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PI3K, RSK, and mTOR signal networks for the GST gene regulation

Cited 29 time in Web of Science Cited 33 time in Scopus
Authors
Kim, Sang Geon; Lee, Seung Jin
Issue Date
2007
Publisher
Oxford University Press
Citation
Toxicol. Sci. 96, 206-213
Keywords
1-Phosphatidylinositol 3-Kinase/genetics/*metabolismAnimalsAntineoplastic Agents/pharmacologyAntioxidants/pharmacologyGene Expression Regulation, Enzymologic/drug effectsGlutathione Transferase/genetics/*metabolismHumansProtein Kinases/genetics/*metabolismRibosomal Protein S6 KinasesSignal Transduction/drug effects/genetics/*physiology
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.
ISSN
1096-6080 (Print)
Language
English
URI
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=17122411

http://hdl.handle.net/10371/23590
DOI
https://doi.org/10.1093/toxsci/kfl175
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College of Medicine/School of Medicine (의과대학/대학원)Program in Clinical Pharmacology (협동과정-임상약리학전공)Journal Papers (저널논문_협동과정-임상약리학전공)
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