{
  "abstract": "DNA polymerase theta (Polθ) plays a pivotal role in the maintenance of stalled replication forks. However, little is known about how Polθ is recruited to the stalled forks. Here we show that PSF3, a member of GINS replicative complex, recruits Polθ to the stalled replication forks. Polθ, which is recruited by interacting with the C-terminal portion of PSF3, restarts the forks, exerts DNA double-strand break end-joining to repair the breaks resulting from collapsed forks in BRCA1/2-deficient and proficient tumor cells, and also fills single-stranded gaps on the replication fork lagging strand in BRCA1/2-deficient tumor cells. Thus, PSF3–Polθ interaction promotes the proliferation of homologous recombination-deficient and proficient tumor cells. Overall, this study highlights an important mechanism of Polθ recruitment to the stalled replication forks to maintain Polθ-dependent fork protection in tumor cells.",
  "abstract_shown": true,
  "affiliations": [
    "Fels Cancer Institute for Personalized Medicine, Lewis Katz School of Medicine, Temple University, Philadelphia, PA 19140",
    "Department of Chemistry, College of Science and Technology, Temple University, Philadelphia, PA 19122",
    "Cancer Signaling and Microenvironment Program, Fox Chase Cancer Center, Philadelphia, PA 19111",
    "Department of Cancer and Cellular Biology, Lewis Katz School of Medicine, Temple University, Philadelphia, PA 19140",
    "Nuclear Dynamics and Cancer Program, Fox Chase Cancer Center, Philadelphia, PA 19111"
  ],
  "article_type": "research article",
  "arxiv": null,
  "author_total": 5,
  "authors": [
    {
      "affs": [
        0
      ],
      "name": "Umeshkumar Vekariya",
      "orcid": "0000-0002-6662-9122"
    },
    {
      "affs": [
        1
      ],
      "name": "Benjamin Lee Prather"
    },
    {
      "affs": [
        2
      ],
      "name": "Roland L. Dunbrack"
    },
    {
      "affs": [
        1
      ],
      "name": "Rongsheng E. Wang",
      "orcid": "0000-0002-5749-7447"
    },
    {
      "affs": [
        0,
        3,
        4
      ],
      "name": "Tomasz Skorski",
      "orcid": "0000-0002-3809-4538"
    }
  ],
  "bibtex": "https://research.draconitic.com/paper/4vzv5n2hjjmnp.bib",
  "cited_by": 0,
  "doi": "10.1073/pnas.2613699123",
  "fulltext_url": "https://pmc.ncbi.nlm.nih.gov/articles/PMC13715820/",
  "id": "4vzv5n2hjjmnp",
  "issns": [
    "0027-8424",
    "1091-6490"
  ],
  "landing_url": "https://doi.org/10.1073/pnas.2613699123",
  "language": "en",
  "licence": "CC-BY-NC-ND-4.0",
  "licence_label": "CC BY-NC-ND 4.0",
  "licence_source": "article",
  "licence_url": "https://creativecommons.org/licenses/by-nc-nd/4.0/",
  "metadata_licence": null,
  "native_subjects": [
    [
      "heading",
      "409"
    ],
    [
      "heading",
      "Biological Sciences"
    ],
    [
      "heading",
      "Cell Biology"
    ],
    [
      "openalex",
      "1312|DNA Repair Mechanisms"
    ]
  ],
  "openalex": "W7222999271",
  "pdf_url": null,
  "pmcid": "PMC13715820",
  "pmid": "42900728",
  "published": "2026-10-20",
  "publisher": "National Academy of Sciences",
  "ris": "https://research.draconitic.com/paper/4vzv5n2hjjmnp.ris",
  "sources": [
    {
      "first_seen": "2026-11-01T12:23:01Z",
      "native_id": "PMC13715820",
      "source": "pmc",
      "url": "https://doi.org/10.1073/pnas.2613699123"
    }
  ],
  "subjects": [
    {
      "field": "biology",
      "origin": "heading:Cell Biology",
      "subfield": "cell-biology"
    }
  ],
  "title": "PSF3 recruits Polθ to stalled replication forks to promote DNA repair",
  "title_text": "PSF3 recruits Polθ to stalled replication forks to promote DNA repair",
  "type": "peer-reviewed",
  "updated_at": "2026-11-01T12:23:01Z",
  "url": "https://research.draconitic.com/paper/4vzv5n2hjjmnp",
  "venue": "Proceedings of the National Academy of Sciences of the United States of America",
  "versions": []
}