ArticleNature communications2025
SART3 promotes homologous recombination repair by stimulating DNA-RNA hybrids removal and DNA end resection.
Article in Nature communications, 2025. 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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Who cites it
1 citing paper in PubMed.
- DDX21 Enhances Radiosensitivity in Head and Neck Squamous Cell Carcinoma by Suppressing MK2-Mediated DNA Damage Response.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
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Authors and funding
13 authors.
Funding
Abstract
DNA-RNA hybrids triggered by double-strand breaks (DSBs) are crucial intermediates during DSB repair, and their timely resolution requires numbers of RNA helicases, including DEAD box 1 (DDX1). However, how these helicases are recruited to DSB-induced hybrids in time remains largely unclear. Here, we revealed that squamous cell carcinoma antigen recognized by T cells 3 (SART3) promotes DDX1 binding to DNA-RNA hybrids at DSBs for optimal homologous recombination (HR) repair. SART3 itself associates with DNA-RNA hybrids and PAR chains and accumulates at DSBs in both PARylation- and DNA-RNA hybrids-dependent fashion. SART3 also associates with DDX1 and is necessary for DDX1 enrichment at DSBs. The defective SART3-DDX1 association observed in cells expressing the cancer-associated variant SART3-R836W impairs not only the accumulation of DDX1, but also hybrid removal and HR efficiency. Moreover, SART3 promotes DNA end resection through enhancing USP15-BARD1 association and BRCA1-BARD1 retention. Together, our study reveals an role of SART3 in DSB repair, rendering SART3 a promising target for cancer therapy.
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