ArticleThe Journal of clinical investigation2013
Fanconi anemia signaling network regulates the spindle assembly checkpoint.
Article in The Journal of clinical investigation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
46 citing papers in PubMed, 68 citations in OpenAlex.
- Integrative proteomics defines FANCA as a multifunctional hub linking DNA repair to translation.iScience · 2026Article
- The periphery of nuclear speckles defines a spatially and temporally regulated compartment of long-lived intron-retained RNAs that resolves during mitosis.Nature cell biology · 2026Article
- Review
- Oncogenic properties of wild-type DNA repair gene FANCA in breast cancer.Cell reports · 2025Article
- PLK1 Inhibition Induces Synthetic Lethality in Fanconi Anemia Pathway-Deficient Acute Myeloid Leukemia.Cancer research communications · 2025Article
- 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
- Identification of new RAD51D-regulating microRNAs that also emerge as potent inhibitors of the Fanconi anemia/homologous recombination pathways.Human molecular genetics · 2022Article
- Cytogenetics in Fanconi Anemia: The Importance of Follow-Up and the Search for New Biomarkers of Genomic Instability.International journal of molecular sciences · 2022Review
- Upregulation of NKG2D ligands impairs hematopoietic stem cell function in Fanconi anemia.The Journal of clinical investigation · 2022Article
- SIK2 kinase synthetic lethality is driven by spindle assembly defects in FANCA-deficient cells.Molecular oncology · 2022Article
- Type-I Interferon Signaling in Fanconi Anemia.Frontiers in cellular and infection microbiology · 2022Review
- Focal Point of Fanconi Anemia Signaling.International journal of molecular sciences · 2021Review
- p53 Activation in Genetic Disorders: Different Routes to the Same Destination.International journal of molecular sciences · 2021Review
- Mitotic Errors Promote Genomic Instability and Leukemia in a Novel Mouse Model of Fanconi Anemia.Frontiers in oncology · 2021Article
- SMC5/6 is required for replication fork stability and faithful chromosome segregation during neurogenesis.eLife · 2020Article
- Evolving insights: how DNA repair pathways impact cancer evolution.Cancer biology & medicine · 2020Review
- Canonical and Noncanonical Roles of Fanconi Anemia Proteins: Implications in Cancer Predisposition.Cancers · 2020Review
- FANCD2 Confers a Malignant Phenotype in Esophageal Squamous Cell Carcinoma by Regulating Cell Cycle Progression.Cancers · 2020Article
- Review
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 3 institutions in 3 countries.
Funding
Abstract
Fanconi anemia (FA) is a heterogenous genetic disease with a high risk of cancer. The FA proteins are essential for interphase DNA damage repair; however, it is incompletely understood why FA-deficient cells also develop gross aneuploidy, leading to cancer. Here, we systematically evaluated the role of the FA proteins in chromosome segregation through functional RNAi screens and analysis of primary cells from patients with FA. We found that FA signaling is essential for the spindle assembly checkpoint and is therefore required for high-fidelity chromosome segregation and prevention of aneuploidy. Furthermore, we discovered that FA proteins differentially localize to key structures of the mitotic apparatus in a cell cycle-dependent manner. The essential role of the FA pathway in mitosis offers a mechanistic explanation for the aneuploidy and malignant transformation known to occur after disruption of FA signaling. Collectively, our findings provide insight into the genetically unstable cancers resulting from inactivation of the FA/BRCA pathway.
Indexed as
Identifiers
What OpenQuestion holds
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.