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- W2049574402 abstract "Cellular DNA undergoes constant assault from a wide range of genotoxic stress. In order to maintain genome integrity, cells develop a repertoire of sophisticated systems to detect DNA damage and mediate cellular responses to DNA damage. Defects in the DNA damage response have been implicated in a variety of disorders including aging and cancer. Tumor suppressor p53 is a key intermediate in DNA damage response by inducing cell-cycle arrest to allow repair or promoting apoptosis to eliminate irreparably damaged cells. A recent study described a novel layer of p53-mediated cellular response to DNA damage, i.e. modulation of cell adhesion and motility. JMY, a p53 co-factor, was demonstrated to be a multifunctional protein that coordinates cell adhesion and motility with nuclear p53 response. These results suggest that abnormal JMY activity and/or localization could contribute to tumor invasion and reveal JMY as a potential therapeutic target." @default.
- W2049574402 created "2016-06-24" @default.
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- W2049574402 date "2010-04-01" @default.
- W2049574402 modified "2023-09-27" @default.
- W2049574402 title "JimMY on the stage" @default.
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- W2049574402 doi "https://doi.org/10.4161/cam.4.2.11368" @default.
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