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Showing 1–4 of 4 results
Advanced filters: Author: Stephanie Panier Clear advanced filters

  • Cancers that arise from epithelial cells often contain tumour cells that have acquired the characteristics of another cell type — a mesenchymal cell. A mouse model of skin cancer offers insights into why such cells resist treatment.

    • Stephanie Panier
    News & Views
    Nature
    Volume: 616, P: 40-42

  • Damage signalling in response to DNA double-strand breaks is under tight negative regulation. These control mechanisms, which include post-translational modifications and changes in chromatin structure, ensure that pathways are spatially and temporally regulated and that they become inactivated when repair is complete.

    • Stephanie Panier
    • Daniel Durocher
    Reviews
    Nature Reviews Molecular Cell Biology
    Volume: 14, P: 661-672

  • When double-strand breaks occur in eukaryotic DNA, the chromatin that protects and organizes the genome must be removed from the vicinity of the break to allow repair factors to bind. Such chromatin displacement involves the addition of ubiquitin groups to histone proteins near the break by the ubiquitin ligases RNF8 and RNF168. Here it is shown that the enzyme OTUB1 prevents RNF168-dependent poly-ubiquitination. Pharmacological targeting of this process might enhance the DNA damage response.

    • Shinichiro Nakada
    • Ikue Tai
    • Daniel Durocher
    Research
    Nature
    Volume: 466, P: 941-946

  • The function of 53BP1 in DNA double-strand break repair is multifaceted, and includes mediator and effector roles. New appreciation of how it is recruited to damaged chromatin, and how it exerts control on pathway choice, has cemented the central role of 53BP1 in genome stability maintenance.

    • Stephanie Panier
    • Simon J. Boulton
    Reviews
    Nature Reviews Molecular Cell Biology
    Volume: 15, P: 7-18