ArticleiScience2019
ERCC1/XPF Is Important for Repair of DNA Double-Strand Breaks Containing Secondary Structures.
Article in iScience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
27 citing papers in PubMed, 43 citations in OpenAlex.
- Archaeal G-quadruplexes: a novel model for understanding unusual DNA/RNA structures across the tree of life.Nucleic acids research · 2026Article
- Break-induced replication is activated to repair R-loop-associated double-strand breaks in SETX-deficient cells.Cell reports · 2025Article
- Role of the nucleotide excision repair endonuclease XPF in the kinetoplastid parasite Trypanosoma brucei.Scientific reports · 2025Article
- Downstream transcription promotes human recurrent CNV associated AT-rich sequence mediated genome rearrangements in yeast.iScience · 2024Article
- mAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Minocycline prevents early age-related cognitive decline in a mouse model of intellectual disability caused by ZBTB18/RP58 haploinsufficiency.Journal of neuroinflammation · 2024Article
- MutSβ protects common fragile sites by facilitating homology-directed repair at DNA double-strand breaks with secondary structures.Nucleic acids research · 2024Article
- A novel algorithm for the virtual screening of extensive small molecule libraries against ERCC1/XPF protein-protein interaction for the identification of resistance-bypassing potential anticancer molecules.Turkish journal of biology = Turk biyoloji dergisi · 2024Article
- APOBEC3G protects the genome of human cultured cells and mice from radiation-induced damage.The FEBS journal · 2023Article
- Multifaceted Influence of Histone Deacetylases on DNA Damage Repair: Implications for Hepatocellular Carcinoma.Journal of clinical and translational hepatology · 2023Review
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- Analysis of representative mutants for key DNA repair pathways on healthspan in Caenorhabditis elegans.Mechanisms of ageing and development · 2021Article
- Homologous recombination within repetitive DNA.Current opinion in genetics & development · 2021Review
- Transcription-Replication Collisions-A Series of Unfortunate Events.Biomolecules · 2021Review
- Intrinsic DNA damage repair deficiency results in progressive microglia loss and replacement.Glia · 2021Article
- ERCC1 mutations impede DNA damage repair and cause liver and kidney dysfunction in patients.The Journal of experimental medicine · 2021Article
- DNA folds threaten genetic stability and can be leveraged for chemotherapy.RSC chemical biology · 2021Review
- Enhancing the activity of platinum-based drugs by improved inhibitors of ERCC1-XPF-mediated DNA repair.Cancer chemotherapy and pharmacology · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 3 countries.
Funding
Abstract
The structure-specific endonuclease ERCC1/XPF plays an important role in nucleotide excision repair and interstrand cross-link repair. In this study, we identified new functions of ERCC1/XPF in DNA double-strand break (DSB) repair. We found that the conserved function of ERCC1/XPF to remove non-homologous sequences at DSBs is a rate-limiting step for homologous recombination in mammalian cells, and more importantly, we uncovered an indispensable role of ERCC1/XPF in repair of DSBs containing DNA secondary structures, including the structure-prone AT-rich DNA sequences derived from common fragile sites and G-quadruplexes (G4s). We also demonstrated a synthetic lethal interaction of XPF with DNA translocase FANCM that is involved in removing DNA secondary structures. Furthermore, inactivation of XPF sensitizes FANCM-deficient cells to G4-interacting compounds. These results suggest an important function of ERCC1/XPF in protecting DNA secondary structures and provide a rationale for targeted treatment of FANCM-deficient tumors through inhibition of XPF.
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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.