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Evaluation of Coupled Nuclear and Cytoplasmic p53 Dynamics
Abstract
The tumor suppressor protein p53 predominantly serves as a sequence specific transcription factor that may be activated upon exposure to diverse stimuli. One potent death inducer, p53-upregulated mediator of apoptosis (PUMA), is transcriptionally induced by p53. Once released into the cytoplasm, PUMA can lead to the activation of Bcl-2 apoptotic network. The cytoplasmic proapoptotic roles of p53 have recently been discovered, and these findings have placed p53 into the chemical interaction network with Bcl-2 family members. PUMA can also relieve p53 from the sequestration of antiapoptotic members. Released p53 further enters the nucleus and induces PUMA expression. We proposed that this positive feedback loop could lead to bistability. Further sensitivity analysis suggested that the system which covers the interactions between p53 and BCL-2 family members is considerably sensitive to p53 production rate. Meanwhile, downstream network components are much more affected by certain parameters than upstream effectors. Therefore, this newly discovered positive feedback loop might play critical roles in apoptotic network.
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