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• W2139061010 abstract "Fibroblast growth factor-19 (FGF-19), a bile acid-responsive enterokine, is secreted by the ileum and regulates a variety of metabolic processes. These studies examined the signal transduction pathways operant in FGF-19-mediated repression of the apical sodium-dependent bile acid transporter (ASBT). Responses to FGF-19 were assessed in Caco-2 and CT-26 cells and in mice where c- fos was conditionally silenced in the intestine by a cre-lox strategy. FGF-19 treatment of Caco-2 cells or wild-type mice led to a significant reduction in ASBT protein expression and enhanced phosphorylation of extracellular signaling kinase 1/2 (ERK1/2), c-Fos, and c-Jun. FGF-19 treatment of Caco-2 cells led to a reduction in activity of the human ASBT promoter and this repression could be blocked by treatment with a mitogen-activated protein kinase/ERK kinase (MEK1/2) inhibitor or by silencing jun kinase 1, jun kinase 2, c- fos, or c- jun. Site directed mutagenesis of a c- fos binding element in the ASBT promoter blocked FGF-19-mediated repression in luciferase reporter constructs. ASBT promoter activity was repressed by FGF-19 in CT-26 cells and this repression could be reduced by MEK1/2 inhibition or silencing c- fos. FGF-19-mediated repression of ASBT protein expression was abrogated in mice where c- fos was conditionally silenced in the intestine. In contrast, ASBT was repressed in the c-Fos expressing gallbladders of the same mice. The studies demonstrate that FGF-19 represses the expression of ASBT in the ileum and gallbladder via a signal transduction pathway involving MEK1/2, ERK1/2, JNK1, JNK2, and c-Fos." @default.
• W2139061010 created "2016-06-24" @default.
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• W2139061010 date "2014-01-15" @default.
• W2139061010 modified "2023-09-25" @default.
• W2139061010 title "c-Fos mediates repression of the apical sodium-dependent bile acid transporter by fibroblast growth factor-19 in mice" @default.
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• W2139061010 doi "https://doi.org/10.1152/ajpgi.00276.2013" @default.
• W2139061010 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3920077" @default.
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