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ToxSci Advance Access originally published online on November 22, 2006
Toxicological Sciences 2007 96(2):206-213; doi:10.1093/toxsci/kfl175
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© The Author 2006. Published by Oxford University Press on behalf of the Society of Toxicology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

PI3K, RSK, and mTOR Signal Networks for the GST Gene Regulation

Sang Geon Kim1 and Seung Jin Lee

College of Pharmacy and Research Institute of Pharmaceutical Sciences, Seoul National University, Seoul 151-742, South Korea

1 To whom correspondence should be addressed. Fax: +822 (872)-1795. E-mail: sgk{at}snu.ac.kr.

Received September 21, 2006; accepted November 20, 2006


  Abstract

The induction of glutathione S-transferases (GST) represents not only cell detoxification and survival but also cancer prevention. In response to various extracellular stimuli, expression of the gene has been shown to be regulated coordinately by activating the transcription factors in a transcriptional or posttranscriptional manner. Cytoprotective agents induce GST and concomitantly activate the PI3K-Akt/ERK-RSK1-mTOR pathways that activate the transcription factors favoring cell viability. The mechanistic basis and cell signaling for the induction of GST induction by prooxidants and toxicants may be different from that by cytoprotective agents. This paper summarizes the molecular mechanisms of the transcriptional induction of the GST gene orchestrated by a series of transcription factors that recruit coactivators or corepressors.

Key Words: CCAAT-enhancer binding protein; glutathione S-transferases; NF-E2-related factor2; hepatocyte nuclear factors; mammalian target of rapamycin; peroxisome proliferator-activated receptors; phosphatidylinositol 3-kinase.


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