Reduced formation of advanced glycation endproducts via interactions between glutathione peroxidase 3 and dihydroxyacetone kinase 1
- Authors
- Lee, Hana; Chi, Seung Wook; Lee, Phil Young; Kang, Sunghyun; Cho, Sayeon; Lee, Chong-Kil; Bae, Kwang-Hee; Park, Byoung Chul; Park, Sung Goo
- Issue Date
- Nov-2009
- Publisher
- ACADEMIC PRESS INC ELSEVIER SCIENCE
- Keywords
- Advanced glycation endproduct; Dihydroxyacetone; Dihydroxyacetone kinase 1; Glutathione peroxidase 3; Oxidative stress
- Citation
- BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, v.389, no.1, pp 177 - 180
- Pages
- 4
- Journal Title
- BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
- Volume
- 389
- Number
- 1
- Start Page
- 177
- End Page
- 180
- URI
- https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/22911
- DOI
- 10.1016/j.bbrc.2009.08.116
- ISSN
- 0006-291X
1090-2104
- Abstract
- Dihydroxyacetone (DHA) induces the formation of advanced glycation endproducts (AGEs), which are involved in several diseases. Earlier, we identified dihydroxyacetone kinase 1 (Dak1) as a candidate glutathione peroxidase 3 (Gpx3)-interacting protein in Saccharomyces cerevisiae. This finding is noteworthy, as no clear evidence on the involvement of oxidative stress systems in DHA-induced AGE formation has been found to date. Here, we demonstrate that Gpx3 interacts with Dak1, alleviates DHA-mediated stress by upregulating Dak activity, and consequently suppresses AGE formation. Based on these results, we propose that defense systems against oxidative stress and DHA-induced AGE formation are related via interactions between Gpx3 and Dak1. (C) 2009 Elsevier Inc. All rights reserved.
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Collections - College of Pharmacy > School of Pharmacy > 1. Journal Articles
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