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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
4
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pubmed:dateCreated |
1996-6-24
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pubmed:abstractText |
The c-jun proto-oncogene plays a vital role in the carcinogenic process. Although numerous works have extensively investigated the induction mechanisms of c-jun by UV, hydrogen peroxide or 12-O-tetradecanoylphorbol-13-acetate, the mechanism induced by alkylating agents has received little attention. In this study, NIH 3T3 cells were exposed to methylmethanesulfonate (MMS), revealing that the agent clearly induced c-jun expression with a peak at 2 h. Pretreatment of cells with various kinase inhibitors, e.g. H7, genistein, herbimycin A and tyrphostin, did not show any significant effects on the MMS-induced c-jun expression. Benzamide, an inhibitor of poly(ADP)-ribosylation, enhanced the MMS-induced DNA breakages, but did not potentiate that agent which elicited c-jun expression. Another experiment showed that this agent transfected and overexpressed an activated v-H-ras gene in NIH 3T3 cells, which became more resistant to MMS-induced DNA damage but expressed the same level of c-jun transcript as compared with NIH 3T3 cells in response to MMS. If intracellular glutathione (GSH) was completely depleted by buthionine sulfoximine (BSO), the MMS-elicited c-jun expression was blocked. Subsequently, re-elevating intracellular GSH by washing off BSO caused the expression of c-jun by MMS to increase proportionately. Based on these findings, we can conclude that the mechanism by which MMS induced c-jun expression does not occur through activation of protein tyrosine kinases or initiation of DNA damage, but is closely related to the intracellular GSH.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Enzyme Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/Glutathione,
http://linkedlifedata.com/resource/pubmed/chemical/Hydrogen Peroxide,
http://linkedlifedata.com/resource/pubmed/chemical/Methyl Methanesulfonate,
http://linkedlifedata.com/resource/pubmed/chemical/Protein Kinase Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Tetradecanoylphorbol Acetate
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pubmed:status |
MEDLINE
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pubmed:month |
Apr
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pubmed:issn |
0143-3334
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
17
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
815-20
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:8625496-3T3 Cells,
pubmed-meshheading:8625496-Animals,
pubmed-meshheading:8625496-DNA Damage,
pubmed-meshheading:8625496-Enzyme Inhibitors,
pubmed-meshheading:8625496-Gene Expression Regulation,
pubmed-meshheading:8625496-Glutathione,
pubmed-meshheading:8625496-Hydrogen Peroxide,
pubmed-meshheading:8625496-Kinetics,
pubmed-meshheading:8625496-Methyl Methanesulfonate,
pubmed-meshheading:8625496-Mice,
pubmed-meshheading:8625496-Protein Kinase Inhibitors,
pubmed-meshheading:8625496-RNA, Messenger,
pubmed-meshheading:8625496-Tetradecanoylphorbol Acetate
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pubmed:year |
1996
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pubmed:articleTitle |
Involvement of glutathione in induction of c-jun proto-oncogene by methylmethanesulfonate in NIH 3T3 cells.
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pubmed:affiliation |
Institute of Toxicology, College of Medicine, National Taiwan University, Taipei.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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