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Modeling of ATM Accumulation and ATM-Mediated Oscillation of p53

A dynamical model to study the accumulation of ATM is proposed in this work. The ATM can accumulate either with low level of DSBs and presence of NBS1 proteins in cells, or with high level of DSBs and absence of NBS1. Both the two ways trigger the cell damage repair system. The interaction in p53 networks responding to DNA damage is discovered in many researches, but the mechanism of initiating oscillation remains unclear. We examine a model shows that the ATM-NBS1 feedback loop exhibits bistability. The bistability has essential roles in the mechanism of initiate oscillation.