Cellular responding DNA damage: An improved modeling of P53 gene regulatory networks under ion radiation (IR)

As a vital anticancer gene, P53 controls the cell cycle arrest and cell apoptosis by regulating a series of genes and their complicated signal pathways. To simulate the self-defensive mechanisms of the cellular responding DNA damage under continuous ion radiation (IR), an improved model of the P53 gene regulatory networks is proposed at single cell level. The model can be used to simulate the kinetics of the double-strand breaks (DSBs) generating and their repair, ataxia telangiectasia mutated (ATM) and ARF activation, as well as the regulations of the P53–MDM2 feedback loop. Also, the model can predict the plausible outcomes of cellular responding DNA damage under different IR dose domains.