We have identified a molecular interaction between the reversibly oxidized form of PTP1B and 14-3-3ζ that regulates PTP1B activity. Destabilizing the transient interaction between 14-3-3ζ and PTP1B, prevented PTP1B inactivation by ROS and decreased EGFR phosphorylation. Our data suggest that destabilizing the interaction between 14-3-3ζ and the reversibly oxidized and inactive form of PTP1B may establish a path to PTP1B activation in cells.
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