INT250050

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Context Info
Confidence 0.48
First Reported 2008
Last Reported 2008
Negated 0
Speculated 0
Reported most in Body
Documents 1
Total Number 9
Disease Relevance 5.76
Pain Relevance 6.53

This is a graph with borders and nodes. Maybe there is an Imagemap used so the nodes may be linking to some Pages.

signal transduction (Gpr143) Golgi apparatus (Gpr143) plasma membrane (Gpr143)
lysosome (Gpr143) signal transducer activity (Gpr143)
Anatomy Link Frequency
neuronal 2
forebrain 1
Gpr143 (Mus musculus)
Pain Link Frequency Relevance Heat
Lasting pain 216 99.56 Very High Very High Very High
Neuronal excitability 27 98.96 Very High Very High Very High
Neurotransmitter 18 98.24 Very High Very High Very High
Anterior cingulate cortex 576 98.20 Very High Very High Very High
Pyramidal cell 108 97.92 Very High Very High Very High
nMDA receptor 45 97.44 Very High Very High Very High
Glutamate 279 97.20 Very High Very High Very High
Acute pain 27 96.72 Very High Very High Very High
IPN 99 95.96 Very High Very High Very High
Pain 63 89.92 High High
Disease Link Frequency Relevance Heat
Targeted Disruption 279 99.58 Very High Very High Very High
Pain 306 99.56 Very High Very High Very High
Inflammatory Pain 99 95.96 Very High Very High Very High
Anxiety Disorder 18 93.16 High High
INFLAMMATION 72 84.56 Quite High
Nociception 18 84.08 Quite High
Drug Dependence 9 73.80 Quite High
Depression 9 5.00 Very Low Very Low Very Low
Disseminated Intravascular Coagulation 9 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
To examine whether heterologous expression of Ap oa1 affects neuronal and synaptic properties of ACC neurons, we compared the neuronal excitability and basal synaptic transmissions in wild-type (WT) and transgenic mice.
Gene_expression (expression) of oa1 in neuronal associated with targeted disruption, neuronal excitability and anterior cingulate cortex
1) Confidence 0.48 Published 2008 Journal Mol Pain Section Body Doc Link PMC2570662 Disease Relevance 0.64 Pain Relevance 0.96
It is well known that Ap oa1 is selectively coupled to Gs protein [38] and activation of heterologous expression of Ap oa1 in HEK293 cells selectively stimulated cAMP synthesis after octopamine application [32].
Gene_expression (expression) of oa1
2) Confidence 0.48 Published 2008 Journal Mol Pain Section Body Doc Link PMC2570662 Disease Relevance 0.56 Pain Relevance 0.39
Using transgenic mice heterologously expressing Ap oa1, we could selectively activate cAMP pathway in the ACC and examine its effect in the synaptic transmission and behavior sensitization.
Gene_expression (expressing) of oa1 associated with targeted disruption and anterior cingulate cortex
3) Confidence 0.48 Published 2008 Journal Mol Pain Section Body Doc Link PMC2570662 Disease Relevance 0.65 Pain Relevance 0.78
Heterologous expression of Ap oa1 receptor in mice forebrain is not affecting either NMDA or non-NMDA receptor-mediated synaptic transmission, suggesting no endogenous activation of Ap oa1 receptor.
Gene_expression (expression) of oa1 in forebrain associated with nmda receptor
4) Confidence 0.48 Published 2008 Journal Mol Pain Section Body Doc Link PMC2570662 Disease Relevance 0.23 Pain Relevance 0.22
Consistently, we have shown here that heterologous expression of Ap oa1 receptor does not affect neuronal excitability and basal synaptic transmission.
Gene_expression (expression) of oa1 in neuronal associated with neuronal excitability
5) Confidence 0.48 Published 2008 Journal Mol Pain Section Body Doc Link PMC2570662 Disease Relevance 0.46 Pain Relevance 0.44
In order to address this question, we took advantage of a novel transgenic mouse model, heterologously expressing an Aplysia octopamine receptor (Ap oa1).
Gene_expression (expressing) of oa1 associated with targeted disruption
6) Confidence 0.37 Published 2008 Journal Mol Pain Section Abstract Doc Link PMC2570662 Disease Relevance 0.73 Pain Relevance 0.88
In the present study, we used novel transgenic mice heterologously expressing Ap oa1 receptors to examine the role of cAMP pathway in synaptic transmission and chronic pain in the ACC.
Gene_expression (expressing) of oa1 associated with targeted disruption, lasting pain and anterior cingulate cortex
7) Confidence 0.37 Published 2008 Journal Mol Pain Section Body Doc Link PMC2570662 Disease Relevance 0.76 Pain Relevance 0.85
We took advantage of transgenic mice heterologously expressing an Aplysia octopamine receptor (Ap oa1) [31].
Gene_expression (expressing) of oa1 associated with targeted disruption
8) Confidence 0.37 Published 2008 Journal Mol Pain Section Body Doc Link PMC2570662 Disease Relevance 1.02 Pain Relevance 1.04
Since Ap oa1 receptor expression is driven by CaMKII?
Gene_expression (expression) of oa1
9) Confidence 0.37 Published 2008 Journal Mol Pain Section Body Doc Link PMC2570662 Disease Relevance 0.71 Pain Relevance 0.98

General Comments

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