FIGURE 7.

Proposed model for ROS homeostatic control by Prx1, Prx5, and c-Myc. Prx1 interacts with the MBII domain of c-Myc (28). The subsequent binding of the complex to prx5 promoter E-box sites results in an overall down-regulation of the prx5 promoter. In the absence of Prx1, however, c-Myc positively regulates the prx5 promoter. Prx1 and Prx5 scavenge ROS primarily in nuclear and cytoplasmic/mitochondrial compartments, respectively. In the absence of Prx1, compensatory increases in Prx5 limit the overall increase in genotoxic ROS. The model accounts for the high levels of nuclear ROS and virtual absence of cytosolic ROS in prx1^-/- MEFs (Fig. 1C).