ArticleCell reports2018
Opposing Roles of FANCJ and HLTF Protect Forks and Restrain Replication during Stress.
Article in Cell reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 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
52 citing papers in PubMed, 73 citations in OpenAlex.
- Rare genetic diseases associated with G-quadruplex-induced replication stress.Communications biology · 2026Review
- Understanding single stranded DNA gaps: from formation to fate.The Biochemical journal · 2026Review
- Targeted CRISPR knockout screening identifies known and novel chemogenomic interactions between DNA damaging agents and DNA repair genes.NAR cancer · 2026Article
- The Genetic and Molecular Analyses of Rare Candidate GermlineInternational journal of molecular sciences · 2026Article
- SLFN11 counteracts the RFWD3-PRIMPOL DNA damage tolerance axis to restrain gapped DNA synthesis in response to replication stress.Nature communications · 2025Article
- Synergistic inhibition of CHK1 and MUS81 to combat replication stress resistance in high-risk neuroblastoma.Scientific reports · 2025Article
- RAD51 is chromatin enriched and targetable in BRCA1-deficient cells.Molecular cell · 2025Article
- Cytosolic DNA and intracellular CaDNA repair · 2025Review
- Mechanisms and regulation of replication fork reversal.DNA repair · 2024Review
- HLTF resolves G4s and promotes G4-induced replication fork slowing to maintain genome stability.Molecular cell · 2024Article
- RAD52 prevents accumulation ofbioRxiv : the preprint server for biology · 2024Article
- Replication stress as a driver of cellular senescence and aging.Communications biology · 2024Review
- A perspective on tumor radiation resistance following high-LET radiation treatment.Journal of cancer research and clinical oncology · 2024Review
- FANCJ promotes PARP1 activity during DNA replication that is essential in BRCA1 deficient cells.Nature communications · 2024Article
- MutSβ-MutLβ-FANCJ axis mediates the restart of DNA replication after fork stalling at cotranscriptional G4/R-loops.Science advances · 2024Article
- FANCJ DNA helicase is recruited to the replisome by AND-1 to ensure genome stability.EMBO reports · 2024Article
- Purification and biochemical characterization of the G4 resolvase and DNA helicase FANCJ.Methods in enzymology · 2024Article
- The nucleolar protein GNL3 prevents resection of stalled replication forks.EMBO reports · 2023Article
- CaMKK2 and CHK1 phosphorylate human STN1 in response to replication stress to protect stalled forks from aberrant resection.Nature communications · 2023Article
- Genome-scale mapping of DNA damage suppressors through phenotypic CRISPR-Cas9 screens.Molecular cell · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
Abstract
The DNA helicase FANCJ is mutated in hereditary breast and ovarian cancer and Fanconi anemia (FA). Nevertheless, how loss of FANCJ translates to disease pathogenesis remains unclear. We addressed this question by analyzing proteins associated with replication forks in cells with or without FANCJ. We demonstrate that FANCJ-knockout (FANCJ-KO) cells have alterations in the replisome that are consistent with enhanced replication stress, including an aberrant accumulation of the fork remodeling factor helicase-like transcription factor (HLTF). Correspondingly, HLTF contributes to fork degradation in FANCJ-KO cells. Unexpectedly, the unrestrained DNA synthesis that characterizes HLTF-deficient cells is FANCJ dependent and correlates with S1 nuclease sensitivity and fork degradation. These results suggest that FANCJ and HLTF promote replication fork integrity, in part by counteracting each other to keep fork remodeling and elongation in check. Indicating one protein compensates for loss of the other, loss of both HLTF and FANCJ causes a more severe replication stress response.
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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.