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Nilsen, H. L.

Publications and source records attributed to Nilsen, H. L..

2 recordsLinked to original sources

A high-throughput screening dataset of small-molecule inhibitors across human DNA glycosylases

The base excision repair pathway removes small base lesions from DNA and is initiated in humans by one of eleven DNA glycosylases with overlapping substrate specificities. Despite their central role in genome maintenance and transcription, systematic datasets describing small-molecule binders or inhibitors of DNA glycosylases are lacking. Here, through a collaborative effort across Scandinavia, we establish a high-throughput biochemical assay platform for human DNA glycosylases and use it to generate a systematic small-molecule screening dataset. A chemogenomic library was screened against nine glycosylases with assays of sufficient quality for hit identification, yielding primary screening and concentration-response data and identifying multiple previously unreported inhibitors. All primary and processed data, along with detailed assay protocols and metadata, are publicly available to support reuse in chemical biology, further compound optimization, assay development and comparative studies of DNA repair enzymes.

biochemistry↗

Recognizing dUTPase as a mitotic factor essential for early embryonic development

dUTPase is universally regarded as a metabolic sanitizing enzyme that protects genomes by preventing the incorporation of uracil into DNA. Despite its essentiality across eukaryotes, no function beyond nucleotide sanitization has been demonstrated. Here, we uncover a conserved, non-canonical role for dUTPase as a regulator of mitosis. Using Drosophila and mouse models, we demonstrate that dUTPase loss causes early embryonic lethality characterized by severe mitotic failure that, cannot be rescued by disabling uracil-DNA repair, uncoupling dUTPase essentiality from DNA repair pathways. Mechanistically, dUTPase dynamically associates with the mitotic spindle and centrosomes, and its depletion induces centrosome amplification and chromosome segregation defects. Beyond cell division, dUTPase dosage bidirectionally controls cell migration, linking its mitotic function to cellular behaviors relevant for metastasis. Together, our findings redefine dUTPase as a moonlighting mitotic factor that coordinates centrosome integrity and spindle dynamics, expanding its known repertoire beyond nucleotide metabolism. HighlightsdUTPase deficiency leads to mitotic defects during early embryonic development in both Drosophila and mouse models dUTPase shows dynamic spatiotemporal localization associated with microtubules through mitosis dUTPase is essential for the normal number and intracellular localization of centrosomes dUTPase deficiency counteracts while its overexpression enhances cell migration

molecular biology↗