ArticleMolecular cell2015
The SLX4 complex is a SUMO E3 ligase that impacts on replication stress outcome and genome stability.
Article in Molecular cell, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 96 papers.
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Who cites it
96 citing papers in PubMed, 135 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
- COSA-1-SLX-4 interaction directly links crossover designation with Holliday junction resolution.Science advances · 2026Article
- Non-covalent SUMO interactions with ligases and effectors: SUMO-interacting motifs and beyond.Essays in biochemistry · 2025Review
- Molecular basis of XPF-ERCC1 targeting to SLX4-dependent DNA repair pathways.Nature communications · 2025Article
- SenExo-cCCT2 Reprograms Senescence Response and Anti-Tumor Immunity Following FOLFIRINOX Chemotherapy in Pancreatic Ductal Adenocarcinoma.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- RNF4 and USP7 coordinate spatial regulation of SLX4 stability within the PML nuclear bodies.Nucleic acids research · 2025Article
- TopBP1 coordinates DNA repair synthesis in mitosis via recruitment of the nuclease scaffold SLX4.Communications biology · 2025Article
- The role of SUMOylation in biomolecular condensate dynamics and protein localization.Cell insight · 2024Review
- Multifaceted roles of SUMO in DNA metabolism.Nucleus (Austin, Tex.) · 2024Review
- Cotton BOP1 mediates SUMOylation of GhBES1 to regulate fibre development and plant architecture.Plant biotechnology journal · 2024Article
- Deciphering the role of post-translational modifications in fanconi anemia proteins and their influence on tumorigenesis.Cancer gene therapy · 2024Review
- Inhibition of topoisomerase 2 catalytic activity impacts the integrity of heterochromatin and repetitive DNA and leads to interlinks between clustered repeats.Nature communications · 2024Article
- SUMO and the DNA damage response.Biochemical Society transactions · 2024Review
- ATR limits Rad18-mediated PCNA monoubiquitination to preserve replication fork and telomerase-independent telomere stability.The EMBO journal · 2024Article
- In silico analysis of several frequent SLX4 mutations appearing in human cancers.microPublication biology · 2024Article
- SUMOylation regulation of ribosome biogenesis: Emerging roles for USP36.Frontiers in RNA research · 2024Article
- The SUMO-NIP45 pathway processes toxic DNA catenanes to prevent mitotic failure.Nature structural & molecular biology · 2023Article
- Comprehensive Interactome Mapping of the DNA Repair Scaffold SLX4 Using Proximity Labeling and Affinity Purification.Journal of proteome research · 2023Article
- Mitotic DNA synthesis in response to replication stress requires the sequential action of DNA polymerases zeta and delta in human cells.Nature communications · 2023Article
36 more citing papers are in PubMed but not listed here.
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Authors and funding
11 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The SLX4 Fanconi anemia protein is a tumor suppressor that may act as a key regulator that engages the cell into specific genome maintenance pathways. Here, we show that the SLX4 complex is a SUMO E3 ligase that SUMOylates SLX4 itself and the XPF subunit of the DNA repair/recombination XPF-ERCC1 endonuclease. This SLX4-dependent activity is mediated by a remarkably specific interaction between SLX4 and the SUMO-charged E2 conjugating enzyme UBC9 and relies not only on newly identified SUMO-interacting motifs (SIMs) in SLX4 but also on its BTB domain. In contrast to its ubiquitin-binding UBZ4 motifs, SLX4 SIMs are dispensable for its DNA interstrand crosslink repair functions. Instead, while detrimental in response to global replication stress, the SUMO E3 ligase activity of the SLX4 complex is critical to prevent mitotic catastrophe following common fragile site expression.
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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.