INT251602

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Context Info
Confidence 0.25
First Reported 2008
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 2
Total Number 2
Disease Relevance 0.05
Pain Relevance 1.34

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

transport (Grin1) plasma membrane (Grin1) enzyme binding (Grin1)
cytoplasm (Grin1)
Grin1 (Mus musculus)
Pain Link Frequency Relevance Heat
opioid receptor 84 99.80 Very High Very High Very High
tolerance 28 99.64 Very High Very High Very High
Glutamate 39 98.40 Very High Very High Very High
Kinase C 39 97.12 Very High Very High Very High
analgesia 4 90.64 High High
Morphine 77 90.24 High High
Analgesic 19 70.60 Quite High
Periaqueductal grey 18 50.60 Quite High
Opioid 14 50.00 Quite Low
imagery 6 49.24 Quite Low
Disease Link Frequency Relevance Heat
Urological Neuroanatomy 18 50.60 Quite High
Sprains And Strains 4 21.48 Low Low
Disease 56 12.76 Low Low
Nociception 7 5.00 Very Low Very Low Very Low
Apoptosis 7 5.00 Very Low Very Low Very Low
Toxicity 4 5.00 Very Low Very Low Very Low
Myelodysplastic Syndromes 4 5.00 Very Low Very Low Very Low
Pain 3 5.00 Very Low Very Low Very Low
Targeted Disruption 3 5.00 Very Low Very Low Very Low
Death 2 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Upon inhibition of these early processes (e.g., Akt or nNOS), the subsequent steps responsible for NMDAR sustained potentiation and MOR tolerance do not occur.
Regulation (responsible) of NMDAR Binding (potentiation) of associated with tolerance and opioid receptor
1) Confidence 0.25 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2890584 Disease Relevance 0.05 Pain Relevance 1.16
Electrophysiology for NMDAR and voltage-gated Ca2+ channels
Regulation (Electrophysiology) of NMDAR Binding (voltage) of
2) Confidence 0.06 Published 2008 Journal Mol Neurodegener Section Body Doc Link PMC2577671 Disease Relevance 0 Pain Relevance 0.18

General Comments

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