INT104855

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Context Info
Confidence 0.06
First Reported 2002
Last Reported 2008
Negated 0
Speculated 0
Reported most in Abstract
Documents 3
Total Number 3
Disease Relevance 1.52
Pain Relevance 1.92

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 (Prkaca, TRPV1) transport (TRPV1) mitochondrion (Prkaca)
Golgi apparatus (Prkaca) protein complex (Prkaca) lipid metabolic process (TRPV1)
Anatomy Link Frequency
gut 1
Prkaca (Mus musculus)
TRPV1 (Homo sapiens)
Pain Link Frequency Relevance Heat
Inflammatory mediators 4 100.00 Very High Very High Very High
bradykinin 3 100.00 Very High Very High Very High
Kinase C 1 99.76 Very High Very High Very High
Nerve growth factor 10 98.80 Very High Very High Very High
Inflammation 21 98.28 Very High Very High Very High
Hyperalgesia 4 95.40 Very High Very High Very High
Stimulus evoked pain 1 95.12 Very High Very High Very High
Pain 20 93.28 High High
Trk A 1 91.56 High High
substance P 15 85.16 High High
Disease Link Frequency Relevance Heat
INFLAMMATION 24 100.00 Very High Very High Very High
Inflammatory Pain 1 96.16 Very High Very High Very High
Hyperalgesia 4 95.40 Very High Very High Very High
Hypersensitivity 3 94.72 High High
Inflammatory Bowel Disease 2 94.20 High High
Injury 2 88.80 High High
Nociception 1 77.92 Quite High
Irritable Bowel Syndrome /

Irritable Bowel Syndrome Super

95 64.00 Quite High
Pain 30 61.92 Quite High
Functional Bowel Disorder 3 50.00 Quite Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Electrophysiological analysis of phosphorylation site mutants clearly pinpoints Ser116 as the residue responsible for PKA-dependent modulation of VR1.
PKA Regulation (modulation) of VR1
1) Confidence 0.06 Published 2002 Journal Neuron Section Abstract Doc Link 12194871 Disease Relevance 0.27 Pain Relevance 0.33
TRPV1 activity is modulated by inflammatory mediators including bradykinin and prostaglandins, probably by cAMP-dependent protein kinase (PKA)- or protein kinase C (PKC)-mediated phosphorylation of the receptor.39 Generally, protein kinase-mediated phoshorylation of the TRPV1 receptor results in sensitisation, and dephosphorylation by protein phosphatases results in desensitisation.40 NGF immunostaining has been difficult to obtain in gut specimens, especially mucosal biopsies as we have used here.
PKA Regulation (modulated) of TRPV1 in gut associated with kinase c, inflammatory mediators, nerve growth factor and bradykinin
2) Confidence 0.04 Published 2008 Journal Gut Section Body Doc Link PMC2564830 Disease Relevance 0.61 Pain Relevance 1.16
Here, we show that modulation of the sensitivity of the heat-activated ion channel TRPV1 by the protein kinases PKA and PKC and by the phosphatase calcineurin depends on the formation of a signaling complex between these enzymes, the scaffolding protein AKAP79/150 and TRPV1.
PKA Regulation (modulation) of TRPV1
3) Confidence 0.02 Published 2008 Journal Neuron Section Abstract Doc Link 18701070 Disease Relevance 0.46 Pain Relevance 0.43

General Comments

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