INT91932

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Context Info
Confidence 0.67
First Reported 2000
Last Reported 2010
Negated 0
Speculated 0
Reported most in Abstract
Documents 18
Total Number 18
Disease Relevance 10.39
Pain Relevance 10.90

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 (Scn10a) transmembrane transport (Scn10a)
Anatomy Link Frequency
DRG 4
neurons 2
trigeminal ganglion 1
ND7/23 1
nerve 1
Scn10a (Rattus norvegicus)
Pain Link Frequency Relevance Heat
sodium channel 55 100.00 Very High Very High Very High
Peripheral nerve injury 26 100.00 Very High Very High Very High
Inflammation 41 99.92 Very High Very High Very High
Pain 22 99.92 Very High Very High Very High
nociceptor 6 99.92 Very High Very High Very High
Trigeminal ganglion neurons 5 99.24 Very High Very High Very High
c fibre 43 99.16 Very High Very High Very High
Inflammatory stimuli 12 99.04 Very High Very High Very High
Eae 26 98.92 Very High Very High Very High
Inflammatory mediators 2 98.64 Very High Very High Very High
Disease Link Frequency Relevance Heat
Nervous System Injury 61 100.00 Very High Very High Very High
Hypersensitivity 23 99.92 Very High Very High Very High
Nociception 21 99.64 Very High Very High Very High
Diabetes Mellitus 3 99.50 Very High Very High Very High
Ganglion Cysts 10 99.04 Very High Very High Very High
Inflammatory Pain 5 98.92 Very High Very High Very High
Channelopathies 1 98.90 Very High Very High Very High
INFLAMMATION 39 98.86 Very High Very High Very High
Neuropathic Pain 23 98.60 Very High Very High Very High
Erythermalgia 2 98.38 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
The results demonstrate that, following FCA injection, Na(V)1.9 expression is upregulated at days 14, 21 and 28 post-FCA, with Na(V)1.7 and Na(V)1.8 showing increased channel expression at days 14 and 28.
Positive_regulation (upregulated) of Na(V)1.8
1) Confidence 0.67 Published 2008 Journal Eur J Pain Section Abstract Doc Link 17950013 Disease Relevance 0.60 Pain Relevance 0.64
Na(v)1.8 mRNA was increased > or =2.5-fold in trigeminal ganglion neurons 1 and 2 weeks after CFA treatment, and Na(v)1.8 protein was increased in the infraorbital nerve over a similar time course.
Positive_regulation (increased) of Na(v)1.8 in neurons associated with ganglion cysts and trigeminal ganglion neurons
2) Confidence 0.67 Published 2008 Journal J Pain Section Abstract Doc Link 18337185 Disease Relevance 1.03 Pain Relevance 1.02
Na(v)1.8 mRNA was increased > or =2.5-fold in trigeminal ganglion neurons 1 and 2 weeks after CFA treatment, and Na(v)1.8 protein was increased in the infraorbital nerve over a similar time course.
Positive_regulation (increased) of Na(v)1.8 in neurons associated with ganglion cysts and trigeminal ganglion neurons
3) Confidence 0.67 Published 2008 Journal J Pain Section Abstract Doc Link 18337185 Disease Relevance 1.01 Pain Relevance 0.95
A similar increase of Na(V)1.8 mRNA was observed when DbcAMP was used to induce persistent hypernociception.
Positive_regulation (increase) of Na(V)1.8
4) Confidence 0.67 Published 2005 Journal Neurosci. Lett. Section Abstract Doc Link 16043287 Disease Relevance 0.23 Pain Relevance 0.39
In this system, beta3 caused a 5-mV hyperpolarizing shift in the threshold of activation of PN3, and a threefold increase in the peak current amplitude when compared with PN3 expressed alone.
Positive_regulation (activation) of PN3
5) Confidence 0.50 Published 2000 Journal Eur. J. Neurosci. Section Abstract Doc Link 11069594 Disease Relevance 0.32 Pain Relevance 0.64
The role of Na(V)1.8 sodium channel in the maintenance of chronic inflammatory hypernociception.
Positive_regulation (role) of Na(V)1.8 associated with inflammation and sodium channel
6) Confidence 0.49 Published 2005 Journal Neurosci. Lett. Section Title Doc Link 16043287 Disease Relevance 0.27 Pain Relevance 0.73
Investigations of gene expression changes in injured trigeminal ganglion neurons of animals with behavioral signs of neuropathic pain demonstrated that the sodium channel alpha-subunit Na(v)1.3-absent in sham-operated animals-was expressed to a limited extent. mRNAs for Na(v)1.8 and Na(v)1.9 were reduced both with respect to proportions of expressing neurons and to intensities, whereas the beta 3 subunit was markedly upregulated. mRNA levels of p11, a regulatory factor that facilitates the surface expression of Na(v)1.8, were unchanged.
Positive_regulation (mRNAs) of Na(v)1.8 in trigeminal ganglion associated with ganglion cysts, sodium channel, neuropathic pain and trigeminal ganglion neurons
7) Confidence 0.49 Published 2005 Journal Pain Section Abstract Doc Link 16297558 Disease Relevance 0.89 Pain Relevance 0.53
