Upregulation of Daxx mediates apoptosis in response to oxidative stress

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Title
Upregulation of Daxx mediates apoptosis in response to oxidative stress
Author(s)
Kyung Soon Kim; Hyun Ah Hwang; S K Chae; H Ha; Ki Sun Kwon
Bibliographic Citation
Journal of Cellular Biochemistry, vol. 96, no. 2, pp. 330-338
Publication Year
2005
Abstract
Oxidative stress induces apoptosis in a variety of cell types by as yet unclear signaling mechanisms. The Daxx protein is reportedly involved in apoptosis through its interactions with Fas, transforming growth factor-β receptor, and promyelocytic leukemia protein (PML). Here, we explored the possible roles of Daxx in oxidative stress-induced apoptosis. We found that both the mRNA and protein levels of Daxx markedly increased when cells underwent apoptosis after H2O2 treatment. Pretreatment with the cell-permeable antioxidant, N-acetyl cysteine, prevented cells from H 2O2-induced Daxx upregulation and subsequent apoptosis, indicating that the endogenous oxidant regulated Daxx expression. Furthermore, suppression of endogenous Daxx expression by antisense oligonucleotide technology inhibited oxidative stress-induced apoptosis in HeLa cells. Taken together, these results suggest that Daxx acts as an intermediary messenger of pro-apoptotic signals triggered by oxidative stress.
Keyword
antisense oligonucleotideapoptosisdaxxoxidative stressredox
ISSN
0730-2312
Publisher
Wiley
DOI
http://dx.doi.org/10.1002/jcb.20545
Type
Article
Appears in Collections:
Division of Research on National Challenges > Aging Research Center > 1. Journal Articles
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