ArticleiScience2026
Genome instability is increased during DNA replication in the presence of the CPD UV photoproduct in transcriptionally active genes.
Article in iScience, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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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1 citing paper in PubMed.
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7 authors.
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No grant is acknowledged in the PubMed record.
Abstract
Ultraviolet (UV) light primarily induces cyclobutane pyrimidine dimers (CPDs) and pyrimidine-pyrimidone (6-4) photoproducts (6-4 PPs) and increases the risk of melanoma developing with genome instability. Here, we show that DNA double-strand breaks (DSBs) associated with genome instability arise during DNA replication in the presence of CPDs. Whereas 6-4PPs, which induce γH2AX expression and cell-cycle arrest, are repaired before the onset of DNA replication, CPDs persist into S phase. We also show that these DSBs are induced in association with transcription-coupled nucleotide excision repair (TC-NER). These DSBs decrease after CPDs were partially repaired in active chromatin regions, but persist in inactive chromatin regions. Structure variants (SVs) and single nucleotide variants (SNVs) associated with the UV-related single-base substitution 7 (SBS7) signature are induced in UV-irradiated cells. Our results point to a pathway that may underlie the genomic alterations observed in human melanoma.
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