ArticleChemical research in toxicology2008
Increased mitochondrial thioredoxin 2 potentiates N-ethylmaleimide-induced cytotoxicity.
Article in Chemical research in toxicology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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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.
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Who cites it
4 citing papers in PubMed, 11 citations in OpenAlex.
- Whole-Cell Fiber-Optic Biosensor for Real-Time, On-Site Sediment and Water Toxicity Assessment: Applications at Contaminated Sites Across Israel.Biosensors · 2025Article
- Enhanced expression of mitochondrial superoxide dismutase leads to prolonged in vivo cell cycle progression and up-regulation of mitochondrial thioredoxin.Free radical biology & medicine · 2010Article
- Reactive species and mitochondrial dysfunction: mechanistic significance of 4-hydroxynonenal.Environmental and molecular mutagenesis · 2010Review
- Mechanisms of pathogenesis in drug hepatotoxicity putting the stress on mitochondria.Molecular interventions · 2010Review
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Thioredoxin 2 (Trx2) is a mitochondrially localized antioxidant and antiapoptotic protein, whose functions are mainly dependent on the conserved cysteines at its redox active center. In the current study, we showed by mass spectrometry that a thiol alkylating agent, N-ethylmaleimide (NEM), alkylated a single cysteine residue in the active center of Trx2. The interaction between NEM and Trx2 in intact cells was confirmed by redox Western analysis. Overexpression of Trx2 in cultured 143B osteosarcoma cells caused increased sensitivity to NEM. Covalent modification by NEM resulted in a dominant-negative effect and increased the interaction between Trx2 and peroxiredoxin 3 (Prx3). Our data suggest that the alkylation of the essential thiol(s) of Trx2 has profound impact on the mitochondrial redox circuitry and that such effects are distinct from the responses to agents causing reversible disulfide bond formation between the vicinal dithiols in the active center.
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Registered trials
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