1
40
2
-
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.
Pages
81–91
Issue
1
Volume
74
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
Rat alpha1-macroglobulin enhances nerve growth factor-promoted neurite outgrowth, TrkA phosphorylation, and gene expression of pheochromocytoma PC12 cells.
Publisher
An entity responsible for making the resource available
Journal of neurochemistry
Date
A point or period of time associated with an event in the lifecycle of the resource
2000
2000-01
Subject
The topic of the resource
Animals; Phosphorylation/drug effects; Rats; Transcription Factors/genetics; Gene Expression/*drug effects; Nerve Growth Factor/*pharmacology; *Immediate-Early Proteins; alpha-Macroglobulins/drug effects/metabolism/*pharmacology; Carrier Proteins; DNA-Binding Proteins/genetics; Early Growth Response Protein 1; Matrix Metalloproteinase 3/metabolism; Membrane Proteins; Nerve Growth Factors/genetics; Neurites/drug effects/*physiology; PC12 Cells/drug effects/metabolism/*physiology; Proto-Oncogene Proteins c-jun/genetics; Serotonin/pharmacology; Sprague-Dawley; Receptor; trkA/*metabolism
Creator
An entity primarily responsible for making the resource
Lee P G; Koo P H
Description
An account of the resource
Monoamine-activated human alpha2-macroglobulin (alpha2M) has been previously demonstrated to inhibit TrkA-, TrkB-, and TrkC-mediated signal transduction. Rat alpha1-macroglobulin (alpha1M) and alpha2M are structural homologues of human alpha2M, but rat alpha1M is distinctly different from rat alpha2M in many ways and its role in the mammalian nervous system is unknown. In this report, monoamine-activated rat alpha1M was demonstrated to enhance in a dose-dependent manner nerve growth factor (NGF)-promoted neurite outgrowth in pheochromocytoma PC12 cells. Monoamine-activated alpha1M by itself, however, was neither neurotrophic nor mitogenic to PC12 cells. To investigate further its possible mode of action, the ability of monoamine-activated alpha1M and normal alpha1M to bind and to activate the NGF receptor (TrkA) was investigated. Monoamine-activated alpha1M formed a more stable complex with TrkA than normal alpha1 M, but the binding of monoamine-activated alpha1M to TrkA was adversely affected by prior stimulation of TrkA with NGF. In addition, monoamine-activated alpha1M enhanced the NGF-promoted TrkA phosphorylation and up-regulated the expression of NGF-inducible immediate-early genes (c-jun and NGFI-A) and delayed-response genes (SCG10 and transin) in PC12 cells; normal alpha1M, in contrast, produced little or no effect. This study demonstrates that alpha1M, the constitutive form of alpha-macroglobulin in the rat, possesses the ability to promote NGF-mediated differentiation in PC12 cells, possibly via its direct action on TrkA receptors and TrkA-mediated signal transduction and gene expression.
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).
*Immediate-Early Proteins
2000
alpha-Macroglobulins/drug effects/metabolism/*pharmacology
Animals
Carrier Proteins
DNA-Binding Proteins/genetics
Early Growth Response Protein 1
Gene Expression/*drug effects
Journal of neurochemistry
Koo P H
Lee P G
Matrix Metalloproteinase 3/metabolism
Membrane Proteins
Nerve Growth Factor/*pharmacology
Nerve Growth Factors/genetics
Neurites/drug effects/*physiology
PC12 Cells/drug effects/metabolism/*physiology
Phosphorylation/drug effects
Proto-Oncogene Proteins c-jun/genetics
Rats
Receptor
Serotonin/pharmacology
Sprague-Dawley
Transcription Factors/genetics
trkA/*metabolism
-
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.
Pages
1402–1412
Issue
9
Volume
42
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
Nuclear receptor-mediated repression of human cholesterol 7alpha-hydroxylase gene transcription by bile acids.
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
2001
2001-09
Subject
The topic of the resource
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
An entity primarily responsible for making the resource
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
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).
*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