INT47992

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Context Info
Confidence 0.78
First Reported 1995
Last Reported 2010
Negated 2
Speculated 0
Reported most in Abstract
Documents 14
Total Number 15
Disease Relevance 4.15
Pain Relevance 3.83

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

transport (Scn8a) plasma membrane (Scn8a) transmembrane transport (Scn8a)
Anatomy Link Frequency
myocytes 1
muscle 1
neurons 1
nervous system 1
Rat2 1
Scn8a (Mus musculus)
Pain Link Frequency Relevance Heat
sodium channel 23 100.00 Very High Very High Very High
Nav1.6 19 100.00 Very High Very High Very High
Nav1.2 11 99.98 Very High Very High Very High
addiction 3 97.40 Very High Very High Very High
Action potential 12 92.96 High High
chemokine 42 82.44 Quite High
tetrodotoxin 14 80.40 Quite High
Pain 2 74.24 Quite High
repetitive firing 2 73.44 Quite High
imagery 10 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Osteochondrodysplasias 27 100.00 Very High Very High Very High
Muscle Weakness 7 98.64 Very High Very High Very High
Muscle Disease 23 96.48 Very High Very High Very High
Neurological Disease 2 96.16 Very High Very High Very High
Thrombocytopenia 2 95.56 Very High Very High Very High
Paralysis 2 93.44 High High
Ataxia 5 92.56 High High
Death 18 91.92 High High
Dystonia 2 91.60 High High
Disease 22 90.24 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
These data suggest that the specialized kinetics of Purkinje Na channels depend directly on Scn8a expression.
Gene_expression (expression) of Scn8a
1) Confidence 0.78 Published 2006 Journal J. Neurophysiol. Section Abstract Doc Link 16687615 Disease Relevance 0.26 Pain Relevance 0.12
To test the effect of cerebellar Na(V)1.6 on motor coordination in mice, we used the Cre-lox system to eliminate Scn8a expression exclusively in Purkinje neurons (Purkinje KO) and/or granule neurons (granule KO).
Gene_expression (expression) of Scn8a in neurons
2) Confidence 0.78 Published 2006 Journal J. Neurophysiol. Section Abstract Doc Link 16687615 Disease Relevance 0.34 Pain Relevance 0.10
The mouse Scn8a sodium channel and its ortholog Na6 in the rat are abundantly expressed in the CNS.
Gene_expression (expressed) of Scn8a associated with sodium channel
3) Confidence 0.77 Published 1998 Journal J. Neurosci. Section Abstract Doc Link 9698304 Disease Relevance 0.37 Pain Relevance 0.20
Mutant med mice are ataxic and lack expression of the Scn8a gene, which encodes the NaV1.6 protein.
Gene_expression (expression) of Scn8a
4) Confidence 0.77 Published 2003 Journal J. Neurosci. Section Abstract Doc Link 12832512 Disease Relevance 0 Pain Relevance 0.28
In this study, we characterized transient (I(NaT)), persistent (I(N)(aP)), and resurgent (I(res)) sodium currents in Na(v)1.6-null mice (med mouse, Na(v)1.6(-/-)) lacking expression of the sodium channel gene Scn8a.
Neg (lacking) Gene_expression (expression) of Scn8a associated with sodium channel
5) Confidence 0.76 Published 2007 Journal J. Neurophysiol. Section Abstract Doc Link 17522178 Disease Relevance 0 Pain Relevance 0.12
The Scn8a gene encodes the voltage-gated Na channel alpha subunit Na(V)1.6, which is widely expressed throughout the nervous system.
Gene_expression (expressed) of Scn8a in nervous system
6) Confidence 0.68 Published 2006 Journal J. Neurophysiol. Section Abstract Doc Link 16687615 Disease Relevance 0.28 Pain Relevance 0.04
Scn8a channels coexpressed with the beta subunits exhibited a persistent current that became larger with increasing depolarization, which was not observed for either Rat1 or Rat2 channels.
Gene_expression (coexpressed) of Scn8a in Rat2
7) Confidence 0.67 Published 1998 Journal J. Neurosci. Section Abstract Doc Link 9698304 Disease Relevance 0.24 Pain Relevance 0.34
Both models started with identical K channel densities and kinetics, but one contained Nav1.2 channels, and the other Nav1.6 channels.
Gene_expression (channels) of Nav1.6 associated with nav1.2 and nav1.6
8) Confidence 0.65 Published 2010 Journal PLoS Computational Biology Section Body Doc Link PMC2924322 Disease Relevance 0 Pain Relevance 1.14
Mutant med mice are ataxic and lack expression of the Scn8a gene, which encodes the NaV1.6 protein.
Gene_expression (expression) of NaV1.6
9) Confidence 0.58 Published 2003 Journal J. Neurosci. Section Abstract Doc Link 12832512 Disease Relevance 0 Pain Relevance 0.28
Patch-clamp experiments were performed to investigate the behavior of voltage-activated inward currents in vas deferens myocytes from Na(V)1.6-null mice (Na(V)1.6(-/-)) lacking the expression of the Na(+) channel gene, Scn8a, and their wild-type littermates (Na(V)1.6(+/+)).
Neg (lacking) Gene_expression (expression) of Scn8a in myocytes
10) Confidence 0.56 Published 2010 Journal J. Cell. Physiol. Section Abstract Doc Link 20054822 Disease Relevance 0 Pain Relevance 0.17
In an MED family with a COL9A3 mutation patients presented with proximal muscle weakness (despite predominantly distal skeletal changes) and mildly elevated levels of creatine kinase (CK; an indicator of muscle degeneration and myopathy).
Gene_expression (mutation) of MED in muscle associated with osteochondrodysplasias, muscle disease and muscle weakness
11) Confidence 0.25 Published 2010 Journal Journal of Biomedicine and Biotechnology Section Body Doc Link PMC2875749 Disease Relevance 1.17 Pain Relevance 0
The med phenotype in mice is due to a mutation in the SCN8A gene resulting in loss of Nav1.6 expression.
Gene_expression (resulting) of SCN8A gene associated with nav1.6
12) Confidence 0.14 Published 2006 Journal Glia Section Abstract Doc Link 16078241 Disease Relevance 0.07 Pain Relevance 0.73
Moreover, HT29 cells expressing variable levels of CXCL12 (Hi and Med) demonstrated decreasing levels of total FAK protein (Figure 2C) coincident with diminished adherence (Figure 2D).
Gene_expression (expressing) of Med
13) Confidence 0.06 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2943927 Disease Relevance 0.25 Pain Relevance 0.12
Moreover, HT29 cells expressing variable levels of CXCL12 (Hi and Med) demonstrated decreasing levels of total FAK protein (Figure 2C) coincident with diminished adherence (Figure 2D).
Gene_expression (expressing) of Med
14) Confidence 0.05 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2943927 Disease Relevance 0.25 Pain Relevance 0.12
Because HAMA developed in all prior patients who received G-CSF with ChL6 RAIT, including patients 1 and 2, who received PBPC, patient 3 was given cyclosporin for 14 days.
Gene_expression (received) of ChL6 in ChL6
15) Confidence 0.01 Published 1995 Journal Cancer Res. Section Abstract Doc Link 7493370 Disease Relevance 0.91 Pain Relevance 0.07

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