A predictive modeling for cellular responding DNA damage under continuous ion radiation (IR)

P53, a vital anticancer gene, controls the cell cycle arrest and cell apoptosis by regulating downstream genes and their complicated signal pathways. To illustrate the cellular self-defense mechanisms in response to acute perturbations at single cell level, a model of P53 stress response networks is proposed under continuous IR. By using combined approaches of systematic analysis, computer sicence and control theory, the model can be used to simulate a series of cellular responding kinetics in fighting against acute IR. Especially, the outcomes of cellular responding DNA damage can be predicted by comparing different simulating results under different IR dose domains.