INT111049

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Context Info
Confidence 0.43
First Reported 2003
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 5
Total Number 10
Disease Relevance 4.39
Pain Relevance 6.25

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
optic nerve 6
14.2 2
oligodendrocyte 2
Nav1 (Mus musculus)
Pain Link Frequency Relevance Heat
Nav1.2 29 100.00 Very High Very High Very High
Nav1.6 23 100.00 Very High Very High Very High
Demyelination 8 98.90 Very High Very High Very High
addiction 54 97.76 Very High Very High Very High
Action potential 27 87.64 High High
Inflammation 27 75.00 Quite High
sodium channel 25 75.00 Quite High
nav1.3 3 72.08 Quite High
Nav1.1 3 71.44 Quite High
dorsal root ganglion 54 66.76 Quite High
Disease Link Frequency Relevance Heat
Death 1 99.52 Very High Very High Very High
Ganglion Cysts 73 99.04 Very High Very High Very High
Demyelinating Disease 16 98.90 Very High Very High Very High
Multiple Sclerosis 21 98.32 Very High Very High Very High
Targeted Disruption 7 84.40 Quite High
Nervous System Injury 2 78.56 Quite High
INFLAMMATION 27 75.00 Quite High
Experimental Autoimmune Encephalomyelitis 3 60.52 Quite High
Nociception 24 54.24 Quite High
Pain 18 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
At 7 months of age, however, Plp/- mice exhibit severe demyelination and oligodendrocyte cell death, leading to a profound reduction in Nav1.6 clusters, loss of the paranodal axoglial apparatus, and a marked increase in Nav1.2.
Negative_regulation (reduction) of Positive_regulation (increase) of Nav1 in oligodendrocyte associated with demyelination, nav1.2, nav1.6 and death
1) Confidence 0.43 Published 2003 Journal J. Neurosci. Res. Section Abstract Doc Link 12898531 Disease Relevance 0.75 Pain Relevance 0.62
These changes within the optic nerve are paralleled by decreased levels of Nav1.6 and increased Nav1.2 protein, together with increased levels of Nav1.2 mRNA, within retinal ganglion cells in EAE.
Negative_regulation (levels) of Positive_regulation (increased) of Nav1 in optic nerve associated with ganglion cysts, multiple sclerosis, nav1.2 and nav1.6
2) Confidence 0.42 Published 2003 Journal Brain Section Abstract Doc Link 12805113 Disease Relevance 1.17 Pain Relevance 1.73
These changes within the optic nerve are paralleled by decreased levels of Nav1.6 and increased Nav1.2 protein, together with increased levels of Nav1.2 mRNA, within retinal ganglion cells in EAE.
Negative_regulation (levels) of Positive_regulation (increased) of Nav1 in optic nerve associated with ganglion cysts, multiple sclerosis, nav1.2 and nav1.6
3) Confidence 0.42 Published 2003 Journal Brain Section Abstract Doc Link 12805113 Disease Relevance 1.18 Pain Relevance 1.75
These changes within the optic nerve are paralleled by decreased levels of Nav1.6 and increased Nav1.2 protein, together with increased levels of Nav1.2 mRNA, within retinal ganglion cells in EAE.
Negative_regulation (levels) of Positive_regulation (increased) of Nav1 in optic nerve associated with ganglion cysts, multiple sclerosis, nav1.2 and nav1.6
4) Confidence 0.42 Published 2003 Journal Brain Section Abstract Doc Link 12805113 Disease Relevance 1.17 Pain Relevance 1.74
The spontaneous augmentation of NaV1.9 was significantly suppressed in the presence of forskolin, and H-89 significantly inhibited this suppressive effect of forskolin (Figure 3).
Negative_regulation (suppressed) of Positive_regulation (augmentation) of NaV1
5) Confidence 0.22 Published 2010 Journal Marine Drugs Section Body Doc Link PMC2857352 Disease Relevance 0 Pain Relevance 0
Thus, apparent suppression of the spontaneous augmentation of NaV1.9 by PMA was largely due to hyperpolarizing shift of the h?
Negative_regulation (suppression) of Positive_regulation (augmentation) of NaV1
6) Confidence 0.22 Published 2010 Journal Marine Drugs Section Body Doc Link PMC2857352 Disease Relevance 0 Pain Relevance 0.05
This suggests that inhibition of the spontaneous augmentation of NaV1.9 by PKA activation was not due to the hyperpolarizing shift of the h?
Negative_regulation (inhibition) of Positive_regulation (augmentation) of NaV1
7) Confidence 0.18 Published 2010 Journal Marine Drugs Section Body Doc Link PMC2857352 Disease Relevance 0 Pain Relevance 0.03
We previously reported that the spontaneous augmentation of NaV1.9 was inhibited by recording with the nystatin-perforated patch clamp technique, and in the presence of intracellular ATP [11,17].
Negative_regulation (inhibited) of Positive_regulation (augmentation) of NaV1
8) Confidence 0.16 Published 2010 Journal Marine Drugs Section Body Doc Link PMC2857352 Disease Relevance 0.12 Pain Relevance 0.21
In the presence of a PKC inhibitor, calphostin C (100 nM), the effect of PMA on the augmentation of NaV1.9 was significantly inhibited (14.2 ± 2.8-fold: n = 10).
Negative_regulation (inhibited) of Positive_regulation (augmentation) of NaV1 in 14.2
9) Confidence 0.16 Published 2010 Journal Marine Drugs Section Body Doc Link PMC2857352 Disease Relevance 0 Pain Relevance 0.11
These results indicate that the spontaneous augmentation of NaV1.9 is suppressed by activation of PKA.
Negative_regulation (suppressed) of Positive_regulation (augmentation) of NaV1
10) Confidence 0.16 Published 2010 Journal Marine Drugs Section Body Doc Link PMC2857352 Disease Relevance 0 Pain Relevance 0

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