Understanding of processes in which calcium signaling is involved is of fundamental importance in systems biology and has many applications in medicine. In this paper we have studied the particular case of the complex calcium-calcineurin-MCIP-NFAT signaling network in cardiac myocytes, the understanding of which is critical for treatment of pathologic hypertrophy and heart failure. By including some most recent experimental findings, we constructed a computational model totally based on biochemical principles. The model can correctly predict the mutant (MCIP1{sup}(-/-)) behavior under different stress such as PO (pressure overload) and CaN{sup}* (activated calcineurin) overexpression.
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