INT9556

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Context Info
Confidence 0.59
First Reported 1992
Last Reported 2010
Negated 0
Speculated 2
Reported most in Body
Documents 47
Total Number 50
Disease Relevance 28.49
Pain Relevance 49.33

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
nerve 2
neuronal 1
sciatic nerve 1
neurons 1
muscle 1
NAV1 (Homo sapiens)
Pain Link Frequency Relevance Heat
Nav1.7 884 100.00 Very High Very High Very High
sodium channel 785 100.00 Very High Very High Very High
nav1.8 206 100.00 Very High Very High Very High
Nav1.1 46 100.00 Very High Very High Very High
Mexiletine 32 99.92 Very High Very High Very High
Trigeminal neuralgia 6 99.84 Very High Very High Very High
diabetic neuropathy 10 99.74 Very High Very High Very High
Paroxysmal extreme pain disorder 332 99.72 Very High Very High Very High
Analgesic 66 99.72 Very High Very High Very High
Lasting pain 72 99.48 Very High Very High Very High
Disease Link Frequency Relevance Heat
Headache 9 99.84 Very High Very High Very High
Diabetic Neuropathy 10 99.74 Very High Very High Very High
Somatoform Disorder 348 99.72 Very High Very High Very High
Neuropathic Pain 235 99.60 Very High Very High Very High
Pain 827 99.48 Very High Very High Very High
Pulpitis 24 99.28 Very High Very High Very High
Neuralgia 7 99.28 Very High Very High Very High
Syndrome 46 99.12 Very High Very High Very High
Facial Pain 22 99.12 Very High Very High Very High
Herpes Simplex Virus Infection 7 99.08 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
We found that Nav1.7 was downregulated in TN (P=0.017) and Nav1.3 was upregulated in these patients (P=0.043).
Negative_regulation (downregulated) of Nav1 associated with nav1.3, trigeminal neuralgia and nav1.7
1) Confidence 0.59 Published 2009 Journal Neuroscience Section Abstract Doc Link 19699781 Disease Relevance 1.07 Pain Relevance 2.01
Recent studies using an Nav1.8 antisense oligonucleotide in an animal model of chronic pain indicated that selective blockade of Nav1.8 was analgesic and could provide effective analgesia with a reduction in the adverse events associated with nonselective VGSC blocking therapeutic agents.
Negative_regulation (blockade) of Nav1 associated with analgesic, lasting pain, sodium channel, nav1.8 and analgesia
2) Confidence 0.58 Published 2008 Journal J. Med. Chem. Section Abstract Doc Link 18176998 Disease Relevance 0.44 Pain Relevance 1.35
Veratridine acts by inhibiting Nav inactivation after spontaneous channel opening and, therefore, it is likely that effects could develop slowly, as channels spontaneously open and then become modified by veratridine.
Negative_regulation (inactivation) of Nav
3) Confidence 0.57 Published 2009 Journal Reprod Biol Endocrinol Section Body Doc Link PMC2724540 Disease Relevance 0.46 Pain Relevance 0.37
Interestingly, the human loss of Nav1.7 function was not replicated in mice, where a conventional knockout is lethal, and a nociceptor-specific knockout (Nassar et al., 2004) develops normally but displays a mild pain phenotype (resistance to inflammatory pain).
Negative_regulation (loss) of Nav1 in nociceptor associated with targeted disruption, pain, ipn, nociceptor and nav1.7
4) Confidence 0.52 Published 2008 Journal The Journal of General Physiology Section Body Doc Link PMC2346569 Disease Relevance 1.21 Pain Relevance 1.13
In contrast, antidepressant serotonin reuptake inhibitors that are not effective in treating post-herpetic neuralgia or diabetic neuropathy were weaker inhibitors of Nav1.7, with in vitro potencies mostly above their therapeutic concentration ranges.
Negative_regulation (inhibitors) of Nav1 associated with neuralgia, antidepressant, diabetic neuropathy, herpes simplex virus infection, nav1.7, serotonin and post herpetic neuralgia
5) Confidence 0.52 Published 2008 Journal The Journal of General Physiology Section Body Doc Link PMC2346569 Disease Relevance 0.77 Pain Relevance 1.73
Inhibition of Nav1.8 by these compounds may underlie their known analgesic effects in animal models.
Negative_regulation (Inhibition) of Nav1 associated with analgesic and nav1.8
6) Confidence 0.49 Published 2005 Journal Eur. J. Pharmacol. Section Abstract Doc Link 16325806 Disease Relevance 0.21 Pain Relevance 1.31
One recent study investigated pain within the orofacial pain region and showed an increase in Nav1.7 expression in pulpitis [22], while another study showed a decrease in Nav1.7 in the neuropathic orofacial pain condition trigeminal neuralgia (TN) [26].
Negative_regulation (decrease) of Nav1 associated with pain, pulpitis, face pain, neuropathic pain and nav1.7
7) Confidence 0.43 Published 2010 Journal BMC Neurosci Section Body Doc Link PMC2890014 Disease Relevance 1.81 Pain Relevance 2.19
A recent investigation in trigeminal neuralgia, a neuropathic pain condition, demonstrated that Nav1.7 levels were decreased.
