LET radiation. Further, FANCD2 facilitated the repair of clustered DSBs in S/G2 cells and proper progression of S-phase. Furthermore, lack of FANCD2 led to a reduced rate of replication fork progression and elevated levels of both replication fork stalling and new origin firing in response to high-LET radiation. Mechanistically, FANCD2 is required for correct recruitment of RPA2 and Rad51 to the sites of clustered DSBs and that is critical for proper processing of clustered DSBs. Significantly, FANCD2-decifient cells exhibited defective chromosome segregation, elevated levels of chromosomal aberrations, and anchorage-independent growth in response to high-LET radiation. These findings establish FANCD2 as a key factor in genome stability maintenance in response to high-LET radiation and as a promising target to improve cancer therapy.
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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.