INT116226

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Context Info
Confidence 0.51
First Reported 2003
Last Reported 2010
Negated 2
Speculated 6
Reported most in Body
Documents 20
Total Number 27
Disease Relevance 14.32
Pain Relevance 25.61

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) cytoplasm (NAV1)
Anatomy Link Frequency
neuron 3
dorsal root ganglia 3
cardiac myocytes 2
plasma 1
vestibule 1
NAV1 (Homo sapiens)
Pain Link Frequency Relevance Heat
Pain 612 100.00 Very High Very High Very High
sodium channel 584 100.00 Very High Very High Very High
Nav1.7 383 100.00 Very High Very High Very High
Paroxysmal extreme pain disorder 154 100.00 Very High Very High Very High
nav1.8 137 100.00 Very High Very High Very High
Nav1.9 49 100.00 Very High Very High Very High
nav1.3 26 100.00 Very High Very High Very High
orphanin 5 100.00 Very High Very High Very High
narcan 2 100.00 Very High Very High Very High
tetrodotoxin 361 99.96 Very High Very High Very High
Disease Link Frequency Relevance Heat
Pain 521 100.00 Very High Very High Very High
Somatoform Disorder 157 100.00 Very High Very High Very High
Nociception 32 100.00 Very High Very High Very High
INFLAMMATION 48 99.80 Very High Very High Very High
Burning Mouth Syndrome 156 99.76 Very High Very High Very High
Frailty 5 99.16 Very High Very High Very High
Sperm Disorder 15 98.96 Very High Very High Very High
Disease 50 98.32 Very High Very High Very High
Erythermalgia 177 98.08 Very High Very High Very High
Inflammatory Pain 32 97.80 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Considering the importance of these regions for channel function [1], it is not surprising that those mutations alter NaV1.7 activity.
Neg (not) Regulation (alter) of NaV1
1) Confidence 0.51 Published 2008 Journal Mol Pain Section Body Doc Link PMC2262064 Disease Relevance 0.27 Pain Relevance 0.15
The combination of spinal and thalamic generation and amplification of pain by Nav1.3 dysregulation contributes to post-SCI chronic pain.
Regulation (dysregulation) of Nav1 in spinal associated with nav1.3, pain, lasting pain and frailty
2) Confidence 0.45 Published 2007 Journal Prog. Brain Res. Section Abstract Doc Link 17618978 Disease Relevance 0.75 Pain Relevance 1.31
Strickland et al. (2008) investigated the changes in expression of Nav1.7, Nav1.8 and Nav1.9 sodium channels in the rat model and showed that the dorsal root ganglia innervating the knee joint had increased expression of all three subtypes up to 28 days after the initial insult [30].
Spec (investigated) Regulation (changes) of Nav1 in dorsal root ganglia associated with sodium channel, nav1.8, nav1.7 and nav1.9
3) Confidence 0.45 Published 2010 Journal BMC Neurosci Section Body Doc Link PMC2890014 Disease Relevance 0.92 Pain Relevance 1.66
Strickland et al. (2008) investigated the changes in expression of Nav1.7, Nav1.8 and Nav1.9 sodium channels in the rat model and showed that the dorsal root ganglia innervating the knee joint had increased expression of all three subtypes up to 28 days after the initial insult [30].
Spec (investigated) Regulation (changes) of Nav1 in dorsal root ganglia associated with sodium channel, nav1.8, nav1.7 and nav1.9
4) Confidence 0.45 Published 2010 Journal BMC Neurosci Section Body Doc Link PMC2890014 Disease Relevance 0.93 Pain Relevance 1.67
Strickland et al. (2008) investigated the changes in expression of Nav1.7, Nav1.8 and Nav1.9 sodium channels in the rat model and showed that the dorsal root ganglia innervating the knee joint had increased expression of all three subtypes up to 28 days after the initial insult [30].
Spec (investigated) Regulation (changes) of Nav1 in dorsal root ganglia associated with sodium channel, nav1.8, nav1.7 and nav1.9
5) Confidence 0.45 Published 2010 Journal BMC Neurosci Section Body Doc Link PMC2890014 Disease Relevance 0.91 Pain Relevance 1.66
It is interesting in this regard that Plassart-Schiess et al. [33] showed that a reduction in temperature produced a similar effect on WT Nav1.4 and Nav1.4/I693T.
Regulation (effect) of Nav1 associated with nav1.7
6) Confidence 0.45 Published 2007 Journal Mol Pain Section Body Doc Link PMC1781932 Disease Relevance 0.83 Pain Relevance 0.97
In an attempt to investigate further the functional role of Nav channels in mature spermatozoa we analyzed the effect of the Nav activator veratridine on sperm motility.
Spec (analyzed) Regulation (effect) of Nav in sperm associated with sperm disorder
7) Confidence 0.44 Published 2009 Journal Reprod Biol Endocrinol Section Body Doc Link PMC2724540 Disease Relevance 0.43 Pain Relevance 0.68
The authors concluded that the tested toxins “exert functional properties resembling local anesthetics with respect to their effect on steady-state inactivation of NaV1.6.”
Regulation (effect) of NaV1 associated with local anesthetic
8) Confidence 0.44 Published 2010 Journal Marine Drugs Section Body Doc Link PMC2866490 Disease Relevance 0 Pain Relevance 0.77
Finally, Nav1.4 and Nav1.5 are muscle sodium channels that control the excitability of the skeletal and cardiac myocytes, respectively.
Regulation (control) of Nav1 in cardiac myocytes associated with sodium channel
9) Confidence 0.44 Published 2003 Journal Genome Biol Section Body Doc Link PMC153452 Disease Relevance 0.18 Pain Relevance 1.56
Finally, Nav1.4 and Nav1.5 are muscle sodium channels that control the excitability of the skeletal and cardiac myocytes, respectively.
Regulation (control) of Nav1 in cardiac myocytes associated with sodium channel
10) Confidence 0.44 Published 2003 Journal Genome Biol Section Body Doc Link PMC153452 Disease Relevance 0.18 Pain Relevance 1.56
In an effort to characterize these interactions, Penzotti et al. [51] undertook a quantitative study of change in binding and unbinding rates with mutations of each of the Nav1.4 vestibule residues known to influence TTX binding and compared them with STX, yielding ??
Regulation (influence) of Nav1 in vestibule associated with tetrodotoxin
11) Confidence 0.42 Published 2010 Journal Marine Drugs Section Body Doc Link PMC2852835 Disease Relevance 0 Pain Relevance 0.93
Computer simulations of the effect of mutant NaV1.7 channels in model DRG neurons have in fact shown that the hyperpolarized shift in the activation of channels is the key factor in inducing neuron hyperexcitability, whereas slow inactivation modulates the effect on the firing frequency of these neurons [22].
Regulation (effect) of NaV1 in neuron associated with hyperexcitability
12) Confidence 0.37 Published 2008 Journal Mol Pain Section Body Doc Link PMC2262064 Disease Relevance 0.39 Pain Relevance 0.22
subunits regulates Nav assembly and activity [13-15].
Regulation (regulates) of Nav associated with sodium channel
13) Confidence 0.32 Published 2010 Journal Mol Neurodegener Section Body Doc Link PMC3022600 Disease Relevance 0.37 Pain Relevance 0.38
Our results indicate that, like many of the previously-reported SCN5A mutations in young children, the F1473C mutation, which appeared de novo in the proband of this study, causes marked changes in Nav1.5 channel inactivation that are predicted to have severe physiological consequences.
Regulation (changes) of Nav1
14) Confidence 0.32 Published 2007 Journal PLoS ONE Section Body Doc Link PMC2082660 Disease Relevance 0 Pain Relevance 0.19
The specific type of fibre expressing Nav1.8, the distribution of Nav1.8 throughout the human dental pulp, and the longitudinal changes in the Nav1.8-immunoreactivity caused by pulpal inflammation, all require further study.


