ArticleMolecular and cellular biology2009
XPF-ERCC1 participates in the Fanconi anemia pathway of cross-link repair.
Article in Molecular and cellular biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 92 papers.
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Who cites it
92 citing papers in PubMed, 139 citations in OpenAlex.
- Phosphorylation by CDK1 switches the function of the human SLX4 SAP domain from DNA binding to MUS81 binding.Nucleic acids research · 2026Article
- Deficiencies in the Fanconi anemia or homologous recombination pathway enhance the antitumor effects of the hypoxia-activated prodrug CP-506.Molecular therapy. Oncology · 2026Article
- Molecular basis of XPF-ERCC1 targeting to SLX4-dependent DNA repair pathways.Nature communications · 2025Article
- FAN1-mediated translesion synthesis and POLQ/HELQ-mediated end joining generate interstrand crosslink-induced mutations.Nature communications · 2025Article
- The Ercc1Aging cell · 2025Article
- Repair of genomic interstrand crosslinks.DNA repair · 2024Review
- Persistent TFIIH binding to non-excised DNA damage causes cell and developmental failure.Nature communications · 2024Article
- p53 regulates diverse tissue-specific outcomes to endogenous DNA damage in mice.Nature communications · 2024Article
- PARP inhibitors in testicular germ cell tumors: what we know and what we are looking for.Frontiers in genetics · 2024Review
- Nucleotide excision repair: a versatile and smart toolkit.Acta biochimica et biophysica Sinica · 2022Review
- Association between ERCC1 Gene Polymorphism (rs11615) and Colorectal Cancer Susceptibility: A Meta-Analysis of Medical Image Fusion and Safety Applications.Computational and mathematical methods in medicine · 2022Article
- Modulation of ERCC1-XPF Heterodimerization InhibitionFrontiers in oncology · 2022Article
- Multiomic analysis identifies CPT1A as a potential therapeutic target in platinum-refractory, high-grade serous ovarian cancer.Cell reports. Medicine · 2021Article
- The Role of RNA in DNA Breaks, Repair and Chromosomal Rearrangements.Biomolecules · 2021Review
- DNA damage-how and why we age?eLife · 2021Review
- Review
- DNA polymerase ι compensates for Fanconi anemia pathway deficiency by countering DNA replication stress.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Exploiting the Microhomology-Mediated End-Joining Pathway in Cancer Therapy.Cancer research · 2020Review
- Targeting Chromosomal Architectural HMGB Proteins Could Be the Next Frontier in Cancer Therapy.Cancer research · 2020Review
- ERCC1-XPF targeting to psoralen-DNA crosslinks depends on XPA and FANCD2.Cellular and molecular life sciences : CMLS · 2020Article
32 more citing papers are in PubMed but not listed here.
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Authors and funding
9 authors at 7 institutions in 3 countries.
Funding
Abstract
Interstrand cross-links (ICLs) prevent DNA strand separation and, therefore, transcription and replication, making them extremely cytotoxic. The precise mechanism by which ICLs are removed from mammalian genomes largely remains elusive. Genetic evidence implicates ATR, the Fanconi anemia proteins, proteins required for homologous recombination, translesion synthesis, and at least two endonucleases, MUS81-EME1 and XPF-ERCC1. ICLs cause replication-dependent DNA double-strand breaks (DSBs), and MUS81-EME1 facilitates DSB formation. The subsequent repair of these DSBs occurs via homologous recombination after the ICL is unhooked by XPF-ERCC1. Here, we examined the effect of the loss of either nuclease on FANCD2 monoubiquitination to determine if the nucleolytic processing of ICLs is required for the activation of the Fanconi anemia pathway. FANCD2 was monoubiquitinated in Mus81(-/-), Ercc1(-/-), and XPF-deficient human, mouse, and hamster cells exposed to cross-linking agents. However, the monoubiquitinated form of FANCD2 persisted longer in XPF-ERCC1-deficient cells than in wild-type cells. Moreover, the levels of chromatin-bound FANCD2 were dramatically reduced and the number of ICL-induced FANCD2 foci significantly lower in XPF-ERCC1-deficient cells. These data demonstrate that the unhooking of an ICL by XPF-ERCC1 is necessary for the stable localization of FANCD2 to the chromatin and subsequent homologous recombination-mediated DSB repair.
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