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Showing 1–8 of 8 results
Advanced filters: Author: Matilde Murga Clear advanced filters

  • Oncogenic activation can generate replicative stress, leading to activation of ATR and Chk1. The hypothesis that these events could be exploited to selectively kill cancer cells is now demonstrated in vivo, using mouse models for cancer development. Myc-driven tumors are shown to be sensitive to ATR deficiency or inhibition of Chk1.

    • Matilde Murga
    • Stefano Campaner
    • Oscar Fernandez-Capetillo
    Research
    Nature Structural & Molecular Biology
    Volume: 18, P: 1331-1335

  • Available ATR inhibitors also show activity against related DNA-damage response kinases such as ATM and DNA-PKcs. Now a cell-based screen leads to the identification of two compounds with potent activity against ATR in tissue culture, including one that is specific for ATR. These compounds are particularly toxic for cells showing oncogene-induced replicative stress, even more so in the absence of p53.

    • Luis I Toledo
    • Matilde Murga
    • Oscar Fernandez-Capetillo
    Research
    Nature Structural & Molecular Biology
    Volume: 18, P: 721-727

  • Oscar Fernandez-Capetillo and colleagues report a mouse model of the human Seckel syndrome characterized by a deficiency in ATR. The Seckel mice show high levels of replicative stress during embryogenesis, and the adults show premature aging.

    • Matilde Murga
    • Samuel Bunting
    • Oscar Fernandez-Capetillo
    Research
    Nature Genetics
    Volume: 41, P: 891-898

  • USP7 deubiquitinase is now shown to prevent ubiquitination of SUMO chains of replisome proteins, thereby regulating DNA replication-fork progression and origin firing.

    • Emilio Lecona
    • Sara Rodriguez-Acebes
    • Oscar Fernandez-Capetillo
    Research
    Nature Structural & Molecular Biology
    Volume: 23, P: 270-277

  • It is shown that p53 is critically involved in preventing the reprogramming of cells carrying various types of DNA damage, including short telomeres, DNA repair deficiencies, or exogenously inflicted DNA damage. Eliminating p53 expression allows efficient reprogramming in the face of DNA damage and the generation of induced pluripotent stem cells carrying persistent DNA damage and chromosomal aberrations.

    • Rosa M. Marión
    • Katerina Strati
    • Maria A. Blasco
    Research
    Nature
    Volume: 460, P: 1149-1153

  • Cyclin-dependent kinase 2 (cdk2) is surprisingly found to suppress senescence induced by the Myc oncogene in various cell types. Inactivation or deletion of cdk2 sensitizes mouse embryonic fibroblasts to Myc-induced senescence via a mechanism requiring pRb and p53.

    • Stefano Campaner
    • Mirko Doni
    • Bruno Amati
    Research
    Nature Cell Biology
    Volume: 12, P: 54-59