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However, oxidation of TXN1 results in an intramolecular disulfide bridge being formed between Cys-32 and Cys-35 and a conformational change in the dithiol oxidoreductase that results in its dissociation from ASK1 and allows the kinase to recruit tumor necrosis factor receptor-associated factor 2 (TRAF2) and TRAF6 to regions adjacent to those to which TXN1 binds (i.e., residues 384β655 of mouse ASK1), thereby forming a high-molecular-mass complex [211]
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J Neuroimmunol (2014) 273(1-2):1β7
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