INT270218

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Context Info
Confidence 0.34
First Reported 2009
Last Reported 2009
Negated 0
Speculated 0
Reported most in Body
Documents 1
Total Number 1
Disease Relevance 0.63
Pain Relevance 0.85

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

Golgi apparatus (P2rx3, Pla2g4a) cytosol (Pla2g4a) aging (Pla2g4a)
endoplasmic reticulum (Pla2g4a) cytoplasmic membrane-bounded vesicle (Pla2g4a) nucleus (Pla2g4a)
Anatomy Link Frequency
neurons 1
P2rx3 (Rattus norvegicus)
Pla2g4a (Rattus norvegicus)
Pain Link Frequency Relevance Heat
dorsal root ganglion 77 99.30 Very High Very High Very High
Neuropathic pain 13 97.48 Very High Very High Very High
Sciatic nerve 1 90.68 High High
Peripheral nervous system 1 86.84 High High
Brush evoked pain 19 84.56 Quite High
qutenza 2 81.64 Quite High
Spinal cord 6 80.68 Quite High
Pain 8 74.64 Quite High
long-term potentiation 1 73.48 Quite High
nMDA receptor 3 71.12 Quite High
Disease Link Frequency Relevance Heat
Ganglion Cysts 78 99.30 Very High Very High Very High
Neuropathic Pain 35 97.48 Very High Very High Very High
Pain 9 74.64 Quite High
Nervous System Injury 44 67.52 Quite High
Injury 5 5.00 Very Low Very Low Very Low
INFLAMMATION 2 5.00 Very Low Very Low Very Low
Hyperalgesia 1 5.00 Very Low Very Low Very Low
Nociception 1 5.00 Very Low Very Low Very Low
Inflammatory Pain 1 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Given the present data showing that cPLA2 and CaMKII are activated via stimulation of P2X3R/P2X2+3R in DRG neurons, this work indicates that P2X3R/P2X2+3R-dependent activation of cPLA2 and CaMKII is enhanced under pathological conditions, such as neuropathic pain.


P2X3R Positive_regulation (activation) of cPLA2 in neurons associated with dorsal root ganglion and neuropathic pain
1) Confidence 0.34 Published 2009 Journal Mol Pain Section Body Doc Link PMC2684092 Disease Relevance 0.63 Pain Relevance 0.85

General Comments

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