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Context Info
Confidence 0.60
First Reported 1997
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 5
Total Number 5
Disease Relevance 4.45
Pain Relevance 3.14

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

transport (Scn10a) plasma membrane (Scn10a) transmembrane transport (Scn10a)
Anatomy Link Frequency
neurons 2
Scn10a (Mus musculus)
Pain Link Frequency Relevance Heat
Pain 217 100.00 Very High Very High Very High
Inflammatory mediators 4 99.80 Very High Very High Very High
Paroxysmal pain 1 98.48 Very High Very High Very High
Arthritis 24 96.64 Very High Very High Very High
sodium channel 18 96.32 Very High Very High Very High
nociceptor 10 94.80 High High
Inflammation 110 93.56 High High
Neurotransmitter 12 93.12 High High
Eae 26 92.52 High High
agonist 20 86.16 High High
Disease Link Frequency Relevance Heat
Pain 227 100.00 Very High Very High Very High
Nociception 15 100.00 Very High Very High Very High
INFLAMMATION 111 99.80 Very High Very High Very High
Targeted Disruption 11 99.14 Very High Very High Very High
Sprains And Strains 133 98.96 Very High Very High Very High
Synovitis 5 98.88 Very High Very High Very High
Experimental Arthritis 7 96.64 Very High Very High Very High
Erythermalgia 1 92.60 High High
Arthritis 24 91.56 High High
Disease 17 89.20 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
In order to delete genes in nociceptive neurons, we generated heterozygous transgenic mice expressing Cre recombinase under the control of the NaV1.8 promoter.
Regulation (control) of NaV1.8 in neurons associated with targeted disruption and nociception
1) Confidence 0.60 Published 2005 Journal Pain Section Abstract Doc Link 15621361 Disease Relevance 0.40 Pain Relevance 0.48
The degree of down-regulation of Scn10a was not identical across strains, but the across strains correlation was not significant for any of the three pain parameters considered.
Regulation (regulation) of Scn10a associated with pain and sprains and strains
2) Confidence 0.42 Published 2009 Journal Mol Pain Section Body Doc Link PMC2649910 Disease Relevance 1.30 Pain Relevance 0.56
These results provide the basis for an evolutionary comparison of sodium channels, the construction and analysis of a mouse SNS null mutant as a direct approach to understanding the biological function of SNS, and the identification of regulatory elements that are responsible for the tissue- and cell-specific expression of SNS.
Regulation (responsible) of SNS associated with sodium channel
3) Confidence 0.39 Published 1997 Journal Genomics Section Abstract Doc Link 9143495 Disease Relevance 0.06 Pain Relevance 0.43
                   SCN10A (NaV1.8), a specific marker for nociceptive
               neurons, is a major contributor to electrogenesis in primary pain pathways, and is
               an important target for inflammatory mediators. 
Regulation (target) of SCN10A in neurons associated with nociception, pain and inflammatory mediators
4) Confidence 0.18 Published 2008 Journal PLoS Genetics Section Body Doc Link PMC2432024 Disease Relevance 1.10 Pain Relevance 0.98
Thus, in experimental models, the proinflammatory influence of the SNS occurs before the onset of synovitis.
Regulation (influence) of SNS associated with synovitis
5) Confidence 0.03 Published 2010 Journal Curr Rheumatol Rep Section Body Doc Link PMC2927688 Disease Relevance 1.58 Pain Relevance 0.70

General Comments

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