INT215519

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Context Info
Confidence 0.86
First Reported 2007
Last Reported 2007
Negated 0
Speculated 0
Reported most in Body
Documents 1
Total Number 2
Disease Relevance 0.39
Pain Relevance 0.69

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

nucleus (Trim33) intracellular (Trim33) DNA binding (Trim33)
ligase activity (Trim33)
Trim33 (Mus musculus)
Pain Link Frequency Relevance Heat
adenocard 82 98.36 Very High Very High Very High
agonist 24 97.12 Very High Very High Very High
Glutamate 64 94.92 High High
antagonist 14 90.48 High High
Dopamine 2 54.80 Quite High
Peripheral nervous system 4 32.80 Quite Low
tetrodotoxin 6 5.00 Very Low Very Low Very Low
Glutamate receptor 6 5.00 Very Low Very Low Very Low
ischemia 4 5.00 Very Low Very Low Very Low
imagery 4 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Pressure And Volume Under Development 52 93.64 High High
Stress 16 83.68 Quite High
Ganglion Cysts 20 67.56 Quite High
Retina Disease 10 5.00 Very Low Very Low Very Low
Targeted Disruption 8 5.00 Very Low Very Low Very Low
Cv Unclassified Under Development 2 5.00 Very Low Very Low Very Low
Ocular Hypertension 2 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
However, it is unclear whether Müller cells also express ectoenzymes that degrade ATP, such as nucleoside triphosphate diphosphohydrolases (NTPDases) or ectonucleotide pyrophosphatase/phosphodiesterases (ENPPs).
Protein_catabolism (degrade) of ecto
1) Confidence 0.86 Published 2007 Journal Purinergic Signal Section Body Doc Link PMC2072913 Disease Relevance 0.23 Pain Relevance 0.09
By rapid degradation, ectonucleotidases are suggested to limit the actions of purinergic receptor agonists.
Protein_catabolism (degradation) of ecto associated with agonist
2) Confidence 0.64 Published 2007 Journal Purinergic Signal Section Body Doc Link PMC2072913 Disease Relevance 0.15 Pain Relevance 0.60

General Comments

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