ArticleOncotarget2014
Basal level of FANCD2 monoubiquitination is required for the maintenance of a sufficient number of licensed-replication origins to fire at a normal rate.
Article in Oncotarget, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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.
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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
24 citing papers in PubMed, 27 citations in OpenAlex.
- FANCD2 restrains fork progression and prevents fragility at early origins upon re-replication.Nature communications · 2026Article
- The Compromised Fanconi Anemia Pathway in Prelamin A-Expressing Cells Contributes to Replication Stress-Induced Genomic Instability.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Fanconi anemia pathway regulation by FANCI in prostate cancer.Frontiers in oncology · 2023Article
- Focal Point of Fanconi Anemia Signaling.International journal of molecular sciences · 2021Review
- Article
- Loss of the Fanconi anemia-associated protein NIPA causes bone marrow failure.The Journal of clinical investigation · 2020Article
- A new look at molecular biology of breast cancer.Cancer biology & therapy · 2019Review
- Specificity for deubiquitination of monoubiquitinated FANCD2 is driven by the N-terminus of USP1.Life science alliance · 2018Article
- Article
- Multifaceted Fanconi Anemia Signaling.Trends in genetics : TIG · 2018Review
- Fanconi anemia FANCD2 and FANCI proteins regulate the nuclear dynamics of splicing factors.The Journal of cell biology · 2017Article
- Fanconi Anemia Signaling and Cancer.Trends in cancer · 2017Review
- Article
- FANCD2 and DNA Damage.International journal of molecular sciences · 2017Review
- Dormant origins as a built-in safeguard in eukaryotic DNA replication against genome instability and disease development.DNA repair · 2017Review
- Involvement of FANCD2 in Energy Metabolism via ATP5α.Scientific reports · 2017Article
- FANCD2 Facilitates Replication through Common Fragile Sites.Molecular cell · 2016Article
- Fanconi Anemia Group D2 Protein Participates in Replication Origin Firing.Chemotherapy · 2016Article
- FANCI is a negative regulator of Akt activation.Cell cycle (Georgetown, Tex.) · 2016Article
- Mutated Fanconi anemia pathway in non-Fanconi anemia cancers.Oncotarget · 2015Article
Corrections and comments
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Authors and funding
8 authors at 5 institutions in 2 countries.
Funding
Abstract
Normal DNA replication starts following the stepwise recruitment of replication initiators to assemble Mini-chromosome Maintenance (MCM) 2-7 protein complexes at an adequate amount of DNA replication origins. Under normal conditions, the monoubiquitination of Fanconi Anemia (FA) group D2 protein (FANCD2) occurs in each S-phase of cell cycle, which is the basal level of FANCD2 monoubiquitination. However, little is known regarding the roles of this basal level of monoubiquitinated FANCD2. Here we show that monoubiquitinated FANCD2 in each S-phase of normal cell cycle is essential for replication origins to fire at a normal rate. We found that the basal level of the monoubiquitinated FANCD2 can interact with replication origins as well as mini-chromosome maintenance protein 3 (MCM3) in an S-phase specific manner to secure an enough number of the licensed-origins to fire. Non-monoubiquitinated FANCD2 or mutant MCM3 lacking AA 477-480 responsible for interacting with FANCD2 can lead to an insufficient amount of licensed origins to fire and, thereby, enlarged intervals between the fired origins. Our results demonstrate that the monoubiquitinated FANCD2 in each S-phase of normal cell cycle is required to maintain an enough number of licensed origins to initiate the normal DNA replication. This finding is the first to provide insights into how FANCD2 functions under normal condition of cell cycle to maintain genome stability, as well as resulting implications in the strategic improvement for the fight against human cancer.
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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.