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Oxidation of thioredoxin reductase in HeLa cells stimulated with tumor necrosis factor-α

Title
Oxidation of thioredoxin reductase in HeLa cells stimulated with tumor necrosis factor-α
Authors
Kim J.-R.Lee S.-M.Cho S.-H.Kim J.-H.Kim B.-H.Kwon J.Choi C.Y.Kim Y.-D.Lee S.-R.
Ewha Authors
이승록
Issue Date
2004
Journal Title
FEBS Letters
ISSN
0014-5793JCR Link
Citation
FEBS Letters vol. 567, no. 41308, pp. 189 - 196
Indexed
SCI; SCIE; SCOPUS WOS scopus
Document Type
Article
Abstract
Stimulation of cells with tumor necrosis factor-α (TNF-α) results in the increase in generation of H2O2 in mitochondria that leads to apoptosis. The effect of H2O2 produced by TNF-α on the redox status of selenocysteine (SeCys) residue essential for mitochondrial thioredoxin reductase (TrxR2) was investigated in HeLa cells. TNF-α caused accumulation of oxidized TrxR2 with a thioselenide bond. The conditional induction of SeCys-deficient TrxR2 resulted in the increased production of H2O2 and apoptosis. These results suggest that the SeCys residue of TrxR2 plays a critical role in cell survival by serving as an electron donor for Trx-II and subsequent peroxiredoxin-III, which is a primary line of defense against H 2O2 in mitochondria. © 2004 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
DOI
10.1016/j.febslet.2004.04.055
Appears in Collections:
자연과학대학 > 생명과학전공 > Journal papers
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