INT196740

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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 8
Disease Relevance 0
Pain Relevance 2.09

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
Calcium channel 16 99.74 Very High Very High Very High
Dopamine 952 97.92 Very High Very High Very High
Glutamate 248 90.72 High High
projection neuron 32 89.04 High High
imagery 24 88.40 High High
nMDA receptor 16 84.80 Quite High
Action potential 32 83.36 Quite High
long-term potentiation 64 73.40 Quite High
dopamine receptor 16 55.96 Quite High
gABA 8 36.96 Quite Low

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Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Furthermore, calcium stimulation alone will reduce both PKAc and phosphoThr34.
Negative_regulation (reduce) of phosphoThr34
1) Confidence 0.01 Published 2006 Journal PLoS Computational Biology Section Body Doc Link PMC1562452 Disease Relevance 0 Pain Relevance 0.20
A persistent calcium elevation has a minimal effect on PKAc and decreases phosphoThr34, whereas a brief transient calcium elevation produces an increase in both PKAc and phosphoThr34.
Negative_regulation (decreases) of phosphoThr34
2) Confidence 0.01 Published 2006 Journal PLoS Computational Biology Section Body Doc Link PMC1562452 Disease Relevance 0 Pain Relevance 0.80
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 (decrease) of phosphoThr34 associated with dopamine
3) Confidence 0.01 Published 2006 Journal PLoS Computational Biology Section Body Doc Link PMC1562452 Disease Relevance 0 Pain Relevance 0.23
The model is based on published biochemical data: the simulated regulation of DARPP-32 phosphorylation by sustained G-protein receptor activation and calcium influx fits experimental data, increasing and decreasing phosphoThr34, respectively (Figures 2 and 3).
Negative_regulation (decreasing) of phosphoThr34
4) Confidence 0.01 Published 2006 Journal PLoS Computational Biology Section Body Doc Link PMC1562452 Disease Relevance 0 Pain Relevance 0.17
This may explain observations that activation of D2 receptors decreases phosphoThr34 and decreases the phosphorylation of PP1 substrates [21,64].
Negative_regulation (decreases) of phosphoThr34
5) Confidence 0.01 Published 2006 Journal PLoS Computational Biology Section Body Doc Link PMC1562452 Disease Relevance 0 Pain Relevance 0.14
In addition, the buildup of phosphoThr34 is decreased (Figure 7B).
Negative_regulation (decreased) of phosphoThr34
6) Confidence 0.01 Published 2006 Journal PLoS Computational Biology Section Body Doc Link PMC1562452 Disease Relevance 0 Pain Relevance 0.17
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 phosphoThr34 associated with calcium channel
7) Confidence 0.01 Published 2006 Journal PLoS Computational Biology Section Body Doc Link PMC1562452 Disease Relevance 0 Pain Relevance 0.20
The decrease in phosphoThr34 caused by elevated calcium is due to PP2B both in the model (Figure 3, dashed lines) and experimentally.
Negative_regulation (decrease) of phosphoThr34
8) Confidence 0.01 Published 2006 Journal PLoS Computational Biology Section Body Doc Link PMC1562452 Disease Relevance 0 Pain Relevance 0.19

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