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Role of sulfiredoxin as a regulator of peroxiredoxin function and regulation of its expression

Title
Role of sulfiredoxin as a regulator of peroxiredoxin function and regulation of its expression
Authors
Jeong W.Bae S.H.Toledano M.B.Rhee S.G.
Ewha Authors
이서구정우진배수한
SCOPUS Author ID
이서구scopusscopus; 정우진scopus
Issue Date
2012
Journal Title
Free Radical Biology and Medicine
ISSN
0891-5849JCR Link
Citation
vol. 53, no. 3, pp. 447 - 456
Indexed
SCI; SCIE; SCOPUS WOS scopus
Abstract
Peroxiredoxins (Prxs) constitute a family of peroxidases in which cysteine serves as the primary site of oxidation during the reduction of peroxides. Members of the 2-Cys Prx subfamily of Prxs (Prx I to IV in mammals) are inactivated via hyperoxidation of the active-site cysteine to sulfinic acid (Cys-SO2H) during catalysis and are reactivated via an ATP-consuming reaction catalyzed by sulfiredoxin (Srx). This reversible hyperoxidation reaction has been proposed to protect H2O2 signaling molecules from premature removal by 2-Cys Prxs or to upregulate the chaperone function of these enzymes. In addition to its sulfinic acid reductase activity, Srx catalyzes the removal of glutathione (deglutathionylation) from modified proteins. The physiological relevance of both the reversible hyperoxidation of 2-Cys Prxs and the deglutathionylation catalyzed by Srx remains unclear. Recent findings have revealed that Srx expression is induced in mammalian cells under a variety of conditions, such as in metabolically stimulated pancreatic β cells, in immunostimulated macrophages, in neuronal cells engaged in synaptic communication, in lung cells exposed to hyperoxia or cigarette smoke, in hepatocytes of ethanol-fed animals, and in several types of cells exposed to chemopreventive agents. Such induction of Srx in mammalian cells is regulated at the transcriptional level, predominantly via activator protein-1 and/or nuclear factor erythroid 2-related factor 2. Srx expression is also regulated at the translational level in Saccharomyces cerevisiae. © 2012 Elsevier Inc. All rights reserved.
DOI
10.1016/j.freeradbiomed.2012.05.020
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일반대학원 > 생명·약학부 > Journal papers
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