INT196119

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Context Info
Confidence 0.38
First Reported 2006
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 2
Total Number 2
Disease Relevance 0.19
Pain Relevance 0.93

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

transport (Trpc3)
Anatomy Link Frequency
liver 1
Trpc3 (Mus musculus)
Pain Link Frequency Relevance Heat
nociceptor 32 92.00 High High
calcitonin gene related peptide 11 88.08 High High
mu opioid receptor 4 86.48 High High
Neuropeptide 4 81.72 Quite High
trigeminal ganglion 75 55.44 Quite High
TRP channel 50 50.00 Quite Low
Central nervous system 3 5.00 Very Low Very Low Very Low
substance P 3 5.00 Very Low Very Low Very Low
Pain 3 5.00 Very Low Very Low Very Low
Somatostatin 3 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Nociception 3 77.96 Quite High
Ganglion Cysts 85 55.44 Quite High
Repression 7 42.92 Quite Low
Targeted Disruption 44 24.72 Low Low
Sprains And Strains 17 17.24 Low Low
Pain 4 5.00 Very Low Very Low Very Low
Death 3 5.00 Very Low Very Low Very Low
Neurodegenerative Disease 3 5.00 Very Low Very Low Very Low
Coronary Heart Disease 2 5.00 Very Low Very Low Very Low
Subacute Sclerosing Panencephalitis 2 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
This is largely in agreement with results from rat tissues [11], only the absence of TRPC3 from rat liver showed a marked difference to our results.
Negative_regulation (absence) of TRPC3 in liver
1) Confidence 0.38 Published 2006 Journal BMC Genomics Section Body Doc Link PMC1557673 Disease Relevance 0 Pain Relevance 0
The expression of multiple sensory markers, including Trpa1, TrpC3, Trpm8, Scn11a and several members of the Mrg family, are Runx1-dependent in the DRG.
Negative_regulation (members) of TrpC3
2) Confidence 0.28 Published 2010 Journal Neural Dev Section Body Doc Link PMC2829025 Disease Relevance 0.19 Pain Relevance 0.93

General Comments

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