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doi:10.1186/s12931-016-0447-z
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The possible mechanistic model anticipates that, in the absence of a stimulus, GSTP1-1 averts IΞΊBΞ± degradation and GSTP1-1-mediated S-glutathionylation shuts down IKK activity, providing a versatile mechanism by which GSTP1-1 represses NF-ΞΊB activation
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