ArticleNature communications2026
DNA-PK driven nucleosome unwrapping enables NHEJ in chromatin.
Article in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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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.
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Abstract
DNA double-strand breaks, one of the most cytotoxic forms of DNA damage, are primarily repaired by non-homologous end joining (NHEJ) in human cells. NHEJ is initiated by the Ku70/80 heterodimer (Ku) and DNA-dependent protein kinase catalytic subunit (DNA-PKcs), followed by factors that bridge and ligate DNA ends. Ku and DNA-PKcs require ~28 base pairs of free duplex DNA, which is often unavailable in chromatin with nucleosomes acting as barriers. The role of DNA-PKcs remains unclear, as previous in vitro studies mainly used naked DNA. Here, in vitro ligation assays show that DNA-PKcs promotes NHEJ on nucleosomes with limited DNA accessibility. Cryo-EM structures of nucleosome-bound Ku and DNA-PKcs reveal that Ku encounters nucleosomal barriers and overcomes them with DNA-PKcs. Distinct structural states support a stepwise model of DNA-PK progressive translocating along nucleosomal DNA, highlighting DNA-PKcs function in chromatin-associated NHEJ in vivo.
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