Using Northern blot analysis and membrane potential measurement, several siRNAs were identified that were capable of a highly-selective attenuation of Na(V)1.8 message as well as functional expression in clonal ND7/23 cells which were stably transfected with the rat Na(V)1.8 gene.
Positive_regulation (attenuation) of Na(V)1.8 in ND7/23
8) Confidence 0.49 Published 2007 Journal Neuroscience Section Abstract Doc Link 17367951 Disease Relevance 0.51 Pain Relevance 0.60
A parallel restoration of the persistent hypernociception and up-regulation of Na(V)1.8 mRNA was observed after the cessation of ODN antisense treatment.
Positive_regulation (up-regulation) of Na(V)1.8
9) Confidence 0.49 Published 2005 Journal Neurosci. Lett. Section Abstract Doc Link 16043287 Disease Relevance 0.19 Pain Relevance 0.50
In addition, during the persistent hypernociceptive state, the PKA and PKCvarepsilon expression and activity in the DRG are up-regulated and the administration of the PKA and PKCvarepsilon inhibitors reduce the hypernociception as well as the Na(V)1.8 mRNA level.
Positive_regulation (up-regulated) of Na(V)1.8 in DRG
10) Confidence 0.45 Published 2009 Journal Biochem. Pharmacol. Section Abstract Doc Link 19073148 Disease Relevance 0.57 Pain Relevance 0.33
In the prostaglandin E(2) (PGE(2))-induced persistent hypernociception, the Na(V)1.8 mRNA in the dorsal root ganglia (DRG) was up-regulated.
Positive_regulation (up-regulated) of Na(V)1.8 in DRG
11) Confidence 0.45 Published 2009 Journal Biochem. Pharmacol. Section Abstract Doc Link 19073148 Disease Relevance 0.41 Pain Relevance 0.30
These data show that, after a period of recurring inflammatory stimuli, an intense and prolonged nociceptive response is elicited by a minimum inflammatory stimulus and that this pro-nociceptive state depends on Na(V)1.8 mRNA up-regulation in the DRG.
Positive_regulation (up-regulation) of Na(V)1.8 in DRG associated with nociception and inflammatory stimuli
12) Confidence 0.45 Published 2009 Journal Biochem. Pharmacol. Section Abstract Doc Link 19073148 Disease Relevance 0.60 Pain Relevance 0.34
Our results show that, in rats with experimental diabetes, there is a significant upregulation of mRNA for the Na(v)1.3, Na(v)1.6, and Na(v)1.9 sodium channels and a downregulation of Na(v)1.8 mRNA 1 and 8 weeks after onset of allodynia.
Positive_regulation (upregulation) of Na(v)1.8 associated with allodynia, diabetes mellitus and sodium channel
13) Confidence 0.45 Published 2002 Journal Ann. Neurol. Section Abstract Doc Link 12447933 Disease Relevance 1.09 Pain Relevance 1.10
Previous work has revealed acute administration of inflammatory mediators, such as Freund's complete adjuvant (FCA) or carrageenan caused an upregulation in the levels of Na(V)1.7 and Na(V)1.8 protein in DRG (dorsal root ganglia) tissue up to 4 days post-insult.
Positive_regulation (upregulation) of Na(V)1.8 in dorsal root ganglia associated with inflammatory mediators
14) Confidence 0.45 Published 2008 Journal Eur J Pain Section Abstract Doc Link 17950013 Disease Relevance 0.59 Pain Relevance 0.67
These data demonstrate a greater involvement of Nav 1.8 in frank nerve injury and inflammatory pain as compared to acute, post-operative or chemotherapy-induced neuropathic pain states.
Positive_regulation (involvement) of Nav 1.8 in nerve associated with nervous system injury, eae and neuropathic pain
15) Confidence 0.30 Published 2006 Journal Pain Section Abstract Doc Link 16545521 Disease Relevance 1.06 Pain Relevance 0.93
Primary erythermalgia as a sodium channelopathy: screening for SCN9A mutations: exclusion of a causal role of SCN10A and SCN11A.
Positive_regulation (role) of SCN10A associated with primary erythermalgia, channelopathies and erythermalgia
16) Confidence 0.21 Published 2008 Journal Arch Dermatol Section Title Doc Link 18347287 Disease Relevance 0.20 Pain Relevance 0.34
To assess the impact of these residues as determinants of pyrethroid sensitivity in another sequence context, we mutated the corresponding positions of the rat pyrethroid-sensitive, TTX-resistant peripheral nerve sodium channel (rNav1.8; also called SNS or PN3) and determined the sensitivity of native and mutated channels expressed in Xenopus oocytes to the pyrethroid insecticide cismethrin.
Positive_regulation (called) of PN3 in oocytes associated with sodium channel
17) Confidence 0.05 Published 2001 Journal Neurotoxicology Section Abstract Doc Link 11829409 Disease Relevance 0 Pain Relevance 0.33
In summary, we have discovered that peripheral nerve injury and activation of TRPV1-expressing C-fibers causes extensive opening of the BSCB and BBB.
Positive_regulation (activation) of peripheral nerve injury in peripheral nerve associated with c fibre, nervous system injury and peripheral nerve injury
18) Confidence 0.01 Published 2010 Journal Mol Pain Section Body Doc Link PMC2984489 Disease Relevance 0.84 Pain Relevance 0.57

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