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Oxidative stress evokes various cellular responses including alteration of gene expression to preserve cellular homeostasis (
1
,
2
). Thioredoxin (TRX) is a small ubiquitous protein with protein thiol-reducing activity and has been shown to function as a cellular antioxidant buffering system in response to oxidative stress and play essential roles in maintenance of cellular function (
3
,
4
). Recently, a growing number of evidence has shown that TRX plays crucial roles in redox regulation of gene expression via either direct or indirect interaction with various transcription factors including NF-κB (
5
), AP-1 (
6
), and PEBP2 (
7
). Alteration in expression and/or subcellular localization of TRX has been indicated to be involved in such redox-dependent control of the transcription factors (
8
,
9
), however, precise mechanisms remain unknown.