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Interestingly, a recent study demonstrated that human glutathione S-transferase P1-1 interacts with the TRAF domain of TRAF2 and specifically down-regulates signaling to MAPKs [32], which together with our present findings suggests that S-glutathionylation of TRAFs or associated protein represents a mechanism by which ROS re-direct and amplify signaling in the innate immune system

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TRF2 was not released, nor was TIN2 (Fig

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