ArticleProceedings of the National Academy of Sciences of the United States of America1997
AP-1 transcriptional activity is regulated by a direct association between thioredoxin and Ref-1.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 216 papers.
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Who cites it
216 citing papers in PubMed.
- Crosstalk of thioredoxin system and programmed cell death: from pathophysiology to novel therapy.Redox biology · 2026Review
- Muscleblind-like proteins dimerize by forming disulfide bonds to regulate alternative splicing and pathogenic RNA foci formation.Nucleic acids research · 2026Article
- APE1 coordinates its disordered region and metal cofactors to drive genome surveillance.Nucleic acids research · 2026Article
- Thioredoxin protects against diabetic hearing loss by regulating TOMM22 mediated mitochondrial autophagy in hair cells and inhibiting microglial M1 polarization.Scientific reports · 2026Article
- APEX1, a transcriptional hub for endochondral ossification and fracture repair.Bone research · 2026Article
- Amniotic extracellular vesicles' effect on equine endometrial cells challenged with LPS: a proteomic analysis.Extracellular vesicles and circulating nucleic acids · 2026Article
- Human P53 Expression in Yeast: Investigating Its Apoptotic Effects.Mini reviews in medicinal chemistry · 2026Review
- APE1/Ref-1 inhibition via APX3330 lowers monocyte/macrophage infiltration without ameliorating the structure and function of dystrophic mdx hindlimb muscles.Physiological reports · 2025Article
- Nanomedicine-Driven Modulation of Reductive Stress for Cancer Therapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- Oxidation-Induced Mixed Disulfide and Cataract Formation: A Review.Antioxidants (Basel, Switzerland) · 2025Review
- Extracellular vesicles deliver thioredoxin to rescue stem cells from senescence and intervertebral disc degenerationActa pharmaceutica Sinica. B · 2025Article
- The Role of Thioredoxin System in Shank3 Mouse Model of Autism.Journal of molecular neuroscience : MN · 2024Article
- Exploring the Thioredoxin System as a Therapeutic Target in Cancer: Mechanisms and Implications.Antioxidants (Basel, Switzerland) · 2024Review
- Thioredoxin (Trx): A redox target and modulator of cellular senescence and aging-related diseases.Redox biology · 2024Review
- Biological and Catalytic Properties of Selenoproteins.International journal of molecular sciences · 2023Review
- The Importance of Thioredoxin-1 in Health and Disease.Antioxidants (Basel, Switzerland) · 2023Review
- Evolutionarily Conserved Role of Thioredoxin Systems in Determining Longevity.Antioxidants (Basel, Switzerland) · 2023Review
- Redox dysregulation as a driver for DNA damage and its relationship to neurodegenerative diseases.Translational neurodegeneration · 2023Review
- Glutathione and Glutaredoxin in Redox Regulation and Cell Signaling of the Lens.Antioxidants (Basel, Switzerland) · 2022Review
- Role of thioredoxin-interacting protein in mediating endothelial dysfunction in hypertension.Genes & diseases · 2022Article
156 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Thioredoxin (TRX) is a pleiotropic cellular factor that has thiol-mediated redox activity and is important in regulation of cellular processes, including proliferation, apoptosis, and gene expression. The activity of several transcription factors is posttranslationally altered by redox modification(s) of specific cysteine residue(s). One such factor is nuclear factor (NF)-kappa B, whose DNA-binding activity is markedly augmented by TRX treatment in vitro. Similarly, the DNA-binding activity of activator protein 1 (AP-1) is modified by a DNA repair enzyme, redox factor 1 (Ref-1), which is identical to a DNA repair enzyme, AP endonuclease. Ref-1 activity is in turn modulated by various redox-active compounds, including TRX. We here report the molecular cascade of redox regulation of AP-1 mediated by TRX and Ref-1. Phorbol 12-myristate 13 acetate efficiently translocated TRX into the HeLa cell nucleus where Ref-1 preexists. This process seems to be essential for AP-1 activation by redox modification because co-overexpression of TRX and Ref-1 in COS-7 cells potentiated AP-1 activity only after TRX was transported into the nucleus by phorbol 12-myristate 13 acetate treatment. To prove the direct active site-mediated association between TRX and Ref-1, we generated a series of substitution-mutant cysteine residues of TRX. In both an in vitro diamide-induced cross-linking study and an in vivo mammalian two-hybrid assay we proved that TRX can associate directly with Ref-1 in the nucleus; also, we demonstrated the requirement of cysteine residues in the TRX catalytic center for the potentiation of AP-1 activity. This report presents an example of a cascade in cellular redox regulation.
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