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As a vital anticancer gene, P53 controls the cell cycle arrest and cell apoptosis by regulating the downstream genes and the complicated signal pathways. To simulate the investigation of the cellular responding continuous Ion Radiation (IR), a model of the P53 gene regulatory networks is proposed. The model can be used to simulate the dynamic processes of the double-strand breaks (DSBs) generating and their repair, ataxia telangiectasia mutated (ATM) and ARF activation, as well as the oscillations in the P53-MDM2 feedback loop under continuous effect of acute IR. Especially, the model can present the plausible outcomes of cellular responding DNA damage induced by continuous IR.
Date of Conference: 6-8 July 2007