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/10.1152/jn.1996.76.5.3038" target="_blank" rel="noreferrer noopener">http://doi.org/10.1152/jn.1996.76.5.3038</a>
Pages
3038–3047
Issue
5
Volume
76
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
Two forms of long-term potentiation in area CA1 activate different signal transduction cascades.
Publisher
An entity responsible for making the resource available
Journal of neurophysiology
Date
A point or period of time associated with an event in the lifecycle of the resource
1996
1996-11
Subject
The topic of the resource
Animals; Hippocampus/drug effects/*physiology; Long-Term Potentiation/drug effects/*physiology; Nifedipine/pharmacology; Rats; Signal Transduction/drug effects/*physiology
Creator
An entity primarily responsible for making the resource
Cavus I; Teyler T
Description
An account of the resource
1. The effects of protein kinase inhibitors on N-methyl-D-aspartate (NMDA)-receptor-mediated, voltage-dependent calcium channel (VDCC)-mediated, and
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1152/jn.1996.76.5.3038" target="_blank" rel="noreferrer noopener">10.1152/jn.1996.76.5.3038</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).
1996
Animals
Cavus I
Hippocampus/drug effects/*physiology
Journal of neurophysiology
Long-Term Potentiation/drug effects/*physiology
Nifedipine/pharmacology
Rats
Signal Transduction/drug effects/*physiology
Teyler T
-
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.
URL Address
<a href="http://doi.org/10.1016/j.expneurol.2017.06.020" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.expneurol.2017.06.020</a>
Pages
1–15
Volume
296
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
Injury-induced gp130 cytokine signaling in peripheral ganglia is reduced in diabetes mellitus.
Publisher
An entity responsible for making the resource available
Experimental neurology
Date
A point or period of time associated with an event in the lifecycle of the resource
2017
2017-10
Subject
The topic of the resource
*Axon regeneration; *Axotomy; *Diabetes; *Neuropathy; *Peripheral nervous system; Animal; Animals; Antibiotics; Antineoplastic/toxicity; Blood Glucose/drug effects; Body Weight/drug effects; Cytokine Receptor gp130/genetics/*metabolism; Cytokines/metabolism; Diabetes Mellitus; Disease Models; Experimental/chemically induced/complications/*pathology; Fasting/blood; Gene Expression Regulation/*physiology; Hyperalgesia/etiology; Hyperglycemia/etiology; Inbred C57BL; Male; Mice; Nerve Degeneration/*etiology/pathology; Nerve Tissue Proteins/metabolism; Pain Measurement; Signal Transduction/drug effects/*physiology; Streptozocin/toxicity; Superior Cervical Ganglion/drug effects/*metabolism; Sweating/drug effects
Creator
An entity primarily responsible for making the resource
Niemi Jon P; Filous Angela R; DeFrancesco Alicia; Lindborg Jane A; Malhotra Nisha A; Wilson Gina N; Zhou Bowen; Crish Samuel D; Zigmond Richard E
Description
An account of the resource
Neuropathy is a major diabetic complication. While the mechanism of this neuropathy is not well understood, it is believed to result in part from deficient nerve regeneration. Work from our laboratory established that gp130 family of cytokines are induced in animals after axonal injury and are involved in the induction of regeneration-associated genes (RAGs) and in the conditioning lesion response. Here, we examine whether a reduction of cytokine signaling occurs in diabetes. Streptozotocin (STZ) was used to destroy pancreatic beta cells, leading to chronic hyperglycemia. Mice were injected with either low doses of STZ (5x60mg/kg) or a single high dose (1x200mg/kg) and examined after three or one month, respectively. Both low and high dose STZ treatment resulted in sustained hyperglycemia and functional deficits associated with the presence of both sensory and autonomic neuropathy. Diabetic mice displayed significantly reduced intraepidermal nerve fiber density and sudomotor function. Furthermore, low and high dose diabetic mice showed significantly reduced tactile touch sensation measured with Von Frey monofilaments. To look at the regenerative and injury-induced responses in diabetic mice, neurons in both superior cervical ganglia (SCG) and the 4th and 5th lumbar dorsal root ganglia (DRG) were unilaterally axotomized. Both high and low dose diabetic mice displayed significantly less axonal regeneration in the sciatic nerve, when measured in vivo, 48h after crush injury. Significantly reduced induction of two gp130 cytokines, leukemia inhibitory factor and interleukin-6, occurred in diabetic animals in SCG 6h after injury compared to controls. Injury-induced expression of interleukin-6 was also found to be significantly reduced in the DRG at 6h after injury in low and high dose diabetic mice. These effects were accompanied by reduced phosphorylation of signal transducer and activator of transcription 3 (STAT3), a downstream effector of the gp130 signaling pathway. We also found decreased induction of several gp130-dependent RAGs, including galanin and vasoactive intestinal peptide. Together, these data suggest a novel mechanism for the decreased response of diabetic sympathetic and sensory neurons to injury.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.expneurol.2017.06.020" target="_blank" rel="noreferrer noopener">10.1016/j.expneurol.2017.06.020</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).
