INT257200

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Context Info
Confidence 0.25
First Reported 2008
Last Reported 2008
Negated 0
Speculated 0
Reported most in Body
Documents 1
Total Number 3
Disease Relevance 0
Pain Relevance 0.94

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

cytosol (Pde5a) signal transduction (Pde5a)
Anatomy Link Frequency
intermediary 1
spike 1
Pde5a (Mus musculus)
Pain Link Frequency Relevance Heat
Action potential 27 98.50 Very High Very High Very High
gABA 21 97.24 Very High Very High Very High
Neurotransmitter 33 96.96 Very High Very High Very High
medulla 6 88.08 High High
tetrodotoxin 9 68.32 Quite High
GABAergic 45 66.40 Quite High
nMDA receptor 81 5.00 Very Low Very Low Very Low
Central nervous system 45 5.00 Very Low Very Low Very Low
long-term potentiation 39 5.00 Very Low Very Low Very Low
Serotonin 33 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Ganglion Cysts 9 10.36 Low Low
Depression 33 5.00 Very Low Very Low Very Low
Increased Venous Pressure Under Development 12 5.00 Very Low Very Low Very Low
Injury 9 5.00 Very Low Very Low Very Low
Targeted Disruption 9 5.00 Very Low Very Low Very Low
Neurodegenerative Disease 6 5.00 Very Low Very Low Very Low
Shock 6 5.00 Very Low Very Low Very Low
Stress 6 5.00 Very Low Very Low Very Low
Cv Unclassified Under Development 6 5.00 Very Low Very Low Very Low
Demyelinating Disease 3 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Interestingly, Kv3 channels, which affect transmitter release by shaping the presynaptic action potential, have been found, when expressed in CHO cells, to be suppressed by the NO–cGMP pathway, not through direct phosphorylation by PKG but through the intermediary of a phosphatase, which probably removes a phosphate group from the channel protein that normally promotes activity (Moreno et al., 2001).
Phosphorylation (phosphorylation) of cGMP in intermediary associated with action potential
1) Confidence 0.25 Published 2008 Journal The European Journal of Neuroscience Section Body Doc Link PMC2610389 Disease Relevance 0 Pain Relevance 0.36
Specifically, stimulation of Ca2+-activated K+ channels by cGMP-dependent phosphorylation enhanced presynaptic spiking by increasing the spike afterhyperpolarization, allowing more Na+ channels to recover from inactivation which, by facilitating spike conduction, increased Ca2+influx in response to trains of stimuli (Klyachko et al., 2001).
Phosphorylation (phosphorylation) of cGMP in spike
2) Confidence 0.19 Published 2008 Journal The European Journal of Neuroscience Section Body Doc Link PMC2610389 Disease Relevance 0 Pain Relevance 0.15
Possibly, therefore, cGMP-dependent phosphorylation directly or indirectly inhibits the channels, resulting in enhanced GABA release.
Phosphorylation (phosphorylation) of cGMP associated with gaba
3) Confidence 0.19 Published 2008 Journal The European Journal of Neuroscience Section Body Doc Link PMC2610389 Disease Relevance 0 Pain Relevance 0.43

General Comments

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