ArticleNucleic acids research2016
FANCJ is essential to maintain microsatellite structure genome-wide during replication stress.
Article in Nucleic acids research, 2016. 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 27 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.
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Who cites it
27 citing papers in PubMed, 36 citations in OpenAlex.
- Rare genetic diseases associated with G-quadruplex-induced replication stress.Communications biology · 2026Review
- Dynamic Assemblies in Genome Maintenance.Advances in experimental medicine and biology · 2026Review
- How DNA secondary structures drive replication fork instability.DNA repair · 2025Review
- Tissue-Specific Effects of the DNA Helicase FANCJ/BRIP1/BACH1 on Repeat Expansion in a Mouse Model of the Fragile X-Related Disorders.International journal of molecular sciences · 2025Article
- Microsatellite break-induced replication generates highly mutagenized extrachromosomal circular DNAs.NAR cancer · 2024Article
- FANCJ DNA helicase is recruited to the replisome by AND-1 to ensure genome stability.EMBO reports · 2024Article
- Article
- Identification of new RAD51D-regulating microRNAs that also emerge as potent inhibitors of the Fanconi anemia/homologous recombination pathways.Human molecular genetics · 2022Article
- Stable G-quadruplex DNA structures promote replication-dependent genome instability.The Journal of biological chemistry · 2022Article
- Replication stress at microsatellites causes DNA double-strand breaks and break-induced replication.The Journal of biological chemistry · 2020Article
- FANCJ helicase promotes DNA end resection by facilitating CtIP recruitment to DNA double-strand breaks.PLoS genetics · 2020Article
- Landscape of BRIP1 molecular lesions in gastrointestinal cancers from published genomic studies.World journal of gastroenterology · 2020Article
- History of DNA Helicases.Genes · 2020Review
- An Arabidopsis FANCJ helicase homologue is required for DNA crosslink repair and rDNA repeat stability.PLoS genetics · 2019Article
- The role of fork stalling and DNA structures in causing chromosome fragility.Genes, chromosomes & cancer · 2019Review
- Deficiency of the Fanconi anemia E2 ubiqitin conjugase UBE2T only partially abrogates Alu-mediated recombination in a new model of homology dependent recombination.Nucleic acids research · 2019Article
- RecQ and Fe-S helicases have unique roles in DNA metabolism dictated by their unwinding directionality, substrate specificity, and protein interactions.Biochemical Society transactions · 2018Review
- BLM's balancing act and the involvement of FANCJ in DNA repair.Cell cycle (Georgetown, Tex.) · 2018Article
- FANCJ helicase controls the balance between short- and long-tract gene conversions between sister chromatids.Nucleic acids research · 2017Article
- A Defective mRNA Cleavage and Polyadenylation Complex Facilitates Expansions of Transcribed (GAA)Cell reports · 2017Article
Corrections and comments
- Erratum issued
Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
Microsatellite DNAs that form non-B structures are implicated in replication fork stalling, DNA double strand breaks (DSBs) and human disease. Fanconi anemia (FA) is an inherited disorder in which mutations in at least nineteen genes are responsible for the phenotypes of genome instability and cancer predisposition. FA pathway proteins are active in the resolution of non-B DNA structures including interstrand crosslinks, G quadruplexes and DNA triplexes. In FANCJ helicase depleted cells, we show that hydroxyurea or aphidicolin treatment leads to loss of microsatellite polymerase chain reaction signals and to chromosome recombination at an ectopic hairpin forming CTG/CAG repeat in the HeLa genome. Moreover, diverse endogenous microsatellite signals were also lost upon replication stress after FANCJ depletion, and in FANCJ null patient cells. The phenotype of microsatellite signal instability is specific for FANCJ apart from the intact FA pathway, and is consistent with DSBs at microsatellites genome-wide in FANCJ depleted cells following replication stress.
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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.