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Text
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Pages
1402–1412
Issue
9
Volume
42
Dublin Core
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Title
A name given to the resource
Nuclear receptor-mediated repression of human cholesterol 7alpha-hydroxylase gene transcription by bile acids.
Publisher
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Journal of lipid research
Date
A point or period of time associated with an event in the lifecycle of the resource
2001
2001-09
Subject
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Humans; Animals; Rats; Cell Line; Transfection; Liver/metabolism; Reverse Transcriptase Polymerase Chain Reaction; DNA/metabolism; CHO Cells; Cricetinae; Cholesterol 7-alpha-Hydroxylase/*genetics; Bile Acids and Salts/*pharmacology; *Membrane Glycoproteins; *Hydroxysteroid Dehydrogenases; Caco-2 Cells; Carrier Proteins/genetics/physiology; DNA-Binding Proteins/drug effects/genetics/physiology; Gene Expression/*drug effects; Kidney; Luciferases/genetics; Recombinant Fusion Proteins/metabolism; Retinoid X Receptors; Taurocholic Acid/pharmacology; Transcription Factors/drug effects/genetics/physiology; Cultured; Receptors; RNA; Genetic/drug effects; Messenger/analysis; Transcription; Genetic; Tumor Cells; Promoter Regions; Embryo; Cytoplasmic and Nuclear/genetics/*physiology; Mammalian; Retinoic Acid/genetics/physiology
Creator
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Chen W; Owsley E; Yang Y; Stroup D; Chiang J Y
Description
An account of the resource
Hydrophobic bile acids strongly repressed transcription of the human cholesterol 7alpha-hydroxylase gene (CYP7A1) in the bile acid biosynthetic pathway in the liver. Farnesoid X receptor (FXR) repressed CYP7A1/Luc reporter activity in a transfection assay in human liver-derived HepG2 cells, but not in human embryonic kidney (HEK) 293 cells. FXR-binding activity was required for bile acid repression of CYP7A1 transcription despite the fact that FXR did not bind to the CYP7A1 promoter. FXR-induced liver-specific factors must be required for mediating bile acid repression. Bile acids and FXR repressed endogenous CYP7A1 but stimulated alpha-fetoprotein transcription factor (FTF) and small heterodimer partner (SHP) mRNA expression in HepG2 cells. Feeding of rats with chenodeoxycholic acid repressed CYP7A1, induced FTF, but had no effect on SHP mRNA expression in the liver. FTF strongly repressed CYP7A1 transcription in a dose-dependent manner, and SHP further inhibited CYP7A1 in HepG2 cells, but not in HEK 293 cells. FXR only moderately stimulated SHP transcription, whereas FTF strongly inhibited SHP transcription in HepG2 cells. Results revealed that FTF was a dominant negative factor that was induced by bile acid-activated FXR to inhibit both CYP7A1 and SHP transcription. Differential regulation of FTF and SHP expression by bile acids may explain the wide variation in CYP7A1 expression and the rate of bile acid synthesis and regulation in different species.
Rights
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Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
*Hydroxysteroid Dehydrogenases
*Membrane Glycoproteins
2001
Animals
Bile Acids and Salts/*pharmacology
Caco-2 Cells
Carrier Proteins/genetics/physiology
Cell Line
Chen W
Chiang J Y
CHO Cells
Cholesterol 7-alpha-Hydroxylase/*genetics
Cricetinae
Cultured
Cytoplasmic and Nuclear/genetics/*physiology
Department of Integrative Medical Sciences
DNA-Binding Proteins/drug effects/genetics/physiology
DNA/metabolism
Embryo
Gene Expression/*drug effects
Genetic
Genetic/drug effects
Humans
Journal of lipid research
Kidney
Liver/metabolism
Luciferases/genetics
Mammalian
Messenger/analysis
NEOMED College of Medicine
Owsley E
Promoter Regions
Rats
Receptors
Recombinant Fusion Proteins/metabolism
Retinoic Acid/genetics/physiology
Retinoid X Receptors
Reverse Transcriptase Polymerase Chain Reaction
RNA
Stroup D
Taurocholic Acid/pharmacology
Transcription
Transcription Factors/drug effects/genetics/physiology
Transfection
Tumor Cells
Yang Y