期刊
TOXICOLOGY LETTERS
卷 199, 期 1, 页码 93-101出版社
ELSEVIER IRELAND LTD
DOI: 10.1016/j.toxlet.2010.08.011
关键词
Glutathione; Keap1-Nrf2 pathway; PYDDT; S-glutathionylation
类别
资金
- Zhejiang Key Science & Technological Program [2009C13028]
- Zhejiang Innovation Program for Graduates [YK2009015]
Keap1-Nrf2 pathway has emerged as a regulator for the endogenous antioxidant response, which is critical in defending cells against carcinogenesis. Herein, we demonstrated that depleting the cellular level of glutathione (GSH) by a novel electrophilic agent 2-(pro-1-ynyl)-5-(5,6-dihydroxypenta-1,3-diynyl) thiophene (PYDDT) could activate Keap1-Nrf2 pathway. In above process, it was found that Keap1 was modified by S-glutathionylation, an important post-translational modification of protein cysteines with critical roles in oxidative stress and signal transduction. We concluded from our findings that conjugation with intracellular GSH by PYDDT might lead to Keap1 S-glutathionylation and was a key event involved in its Nrf2 inducing activity. (C) 2010 Elsevier Ireland Ltd. All rights reserved.
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