ArticleDNA repair2015
Physical interaction between SLX4 (FANCP) and XPF (FANCQ) proteins and biological consequences of interaction-defective missense mutations.
Article in DNA repair, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 18 citations in OpenAlex.
- Molecular basis of XPF-ERCC1 targeting to SLX4-dependent DNA repair pathways.Nature communications · 2025Article
- Machine learning-driven prediction of substrates for enzymes introducing or removing protein post-translational modifications.Communications chemistry · 2025Article
- Computed cancer interactome explains the effects of somatic mutations in cancers.Protein science : a publication of the Protein Society · 2022Article
- Exploring the Structures and Functions of Macromolecular SLX4-Nuclease Complexes in Genome Stability.Frontiers in genetics · 2021Review
- SLX4IP acts with SLX4 and XPF-ERCC1 to promote interstrand crosslink repair.Nucleic acids research · 2019Article
- The role of SLX4 and its associated nucleases in DNA interstrand crosslink repair.Nucleic acids research · 2019Article
- Functional Comparison of XPF Missense Mutations Associated to Multiple DNA Repair Disorders.Genes · 2019Article
- Recruitment and positioning determine the specific role of the XPF-ERCC1 endonuclease in interstrand crosslink repair.The EMBO journal · 2017Article
- Cho Endonuclease Functions during DNA Interstrand Cross-Link Repair in Escherichia coli.Journal of bacteriology · 2016Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
SLX4 (FANCP) and XPF (FANCQ) proteins interact with each other and play a vital role in the Fanconi anemia (FA) DNA repair pathway. We have identified a SLX4 region and several amino acid residues that are responsible for this interaction. The study has revealed that the global minor allele, SLX4(Y546C), is defective in this interaction and cannot complement Fancp knockout mouse cells in mitomycin C-induced cytotoxicity or chromosomal aberrations. These results highly suggest this allele, as well as SLX4(L530Q), to be pathogenic. The interacting partner XPF is involved in various DNA repair pathways, and certain XPF mutations cause progeria, Cockayne syndrome (CS), and/or FA phenotypes. Because several atypical xeroderma pigmentosum (XP) phenotype-causing XPF missense mutations are located in the SLX4-interacting region, we suspected the disruption of the interaction with SLX4 in these XPF mutants, thereby causing severer phenotypes. The immunoprecipitation assay of cell extracts revealed that those XPF mutations, except XPF(C236R), located in the SLX4-interacting region cause instability of XPF protein, which could be the reason for the FA, progeria and/or CS phenotypes.
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Registered trials
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