ArticleNature genetics2011
SLX4, a coordinator of structure-specific endonucleases, is mutated in a new Fanconi anemia subtype.
Article in Nature genetics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 188 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
188 citing papers in PubMed, 297 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
- Dual-site phosphorylation of SLX4 stabilizes the SLX4-MUS81 interface to promote mitotic SMX assembly and genome protection.Nucleic acids research · 2026Article
- Insights and modulation of RNA polymerase-dependent R-loop and dsRNA in Fanconi anemia hematopoietic stem cells.JCI insight · 2026Article
- SLX1 Inhibition Enhances Olaparib Sensitivity by Impairing Homologous Recombination Repair in Breast Cancer.International journal of molecular sciences · 2025Article
- The CIP2A-TOPBP1 axis facilitates mitotic DNA repair via MiDAS and MMEJ.Nature communications · 2025Article
- Inherited Predispositions to Myeloid Neoplasms: Pathogenesis and Clinical Implications.Annual review of pathology · 2025Review
- Mitotic DNA Synthesis in Untransformed Human Cells Preserves Common Fragile Site Stability via a FANCD2-Driven Mechanism That Requires HELQ.Journal of molecular biology · 2023Article
- Comprehensive Interactome Mapping of the DNA Repair Scaffold SLX4 Using Proximity Labeling and Affinity Purification.Journal of proteome research · 2023Article
- Review
- PARP Inhibitors and Proteins Interacting with SLX4.Cancers · 2023Review
- Partial Response to Crizotinib in a Lung Adenocarcinoma Patient with a Novel FBXO11 (Intergenic)-ALK (Exon 20-29) Fusion.OncoTargets and therapy · 2023Article
- Article
- Article
- The structure-specific endonuclease complex SLX4-XPF regulates Tus-Ter-induced homologous recombination.Nature structural & molecular biology · 2022Article
- Pembrolizumab activity in patients with Fanconi anemia repair pathway competent and deficient tumors.Biomarker research · 2022Article
- SLX4 dampens MutSα-dependent mismatch repair.Nucleic acids research · 2022Article
- MRE11-dependent instability in mitochondrial DNA fork protection activates a cGAS immune signaling pathway.Science advances · 2021Article
- RNF168 E3 ligase participates in ubiquitin signaling and recruitment of SLX4 during DNA crosslink repair.Cell reports · 2021Article
- Detection and analysis of common pathogenic germline mutations in Peutz-Jeghers syndrome.World journal of gastroenterology · 2021Article
- Coordinated roles of SLX4 and MutSβ in DNA repair and the maintenance of genome stability.Critical reviews in biochemistry and molecular biology · 2021Review
128 more citing papers are in PubMed but not listed here.
Corrections and comments
- Commented on by
- Commented on by
Authors and funding
16 authors at 6 institutions in 3 countries.
Funding
Abstract
DNA interstrand crosslink repair requires several classes of proteins, including structure-specific endonucleases and Fanconi anemia proteins. SLX4, which coordinates three separate endonucleases, was recently recognized as an important regulator of DNA repair. Here we report the first human individuals found to have biallelic mutations in SLX4. These individuals, who were previously diagnosed as having Fanconi anemia, add SLX4 as an essential component to the FA-BRCA genome maintenance pathway.
Indexed as
Identifiers
What OpenQuestion holds
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.