English  |  正體中文  |  简体中文  |  Items with full text/Total items : 28607/40644
Visitors : 5280664      Online Users : 534
RC Version 4.0 © Powered By DSPACE, MIT. Enhanced by NTU Library IR team.
Scope Adv. Search

Please use this identifier to cite or link to this item: http://ntour.ntou.edu.tw:8080/ir/handle/987654321/45547

Title: Loss of the Oxidative Stress Sensor NPGPx Compromises GRP78 Chaperone Activity and Induces Systemic Disease.
Authors: Pei-Chi Wei;Yi-Hsuan Hsieh;Mei-I. Su;Xianzhi Jiang;Pang-Hung Hsu;Wen-Ting Lo;Jui-Yun Weng;Yung-Ming Jeng;Ju-Ming Wang;Phang-lang Chen;Yi-Cheng Chang;Kuo-Fen Lee;Ming-Daw Tsai;Jin-Yuh Shew;Wen-Hwa Lee
Contributors: 國立臺灣海洋大學:生命科學系
Date: 2012
Issue Date: 2018-03-26T05:57:29Z
Publisher: Molecular Cells
Abstract: Abstract: NPGPx is a member of the glutathione peroxidase (GPx) family; however, it lacks GPx enzymatic activity due to the absence of a critical selenocysteine residue, rendering its function an enigma. Here, we show that NPGPx is a newly identified stress sensor that transmits oxidative stress signals by forming the disulfide bond between its Cys57 and Cys86 residues. This oxidized form of NPGPx binds to glucose-regulated protein (GRP)78 and forms covalent bonding intermediates between Cys86 of NPGPx and Cys41/Cys420 of GRP78. Subsequently, the formation of the disulfide bond between Cys41 and Cys420 of GRP78 enhances its chaperone activity. NPGPx-deficient cells display increased reactive oxygen species, accumulated misfolded proteins, and impaired GRP78 chaperone activity. Complete loss of NPGPx in animals causes systemic oxidative stress, increases carcinogenesis, and shortens life span. These results suggest that NPGPx is essential for releasing excessive ER stress by enhancing GRP78 chaperone activity to maintain physiological homeostasis.
URI: http://ntour.ntou.edu.tw:8080/ir/handle/987654321/45547
Appears in Collections:[生命科學系] 期刊論文

Files in This Item:

File Description SizeFormat

All items in NTOUR are protected by copyright, with all rights reserved.


著作權政策宣告: 本網站之內容為國立臺灣海洋大學所收錄之機構典藏,無償提供學術研究與公眾教育等公益性使用,請合理使用本網站之內容,以尊重著作權人之權益。
網站維護: 海大圖資處 圖書系統組
DSpace Software Copyright © 2002-2004  MIT &  Hewlett-Packard  /   Enhanced by   NTU Library IR team Copyright ©   - Feedback