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Showing 1–7 of 7 results
Advanced filters: Author: Rimma Belotserkovskaya Clear advanced filters

  • Although loss of BRCA1 leads to defects in DNA double-strand break repair by homologous recombination (HR) and renders cells hypersensitive to PARP inhibitors, resistance to the drugs can arise. Here the authors reveal that PALB2 chromatin recruitment restores HR in BRCA1-deficient cells depleted of 53BP1.

    • Rimma Belotserkovskaya
    • Elisenda Raga Gil
    • Stephen P. Jackson
    ResearchOpen Access
    Nature Communications
    Volume: 11, P: 1-11

  • MDC1 and H2AX interact and accumulate at sites of DNA damage, functioning to recruit additional factors involved in the repair process. Here the authors uncover a function for MDC1 that is independent of the presence of H2AX and is mediated through its PST-repeat region.

    • Israel Salguero
    • Rimma Belotserkovskaya
    • Stephen P. Jackson
    ResearchOpen Access
    Nature Communications
    Volume: 10, P: 1-11

  • ATR inhibitors are being developed for treating cancers, but mechanisms that determine their efficacy are unclear. Here, the authors show that transcription factor KLF5 loss sensitizes cells to ATR inhibition through regulating BRD4 chromatin recruitment. This work also identifies KLF5 as a potential target for treating ARID1A-deficient cancers.

    • Samah W. Awwad
    • Colm Doyle
    • Stephen P. Jackson
    ResearchOpen Access
    Nature Communications
    Volume: 16, P: 1-16

  • CtIP helps maintain genomic stability by promoting DNA double-strand-break repair. Structural and biophysical analyses now show that the N terminus of human CtIP forms a tetrameric structure that is required for resection of broken DNA ends to permit their repair by homologous recombination.

    • Owen R Davies
    • Josep V Forment
    • Luca Pellegrini
    Research
    Nature Structural & Molecular Biology
    Volume: 22, P: 150-157

  • Following the formation of a DNA double-strand break (DSB), cells activate the DNA-damage response and recruit a number of proteins to the lesion. Some of these proteins are modified by the attachment of small ubiquitin-related modifier (SUMO). Here, SUMO1, SUMO2 and SUMO3 are shown to accumulate at DSB sites in mammalian cells. SUMO1 and SUMO2/3 accrual requires the E3 ligase enzymes PIAS4 and PIAS1, which promote DSB repair.

    • Yaron Galanty
    • Rimma Belotserkovskaya
    • Stephen P. Jackson
    Research
    Nature
    Volume: 462, P: 935-939

  • A recent study published in Science reveals the mechanism and biological importance of DNA damage response abrogation in mitotic cells.

    • Rimma Belotserkovskaya
    • Stephen P Jackson
    Research Highlights
    Cell Research
    Volume: 24, P: 781-782