INT116321

From wiki-pain
Jump to: navigation, search
Context Info
Confidence 0.62
First Reported 2004
Last Reported 2011
Negated 4
Speculated 4
Reported most in Body
Documents 38
Total Number 42
Disease Relevance 26.62
Pain Relevance 37.97

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

cell differentiation (Nav1) cytoskeleton (Nav1) cytoplasm (Nav1)
Anatomy Link Frequency
peripheral nerve 5
neuronal 3
muscle 1
brain 1
nociceptor 1
Nav1 (Mus musculus)
Pain Link Frequency Relevance Heat
Nav1.7 631 100.00 Very High Very High Very High
nav1.8 631 100.00 Very High Very High Very High
sodium channel 320 100.00 Very High Very High Very High
tetrodotoxin 248 100.00 Very High Very High Very High
nav1.3 168 100.00 Very High Very High Very High
Nav1.9 106 100.00 Very High Very High Very High
Nav1.2 36 100.00 Very High Very High Very High
Nav1.6 25 100.00 Very High Very High Very High
nociceptor 190 99.98 Very High Very High Very High
Analgesic 11 99.80 Very High Very High Very High
Disease Link Frequency Relevance Heat
Disease 79 99.98 Very High Very High Very High
Targeted Disruption 450 99.88 Very High Very High Very High
Heart Arrhythmia 32 99.80 Very High Very High Very High
Neuropathic Pain 361 99.72 Very High Very High Very High
Poisoning 2 99.46 Very High Very High Very High
Pain 313 99.44 Very High Very High Very High
Inflammatory Pain 126 99.28 Very High Very High Very High
INFLAMMATION 531 99.04 Very High Very High Very High
Ganglion Cysts 97 99.04 Very High Very High Very High
Febrile Convulsions 63 98.96 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
In addition our results rule out Nav1.7 up-regulation in the Nav1.8 knockout as the reason behind the discrepancy between the finding of Kerr et al [17] and Lai et al [18].
Regulation (regulation) of Nav1 associated with targeted disruption, nav1.8 and nav1.7
1) Confidence 0.62 Published 2005 Journal Mol Pain Section Body Doc Link PMC1215513 Disease Relevance 1.28 Pain Relevance 2.34
In addition our results rule out Nav1.7 up-regulation in the Nav1.8 knockout as the reason behind the discrepancy between the finding of Kerr et al [17] and Lai et al [18].
Regulation (regulation) of Nav1 associated with targeted disruption, nav1.8 and nav1.7
2) Confidence 0.62 Published 2005 Journal Mol Pain Section Body Doc Link PMC1215513 Disease Relevance 1.29 Pain Relevance 2.34
However, real-time PCR results in our study showed no transcriptional change in ASIC3, Nav1.6, Nav1.7, and Nav1.8 mRNA level following inflammation.
Neg (no) Regulation (change) of Nav1 associated with inflammation, nav1.8, nav1.7 and nav1.6
3) Confidence 0.60 Published 2009 Journal Mol Pain Section Body Doc Link PMC2632618 Disease Relevance 1.23 Pain Relevance 1.51
However, real-time PCR results in our study showed no transcriptional change in ASIC3, Nav1.6, Nav1.7, and Nav1.8 mRNA level following inflammation.
Neg (no) Regulation (change) of Nav1 associated with inflammation, nav1.8, nav1.7 and nav1.6
4) Confidence 0.60 Published 2009 Journal Mol Pain Section Body Doc Link PMC2632618 Disease Relevance 1.23 Pain Relevance 1.52
However, real-time PCR results in our study showed no transcriptional change in ASIC3, Nav1.6, Nav1.7, and Nav1.8 mRNA level following inflammation.
Neg (no) Regulation (change) of Nav1 associated with inflammation, nav1.8, nav1.7 and nav1.6
5) Confidence 0.60 Published 2009 Journal Mol Pain Section Body Doc Link PMC2632618 Disease Relevance 1.23 Pain Relevance 1.51
The poison Dart frog's batrachotoxin modulates Nav1.8.
Regulation (modulates) of Nav1 associated with nav1.8 and poisoning
6) Confidence 0.54 Published 2004 Journal FEBS Lett. Section Title Doc Link 15527793 Disease Relevance 0.46 Pain Relevance 0.38
This study presents, for the first time, evidence that calmodulin associates with a sodium channel, Nav1.8, in native neurons, and demonstrates a regulation of Nav1.8 currents that can significantly affect electrogenesis of DRG neurons in which Nav1.8 is normally expressed.
Regulation (regulation) of Nav1 in DRG associated with dorsal root ganglion, sodium channel and nav1.8
7) Confidence 0.53 Published 2006 Journal J. Neurophysiol. Section Abstract Doc Link 16598065 Disease Relevance 0.29 Pain Relevance 1.05
From all the above, our results indicate that Nav1.8 and Nav1.7 subunits contribute to the excitability of peripheral nerve terminals and their modulation is critical for peripheral sensitisation in inflammatory pain

