INT97366

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Context Info
Confidence 0.62
First Reported 2001
Last Reported 2010
Negated 11
Speculated 4
Reported most in Body
Documents 38
Total Number 43
Disease Relevance 23.63
Pain Relevance 38.17

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

Anatomy Link Frequency
sensory neurons 3
nerve 3
neurons 3
brain 2
HEK 2
Nav1 (Rattus norvegicus)
Pain Link Frequency Relevance Heat
dorsal root ganglion 904 100.00 Very High Very High Very High
nav1.8 818 100.00 Very High Very High Very High
sodium channel 320 100.00 Very High Very High Very High
nav1.3 213 100.00 Very High Very High Very High
Nav1.6 118 100.00 Very High Very High Very High
Nav1.2 61 100.00 Very High Very High Very High
Nav1.9 51 100.00 Very High Very High Very High
Nav1.1 38 100.00 Very High Very High Very High
Gabapentin 7 100.00 Very High Very High Very High
beta nociceptor 2 99.96 Very High Very High Very High
Disease Link Frequency Relevance Heat
Ganglion Cysts 916 100.00 Very High Very High Very High
Nerve Compression Syndromes 496 99.84 Very High Very High Very High
INFLAMMATION 97 99.80 Very High Very High Very High
Pain 311 99.76 Very High Very High Very High
Nervous System Injury 209 99.72 Very High Very High Very High
Injury 918 99.68 Very High Very High Very High
Cancer Pain 120 99.44 Very High Very High Very High
Neuropathic Pain 362 99.12 Very High Very High Very High
Nociception 164 98.88 Very High Very High Very High
Cancer 205 96.64 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
These data indicate that Nav1.8 and Nav1.9 subunits are transported to the periphery in normal animals and are differentially regulated during inflammation.
Regulation (regulated) of Nav1 associated with inflammation, nav1.8 and nav1.9
1) Confidence 0.62 Published 2004 Journal Neurosci. Lett. Section Abstract Doc Link 14729231 Disease Relevance 0.19 Pain Relevance 1.52
These data indicate that Nav1.8 and Nav1.9 subunits are transported to the periphery in normal animals and are differentially regulated during inflammation.
Regulation (regulated) of Nav1 associated with inflammation, nav1.8 and nav1.9
2) Confidence 0.62 Published 2004 Journal Neurosci. Lett. Section Abstract Doc Link 14729231 Disease Relevance 0.19 Pain Relevance 1.52
Algogens released from a tumor or its surrounding tissue and transported all over the body, such as endothelin-1 [33], prostaglandins [34] and ATP [35], may directly or indirectly sensitize and/or excite primary afferent nociceptors and therefore interact with the proteins that regulate Nav1.8.
Regulation (regulate) of Nav1 in body associated with cancer, nociceptor and nav1.8
3) Confidence 0.62 Published 2010 Journal BMC Cancer Section Body Doc Link PMC2894792 Disease Relevance 1.13 Pain Relevance 1.07
Intracellular Nav1.8 domains interact widely with many proteins and immunoprecipitation assays have confirmed that some of these proteins may regulate Nav1.8 in vivo [32].
Spec (may) Regulation (regulate) of Nav1 associated with nav1.8
4) Confidence 0.62 Published 2010 Journal BMC Cancer Section Body Doc Link PMC2894792 Disease Relevance 0.89 Pain Relevance 1.10
There were no concomitant changes in the mRNAs for Nav1.1 and Nav1.6.
Neg (no) Regulation (changes) of Nav1 associated with nav1.1 and nav1.6
5) Confidence 0.61 Published 2003 Journal Brain Res. Mol. Brain Res. Section Abstract Doc Link 12941467 Disease Relevance 0 Pain Relevance 1.11
These suggested the diverse mechanisms underlying modulation of Nav1.8 by the different proinflammatory agents.
Regulation (modulation) of Nav1.8 associated with nav1.8
6) Confidence 0.54 Published 2009 Journal Mol Pain Section Body Doc Link PMC2715383 Disease Relevance 0.42 Pain Relevance 1.55
Here, we studied the effect of such prolonged exposure to gabapentin on a rat sodium channel, Nav1.2.
Regulation (effect) of Nav1 associated with nav1.2, sodium channel and gabapentin
7) Confidence 0.45 Published 2006 Journal Epilepsy Res. Section Abstract Doc Link 16621448 Disease Relevance 0 Pain Relevance 1.10
We observed no changes in the expression of neuronal sodium channels Nav1.1, Nav1.2, or Nav1.6 in VPL neurons, although we can not rule out a contribution of other channels that could have an affect on firing thresholds [19,20].
Neg (no) Regulation (changes) of Nav1 in neurons associated with nav1.1, nav1.2, sodium channel and nav1.6
8) Confidence 0.45 Published 2006 Journal Mol Pain Section Body Doc Link PMC1563449 Disease Relevance 0.91 Pain Relevance 1.24
