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- W2008064286 abstract "The mechanism by which treatment of mice with CCl4 induces an increase in choline kinase α has been investigated. Nuclear run on assays demonstrated a major increase in the transcript for choline kinase α in livers from mice 3 h and 6 h after administration of CCl4 compared to vehicle (olive oil). 5′deletion analyses of choline kinase α promoter-luciferase constructs expressed in Hepa-1 cells identified a promoter element between − 875 and − 866 that was nearly identical to an AP-1 consensus site. Mutation of this AP-1 site caused a striking decrease in the expression of choline kinase α promoter-luciferase constructs. Electromobility shift assays with nuclear extracts from mouse liver demonstrated that c-Jun, but not c-fos, bound oligonucleotides with the AP-1 site. The amount of c-jun bound was greatly increased when hepatic nuclear extracts from mice treated with CCl4 were used. Chromatin immunoprecipitation assays confirmed that c-jun binds to the choline kinase α promoter. The results from these studies provide strong evidence that the choline kinase α promoter has a distal element (− 875/− 867) that binds c-jun and the binding of c-jun is enhanced by treatment with CCl4." @default.
- W2008064286 created "2016-06-24" @default.
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- W2008064286 date "2007-09-01" @default.
- W2008064286 modified "2023-10-18" @default.
- W2008064286 title "Induction of choline kinase alpha by carbon tetrachloride (CCl4) occurs via increased binding of c-jun to an AP-1 element" @default.
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- W2008064286 doi "https://doi.org/10.1016/j.bbalip.2007.07.003" @default.
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