Mechanism of the Nrf2/Keap1/ARE signaling system

被引：202
|
作者：
Tkachev, V. O. [1 ,2 ]
Menshchikova, E. B. [1 ]
Zenkov, N. K. [1 ]
机构：
[1] Russian Acad Med Sci, Siberian Branch, Sci Ctr Clin & Expt Med, Novosibirsk 630117, Russia
[2] Russian Acad Med Sci, Siberian Branch, Inst Clin Immunol, Novosibirsk 630094, Russia
来源：
BIOCHEMISTRY-MOSCOW | 2011年 / 76卷 / 04期
基金：
俄罗斯基础研究基金会;
关键词：
redox regulation; Nrf2; Keap1; antioxidant-respons(iv)e element (ARE); ANTIOXIDANT-RESPONSE ELEMENT; TRANSCRIPTION FACTOR NRF2; HEME OXYGENASE-1 GENE; OXIDATIVE STRESS; MEDIATED EXPRESSION; NUCLEAR EXPORT; SENSOR KEAP1; DNA-BINDING; PHOSPHATIDYLINOSITOL; 3-KINASE/AKT; CHEMOPREVENTIVE AGENTS;
D O I：
10.1134/S0006297911040031
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
Nrf2 regulates expression of genes containing antioxidant-respons(iv)e element (ARE) in their promoters and plays a pivotal role among all redox-sensitive transcription factors. Nrf2 is constitutively controlled by repressor protein Keap1, which acts as a molecular sensor of disturbances in cellular homeostasis. These molecular patterns are in close inter-connection and function as parts of the integrated redox-sensitive signaling system Nrf2/Keap1/ARE. Depending on cellular redox balance, activity of this signaling system changes at the levels of transcription, translation, posttranslational modification, nuclear translocation of transcription factor, and its binding to ARE-driven gene promoters. This review summarizes current conceptions of Nrf2/Keap1/ARE induction and inactivation.
引用
收藏
页码：407 / 422
页数：16
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