ArticleNature communications2026
Discovery of an Endonuclease G-inhibitory Ku80-peptide protecting against leukemogenic rearrangements at the MLL breakpoint cluster.
Article in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Pathway and Mechanism for the Biodegradation of Inosine and Guanosine byFoods (Basel, Switzerland) · 2026Article
Corrections and comments
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Authors and funding
13 authors.
Funding
Abstract
Endonuclease G (EndoG) is an evolutionarily conserved enzyme that cleaves the Mixed Lineage Leukemia breakpoint cluster region (MLLbcr) under sublethal chemotherapeutic treatment conditions, causing leukemogenic chromosomal rearrangements. While endogenous inhibitors (EndoGI) control EndoG in lower organisms, no such EndoGI has been identified in mammalian cells. Due to the structural similarity of EndoGI from Drosophila melanogaster to the C-terminus (Ct) of human Ku80, we perform immunoprecipitation, surface plasmon resonance analysis and 3D molecular modeling, revealing binding of human EndoG to Ku80-Ct putatively between amino acid 110-184. Docking modeling predicts EndoGI-like peptides clustering around residues 686-707 of Ku80. Our experimental studies provide evidence that Ku80-Ct and 28-mer peptide Ku3 reduce MLLbcr breakage after doxorubicin treatment independently of DNA-PK activity. Proximity ligation and single molecule tracking studies show that Ku3 antagonizes Ku80-EndoG association and modulates chromatin-binding of EndoG. Such MLLbcr protection blocks EndoG´s pro-tumorigenic functions without limiting cytotoxicity, pursued for co-treatments that reduce secondary leukemia, a severe side effect of chemotherapy.
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Registered trials
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