When NRF2 Talks, Who's Listening?

被引：512

作者：

Wakabayashi, Nobunao ^{[1
,2
]}

Slocum, Stephen L. ^{[1
,3
]}

Skoko, John J. ^{[1
,4
]}

Shin, Soona ^{[1
,4
]}

Kensler, Thomas W. ^{[1
,4
]}

机构：

[1] Univ Pittsburgh, Dept Pharmacol & Chem Biol, Pittsburgh, PA 15261 USA

[2] Johns Hopkins Univ, Sch Med, Dept Environm Hlth Sci, Baltimore, MD USA

[3] Johns Hopkins Univ, Dept Biochem & Mol Biol, Bloomberg Sch Publ Hlth, Baltimore, MD USA

[4] Johns Hopkins Univ, Sch Med, Dept Pharmacol & Mol Sci, Baltimore, MD 21205 USA

来源：

ANTIOXIDANTS & REDOX SIGNALING | 2010年 / 13卷 / 11期

关键词：

NF-KAPPA-B; ARYL-HYDROCARBON RECEPTOR; ANTIOXIDANT RESPONSE ELEMENT; TRANSCRIPTION FACTOR NRF2; NITRIC-OXIDE SYNTHASE; HEME OXYGENASE-1 INDUCTION; GENE-EXPRESSION; ENDOTHELIAL-CELLS; OXIDATIVE STRESS; IN-VITRO;

D O I：

10.1089/ars.2010.3216

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：

Activation of the KEAP1-NRF2 signaling pathway is an adaptive response to environmental and endogenous stresses and serves to render animals resistant to chemical carcinogenesis and other forms of toxicity, whereas disruption of the pathway exacerbates these outcomes. This pathway, which can be activated by sulfhydryl-reactive, small-molecule pharmacologic agents, regulates the inducible expression of an extended battery of cytoprotective genes, often by direct binding of the transcription factor to antioxidant response elements in the promoter regions of target genes. However, it is becoming evident that some of the protective effects may be mediated indirectly through cross talk with additional pathways affecting cell survival and other aspects of cell fate. These interactions provide a multi-tiered, integrated response to chemical stresses. This review highlights recent observations on the molecular interactions and their functional consequences between NRF2 and the arylhydrocarbon receptor (AhR), NF-kappa B, p53, and Notch1 signaling pathways. Antioxid. Redox Signal. 13, 1649-1663.

引用

页码：1649 / 1663

页数：15

共 168 条

[1] Triterpenoid CDDO-Me blocks the NF-κB pathway by direct inhibition of IKKβ on Cys-179 [J].