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• W2130698963 abstract "The tumor suppressor protein p53 plays a central role in the multiple response pathways activated by DNA damage. In particular, p53 is involved in both the pro-survival response of cell cycle arrest and DNA repair, and the pro-death response of apoptosis. How does the p53 network coordinate the different pathways that lead to the opposite cell fates and what is its strategy in making the life-death decisions? To address these questions, we develop an integrated mathematical model that embraces three key modules of the p53 network: p53 core regulation, p53-induced cell cycle arrest and p53-dependent apoptosis initiation. Our analyses reveal that different aspects of the nuclear p53 dynamic profile are being used to differentially regulate the pro-survival and the pro-death modules. While the activation of the pro-survival module is dependent on the current or recent status of the DNA damage, the activation of the pro-death module relies on the accumulation or integration of the damage level over time. Thus, the cell will take the death fate if it cannot recover from the damage within a time period that is inversely proportional to the damage level. This adaptive timer strategy is likely to be adopted in other stress response systems." @default.
• W2130698963 created "2016-06-24" @default.
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• W2130698963 date "2011-02-01" @default.
• W2130698963 modified "2023-09-26" @default.
• W2130698963 title "Decision making of the p53 network: Death by integration" @default.
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• W2130698963 doi "https://doi.org/10.1016/j.jtbi.2010.11.041" @default.
• W2130698963 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4121385" @default.
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• W2130698963 hasPublicationYear "2011" @default.
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