Fig. 6

PRDX1 acts as a gatekeeper of JNK activity in the transition of benign fibroblasts into CAFs under rising levels of H₂O₂. PRDX1 controls JNK activation under low H₂O₂ levels through protecting PTEN from inactivation by H₂O₂. As H₂O₂ levels rise, PRDX1 dissociates from PTEN resulting in reversible PTEN inactivation [29, 30] and JNK phosphorylation and activation [31]. Under these circumstances, PRDX1 binds associates with JNK and inhibits JNK activation. Therefore, it is proposed that PRDX1 controls JNK activity on two levels: first, by promoting PTEN activity and secondly, by binding directly to JNK