ReviewThe Biochemical journal2000
Thioredoxin reductase.
Review in The Biochemical journal, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 297 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
297 citing papers in PubMed, 290 citations in OpenAlex.
- Thioredoxin reductase-1 facilitates cellular plasticity and stemness mediated by TGF-β1 in non-small cell lung cancer.Cancer biology & therapy · 2026Article
- Glutathione Relevance in the Response of CiliateBiology · 2026Article
- Disulfidptosis: molecular mechanisms and therapeutic targets.Signal transduction and targeted therapy · 2026Review
- Article
- A Crystalline and Thermally Stable Selenocysteine Selenenic Acid.Angewandte Chemie (International ed. in English) · 2026Article
- Crosstalk of thioredoxin system and programmed cell death: from pathophysiology to novel therapy.Redox biology · 2026Review
- Redox regulation of EGFR activation by thioredoxin reductase 3 drives resistance to EGFR inhibitors in triple-negative breast cancer.Cell death discovery · 2026Article
- A next-generation multimetal complex induces immunogenic cell death with distinct transcriptomic signatures.Chemical communications (Cambridge, England) · 2026Article
- Targeting glioblastoma multiforme with Demethoxycurcumin and its analogues: current evidence and future directions.Molecular biology reports · 2026Review
- Familial glucocorticoid deficiency due to a novelFrontiers in endocrinology · 2026Article
- Unlocking Protein Evolution Insights: Efficient and Interpretable Mutational Effect Predictions with GEMME.Methods in molecular biology (Clifton, N.J.) · 2026Article
- Arsenome, Arsenobolome, and Arsenobiolome.International journal of molecular sciences · 2025Review
- Ambroxol mitigates cyclophosphamide-induced liver injury by suppressing TLR-4/NF-κB signaling and oxidative stress and upregulating cytoglobin, TXNRD1 and HMGB1.World journal of gastroenterology · 2025Article
- Optimizing Selenium Polysaccharide Supplementation: Impacts on Growth, Oxidative Stress, and Tissue Selenium in Juvenile Large Yellow Croaker (Animals : an open access journal from MDPI · 2025Article
- Loss of STARD7 Triggers Metabolic Reprogramming and Cell Cycle Arrest in Breast Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Phylotaxonomic analysis uncovers underestimated species diversity within the genus Rossellomorea with description of selenium-resistant Rossellomorea yichunensis sp. nov.BMC microbiology · 2025Article
- Article
- Alzheimer's Disease Pathogenic Mechanisms: Linking Redox Homeostasis and Mitochondria-Associated Metabolic Pathways Through Nuclear Factor Erythroid 2-Related Factor 2 (Nrf2).Antioxidants (Basel, Switzerland) · 2025Review
- Oxidant-Based Cytotoxic Agents During Aging: From Disturbed Energy Metabolism to Chronic Inflammation and Disease Progression.Biomolecules · 2025Review
- Selenium nutritional status and thyroid dysfunction.Archives of endocrinology and metabolism · 2025Review
237 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The mammalian thioredoxin reductases (TrxRs) are a family of selenium-containing pyridine nucleotide-disulphide oxidoreductases with mechanistic and sequence identity, including a conserved -Cys-Val-Asn-Val-Gly-Cys- redox catalytic site, to glutathione reductases. TrxRs catalyse the NADPH-dependent reduction of the redox protein thioredoxin (Trx), as well as of other endogenous and exogenous compounds. The broad substrate specificity of mammalian TrxRs is due to a second redox-active site, a C-terminal -Cys-SeCys- (where SeCys is selenocysteine), that is not found in glutathione reductase or Escherichia coli TrxR. There are currently two confirmed forms of mammalian TrxRs, TrxR1 and TrxR2, and it is possible that other forms will be identified. The availability of Se is a key factor determining TrxR activity both in cell culture and in vivo, and the mechanism(s) for the incorporation of Se into TrxRs, as well as the regulation of TrxR activity, have only recently begun to be investigated. The importance of Trx to many aspects of cell function make it likely that TrxRs also play a role in protection against oxidant injury, cell growth and transformation, and the recycling of ascorbate from its oxidized form. Since TrxRs are able to reduce a number of substrates other than Trx, it is likely that additional biological effects will be discovered for TrxR. Furthermore, inhibiting TrxR with drugs may lead to new treatments for human diseases such as cancer, AIDS and autoimmune diseases.
Indexed as
Identifiers
10657232PMC1220815W4299903067What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.