INT143450

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Context Info
Confidence 0.43
First Reported 2007
Last Reported 2010
Negated 1
Speculated 0
Reported most in Body
Documents 3
Total Number 8
Disease Relevance 2.71
Pain Relevance 0.88

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

transport (Scn5a) plasma membrane (Scn5a) transmembrane transport (Scn5a)
Anatomy Link Frequency
neurons 1
hearts 1
Scn5a (Mus musculus)
Pain Link Frequency Relevance Heat
nav1.3 13 100.00 Very High Very High Very High
Nav1.1 3 100.00 Very High Very High Very High
Nav1.6 1 100.00 Very High Very High Very High
Nav1.2 1 100.00 Very High Very High Very High
nav1.8 1 99.84 Very High Very High Very High
imagery 30 78.56 Quite High
sodium channel 2 75.00 Quite High
Action potential 64 72.68 Quite High
fibrosis 132 72.40 Quite High
anesthesia 6 7.76 Low Low
Disease Link Frequency Relevance Heat
Targeted Disruption 31 100.00 Very High Very High Very High
Heart Arrhythmia 105 97.08 Very High Very High Very High
Arrhythmias 2 Under Development 162 96.04 Very High Very High Very High
Aging 60 93.34 High High
Channelopathies 6 93.28 High High
Heart Disease 6 79.28 Quite High
Disease 24 75.00 Quite High
Fibrosis 114 72.40 Quite High
Cv General 2 Under Development 6 71.20 Quite High
Heart Rate Under Development 30 39.20 Quite Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
A mouse model with targeted disruption of Scn5a has been established [9].
Negative_regulation (disruption) of Scn5a associated with targeted disruption
1) Confidence 0.43 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2824822 Disease Relevance 0.84 Pain Relevance 0.06
We investigated the mechanisms of this heterogeneity in a mouse model with heterozygous targeted disruption of Scn5a (Scn5a+/?
Negative_regulation (disruption) of Scn5a associated with targeted disruption
2) Confidence 0.43 Published 2010 Journal PLoS ONE Section Abstract Doc Link PMC2824822 Disease Relevance 0.60 Pain Relevance 0
mice, global Nav1.5 protein was reduced by 50±4% in ventricular lysates of animals with a severe phenotype versus WT littermates (p<0.001) and by only 21±7% for animals with a mild phenotype (p<0.05 versus severe phenotype, NS versus WT; Figure 6).
Negative_regulation (reduced) of Nav1.5 protein
3) Confidence 0.43 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2824822 Disease Relevance 0 Pain Relevance 0.12
We investigated the mechanisms of this heterogeneity in a mouse model with heterozygous targeted disruption of Scn5a (Scn5a+/?
Negative_regulation (disruption) of Scn5a associated with targeted disruption
4) Confidence 0.43 Published 2010 Journal PLoS ONE Section Abstract Doc Link PMC2824822 Disease Relevance 0.60 Pain Relevance 0
Our study points to a key similarity between Scn5a+/?
Negative_regulation (similarity) of Scn5a
5) Confidence 0.43 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2824822 Disease Relevance 0.23 Pain Relevance 0
mice with severe ventricular conduction defects, exhibit more myocardial rearrangements with aging than mice with a mild phenotype; (iii) only old mice with a severe phenotype have a markedly reduced conduction reserve and show spontaneous ventricular arrhythmias; (iv) symptomatic BrS patients carrying SCN5A mutations have more pronounced conduction slowing than asymptomatic patients; and (v) the expressivity of the conduction deficit in Scn5a+/?
Negative_regulation (deficit) of Scn5a associated with aging, heart arrhythmia and arrhythmias 2 under development
6) Confidence 0.43 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2824822 Disease Relevance 0.35 Pain Relevance 0.10
RT-PCR analysis detected Nav1.1, Nav1.2 and Nav1.6, but not Nav1.3, Nav1.4, Nav 1.5 or Nav1.8 Na+ channel alpha subunit gene expression in cultured Purkinje neurons, as observed in vivo.
Neg (not) Negative_regulation (detected) of Nav 1.5 in neurons associated with nav1.3, nav1.1, nav1.2, nav1.8 and nav1.6
7) Confidence 0.41 Published 2007 Journal J. Neurochem. Section Abstract Doc Link 17448145 Disease Relevance 0.07 Pain Relevance 0.60
In conclusion, we have for the first time associated the lack of the Scn3b gene with a ventricular arrhythmogenesis in intact perfused hearts whose features are similar to those shown in Scn5a+/?
Negative_regulation (shown) of Scn5a in hearts
8) Confidence 0.40 Published 2008 Journal Prog Biophys Mol Biol Section Body Doc Link PMC2764399 Disease Relevance 0 Pain Relevance 0

General Comments

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