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. Author manuscript; available in PMC: 2013 Dec 18.
Published in final edited form as: Biochemistry. 2012 Dec 5;51(50):9954–9965. doi: 10.1021/bi301441e

Figure 4.

Figure 4

Redox regulation of peroxiredoxins (Prxs) during EGFR signaling. Receptor activation results in localized phosphorylation and inactivation of peroxiredoxin I (PrxI) by PTKs, such as the redox-regulated cytoplasmic Src (c-Src). Deactivation of PrxI diminishes the redox-buffering capacity adjacent to the cell membrane, allowing for a transient and localized increase in H2O2 levels for signal transduction. Additionally, elevated H2O2 concentrations can inactivate Prx2 by oxidation of its catalytic cysteine to sulfinic acid.