ReviewGenes2019
Holding All the Cards-How Fanconi Anemia Proteins Deal with Replication Stress and Preserve Genomic Stability.
Review in Genes, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 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
34 citing papers in PubMed, 57 citations in OpenAlex.
- Loss of the RAD-51 isoform A redirects DNA repair and preserves genome stability in FANCD2-deficient Caenorhabditis elegans.BMC biology · 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
- 8-Oxoguanine Disrupts G-Quadruplex DNA Stability and Modulates FANCJ AKKQ Peptide Binding.Molecules (Basel, Switzerland) · 2025Article
- Replication stress as a driver of cellular senescence and aging.Communications biology · 2024Review
- Reversion from basal histone H4 hypoacetylation at the replication fork increases DNA damage in FANCA deficient cells.PloS one · 2024Article
- Discovery of a new hereditary RECQ helicase disorder RECON syndrome positions the replication stress response and genome homeostasis as centrally important processes in aging and age-related disease.Ageing research reviews · 2023Review
- Maintenance of genome integrity by the late-acting cytoplasmic iron-sulfur assembly (CIA) complex.Frontiers in genetics · 2023Review
- Regulator of telomere elongation helicase 1 gene and its association with malignancy.Cancer reports (Hoboken, N.J.) · 2023Review
- Genotype-phenotype and outcome associations in patients with Fanconi anemia: the National Cancer Institute cohort.Haematologica · 2023Article
- Dual targeting of Saccharomyces cerevisiae Pso2 to mitochondria and the nucleus, and its functional relevance in the repair of DNA interstrand crosslinks.G3 (Bethesda, Md.) · 2022Article
- Review
- DNA damage responses that enhance resilience to replication stress.Cellular and molecular life sciences : CMLS · 2021Review
- Uncovering cancer vulnerabilities by machine learning prediction of synthetic lethality.Molecular cancer · 2021Article
- Comprehensive Mutational Analysis of the BRCA1-Associated DNA Helicase and Tumor-Suppressor FANCJ/BACH1/BRIP1.Molecular cancer research : MCR · 2021Article
- DNA folds threaten genetic stability and can be leveraged for chemotherapy.RSC chemical biology · 2021Review
- Formation and repair of unavoidable, endogenous interstrand cross-links in cellular DNA.DNA repair · 2021Review
- DCAF14 promotes stalled fork stability to maintain genome integrity.Cell reports · 2021Article
- SLX4-XPF mediates DNA damage responses to replication stress induced by DNA-protein interactions.The Journal of cell biology · 2021Article
- DNA Repair in Huntington's Disease and Spinocerebellar Ataxias: Somatic Instability and Alternative Hypotheses.Journal of Huntington's disease · 2021Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Fanconi anemia (FA) is a hereditary chromosomal instability disorder often displaying congenital abnormalities and characterized by a predisposition to progressive bone marrow failure (BMF) and cancer. Over the last 25 years since the discovery of the first linkage of genetic mutations to FA, its molecular genetic landscape has expanded tremendously as it became apparent that FA is a disease characterized by a defect in a specific DNA repair pathway responsible for the correction of covalent cross-links between the two complementary strands of the DNA double helix. This pathway has become increasingly complex, with the discovery of now over 20 FA-linked genes implicated in interstrand cross-link (ICL) repair. Moreover, gene products known to be involved in double-strand break (DSB) repair, mismatch repair (MMR), and nucleotide excision repair (NER) play roles in the ICL response and repair of associated DNA damage. While ICL repair is predominantly coupled with DNA replication, it also can occur in non-replicating cells. DNA damage accumulation and hematopoietic stem cell failure are thought to contribute to the increased inflammation and oxidative stress prevalent in FA. Adding to its confounding nature, certain FA gene products are also engaged in the response to replication stress, caused endogenously or by agents other than ICL-inducing drugs. In this review, we discuss the mechanistic aspects of the FA pathway and the molecular defects leading to elevated replication stress believed to underlie the cellular phenotypes and clinical features of FA.
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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.