INT111018

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Context Info
Confidence 0.30
First Reported 2003
Last Reported 2009
Negated 0
Speculated 0
Reported most in Abstract
Documents 5
Total Number 5
Disease Relevance 3.11
Pain Relevance 2.02

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

signal transduction (F2rl1) plasma membrane (F2rl1) signal transducer activity (F2rl1)
Anatomy Link Frequency
macrophages 1
monocyte 1
endothelial cells 1
neurons 1
F2rl1 (Mus musculus)
Pain Link Frequency Relevance Heat
agonist 7 100.00 Very High Very High Very High
Inflammation 64 99.98 Very High Very High Very High
substance P 36 99.30 Very High Very High Very High
chemokine 3 98.46 Very High Very High Very High
Hyperalgesia 1 92.48 High High
antagonist 5 90.32 High High
Angina 3 86.56 High High
qutenza 7 83.88 Quite High
Central nervous system 4 76.80 Quite High
cytokine 15 74.00 Quite High
Disease Link Frequency Relevance Heat
INFLAMMATION 56 99.98 Very High Very High Very High
Atherosclerotic Plaque 3 98.94 Very High Very High Very High
Atherosclerosis 15 98.36 Very High Very High Very High
Hyperalgesia 1 92.48 High High
Cv General 3 Under Development 3 86.56 High High
Vasculitis 3 85.32 High High
Necrosis 7 82.64 Quite High
Cancer 7 82.28 Quite High
Disease 5 13.76 Low Low
Hypersensitivity 4 13.40 Low Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
In addition, desensitizing neurokinin receptors with substance P and/or neurokinin A decreased the PAR-2 agonist-evoked contraction.
PAR-2 Binding (contraction) of associated with agonist and substance p
1) Confidence 0.30 Published 2003 Journal Am. J. Physiol. Gastrointest. Liver Physiol. Section Abstract Doc Link 12801882 Disease Relevance 0 Pain Relevance 0.48
We also found that LIGHT, LIGHT receptors, and PAR-2 showed enhanced expression, and, to some degree, colocalization in endothelial cells and macrophages, in the atherosclerotic plaques of ApoE(-/-) mice, suggesting that the inflammatory interaction between LIGHT and PAR-2 also may be operating in vivo within an atherosclerotic lesion.
PAR-2 Binding (interaction) of in macrophages associated with atherosclerotic plaque, inflammation and atherosclerosis
2) Confidence 0.16 Published 2009 Journal Circ. Res. Section Abstract Doc Link 19023130 Disease Relevance 0.88 Pain Relevance 0.34
We also found that LIGHT acted synergistically with PAR-2 activation to promote enhanced release of the proatherogenic chemokines interleukin-8 and monocyte chemoattractant protein-1, underscoring that the interaction between LIGHT and PAR-2 is biologically active, promoting potent inflammatory effects.
PAR-2 Binding (interaction) of in monocyte associated with chemokine and inflammation
3) Confidence 0.16 Published 2009 Journal Circ. Res. Section Abstract Doc Link 19023130 Disease Relevance 1.10 Pain Relevance 0.40
They hypothesized that tryptase excites neurons through PAR2 because activation of PAR2 with trypsin or peptide agonists strongly desensitizes the response to tryptase.
PAR2 Binding (activation) of in neurons associated with agonist
4) Confidence 0.06 Published 2005 Journal Allergy Asthma Clin Immunol Section Body Doc Link PMC2877069 Disease Relevance 0.26 Pain Relevance 0.46
We also found that LIGHT, LIGHT receptors, and PAR-2 showed enhanced expression, and, to some degree, colocalization in endothelial cells and macrophages, in the atherosclerotic plaques of ApoE(-/-) mice, suggesting that the inflammatory interaction between LIGHT and PAR-2 also may be operating in vivo within an atherosclerotic lesion.
PAR-2 Binding (interaction) of in endothelial cells associated with atherosclerotic plaque, inflammation and atherosclerosis
5) Confidence 0.05 Published 2009 Journal Circ. Res. Section Abstract Doc Link 19023130 Disease Relevance 0.88 Pain Relevance 0.34

General Comments

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