1
40
4
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1210/me.2009-0482" target="_blank" rel="noreferrer noopener">http://doi.org/10.1210/me.2009-0482</a>
Pages
1151–1164
Issue
6
Volume
24
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
A novel bile acid-activated vitamin D receptor signaling in human hepatocytes.
Publisher
An entity responsible for making the resource available
Molecular endocrinology (Baltimore, Md.)
Date
A point or period of time associated with an event in the lifecycle of the resource
2010
2010-06
Subject
The topic of the resource
Calcitriol/*metabolism; Calcitriol/pharmacology; Cell Membrane/drug effects/metabolism; Cell Nucleus/drug effects/metabolism; Cholesterol 7-alpha-Hydroxylase/antagonists & inhibitors/genetics; Enzyme Activation/drug effects; Extracellular Signal-Regulated MAP Kinases/antagonists & inhibitors; Genetic/genetics; Hep G2 Cells; Hepatocyte Nuclear Factor 4/metabolism; Hepatocytes/*drug effects/enzymology/*metabolism; Humans; Intracellular Space/drug effects/metabolism; Ligands; Lithocholic Acid/*pharmacology; Mitogen-Activated Protein Kinase Kinases/metabolism; Phosphorylation/drug effects; Phosphotyrosine/metabolism; Promoter Regions; Protein Kinase Inhibitors/pharmacology; Protein Transport/drug effects; Proto-Oncogene Proteins c-raf/metabolism; Receptors; Retinoid X Receptor alpha/metabolism; Signal Transduction/*drug effects; src-Family Kinases/metabolism; Steroid Hydroxylases/genetics/metabolism; Vitamin D3 24-Hydroxylase
Creator
An entity primarily responsible for making the resource
Han Shuxin; Li Tiangang; Ellis Ewa; Strom Stephen; Chiang John Y L
Description
An account of the resource
Vitamin D receptor (VDR) is activated by natural ligands, 1alpha,
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1210/me.2009-0482" target="_blank" rel="noreferrer noopener">10.1210/me.2009-0482</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2010
Calcitriol/*metabolism
Calcitriol/pharmacology
Cell Membrane/drug effects/metabolism
Cell Nucleus/drug effects/metabolism
Chiang John Y L
Cholesterol 7-alpha-Hydroxylase/antagonists & inhibitors/genetics
Department of Integrative Medical Sciences
Ellis Ewa
Enzyme Activation/drug effects
Extracellular Signal-Regulated MAP Kinases/antagonists & inhibitors
Genetic/genetics
Han Shuxin
Hep G2 Cells
Hepatocyte Nuclear Factor 4/metabolism
Hepatocytes/*drug effects/enzymology/*metabolism
Humans
Intracellular Space/drug effects/metabolism
Li Tiangang
Ligands
Lithocholic Acid/*pharmacology
Mitogen-Activated Protein Kinase Kinases/metabolism
Molecular endocrinology (Baltimore, Md.)
NEOMED College of Medicine
Phosphorylation/drug effects
Phosphotyrosine/metabolism
Promoter Regions
Protein Kinase Inhibitors/pharmacology
Protein Transport/drug effects
Proto-Oncogene Proteins c-raf/metabolism
Receptors
Retinoid X Receptor alpha/metabolism
Signal Transduction/*drug effects
src-Family Kinases/metabolism
Steroid Hydroxylases/genetics/metabolism
Strom Stephen
Vitamin D3 24-Hydroxylase
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1194/jlr.M002782" target="_blank" rel="noreferrer noopener">http://doi.org/10.1194/jlr.M002782</a>
Pages
832–842
Issue
4
Volume
51
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Glucose stimulates cholesterol 7alpha-hydroxylase gene transcription in human hepatocytes.
