ArticleCell reports2026
Bypass of LANA-DNA crosslinks by Polη ensures KSHV genome maintenance and tumor growth.
Article in Cell reports, 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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6 authors.
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Abstract
Episome maintenance of Kaposi's sarcoma-associated herpesvirus (KSHV) requires LANA protein binding to the viral terminal repeat (TR) DNA. Here, we show that LANA forms cell cycle-dependent DNA-protein crosslinks (DPCs) within the TR. Targeted shRNA screening identified translesional repair DNA polymerase Polη as necessary for the stability of KSHV TR DNA and viral episome maintenance. We found that Polη binds LANA and colocalizes with LANA nuclear bodies. Inhibiting the enzymatic activity of Polη by small molecule PNR-07-02 provided selective cell killing of KSHV
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