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Redox control of cellular function by thioredoxin; a new therapeutic direction in host defence

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Nishinaka Y., Nakamura H., Masutani H., Yodoi J.
Archivum Immunologiae et Therapiae Experimentalis
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2001
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vol. 49
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issue 4
285-292
EN
Compelling evidence has suggested that oxidative stress mediates various cellular reponses, and control of reduction/oxidation (redox) is importan in maintaining the homeostatsis of an organism. The thioredoxin (TRX) system, along with as well as the glutathione system, is one of the key system in controling cellular redox statuts. TRX is a small ubiquitous protein with the redox-active site sequence -Cys-Gly-Pro-Cys-. It has been demonstrated to be a multifunctional protein, which has regulatory roles in cellular signaling and gene transcription in addition to cytoprotective activities through the quenching of reactive oxygen species. Various oxidative stimuli, such as as UV irradiation, cytokines and some chemicals, promptly induce the xpression of TRX. Overexpression of TRX correlates with a wide variety of oxidative stress conditions and, in some cases, TRX has shown promising effects for clinical use, for instance in the attenuation of tissue injury in ischemia reperfusion models. The modulation of TRX functions in association with other redox-regulatory should give us a new therapeutic strategy in the treatment of oxidative stress-mediated disorders and diseases.
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