Negative_regulation (decreased) of Nav1 associated with face pain, neuropathic pain and nav1.7
8) Confidence 0.43 Published 2010 Journal BMC Neurosci Section Body Doc Link PMC2890014 Disease Relevance 1.56 Pain Relevance 2.30
Both voltage-activated and deltamethrin-activated human Nav1.8 were inhibited by the sodium channel blockers BIII 890 CL, NW-1029, and mexiletine.
Negative_regulation (inhibited) of Nav1 associated with sodium channel, mexiletine and nav1.8
9) Confidence 0.43 Published 2005 Journal Eur. J. Pharmacol. Section Abstract Doc Link 16325806 Disease Relevance 0.22 Pain Relevance 1.34
On the other hand, block of Nav1.1 and Nav1.5 may contribute to the proconvulsive and proarrhythmic adverse reactions, especially observed during overdose.
Negative_regulation (block) of Nav1 associated with adverse drug reaction, nav1.1 and overdose
10) Confidence 0.43 Published 2009 Journal Pain Section Abstract Doc Link 19217209 Disease Relevance 0.39 Pain Relevance 1.41
On the other hand, block of Nav1.1 and Nav1.5 may contribute to the proconvulsive and proarrhythmic adverse reactions, especially observed during overdose.
Negative_regulation (block) of Nav1 associated with adverse drug reaction, nav1.1 and overdose
11) Confidence 0.43 Published 2009 Journal Pain Section Abstract Doc Link 19217209 Disease Relevance 0.39 Pain Relevance 1.41
Ranolazine also blocks wild-type Nav1.7 and Nav1.8 channels in a use-dependent manner.
Negative_regulation (blocks) of Nav1 associated with nav1.8 and nav1.7
12) Confidence 0.43 Published 2010 Journal Mol Pain Section Abstract Doc Link 20529343 Disease Relevance 0.56 Pain Relevance 1.47
Ranolazine also blocks wild-type Nav1.7 and Nav1.8 channels in a use-dependent manner.
Negative_regulation (blocks) of Nav1 associated with nav1.8 and nav1.7
13) Confidence 0.43 Published 2010 Journal Mol Pain Section Abstract Doc Link 20529343 Disease Relevance 0.56 Pain Relevance 1.47
Because these drugs can have adverse effects that limit their efficacy, more potent and selective Nav1 inhibitors are being pursued.
Negative_regulation (inhibitors) of Nav1 associated with sodium channel
14) Confidence 0.42 Published 2007 Journal Biochemistry Section Abstract Doc Link 18027973 Disease Relevance 0.44 Pain Relevance 0.94
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.”
Negative_regulation (inactivation) of NaV1 associated with local anesthetic
15) Confidence 0.42 Published 2010 Journal Marine Drugs Section Body Doc Link PMC2866490 Disease Relevance 0 Pain Relevance 0.76
It has been proposed that the high probability of slow inactivation of hNaV1.4 channels has a physiological role in muscle fatigue [112].
Negative_regulation (inactivation) of NaV1 in muscle associated with fatigue
16) Confidence 0.42 Published 2010 Journal Marine Drugs Section Body Doc Link PMC2866490 Disease Relevance 0.28 Pain Relevance 0.13
A UHTS campaign, using the membrane potential–based assay described to screen for inhibitors of Nav1.7, discovered the novel 1-benzazepin-2-one channel inhibitors (Hoyt et al., 2007; Williams et al., 2007).
Negative_regulation (inhibitors) of Nav1 associated with nav1.7
17) Confidence 0.39 Published 2008 Journal The Journal of General Physiology Section Body Doc Link PMC2346569 Disease Relevance 0.48 Pain Relevance 0.73
Similarly, tricyclic antidepressants, such as amitriptyline, which are efficacious in treating neuropathic pain, possess a broad spectrum of pharmacological activities including inhibition of Nav1 channels.
Negative_regulation (inhibition) of Nav1 associated with neuropathic pain, endep and tricyclic antidepressant
18) Confidence 0.39 Published 2008 Journal The Journal of General Physiology Section Body Doc Link PMC2346569 Disease Relevance 0.67 Pain Relevance 1.53
These data obtained with CDA54 strongly suggested that inhibition of PNS sodium channels alone is efficacious in animal models of neuropathic pain, and that limiting CNS exposures of Nav1 inhibitors is a viable approach to developing Nav1 inhibitors with an improved therapeutic index.
Negative_regulation (inhibitors) of Nav1 associated with peripheral nervous system, neuropathic pain and sodium channel
19) Confidence 0.38 Published 2008 Journal The Journal of General Physiology Section Body Doc Link PMC2346569 Disease Relevance 0.49 Pain Relevance 0.58
A comparison between therapeutic efficacy and ability to inhibit Nav1.7 channels for two classes of antidepressants, tricyclics and serotonin reuptake inhibitors, suggests a role of sodium channel inhibition in the efficacy of these compounds in treating neuropathic pain (Dick et al., 2007).
Negative_regulation (inhibit) of Nav1 associated with antidepressant, neuropathic pain, sodium channel, serotonin and nav1.7
20) Confidence 0.38 Published 2008 Journal The Journal of General Physiology Section Body Doc Link PMC2346569 Disease Relevance 0.78 Pain Relevance 1.58

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