First, if we assume that Nav1.3 enables a neuron to fire at higher-than-normal frequencies, it is possible that VPL neurons are upregulating Nav1.3 in order to accommodate high-frequency information received from the spinal cord.
Spec (possible) Regulation (upregulating) of Nav1 in spinal cord associated with nav1.3 and spinal cord
9) Confidence 0.45 Published 2006 Journal Mol Pain Section Body Doc Link PMC1563449 Disease Relevance 0.46 Pain Relevance 1.09
We observed no changes in the expression of neuronal sodium channels Nav1.1, Nav1.2, or Nav1.6 in VPL neurons, although we can not rule out a contribution of other channels that could have an affect on firing thresholds [19,20].
Neg (no) Regulation (changes) of Nav1 in neurons associated with nav1.1, nav1.2, sodium channel and nav1.6
10) Confidence 0.45 Published 2006 Journal Mol Pain Section Body Doc Link PMC1563449 Disease Relevance 0.92 Pain Relevance 1.25
We observed no changes in the expression of neuronal sodium channels Nav1.1, Nav1.2, or Nav1.6 in VPL neurons, although we can not rule out a contribution of other channels that could have an affect on firing thresholds [19,20].
Neg (no) Regulation (changes) of Nav1 in neurons associated with nav1.1, nav1.2, sodium channel and nav1.6
11) Confidence 0.45 Published 2006 Journal Mol Pain Section Body Doc Link PMC1563449 Disease Relevance 0.91 Pain Relevance 1.24
Quantitative evaluation of Nav1.6 and caspr immunofluorescence staining intensities and nodal gap axial length within single caspr-identified typical nodes in normal vs. lesioned IONs
Regulation (intensities) of Nav1.6 in nodes associated with nav1.6
12) Confidence 0.45 Published 2007 Journal BMC Neurosci Section Body Doc Link PMC1941742 Disease Relevance 0 Pain Relevance 0.66
In addtion, Nav1.8 activity is likely to be up-regulated through other post-translational regulatory mechanisms such as the distribution of the channel proteins or protein phosphorylation[14].
Spec (likely) Regulation (regulated) of Nav1 associated with nav1.8
13) Confidence 0.45 Published 2010 Journal BMC Cancer Section Body Doc Link PMC2894792 Disease Relevance 1.33 Pain Relevance 1.57
Changes in the expression, trafficking, and redistribution of Nav1.8 in chronic pain models are considered to account for abnormal firing and the generation of ectopic activity in afferent nerves [11].
Regulation (Changes) of Nav1 in nerves associated with lasting pain, ectopic activity and nav1.8
14) Confidence 0.45 Published 2010 Journal BMC Cancer Section Body Doc Link PMC2894792 Disease Relevance 1.12 Pain Relevance 2.45
There were no concomitant changes in the mRNAs for Nav1.1 and Nav1.6.
Neg (no) Regulation (changes) of Nav1 associated with nav1.1 and nav1.6
15) Confidence 0.45 Published 2003 Journal Brain Res. Mol. Brain Res. Section Abstract Doc Link 12941467 Disease Relevance 0 Pain Relevance 1.11
Moreover, consistent with the idea that cellular factors can modulate the properties of Nav1.3, the repriming kinetics were twofold faster in the neurons than in the HEK 293 cells.
Regulation (modulate) of Nav1 in HEK associated with nav1.3
16) Confidence 0.45 Published 2001 Journal J. Neurosci. Section Abstract Doc Link 11487618 Disease Relevance 0.34 Pain Relevance 1.18
However, the physiological role of Nav channels in vivo has remained an open question.
Regulation (role) of Nav
17) Confidence 0.43 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2752992 Disease Relevance 0 Pain Relevance 0.31
These findings suggest that in Aalpha/beta nociceptors, influences of NGF on expression levels of Nav1.8 are related to, and perhaps limited by, expression levels of trkA.
Regulation (influences) of Nav1 in nociceptors associated with nav1.8 and beta nociceptor
18) Confidence 0.42 Published 2005 Journal J. Neurosci. Section Abstract Doc Link 15888662 Disease Relevance 0.20 Pain Relevance 1.47
In the present study, we detected ipsilaterally decreased DRG NaV1.8 immunoreactivity (Fig. 3), but NaV1.8 mRNA levels in the DRG were not affected by SNE injury (Figs. 4 &5).
Neg (not) Regulation (affected) of NaV1 associated with dorsal root ganglion, injury and nerve compression syndromes
19) Confidence 0.41 Published 2009 Journal Mol Pain Section Body Doc Link PMC2667430 Disease Relevance 2.05 Pain Relevance 0.90
It is conceivable that the modulation of Nav1.8 by NK-1 activation may contribute to peripheral sensitization of pain pathway.
Regulation (modulation) of Nav1.8 associated with pain, peripheral sensitization and nav1.8
20) Confidence 0.39 Published 2009 Journal Mol Pain Section Body Doc Link PMC2715383 Disease Relevance 0.53 Pain Relevance 1.34

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