Regulation (changes) of Nav1.8-immunoreactivity in dental pulp associated with inflammation and nav1.8
15) Confidence 0.27 Published 2005 Journal BMC Oral Health Section Body Doc Link PMC1183220 Disease Relevance 0.58 Pain Relevance 1.22
Further studies of the time-course of the disease, and severity of pain and/or inflammation, are necessary to elucidate the role and regulation of Nav1.8 ion channels in the pathophysiology of trigeminal pain.
Regulation (regulation) of Nav1 associated with pain, inflammation, nav1.8 and disease
16) Confidence 0.27 Published 2005 Journal BMC Oral Health Section Body Doc Link PMC1183220 Disease Relevance 0.74 Pain Relevance 1.31
Our essential result and hypothesis to follow are that EGF induced upregulation of Nav1.7 mRNA and VGSC protein synthesis, most of which was inserted in plasma membrane and led to the observed enhancement of MCBs.
Regulation (upregulation) of Nav1 in plasma associated with sodium channel and nav1.7
17) Confidence 0.25 Published 2007 Journal Mol Cancer Section Body Doc Link PMC2211503 Disease Relevance 0.56 Pain Relevance 0.32
In the absence of molecular selectivity for one Nav1 subtype, it is possible to specifically target Nav1 channels in a given conformational state while preserving sodium channel–dependent impulse conduction.
Spec (possible) Regulation (target) of Nav1 associated with sodium channel
18) Confidence 0.24 Published 2008 Journal The Journal of General Physiology Section Body Doc Link PMC2346569 Disease Relevance 0.73 Pain Relevance 1.81
Our previous work also did not show a significant change in another sodium channel isoform Nav1.8 in BMS, whereas the levels of the heat and capsaicin receptor, transient receptor potential Vanilloid (TRPV1), were increased [31].
Regulation (change) of Nav1 associated with qutenza, burning mouth syndrome, sodium channel and nav1.8
19) Confidence 0.24 Published 2010 Journal BMC Neurosci Section Body Doc Link PMC2890014 Disease Relevance 2.02 Pain Relevance 1.76
We could not detect any significant changes in the levels of Nav?
Neg (not) Regulation (changes) of Nav associated with sodium channel
20) Confidence 0.19 Published 2010 Journal Mol Neurodegener Section Body Doc Link PMC3022600 Disease Relevance 0.06 Pain Relevance 0.63

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