INT195917

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Context Info
Confidence 0.52
First Reported 2006
Last Reported 2008
Negated 0
Speculated 0
Reported most in Body
Documents 2
Total Number 2
Disease Relevance 1.86
Pain Relevance 2.29

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

cytosol (Trpv1) transport (Trpv1) plasma membrane (Trpv1)
transmembrane transport (Trpv1) lipid metabolic process (Trpv1)
Anatomy Link Frequency
PGE2 2
Trpv1 (Mus musculus)
Pain Link Frequency Relevance Heat
Inflammation 47 99.76 Very High Very High Very High
Thermal hyperalgesia 11 99.12 Very High Very High Very High
antagonist 41 97.92 Very High Very High Very High
analgesia 11 97.32 Very High Very High Very High
Pain 92 97.04 Very High Very High Very High
agonist 46 93.92 High High
Hyperalgesia 25 91.00 High High
Lasting pain 5 85.12 High High
central sensitization 6 84.32 Quite High
Eae 5 83.28 Quite High
Disease Link Frequency Relevance Heat
INFLAMMATION 45 99.76 Very High Very High Very High
Hyperalgesia 39 99.12 Very High Very High Very High
Pain 97 97.04 Very High Very High Very High
Nociception 27 93.52 High High
Inflammatory Pain 8 83.28 Quite High
Neuropathic Pain 25 5.00 Very Low Very Low Very Low
Targeted Disruption 23 5.00 Very Low Very Low Very Low
Disease 17 5.00 Very Low Very Low Very Low
Ganglion Cysts 11 5.00 Very Low Very Low Very Low
Headache 6 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Also, identification of specific second messenger molecules that regulate phosphorylation of TRPV1 has been the focus of intense research, to exploit a broader approach to pain treatment.
Regulation (regulate) of Phosphorylation (phosphorylation) of TRPV1 associated with pain
1) Confidence 0.52 Published 2008 Journal Current Neuropharmacology Section Abstract Doc Link PMC2645548 Disease Relevance 0.64 Pain Relevance 1.42
Phosphorylation of the TRPV1 by numerous kinases, including cAMP-dependent protein kinase A (PKA), can regulate function of the receptor [6-8]. cAMP levels are elevated in inflamed tissues [9,10] and the cAMP/PKA pathway appears to be essential in sensitizing inflammatory nociception and contributes to the development of inflammatory hyperalgesia induced by proinflammatory mediators such as prostaglandin E2 (PGE2) [9,11].
Regulation (regulate) of Phosphorylation (Phosphorylation) of TRPV1 in PGE2 associated with nociception, hyperalgesia and inflammation
2) Confidence 0.22 Published 2006 Journal Mol Pain Section Body Doc Link PMC1553434 Disease Relevance 1.22 Pain Relevance 0.87

General Comments

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