Publisher
An entity responsible for making the resource available
Journal of lipid research
Date
A point or period of time associated with an event in the lifecycle of the resource
2010
2010-04
Subject
The topic of the resource
*Gene Expression Regulation; Acetylation; AMP-Activated Protein Kinases/metabolism; ATP Citrate (pro-S)-Lyase/genetics/metabolism; Bile Acids and Salts/metabolism; Cells; Cholesterol 7-alpha-Hydroxylase/genetics/*metabolism; Cultured; DNA-Binding Proteins/metabolism; Enzymologic; Epigenesis; Genes; Genetic; Glucose/*administration & dosage; Hep G2 Cells; Hepatocyte Nuclear Factor 4/metabolism; Hepatocytes/*enzymology/metabolism; Histones/metabolism; Humans; Hyperglycemia/enzymology/*metabolism; Messenger/metabolism; Methylation; Reporter; RNA; RNA Interference
Creator
An entity primarily responsible for making the resource
Li Tiangang; Chanda Dipanjan; Zhang Yanqiao; Choi Hueng-Sik; Chiang John Y L
Description
An account of the resource
Bile acids play important roles in the regulation of lipid, glucose, and energy homeostasis. Recent studies suggest that glucose regulates gene transcription in the liver. The aim of this study was to investigate the potential role of glucose in regulation of bile acid synthesis in human hepatocytes. High glucose stimulated bile acid synthesis and induced mRNA expression of cholesterol 7alpha-hydroxylase (CYP7A1), the key regulatory gene in bile acid synthesis. Activation of an AMP-activated protein kinase (AMPK) decreased CYP7A1 mRNA, hepatocyte nuclear factor 4alpha (HNF4alpha) protein, and binding to CYP7A1 chromatin. Glucose increased ATP levels to inhibit AMPK and induce HNF4alpha to stimulate CYP7A1 gene transcription. Furthermore, glucose increased histone acetylation and decreased H3K9 di- and tri-methylation in the CYP7A1 chromatin. Knockdown of ATP-citrate lyase, which converts citrate to acetyl-CoA, decreased histone acetylation and attenuated glucose induction of CYP7A1 mRNA expression. These results suggest that glucose signaling also induces CYP7A1 gene transcription by epigenetic regulation of the histone acetylation status. This study uncovers a novel link between hepatic glucose metabolism and bile acid synthesis. Glucose induction of bile acid synthesis may have an important implication in metabolic control of glucose, lipid, and energy homeostasis under normal and diabetic conditions.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1194/jlr.M002782" target="_blank" rel="noreferrer noopener">10.1194/jlr.M002782</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
*Gene Expression Regulation
2010
Acetylation
AMP-Activated Protein Kinases/metabolism
ATP Citrate (pro-S)-Lyase/genetics/metabolism
Bile Acids and Salts/metabolism
Cells
Chanda Dipanjan
Chiang John Y L
Choi Hueng-Sik
Cholesterol 7-alpha-Hydroxylase/genetics/*metabolism
Cultured
Department of Integrative Medical Sciences
DNA-Binding Proteins/metabolism
Enzymologic
Epigenesis
Genes
Genetic
Glucose/*administration & dosage
Hep G2 Cells
Hepatocyte Nuclear Factor 4/metabolism
Hepatocytes/*enzymology/metabolism
Histones/metabolism
Humans
Hyperglycemia/enzymology/*metabolism
Journal of lipid research
Li Tiangang
Messenger/metabolism
Methylation
NEOMED College of Medicine
Reporter
RNA
RNA Interference
Zhang Yanqiao
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1074/jbc.M109.083899" target="_blank" rel="noreferrer noopener">http://doi.org/10.1074/jbc.M109.083899</a>
Pages
3035–3043
Issue
5
Volume
285
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Identification of novel pathways that control farnesoid X receptor-mediated hypocholesterolemia.
