作者: Eléonore Toufektchan , Franck Toledo
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摘要: The p53 protein has been extensively studied for its capacity to prevent proliferation of cells with a damaged genome. Surprisingly, however, our recent analysis mice expressing hyperactive mutant that lacks the C-terminal domain revealed increased activity may alter genome maintenance. We showed downregulates genes essential telomere metabolism, DNA repair, and centromere structure sustained leads phenotypic traits associated dyskeratosis congenita Fanconi anemia. This downregulation is largely conserved in human cells, which suggests findings could be relevant better understand processes involved bone marrow failure as well aging tumor suppression.