INT55038

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Context Info
Confidence 0.77
First Reported 1994
Last Reported 2010
Negated 2
Speculated 0
Reported most in Body
Documents 10
Total Number 41
Disease Relevance 28.79
Pain Relevance 9.80

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

lyase activity (Adcy8)
Anatomy Link Frequency
forebrain 11
hippocampus 2
insular cortex 1
nerve 1
neurons 1
Adcy8 (Mus musculus)
Pain Link Frequency Relevance Heat
nMDA receptor 46 100.00 Very High Very High Very High
Pain 180 99.80 Very High Very High Very High
Eae 178 99.68 Very High Very High Very High
Anterior cingulate cortex 132 99.68 Very High Very High Very High
Hippocampus 891 99.40 Very High Very High Very High
Inflammation 49 99.32 Very High Very High Very High
allodynia 65 99.04 Very High Very High Very High
Glutamate 21 99.00 Very High Very High Very High
withdrawal 10 98.92 Very High Very High Very High
Thalamus 65 98.88 Very High Very High Very High
Disease Link Frequency Relevance Heat
Cognitive Disorder 258 99.84 Very High Very High Very High
Targeted Disruption 3149 99.80 Very High Very High Very High
Myalgia 29 99.80 Very High Very High Very High
Nervous System Injury 20 99.60 Very High Very High Very High
INFLAMMATION 53 99.32 Very High Very High Very High
Pain 243 99.08 Very High Very High Very High
Anxiety Disorder 2104 99.06 Very High Very High Very High
Neuropathic Pain 99 99.04 Very High Very High Very High
Death 2 98.58 Very High Very High Very High
Nociception 39 98.38 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
We used a doxycycline-regulated system (e.g. tetracycline-off system) to restore AC8 expression in a temporally regulated fashion.
Gene_expression (expression) of AC8
1) Confidence 0.77 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2954788 Disease Relevance 0.70 Pain Relevance 0.31
To evaluate the role of Ca2+-stimulated AC activity during short-term memory, we restored AC8 expression during novel object recognition and compared our results with DKO and WT mice.
Gene_expression (expression) of AC8 associated with targeted disruption, cognitive disorder and eae
2) Confidence 0.77 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2954788 Disease Relevance 0.94 Pain Relevance 0.05
We find that AC8 expression begins to turn on two weeks after taking mice off doxycycline, and conversely, AC8 expression is turned off completely after 2 wk on doxycycline (Fig. 5B).
Gene_expression (expression) of AC8
3) Confidence 0.77 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2954788 Disease Relevance 0.48 Pain Relevance 0.27
To functionally test the temporal role of AC activity during CF learning, we restored Ca2+-stimulated AC function at different time points during behavioral testing with a transgenic model of AC8 expression.
Gene_expression (expression) of AC8 associated with targeted disruption and anxiety disorder
4) Confidence 0.77 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2954788 Disease Relevance 0.79 Pain Relevance 0.28
Importantly, AC8 rescue mice on doxycycline show no Ca2+-stimulated AC activity, confirming that doxycycline efficiently represses AC8 transgene expression.


Gene_expression (expression) of AC8 transgene
5) Confidence 0.77 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2954788 Disease Relevance 0.37 Pain Relevance 0.17
Doxycycline was given or removed for at least 2 wk, in most cases a month, in between testing to allow for AC8 expression to be turned on or off effectively.


