1
40
3
-
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/10.1002/(SICI)1097-4547(19960201)43:3%3C282::AID-JNR3%3E3.0.CO;2-F" target="_blank" rel="noreferrer noopener">http://doi.org/10.1002/(SICI)1097-4547(19960201)43:3%3C282::AID-JNR3%3E3.0.CO;2-F</a>
Pages
282–288
Issue
3
Volume
43
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
Inhibition of long-term potentiation development in rat hippocampal slice by alpha 2-macroglobulin, an acute-phase protein in the brain.
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
1996
1996-02
Subject
The topic of the resource
alpha-Macroglobulins/*pharmacology; Animals; Electric Stimulation; Hippocampus/drug effects/*physiology; Humans; In Vitro Techniques; Long-Term Potentiation/*drug effects; Methylamines/pharmacology; Neurites/drug effects/*physiology; Pyramidal Cells/drug effects/physiology; Rats; Synapses/drug effects/physiology; Synaptic Transmission/drug effects; Time Factors
Creator
An entity primarily responsible for making the resource
Cavus I; Koo P H; Teyler T J
Description
An account of the resource
Alpha-2-macroglobulin (alpha 2M) in the rat and human brain is an acute-phase protein synthesized primarily by astrocytes, and it has been implicated in Alzheimer's disease and other neuropathological processes. The activated forms of alpha 2M, but not the native form, can suppress the neurite outgrowth of the central neurons, presumably through binding to neurotrophic factors and through direct inhibition of neurotrophic factor receptor signal transduction. Since neurotrophic factors are known to be involved in synaptic plasticity, we tested the effect of both the native and methylamine-activated (MA-alpha 2M) forms of alpha 2M on long-term potentiation (LTP) in area CA1 of adult rat hippocampal slice. Neither native alpha 2M nor MA-alpha 2M had an effect on baseline synaptic transmission. LTP induced by 200-Hz trains in the presence of 1.4 microM or 0.14 microM native alpha 2M was indistinguishable from control LTP. Although the presence of MA-alpha 2M at the same concentrations did not interfere with LTP induction, the development and maintenance of potentiation was blocked in a concentration-dependent time course. Results of this study indicate that the accumulation and activation of alpha 2M with inflammatory neuropathologies such as Alzheimer's disease can inhibit synaptic plasticity, which might partly account for the memory deficits seen in these patients.
Identifier
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<a href="http://doi.org/10.1002/(SICI)1097-4547(19960201)43:3%3C282::AID-JNR3%3E3.0.CO;2-F" target="_blank" rel="noreferrer noopener">10.1002/(SICI)1097-4547(19960201)43:3%3C282::AID-JNR3%3E3.0.CO;2-F</a>
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).
1996
alpha-Macroglobulins/*pharmacology
Animals
Cavus I
Electric Stimulation
Hippocampus/drug effects/*physiology
Humans
In Vitro Techniques
Journal of neuroscience research
Koo P H
Long-Term Potentiation/*drug effects
Methylamines/pharmacology
Neurites/drug effects/*physiology
Pyramidal Cells/drug effects/physiology
Rats
Synapses/drug effects/physiology
Synaptic Transmission/drug effects
Teyler T J
Time Factors
-
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
5369–5376
Issue
7
Volume
269
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
Monoamine-activated alpha 2-macroglobulin binds trk receptor and inhibits nerve growth factor-stimulated trk phosphorylation and signal transduction.
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
1994
1994-02
Subject
The topic of the resource
Humans; Male; Animals; Mice; Signal Transduction/drug effects/*physiology; Phosphorylation; PC12 Cells; Protein-Serine-Threonine Kinases/metabolism; Neurites/drug effects/*physiology; Nerve Growth Factors/*pharmacology; Adrenal Gland Neoplasms; alpha-Macroglobulins/isolation & purification/*metabolism/pharmacology; ErbB Receptors/isolation & purification/metabolism; Fibrinolysin/metabolism; Mitogen-Activated Protein Kinase 1; Pheochromocytoma; Protein-Tyrosine Kinases/metabolism; Proto-Oncogene Proteins/drug effects/isolation & purification/*metabolism; Receptor Protein-Tyrosine Kinases/drug effects/isolation & purification/*metabolism; Serotonin/*metabolism/pharmacology; Receptors; Receptor; Nerve Growth Factor/drug effects/isolation & purification/*metabolism; Platelet-Derived Growth Factor/isolation & purification/metabolism; trkA
Creator
An entity primarily responsible for making the resource
Koo P H; Qiu W S
Description
An account of the resource
Monoamine-activated alpha 2-macroglobulin (alpha 2M) has been shown to inhibit beta-nerve growth factor (NGF)-promoted neurite outgrowth and the survival of embryonic sensory and forebrain neurons, whereas normal alpha 2M has little or no such activity. The objective of this study is to elucidate the mechanism of inhibition by monoamine-activated alpha 2M. Methylamine-activated alpha 2M (MA-alpha 2M) and serotonin-activated alpha 2M (5HT-alpha 2M) dose dependently inhibit NGF-promoted neurite outgrowth of the pheochromocytoma PC12 cell and its subline PC12(6-24) which overexpresses human trk protooncogene product, but have no effect on their viability, and this inhibition can be blocked by high concentrations of NGF. The binding of MA-alpha 2M to trk, which is a part of high-affinity NGF receptor, was studied with PC12(6-24) cells and NIH-3T3 fibroblasts expressing trk (trk-3T3). In each case MA-alpha 2M readily forms stable complexes with trk in vivo, whereas normal alpha 2M does not. Both
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).
1994
Adrenal Gland Neoplasms
alpha-Macroglobulins/isolation & purification/*metabolism/pharmacology
Animals
ErbB Receptors/isolation & purification/metabolism
Fibrinolysin/metabolism
Humans
Koo P H
Male
Mice
Mitogen-Activated Protein Kinase 1
Nerve Growth Factor/drug effects/isolation & purification/*metabolism
Nerve Growth Factors/*pharmacology
Neurites/drug effects/*physiology
PC12 Cells
Pheochromocytoma
Phosphorylation
Platelet-Derived Growth Factor/isolation & purification/metabolism
Protein-Serine-Threonine Kinases/metabolism
Protein-Tyrosine Kinases/metabolism
Proto-Oncogene Proteins/drug effects/isolation & purification/*metabolism
Qiu W S
Receptor
Receptor Protein-Tyrosine Kinases/drug effects/isolation & purification/*metabolism
Receptors
Serotonin/*metabolism/pharmacology
Signal Transduction/drug effects/*physiology
The Journal of biological chemistry
trkA
-
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