E
Elias S.J. Arnér
Researcher at Karolinska Institutet
Publications - 208
Citations - 18978
Elias S.J. Arnér is an academic researcher from Karolinska Institutet. The author has contributed to research in topics: Thioredoxin reductase & Thioredoxin. The author has an hindex of 58, co-authored 192 publications receiving 16579 citations. Previous affiliations of Elias S.J. Arnér include City University of New York.
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Journal ArticleDOI
Regulation of the mammalian selenoprotein thioredoxin reductase 1 in relation to cellular phenotype, growth, and signaling events.
TL;DR: The current knowledge of different levels of TrxR1 regulation in diverse cell types and in response to growth and signaling events is summarized.
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Crystal Structure and Catalysis of the Selenoprotein Thioredoxin Reductase 1
TL;DR: The crystal structure of catalytically active rat thioredoxin reductase 1 (TrxR1) is presented, revealing surprises at the C-terminal Sec-containing active site, and it is demonstrated that a recombinant selenoprotein TrxR can be produced in high amount and sufficient purity to enable crystal structure determination, which suggests that additional structural studies of these types of proteins are feasible.
Journal ArticleDOI
Rapid Induction of Cell Death by Selenium-compromised Thioredoxin Reductase 1 but Not by the Fully Active Enzyme Containing Selenocysteine
Karin Anestål,Elias S.J. Arnér +1 more
TL;DR: In this article, a two-amino acid-truncated C-terminal -GlyCys-Sec-Gly-COOH motif was found to promote cell death.
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Cell Death by SecTRAPs: Thioredoxin Reductase as a Prooxidant Killer of Cells
TL;DR: In this paper, the authors showed that SecTRAPs are prooxidant killers of cells, triggering mechanisms beyond those of a mere loss of thioredoxin reductase activity.
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The thioredoxin reductase inhibitor auranofin triggers apoptosis through a Bax/Bak-dependent process that involves peroxiredoxin 3 oxidation.
TL;DR: It is concluded that auranofin induces apoptosis in cells through a Bax/Bak-dependent mechanism associated with selective disruption of mitochondrial redox homeostasis in conjunction with oxidation of Prx3.