Gene_expression (expression) of AC8
6) Confidence 0.77 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2954788 Disease Relevance 0.74 Pain Relevance 0.05
After confirming that our AC8 rescue system was able to restore AC8 expression and activity to the forebrain, we turned AC8 activity on and off at different time points throughout CF testing.
Gene_expression (expression) of AC8 in forebrain associated with anxiety disorder
7) Confidence 0.77 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2954788 Disease Relevance 0.35 Pain Relevance 0.16
To confirm that the founder lines were capable of inducible AC8 cDNA expression, they were mated with tTAluc mice [22], which express tTA in many tissues with no detectable endogenous AC8 expression, allowing us to establish that the transgene was expressed (data not shown).
Neg (no) Gene_expression (expression) of AC8
8) Confidence 0.77 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2954788 Disease Relevance 0.29 Pain Relevance 0
Restoration of AC8 expression in the forebrain of DKO mice elicits a response comparable to WT mice.
Gene_expression (expression) of AC8 in forebrain associated with targeted disruption
9) Confidence 0.77 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2954788 Disease Relevance 0.98 Pain Relevance 0.05
To confirm that the founder lines were capable of inducible AC8 cDNA expression, they were mated with tTAluc mice [22], which express tTA in many tissues with no detectable endogenous AC8 expression, allowing us to establish that the transgene was expressed (data not shown).
Gene_expression (expression) of AC8
10) Confidence 0.77 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2954788 Disease Relevance 0.29 Pain Relevance 0
To investigate if Ca2+-stimulated AC activity was needed just for retrieval, rather than retention, we turned AC8 expression on again and tested mice two weeks later (1.5 mo after training).
Gene_expression (expression) of AC8
11) Confidence 0.77 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2954788 Disease Relevance 0.57 Pain Relevance 0.03
Once inducible expression of the AC8 cDNA was established, mice were mated with CaMKII-tTA mice (CaMKII-tTA mice from Jackson Laboratories) [23], which have tTA under control of the CaMKII forebrain-specific promoter.
Gene_expression (expression) of AC8 in forebrain
12) Confidence 0.77 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2954788 Disease Relevance 0.34 Pain Relevance 0
We find that AC8 expression begins to turn on two weeks after taking mice off doxycycline, and conversely, AC8 expression is turned off completely after 2 wk on doxycycline (Fig. 5B).
Gene_expression (expression) of AC8
13) Confidence 0.77 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2954788 Disease Relevance 0.50 Pain Relevance 0.27
Additionally, we recapitulate the novel object recognition data with DKO mice showing impairments, but also provide evidence that memory can be restored if AC8 expression is turned on in the forebrain before training.
Gene_expression (expression) of AC8 in forebrain associated with targeted disruption, cognitive disorder and eae
14) Confidence 0.77 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2954788 Disease Relevance 1.08 Pain Relevance 0.08
To produce forebrain-specific, inducible AC8 expression mice (AC8 rescue) on a DKO background, a tetracycline-off system was used to allow for temporal control over AC8 cDNA expression.
Gene_expression (expression) of AC8 in forebrain associated with targeted disruption
15) Confidence 0.77 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2954788 Disease Relevance 0.37 Pain Relevance 0
We generated a system where AC8 is expressed in the forebrain of mice on a DKO background (AC8 rescue mice).
Gene_expression (expressed) of AC8 in forebrain associated with targeted disruption
16) Confidence 0.77 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2954788 Disease Relevance 0.78 Pain Relevance 0.28
Our data support these findings as AC8 rescue mice that have AC8 turned off during the consolidation CF training period show memory impairment, while AC8 transgene expression throughout training and testing restores long-term conditioned responses.
Gene_expression (expression) of AC8 transgene associated with cognitive disorder and anxiety disorder
17) Confidence 0.77 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2954788 Disease Relevance 1.24 Pain Relevance 0.09
Suggesting that Ca2+-stimulated AC activity is necessary during memory retention, we found that AC8 expression for two weeks after the 1 mo testing session was unable to rescue CF memory at 1.5 mo (Fig. 6D).
Gene_expression (expression) of AC8 associated with anxiety disorder
18) Confidence 0.77 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2954788 Disease Relevance 0.65 Pain Relevance 0.03
Although expression of AC8 protein in the AC8 rescue mice appears higher than what is present endogenously within the WT mice (Fig. 5A), we found that that overall Ca2+-stimulated AC activity was recovered to approximately 50% and 30% of WT levels in the cortex (Fig. 5C) and hippocampus (Fig. 5D), respectively.
Gene_expression (expression) of AC8 in hippocampus associated with hippocampus
19) Confidence 0.77 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2954788 Disease Relevance 0.39 Pain Relevance 0.22
AC1 and AC8 are highly expressed in the anterior cingulate cortex (ACC), and contribute to inflammation-induced activation of CREB.
Gene_expression (expressed) of AC8 in cingulate cortex associated with inflammation and anterior cingulate cortex
20) Confidence 0.76 Published 2002 Journal Neuron Section Abstract Doc Link 12441059 Disease Relevance 0.74 Pain Relevance 0.62

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