摘要
Radiotherapy can cause DNA damage into cells, triggering the cell cycle arrest and cell apop-tosis through complicated interactions among vital genes and their signal pathways. In order to in-depth study the complicated cellular res- ponses under such a circumstance, a novel mo- del for P53 stress response networks is pro- posed. It can be successfully used to simulate the dynamic processes of DNA damage trans-ferring, ATM and ARF activation, regulations of P53-MDM2 feedback loop, as well as the toxins degradation. Particularly, it has become feasible to predict the outcomes of cellular response in fighting against genome stresses. Consequently, the new model has provided a reasonable framework for analyzing the complicated regu-lations of P53 stress response networks, as well as investigating the mechanisms of the cellular self-defense under radiotherapy.
Radiotherapy can cause DNA damage into cells, triggering the cell cycle arrest and cell apop-tosis through complicated interactions among vital genes and their signal pathways. In order to in-depth study the complicated cellular res- ponses under such a circumstance, a novel mo- del for P53 stress response networks is pro- posed. It can be successfully used to simulate the dynamic processes of DNA damage trans-ferring, ATM and ARF activation, regulations of P53-MDM2 feedback loop, as well as the toxins degradation. Particularly, it has become feasible to predict the outcomes of cellular response in fighting against genome stresses. Consequently, the new model has provided a reasonable framework for analyzing the complicated regu-lations of P53 stress response networks, as well as investigating the mechanisms of the cellular self-defense under radiotherapy.
