INT220763

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Context Info
Confidence 0.29
First Reported 2007
Last Reported 2009
Negated 0
Speculated 1
Reported most in Body
Documents 3
Total Number 4
Disease Relevance 0.84
Pain Relevance 1.22

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

nucleoplasm (PRKCA) mitochondrion (PRKCA) small molecule metabolic process (PRKCA)
endoplasmic reticulum (PRKCA) enzyme binding (PRKCA) cytoplasm (PRKCA)
Anatomy Link Frequency
neuronal 2
neurons 2
PRKCA (Homo sapiens)
Pain Link Frequency Relevance Heat
Kinase C 130 100.00 Very High Very High Very High
Neuronal excitability 4 99.96 Very High Very High Very High
sodium channel 82 99.50 Very High Very High Very High
tetrodotoxin 25 91.12 High High
Neurotransmitter 2 85.60 High High
agonist 84 78.52 Quite High
Nav1.7 13 65.08 Quite High
antagonist 5 57.00 Quite High
Central nervous system 20 5.00 Very Low Very Low Very Low
Nerve growth factor 6 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Reprotox - General 1 54 87.96 High High
Virus Diseases 178 85.00 Quite High
Adhesions 4 78.16 Quite High
Infection 58 68.96 Quite High
Borna Disease 8 50.00 Quite Low
Cancer 2 5.12 Low Low
Disease 12 5.00 Very Low Very Low Very Low
Neurological Disease 8 5.00 Very Low Very Low Very Low
Cognitive Disorder 6 5.00 Very Low Very Low Very Low
Viral Infection 6 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Indeed, PKC phosphorylation of SNAP-25, by promoting inhibition of VGCCs decreases calcium signaling and controls neuronal excitability.
Regulation (controls) of Phosphorylation (phosphorylation) of PKC in neuronal associated with kinase c and neuronal excitability
1) Confidence 0.29 Published 2009 Journal PLoS Pathogens Section Body Doc Link PMC2673689 Disease Relevance 0.07 Pain Relevance 0.32
Consistent with our previous reports, we showed by quantitative Western blot analysis that the phosphorylation of these two neuronal PKC targets was significantly impaired in neurons infected with rBDV-wt (Figure 2A and 2B).
Regulation (targets) of Phosphorylation (phosphorylation) of PKC in neurons associated with kinase c
2) Confidence 0.17 Published 2009 Journal PLoS Pathogens Section Body Doc Link PMC2673689 Disease Relevance 0.30 Pain Relevance 0.33
It is noteworthy that Ser329 has previously been identified as a target residue for PKA phosphorylation [33] while Ser331 was identified as a target for PKG phosphorylation [35] and Thr337 as a target for PKC phosphorylation [32].
Regulation (target) of Phosphorylation (phosphorylation) of PKC
3) Confidence 0.12 Published 2007 Journal Biochim Biophys Acta Section Body Doc Link PMC2680961 Disease Relevance 0 Pain Relevance 0.04
It is possible that VGSC expression/activity was controlled at a variety of levels from transcription to post-translation, including mRNA stability and phosphorylation by PKC or PKA [e.g. [33]].
Spec (possible) Regulation (controlled) of Phosphorylation (phosphorylation) of PKC associated with sodium channel
4) Confidence 0.06 Published 2007 Journal Mol Cancer Section Body Doc Link PMC2211503 Disease Relevance 0.47 Pain Relevance 0.54

General Comments

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