Redox regulation by thioredoxin superfamily; protection against oxidative stress and aging

Free Radic Res. 2000 Dec;33(6):851-5. doi: 10.1080/10715760000301361.

Abstract

Thioredoxin (TRX) is a 12 kD protein with redox-active dithiol in the active site; -Cys-Gly-Pro-Cys-. We originally cloned human TRX as adult T cell leukemia derived factor (ADF) produced by HTLV-I transformed cells. TRX and related molecules maintain a cellular reducing enviroment, working in concert with the glutathione system. Physiologically, TRX has cytoprotective effects against oxidative stress. TRX promotes DNA binding of transcription factors such as NF-kB, AP-1, p53, and PEBP-2. The TRX superfamily, including thioredoxin-2 (mitochondrial thioredoxin) and glutaredoxin, are involved in biologically important phenomena via the redox-regulating system. Thioredoxin-binding protein-2, which we recently identified by a yeast two-hybrid system, is a type of endogenous modulator of TRX activity. TRX is secreted from the cells and exhibits cytokine-like and chemokine-like activities. Redox regulation by TRX plays a crucial role in biological responses against oxidative stress.

Publication types

  • Review

MeSH terms

  • Aging*
  • Animals
  • DNA / metabolism
  • Homeostasis*
  • Humans
  • Mice
  • Mice, Knockout
  • Mice, Transgenic
  • Oxidation-Reduction*
  • Oxidative Stress*
  • Thioredoxins / metabolism*
  • Thioredoxins / pharmacology
  • Transcription Factors / metabolism

Substances

  • Transcription Factors
  • Thioredoxins
  • DNA