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/10.1046/j.1471-4159.2000.0740081.x" target="_blank" rel="noreferrer noopener">http://doi.org/10.1046/j.1471-4159.2000.0740081.x</a>
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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).
Pages
81-91
Issue
1
Volume
74
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Dublin Core
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Title
A name given to the resource
Rat Alpha(1)-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
alpha-2-macroglobulin receptor; alpha-macroglobulins; alpha(2)-macroglobulin; Biochemistry & Molecular Biology; caudate putamen; cerebral cortical-neurons; choline-acetyltransferase; delayed-response genes; immediate-early genes; myelin-associated glycoprotein; nerve growth factor receptor; neurite-promoting factor; Neurosciences & Neurology; ngf receptor; protein; signal; signal-transduction; transduction
Creator
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Lee P G; Koo P H
Description
An account of the resource
Monoamine-activated human alpha(2)-macroglobulin (alpha(2)M) has been previously demonstrated to inhibit TrkA-, TrkB-, and TrkC-mediated signal transduction. Rat alpha(1),-macroglobulin (alpha(1)M) and alpha(2)M are structural homologues of human alpha(2)M, but rat alpha(1)M is distinctly different from rat alpha(2)M in many ways and its role in the mammalian nervous system is unknown. In this report, monoamine-activated rat alpha(1)M was demonstrated to enhance in a dose-dependent manner nerve growth factor (NGF)-promoted neurite outgrowth in pheochromocytoma PC12 cells. Monoamine-activated alpha(1)M by itself, however, was neither neurotrophic nor mitogenic to PC12 cells. To investigate further its possible mode of action, the ability of monoamine-activated alpha(1)M and normal alpha(1)M to bind and to activate the NGF receptor (TrkA) was investigated. Monoamine-activated alpha(1)M formed a more stable complex with TrkA than normal alpha(1)M, but the binding of mono-amina-activated alpha(1)M to TrkA was adversely affected by prior stimulation of TrkA with NGF. In addition, monoamine-activated alpha(1)M 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 alpha(1)M, in contrast, produced little or no effect, This study demonstrates that alpha(1)M, the constitutive form of ar-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.
Identifier
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<a href="http://doi.org/10.1046/j.1471-4159.2000.0740081.x" target="_blank" rel="noreferrer noopener">10.1046/j.1471-4159.2000.0740081.x</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article or Conference Abstract Publication
2000
alpha-2-macroglobulin receptor
alpha-macroglobulins
alpha(2)-macroglobulin
Biochemistry & Molecular Biology
caudate putamen
cerebral cortical-neurons
choline-acetyltransferase
delayed-response genes
immediate-early genes
Journal Article or Conference Abstract Publication
Journal of neurochemistry
Koo P H
Lee P G
myelin-associated glycoprotein
nerve growth factor receptor
neurite-promoting factor
Neurosciences & Neurology
ngf receptor
Protein
signal
signal-transduction
Transduction
-
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
n/a
Rights
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Pages
A973-A973
Issue
9
Volume
11
Search for Full-text
Locate full-text within NEOMED Library's e-journal collections
<p>Users with a NEOMED Library login can search for full-text journal articles at the following url: <a href="https://libraryguides.neomed.edu/home">https://libraryguides.neomed.edu/home</a></p>
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Title
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Alpha-2-macroglobulin Homologues Mediating Nerve Degeneration And Regeneration
Publisher
An entity responsible for making the resource available
Faseb Journal
Date
A point or period of time associated with an event in the lifecycle of the resource
1997
1997-07
Subject
The topic of the resource
Biochemistry & Molecular Biology; Cell Biology; Life Sciences & Biomedicine - Other; Topics
Creator
An entity primarily responsible for making the resource
Lee P G; Hu Y Q; Liebl D J; Koo P H
Identifier
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n/a
Format
The file format, physical medium, or dimensions of the resource
Journal Article or Conference Abstract Publication
1997
Biochemistry & Molecular Biology
Cell Biology
Faseb Journal
Hu Y Q
Journal Article or Conference Abstract Publication
Koo P H
Lee P G
Liebl D J
Life Sciences & Biomedicine - Other
Topics
-
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
872–883
Issue
6
Volume
57
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 alpha(2)-macroglobulin inhibits NGF-promoted neurite outgrowth, TrK phosphorylation, and gene expression of pheochromocytoma PC12 cells.
Publisher
An entity responsible for making the resource available
Journal of neuroscience research
Date
A point or period of time associated with an event in the lifecycle of the resource
1999
1999-09
Subject
The topic of the resource
Animals; Rats; Gene Expression Regulation; Phosphorylation; PC12 Cells; Proto-Oncogene Proteins c-jun/genetics; Adrenal Gland Neoplasms/metabolism; alpha-Macroglobulins/*pharmacology; Nerve Growth Factors/*antagonists & inhibitors; Neurites/*drug effects; Pheochromocytoma/metabolism; Sprague-Dawley; Receptor; Neoplastic/*drug effects; trkA/*metabolism
Creator
An entity primarily responsible for making the resource
Lee P G; Koo P H
Description
An account of the resource
Rat alpha-1-macroglobulin (alpha(1)M) and alpha-2-macroglobulin (alpha(2)M) are murine homologs of human alpha(2)M, and rat alpha(2)M is generally known as an acute-phase protein. Monoamine-activated forms of human alpha(2)M have been shown to inhibit various neuronal functions, but the effect of rat alpha(1)M and acute-phase alpha(2)M on neurons is largely unknown. In this report, rat serotonin-activated alpha(2)M (5HT-alpha(2)M) has been demonstrated to inhibit nerve growth factor (NGF)-promoted neurite extension in pheochromocytoma PC12 cells, and we investigated its possible mechanism of action including its effect on NGF-promoted signal transduction and gene expression in these cells. Especially in the absence of NGF, 5HT-alpha(2)M was found to bind to TrkA (the high-affinity receptor for NGF) much better than normal alpha(2)M (N-alpha(2)M).
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).
1999
Adrenal Gland Neoplasms/metabolism
alpha-Macroglobulins/*pharmacology
Animals
Gene Expression Regulation
Journal of neuroscience research
Koo P H
Lee P G
Neoplastic/*drug effects
Nerve Growth Factors/*antagonists & inhibitors
Neurites/*drug effects
PC12 Cells
Pheochromocytoma/metabolism
Phosphorylation
Proto-Oncogene Proteins c-jun/genetics
Rats
Receptor
Sprague-Dawley
trkA/*metabolism