Publisher
An entity responsible for making the resource available
The Journal of biological chemistry
Date
A point or period of time associated with an event in the lifecycle of the resource
2010
2010-01
Subject
The topic of the resource
Absorption; Animals; Biological; Cell Line; Cholesterol/*metabolism; Class B/*genetics/metabolism; Coronary Disease/metabolism; Cytoplasmic and Nuclear/*metabolism; Glucose/metabolism; Hepatocyte Nuclear Factor 4/metabolism; Homeostasis; Humans; Lipoproteins/metabolism; Liver/metabolism; Mice; Models; Receptors; Scavenger Receptors
Creator
An entity primarily responsible for making the resource
Zhang Yanqiao; Yin Liya; Anderson Jody; Ma Huiyan; Gonzalez Frank J; Willson Timothy M; Edwards Peter A
Description
An account of the resource
Farnesoid X receptor (FXR) plays important regulatory roles in bile acid, lipoprotein, and glucose homeostasis. Here, we have utilized Fxr(-/-) mice and mice deficient in scavenger receptor class B type I (SR-BI), together with an
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1074/jbc.M109.083899" target="_blank" rel="noreferrer noopener">10.1074/jbc.M109.083899</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2010
Absorption
Anderson Jody
Animals
Biological
Cell Line
Cholesterol/*metabolism
Class B/*genetics/metabolism
Coronary Disease/metabolism
Cytoplasmic and Nuclear/*metabolism
Department of Integrative Medical Sciences
Edwards Peter A
Glucose/metabolism
Gonzalez Frank J
Hepatocyte Nuclear Factor 4/metabolism
Homeostasis
Humans
Lipoproteins/metabolism
Liver/metabolism
Ma Huiyan
Mice
Models
NEOMED College of Medicine
Receptors
Scavenger Receptors
The Journal of biological chemistry
Willson Timothy M
Yin Liya
Zhang Yanqiao
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1053/j.gastro.2007.08.042" target="_blank" rel="noreferrer noopener">http://doi.org/10.1053/j.gastro.2007.08.042</a>
Pages
1660–1669
Issue
5
Volume
133
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
A novel role of transforming growth factor beta1 in transcriptional repression of human cholesterol 7alpha-hydroxylase gene.
Publisher
An entity responsible for making the resource available
Gastroenterology
Date
A point or period of time associated with an event in the lifecycle of the resource
2007
2007-11
Subject
The topic of the resource
Bile Acids and Salts/metabolism; Carcinoma; Cell Line; Cells; Cholesterol 7-alpha-Hydroxylase/*genetics/*metabolism; Cultured; Enzyme Inhibitors/pharmacology; Genetic/drug effects/*physiology; Hepatocellular/*metabolism/pathology; Hepatocyte Nuclear Factor 4/metabolism; Hepatocytes/drug effects/*metabolism/pathology; Humans; Hydroxamic Acids/pharmacology; Liver Neoplasms/*metabolism/pathology; Messenger/metabolism; RNA; Signal Transduction/physiology; Smad3 Protein/metabolism; Transcription; Transforming Growth Factor beta1/*metabolism; Tumor
Creator
An entity primarily responsible for making the resource
Li Tiangang; Chiang John Y L
Description
An account of the resource
BACKGROUND & AIMS: Inhibition of cholesterol 7alpha-hydroxylase (CYP7A1) by bile acids and inflammatory cytokines provides an important mechanism to protect hepatocytes from bile acid toxicity during cholestasis. Transforming growth factor beta1 (TGFbeta1) released by hepatic stellate cells during chronic liver injury plays a critical role in liver inflammation and fibrogenesis. The objective of this study is to investigate the role of TGFbeta1 in hepatic bile acid synthesis. METHODS: mRNA expressions in primary human hepatocytes and HepG2 cells were measured by quantitative real-time polymerase chain reaction. Reporter assay, glutathione-S-transferase pull-down assay, adenovirus-mediated gene transduction, and chromatin immunoprecipitation assay were used to study the mechanism of TGFbeta1 regulation of CYP7A1 gene transcription. RESULTS: TGFbeta1 inhibited the mRNA expression of CYP7A1 and bile acid synthesis in HepG2 cells and primary human hepatocytes. Mothers against decapentaplegic homolog (Smad3) inhibited both CYP7A1 promoter activity and mRNA expression by inhibiting
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1053/j.gastro.2007.08.042" target="_blank" rel="noreferrer noopener">10.1053/j.gastro.2007.08.042</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2007
Bile Acids and Salts/metabolism
Carcinoma
Cell Line
Cells
Chiang John Y L
Cholesterol 7-alpha-Hydroxylase/*genetics/*metabolism
Cultured
Department of Integrative Medical Sciences
Enzyme Inhibitors/pharmacology
Gastroenterology
Genetic/drug effects/*physiology
Hepatocellular/*metabolism/pathology
Hepatocyte Nuclear Factor 4/metabolism
Hepatocytes/drug effects/*metabolism/pathology
Humans
Hydroxamic Acids/pharmacology
Li Tiangang
Liver Neoplasms/*metabolism/pathology
Messenger/metabolism
NEOMED College of Medicine
RNA
Signal Transduction/physiology
Smad3 Protein/metabolism
Transcription
Transforming Growth Factor beta1/*metabolism
Tumor