*Axon regeneration
*Axotomy
*Diabetes
*Neuropathy
*Peripheral nervous system
2017
Animal
Animals
Antibiotics
Antineoplastic/toxicity
Blood Glucose/drug effects
Body Weight/drug effects
Crish Samuel D
Cytokine Receptor gp130/genetics/*metabolism
Cytokines/metabolism
DeFrancesco Alicia
Department of Pharmaceutical Sciences
Diabetes Mellitus
Disease Models
Experimental neurology
Experimental/chemically induced/complications/*pathology
Fasting/blood
Filous Angela R
Gene Expression Regulation/*physiology
Hyperalgesia/etiology
Hyperglycemia/etiology
Inbred C57BL
Lindborg Jane A
Male
Malhotra Nisha A
Mice
NEOMED College of Pharmacy
Nerve Degeneration/*etiology/pathology
Nerve Tissue Proteins/metabolism
Niemi Jon P
Pain Measurement
Signal Transduction/drug effects/*physiology
Streptozocin/toxicity
Superior Cervical Ganglion/drug effects/*metabolism
Sweating/drug effects
Wilson Gina N
Zhou Bowen
Zigmond Richard E
-
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
213–220
Issue
1
Volume
71
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 phosphorylation of TrkB and TrkC and their signal transduction by alpha2-macroglobulin.
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
1998
1998-07
Subject
The topic of the resource
Humans; Animals; Mice; Signal Transduction/drug effects/*physiology; Phosphorylation; Mitogen-Activated Protein Kinase 1/metabolism; Antineoplastic Agents/pharmacology; Type C Phospholipases/metabolism; Cell Differentiation/drug effects; Neuroprotective Agents/*metabolism; Neuroblastoma; alpha-Macroglobulins/*pharmacology; *Mitogen-Activated Protein Kinases; 3T3 Cells/chemistry/cytology/enzymology; Brain-Derived Neurotrophic Factor/pharmacology; Calcium-Calmodulin-Dependent Protein Kinases/metabolism; Isoenzymes/metabolism; Mitogen-Activated Protein Kinase 3; Nerve Growth Factors/pharmacology; Neurotrophin 3; Phospholipase C gamma; Receptor Protein-Tyrosine Kinases/*metabolism; Serotonin/metabolism; Tretinoin/pharmacology; Ciliary Neurotrophic Factor; Receptors; Receptor; Tumor Cells; Cultured/chemistry/cytology/enzymology; Nerve Growth Factor/*metabolism; trkC
Creator
An entity primarily responsible for making the resource
Hu Y Q; Koo P H
Description
An account of the resource
Monoamine-activated alpha2-macroglobulin (alpha2M) was shown to reduce the dopamine concentration in corpus striatum of adult rat brains and inhibit other neuronal functions in vivo and in vitro. As brain-derived neurotrophic factor, neurotrophin-4, and neurotrophin-3 are important neurotrophic factors for dopaminergic neurons, the effect of monoamine-activated alpha2M on signal transduction by trkB and trkC was investigated. The results show that monoamine-activated alpha2M binds to trkB and inhibits brain-derived neurotrophic factor/neurotrophin-4-promoted autophosphorylation of trkB in a dose-dependent manner in both trkB-expressing NIH3T3 (NIH3T3-trkB) and human neuroblastoma
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).
*Mitogen-Activated Protein Kinases
1998
3T3 Cells/chemistry/cytology/enzymology
alpha-Macroglobulins/*pharmacology
Animals
Antineoplastic Agents/pharmacology
Brain-Derived Neurotrophic Factor/pharmacology
Calcium-Calmodulin-Dependent Protein Kinases/metabolism
Cell Differentiation/drug effects
Ciliary Neurotrophic Factor
Cultured/chemistry/cytology/enzymology
Hu Y Q
Humans
Isoenzymes/metabolism
Journal of neurochemistry
Koo P H
Mice
Mitogen-Activated Protein Kinase 1/metabolism
Mitogen-Activated Protein Kinase 3
Nerve Growth Factor/*metabolism
Nerve Growth Factors/pharmacology
Neuroblastoma
Neuroprotective Agents/*metabolism
Neurotrophin 3
Phospholipase C gamma
Phosphorylation
Receptor
Receptor Protein-Tyrosine Kinases/*metabolism
Receptors
Serotonin/metabolism
Signal Transduction/drug effects/*physiology
Tretinoin/pharmacology
trkC
Tumor Cells
Type C Phospholipases/metabolism