INT196756

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Context Info
Confidence 0.01
First Reported 2006
Last Reported 2006
Negated 0
Speculated 0
Reported most in Body
Documents 1
Total Number 2
Disease Relevance 0
Pain Relevance 0.47

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

phosphatase activity (Phospho1) cellular_component (Phospho1) biological_process (Phospho1)
Phospho1 (Mus musculus)
Pain Link Frequency Relevance Heat
Dopamine 238 99.98 Very High Very High Very High
Calcium channel 4 99.74 Very High Very High Very High
Action potential 8 61.92 Quite High
agonist 2 34.76 Quite Low
Glutamate 62 5.00 Very Low Very Low Very Low
long-term potentiation 16 5.00 Very Low Very Low Very Low
projection neuron 8 5.00 Very Low Very Low Very Low
Neurotransmitter 6 5.00 Very Low Very Low Very Low
imagery 6 5.00 Very Low Very Low Very Low
nMDA receptor 4 5.00 Very Low Very Low Very Low

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Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Figure 6D shows that now calcium alone (blue lines) produces a decrease in both PKAc and phosphoThr34 (qualitatively similar to that observed with the feedback loop eliminated), and calcium paired with dopamine inhibits the production of PKAc and phosphoThr34 (red lines), again similar to that observed with the feedback loop eliminated.
Negative_regulation (inhibits) of Gene_expression (production) of phosphoThr34 associated with dopamine
1) Confidence 0.01 Published 2006 Journal PLoS Computational Biology Section Body Doc Link PMC1562452 Disease Relevance 0 Pain Relevance 0.27
A sustained increase in intracellular calcium concentration, as results from prolonged activation of NMDA or voltage-dependent calcium channels, leads to a decrease in the levels of phosphoThr34.
Negative_regulation (decrease) of Gene_expression (levels) of phosphoThr34 associated with calcium channel
2) Confidence 0.01 Published 2006 Journal PLoS Computational Biology Section Body Doc Link PMC1562452 Disease Relevance 0 Pain Relevance 0.20

General Comments

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