Neuropathic pain

Regulation (contribute) of Nav1 in peripheral nerve associated with eae, neuropathic pain, nav1.8 and nav1.7
8) Confidence 0.45 Published 2005 Journal Mol Pain Section Body Doc Link PMC1215513 Disease Relevance 1.01 Pain Relevance 2.32
From all the above, our results indicate that Nav1.8 and Nav1.7 subunits contribute to the excitability of peripheral nerve terminals and their modulation is critical for peripheral sensitisation in inflammatory pain

Neuropathic pain

Regulation (contribute) of Nav1 in peripheral nerve associated with eae, neuropathic pain, nav1.8 and nav1.7
9) Confidence 0.45 Published 2005 Journal Mol Pain Section Body Doc Link PMC1215513 Disease Relevance 1.01 Pain Relevance 2.33
GDNF reverses the up-regulation of Nav1.3 and neuropathic pain behaviour [19], and antisense oligonucleotides against Nav1.3 sequence reverse neuropathic pain behaviour [20,21].
Regulation (regulation) of Nav1 associated with nav1.3 and neuropathic pain
10) Confidence 0.45 Published 2006 Journal Mol Pain Section Body Doc Link PMC1630424 Disease Relevance 0.57 Pain Relevance 1.59
The balance of effect of Nav 1.8 deletion and compensatory increases may actually be masking less prominent roles for Nav 1.8 in the transmission of thermal stimuli.
Regulation (effect) of Nav
11) Confidence 0.44 Published 2006 Journal Mol Pain Section Body Doc Link PMC1403745 Disease Relevance 0.29 Pain Relevance 0.12
Deregulation, by the absence of dystrophin, of Nav1.4 activity leading to Na+ overload is likely connected with multiple other changes reported in mdx fibers.
Regulation (Deregulation) of Nav1
12) Confidence 0.44 Published 2008 Journal The Journal of General Physiology Section Body Doc Link PMC2483333 Disease Relevance 0.16 Pain Relevance 0
Thus, it can be argued that changes in Nav1.4 gating properties significantly affect the Na+ balance in FBD muscle fibers, producing an important long-term effect even in nonexercised muscle.
Regulation (changes) of Nav1 in muscle
13) Confidence 0.44 Published 2008 Journal The Journal of General Physiology Section Body Doc Link PMC2483333 Disease Relevance 0.11 Pain Relevance 0
To assess how these changes in Nav1.4 gating properties influence [Na+] under the sarcolemma, we measured the reversal potential for Na+.
Regulation (changes) of Nav1
14) Confidence 0.44 Published 2008 Journal The Journal of General Physiology Section Body Doc Link PMC2483333 Disease Relevance 0 Pain Relevance 0.04
The up-regulation of Nav1.9 on day 2 with intraplantar carrageenan-induced inflammation was significant and ASIC3 dependent.
Regulation (regulation) of Nav1 associated with inflammation and nav1.9
15) Confidence 0.44 Published 2009 Journal Mol Pain Section Body Doc Link PMC2632618 Disease Relevance 0.65 Pain Relevance 0.91
To test this hypothesis, we investigated the effect of S241A and S241L substitutions on the gating properties of Nav1.7.
Spec (investigated) Regulation (effect) of Nav1 associated with nav1.7
16) Confidence 0.44 Published 2006 Journal J. Biol. Chem. Section Abstract Doc Link 17008310 Disease Relevance 0.49 Pain Relevance 0.65
Whether the substrate for arrhythmias in SCN5A-related BrS patients relies essentially on Nav1.5 dysfunction or involves additional myocardial rearrangements is unclear.
Regulation (relies) of Nav1 associated with heart arrhythmia
17) Confidence 0.40 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2824822 Disease Relevance 0.91 Pain Relevance 0.14
There was no difference between the Nav1.8 and the DKO mice in this test, figure 3d, and similar results have been obtained with the nociceptor-specific Nav1.7 knockout [13]

Inflammatory pain behaviour

Regulation (specific) of Nav1 in nociceptor associated with targeted disruption, eae, nociceptor, nav1.8 and nav1.7
18) Confidence 0.40 Published 2005 Journal Mol Pain Section Body Doc Link PMC1215513 Disease Relevance 1.04 Pain Relevance 1.23
It may be speculated that a decrease in the number of sarcolemmal Na+ channels could trigger changes in the expression/interaction of proteins that remain to be indentified altering Nav1.5 biophysical properties.
Regulation (altering) of Nav1
19) Confidence 0.35 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2824822 Disease Relevance 0.13 Pain Relevance 0
Although skeletal muscle channels (Nav1.4) were strongly affected by Tz1, the neuronal channels Nav1.6 and Nav1.2 were less sensitive, and the cardiac Nav1.5 and the peripheral nerve channel Nav1.7 were essentially insensitive.
Regulation (affected) of Nav1 in neuronal associated with nav1.2, nav1.7 and nav1.6
20) Confidence 0.34 Published 2006 Journal Mol. Pharmacol. Section Abstract Doc Link 16638971 Disease Relevance 0 Pain Relevance 0.53

General Comments

This test has worked.

Personal tools
Namespaces

Variants
Actions
Navigation
Toolbox