INT231300

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Context Info
Confidence 0.39
First Reported 2008
Last Reported 2008
Negated 1
Speculated 0
Reported most in Body
Documents 1
Total Number 1
Disease Relevance 0.16
Pain Relevance 0.05

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

plasma membrane (Grin2b, Prnp) transport (Grin2b) Golgi apparatus (Prnp)
endoplasmic reticulum (Prnp) embryo development (Grin2b) cytoplasm (Prnp)
Grin2b (Mus musculus)
Prnp (Mus musculus)
Pain Link Frequency Relevance Heat
agonist 3 92.56 High High
tetrodotoxin 6 30.84 Quite Low
Glutamate 9 5.00 Very Low Very Low Very Low
imagery 6 5.00 Very Low Very Low Very Low
Neuronal excitability 5 5.00 Very Low Very Low Very Low
Hippocampus 5 5.00 Very Low Very Low Very Low
GABAergic 4 5.00 Very Low Very Low Very Low
antagonist 3 5.00 Very Low Very Low Very Low
hyperexcitability 2 5.00 Very Low Very Low Very Low
ketamine 2 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Targeted Disruption 10 99.78 Very High Very High Very High
Death 13 5.00 Very Low Very Low Very Low
Prion Diseases 6 5.00 Very Low Very Low Very Low
Toxicity 4 5.00 Very Low Very Low Very Low
Convulsion 4 5.00 Very Low Very Low Very Low
Stroke 4 5.00 Very Low Very Low Very Low
Myelodysplastic Syndromes 3 5.00 Very Low Very Low Very Low
Scrapie 3 5.00 Very Low Very Low Very Low
Disease 3 5.00 Very Low Very Low Very Low
Sprains And Strains 2 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Collectively, these data are consistent with an NMDAR hyperfunction upon knockout of native PrPC, which is not caused by an augmentation of NR2B-containing receptors.
Positive_regulation (augmentation) of NR2B-containing Neg (not) Positive_regulation (caused) of PrPC associated with targeted disruption
1) Confidence 0.39 Published 2008 Journal The Journal of Cell Biology Section Body Doc Link PMC2364707 Disease Relevance 0.16 Pain Relevance 0.05

General Comments

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