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Showing 1–10 of 10 results
Advanced filters: Author: "Madalena Tarsounas" Clear advanced filters

  • Germline mutations in BRCA1 or BRCA2 tumour suppressor genes predispose to different cancers, as does oncogene activation. Here the authors reveal that aberrant transcription of specific genes triggered by activation of the oncogene β-catenin causes replication failure and cell death in the context of BRCA1/2 deficiency.

    • Rebecca A. Dagg
    • Gijs Zonderland
    • Madalena Tarsounas
    ResearchOpen Access
    Nature Communications
    Volume: 12, P: 1-17

  • Probing the synthetic lethal effect of FANCD2 deletion in BRCA2-deficient cells reveals independent roles of FANCD2 and BRCA2 in stabilizing stalled replication forks to maintain genome stability and promote cell survival.

    • Johanna Michl
    • Jutta Zimmer
    • Madalena Tarsounas
    Research
    Nature Structural & Molecular Biology
    Volume: 23, P: 755-757

  • BRCA2 plays important roles in cell physiology by promoting DNA replication and DNA double-strand breaks repair. Here the authors, reveal the impact of BRCA2 depletion on the cell transcriptional program with activation of the innate immune response that is potentiated by PARP inhibitor treatments.

    • Timo Reisländer
    • Emilia Puig Lombardi
    • Madalena Tarsounas
    ResearchOpen Access
    Nature Communications
    Volume: 10, P: 1-13

  • BRCA2-deficient cells fail to complete replication in S-phase, which results in DNA bridges and chromosome mis-segregation at mitosis. Here the authors show that MUS81 helps BRCA2-deficient cells survive replication stress by activating mitotic DNA synthesis and resolving mitotic DNA bridges.

    • Xianning Lai
    • Ronan Broderick
    • Madalena Tarsounas
    ResearchOpen Access
    Nature Communications
    Volume: 8, P: 1-13

  • The tumour suppressor ARF regulates p53 levels; however, in contrast to p53, ARF has not been implicated in the response to DNA damage. In this study, Carlos et al.show that single-stranded DNA formed in BRCA2-null cells triggers a DNA damage response leading to the activation of ARF and senescence.

    • Ana Rita Carlos
    • Jose Miguel Escandell
    • Madalena Tarsounas
    Research
    Nature Communications
    Volume: 4, P: 1-14

  • Crystallographic analysis depicting the interaction of the kinase inhibitor SCH772984 with ERK1/2 reveals a unique binding pocket distinct from off-targets such as haspin and is associated with slow binding kinetics and prolonged inhibitory activity.

    • Apirat Chaikuad
    • Eliana M C Tacconi
    • Stefan Knapp
    Research
    Nature Chemical Biology
    Volume: 10, P: 853-860

  • A transposon mutagenesis screen indicates that loss of 53BP1 expression rescues the clonal growth defect of BRCA1 null cells. 53BP1 deficiency is shown to abrogate the cell cycle arrest triggered in the absence of BRCA1 and to partially restore homologous recombination. The potential clinical implications of these findings are supported by the reduction of 53BP1 expression in sporadic triple-negative and BRCA-associated breast cancers.

    • Peter Bouwman
    • Amal Aly
    • Jos Jonkers
    Research
    Nature Structural & Molecular Biology
    Volume: 17, P: 688-695

  • Mutations in BRCA2 are associated with higher susceptibility to some forms of cancer. BRCA2 is known to play a central role in the repair of DNA breaks via homologous recombination. Now a role for BRCA2 in telomere integrity is revealed, indicating that BRCA2 can contribute to genome stability in multiple ways.

    • Sophie Badie
    • Jose M Escandell
    • Madalena Tarsounas
    Research
    Nature Structural & Molecular Biology
    Volume: 17, P: 1461-1469

  • Genes encoding DNA damage response factors are frequently mutated in cancer, causing genomic instability and presenting opportunities for therapeutic intervention. This Review discusses state-of-the-art strategies for DNA damage response inactivation using small-molecule inhibitors.

    • Florian J. Groelly
    • Matthew Fawkes
    • Madalena Tarsounas
    Reviews
    Nature Reviews Cancer
    Volume: 23, P: 78-94

  • BRCA1 and its partner BARD1 support repair of double-strand breaks by homologous recombination and protect replication forks from damage. Recent studies have improved our understanding of the molecular mechanisms of these tumour-suppressive functions of BRCA1–BARD1 and how they are subverted in therapy-resistant cancers.

    • Madalena Tarsounas
    • Patrick Sung
    Reviews
    Nature Reviews Molecular Cell Biology
    Volume: 21, P: 284-299