INT196687

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Context Info
Confidence 0.06
First Reported 2006
Last Reported 2010
Negated 0
Speculated 1
Reported most in Body
Documents 6
Total Number 13
Disease Relevance 3.85
Pain Relevance 1.32

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

plasma membrane (SCNN1G)
Anatomy Link Frequency
vesicles 1
SCNN1G (Homo sapiens)
Pain Link Frequency Relevance Heat
agonist 37 99.46 Very High Very High Very High
fibrosis 43 99.20 Very High Very High Very High
bradykinin 60 96.84 Very High Very High Very High
Kinase C 12 96.72 Very High Very High Very High
Dopamine 6 93.68 High High
cytokine 126 91.68 High High
aspirin 6 86.80 High High
cINOD 6 86.08 High High
Inflammatory mediators 120 83.80 Quite High
Inflammation 204 76.24 Quite High
Disease Link Frequency Relevance Heat
Cystic Fibrosis 43 99.20 Very High Very High Very High
Natriuresis 12 98.04 Very High Very High Very High
Heart Rate Under Development 94 97.44 Very High Very High Very High
Colitis 18 92.60 High High
Sepsis 24 89.60 High High
Diarrhoea 48 88.80 High High
Inflammatory Bowel Disease 24 86.36 High High
INFLAMMATION 336 85.84 High High
Pneumonia 6 80.36 Quite High
Bacterial Pneumonia 6 77.08 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Increased extrusion of K+ ions in the presence of 1-EBIO may locally build up an electrical gradient resulting in elevated ENaC activity.
Positive_regulation (resulting) of ENaC
1) Confidence 0.06 Published 2010 Journal Respir Res Section Body Doc Link PMC2889873 Disease Relevance 0.06 Pain Relevance 0
Intriguingly, K Ca3.1 channel opener still activated ENaC.
Positive_regulation (activated) of ENaC
2) Confidence 0.06 Published 2010 Journal Respir Res Section Body Doc Link PMC2889873 Disease Relevance 0.07 Pain Relevance 0
Another possibility is that 1-EBIO directly stimulates ENaC.
Positive_regulation (stimulates) of ENaC
3) Confidence 0.05 Published 2010 Journal Respir Res Section Body Doc Link PMC2889873 Disease Relevance 0.06 Pain Relevance 0.03
This lack of response to aldosterone could be reproduced by incubation of healthy human colonic tissue with TNF and IFN gamma, which reduced electrogenic sodium transport and lead to a reduced upregulation of ENaC mRNA [89].
Positive_regulation (upregulation) of ENaC
4) Confidence 0.05 Published 2006 Journal J Inflamm (Lond) Section Body Doc Link PMC1562419 Disease Relevance 0.14 Pain Relevance 0.03
In isolated congenital CFTR dysfunction (cystic fibrosis) an increase in sodium transport by an increase in apical ENaC and basolateral Na/K ATPase activity in the airways can compensate for a reduction in alveolar chloride and sodium transport.
Positive_regulation (increase) of ENaC associated with fibrosis and cystic fibrosis
5) Confidence 0.04 Published 2006 Journal J Inflamm (Lond) Section Body Doc Link PMC1562419 Disease Relevance 0.98 Pain Relevance 0.13
K+ channel openers restore the suppressed ENaC activity in vitro to a significant extent.
Positive_regulation (restore) of ENaC
6) Confidence 0.04 Published 2010 Journal Respir Res Section Body Doc Link PMC2889873 Disease Relevance 0 Pain Relevance 0.03
Increased extrusion of K+ ions in the presence of 1-EBIO may locally build up an electrical gradient resulting in elevated ENaC activity.
Positive_regulation (elevated) of ENaC
7) Confidence 0.04 Published 2010 Journal Respir Res Section Body Doc Link PMC2889873 Disease Relevance 0.06 Pain Relevance 0
If the K+ channel openers restore the depressed ENaC and Na+/K+-ATPase by stimulating K+ influx which facilitates Na+/K+-ATPase in intact cells, no effects on ENaC should be observed in basolateral permeabilized monolayers.
Positive_regulation (restore) of ENaC
8) Confidence 0.04 Published 2010 Journal Respir Res Section Body Doc Link PMC2889873 Disease Relevance 0.08 Pain Relevance 0
The residual ENaC currents were no longer sensitive to verapamil under these Ca2+-depletion conditions (the ENaC current even increased by 0.4 ± 1.5% after correction of the run-down slope, P>0.05 compared with basal current, n = 4, Fig. 9D).
Positive_regulation (increased) of ENaC
9) Confidence 0.04 Published 2010 Journal Respir Res Section Body Doc Link PMC2889873 Disease Relevance 0 Pain Relevance 0
STNFR1 seemed to modulate TNF function by diverting it from classical TNF receptors to an alternative receptor activating ENaC [21].
Positive_regulation (activating) of ENaC
10) Confidence 0.03 Published 2006 Journal J Inflamm (Lond) Section Body Doc Link PMC1562419 Disease Relevance 0.82 Pain Relevance 0.09
This is for beta agonists achieved by cAMP mediated activation of Na/K ATPase function and subsequently ENaC function.
Positive_regulation (activation) of ENaC associated with agonist
11) Confidence 0.03 Published 2006 Journal J Inflamm (Lond) Section Body Doc Link PMC1562419 Disease Relevance 0.64 Pain Relevance 0.36
This effect is mediated by inhibition of ENaC and Na/K ATPase activity possibly mediated by an increase in intracellular calcium and/or pH.
Spec (possibly) Positive_regulation (mediated) of ENaC
12) Confidence 0.03 Published 2006 Journal J Inflamm (Lond) Section Body Doc Link PMC1562419 Disease Relevance 0.10 Pain Relevance 0.31
The effect was achieved partly by increase of trafficking of ENaC containing intracellular vesicles to the apical membrane leading to increased insertion of the channel and partly by activation of ENaC through extracellular signal-regulated kinase, phosphatidylinositol 3-kinase and protein kinase C [124].
Positive_regulation (activation) of ENaC in vesicles associated with kinase c
13) Confidence 0.03 Published 2006 Journal J Inflamm (Lond) Section Body Doc Link PMC1562419 Disease Relevance 0.87 Pain Relevance 0.35

General Comments

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