INT118518

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Context Info
Confidence 0.56
First Reported 2004
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 7
Total Number 11
Disease Relevance 5.31
Pain Relevance 2.59

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

mitochondrion (Slc8a1) plasma membrane (Slc8a1) transmembrane transport (Slc8a1)
response to stress (Slc8a1)
Anatomy Link Frequency
neuronal 4
cardiomyocytes 1
neurons 1
heart 1
Slc8a1 (Rattus norvegicus)
Pain Link Frequency Relevance Heat
Potency 6 99.56 Very High Very High Very High
ischemia 285 99.24 Very High Very High Very High
nMDA receptor 177 99.16 Very High Very High Very High
Glutamate 380 97.96 Very High Very High Very High
Glutamate receptor 17 92.80 High High
antagonist 7 83.36 Quite High
action potential duration 6 76.80 Quite High
Inflammation 5 75.00 Quite High
Central nervous system 7 68.84 Quite High
bDMF 15 67.72 Quite High
Disease Link Frequency Relevance Heat
Brain Hemorrhage 190 99.24 Very High Very High Very High
Stress 32 99.16 Very High Very High Very High
Cv Unclassified Under Development 81 98.76 Very High Very High Very High
Hypoxia 121 98.74 Very High Very High Very High
Death 193 98.60 Very High Very High Very High
Injury 81 96.64 Very High Very High Very High
Diabetes Mellitus 76 96.32 Very High Very High Very High
Myocardial Infarction 8 95.06 Very High Very High Very High
Apoptosis 249 90.08 High High
Body Weight 4 89.28 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
The most remarkable decrease of neural (NeuN) and astroglial protein (GFAP) 24 h after focal cerebral ischemia supports evidence demonstrating that increased NCX1 and NR2B-containing NMDA receptor is closely associated with Ca2+-dependent neuronal injury in the penumbra.
Positive_regulation (increased) of NCX1 in neuronal associated with brain hemorrhage, nmda receptor, ischemia and injury
1) Confidence 0.56 Published 2010 Journal Anatomy & Cell Biology Section Body Doc Link PMC3015038 Disease Relevance 0.57 Pain Relevance 0.34
These findings imply that intracellular Na+ accumulation via decreased Na+/K+-ATPase exacerbate the Ca2+ overload cooperated by the increased NCX1 and NR2B-containing NMDA receptor which may play an important role in the pathogenesis of the penumbra.



Positive_regulation (increased) of NCX1 associated with nmda receptor
2) Confidence 0.38 Published 2010 Journal Anatomy & Cell Biology Section Abstract Doc Link PMC3015038 Disease Relevance 0.44 Pain Relevance 0.37
Therefore, intracellular Na+ accumulation plays a critical role in NCX1 and/or NMDA-induced neuronal cell death by participating in mechanisms that brings about Ca2+ overload and accelerates glutamate release from the astrocytes.
Positive_regulation (accumulation) of NCX1 in neuronal associated with glutamate and death
3) Confidence 0.38 Published 2010 Journal Anatomy & Cell Biology Section Body Doc Link PMC3015038 Disease Relevance 0.32 Pain Relevance 0.35
Our results suggest that increased reverse NCX1 in the penumbra participates in Na+/K+-ATPase-dependent amplification of NMDA-induced Ca2+ influx in ischemic depolarized neuronal cells.


Positive_regulation (increased) of NCX1 in neuronal
4) Confidence 0.33 Published 2010 Journal Anatomy & Cell Biology Section Body Doc Link PMC3015038 Disease Relevance 0.43 Pain Relevance 0.18
In particular, ouabain-induced drop in the driving force of Ca2+ influx via NMDA channels was offset by an increased driving force of reverse NCX1 (Czyz et al., 2002).
Positive_regulation (increased) of NCX1
5) Confidence 0.33 Published 2010 Journal Anatomy & Cell Biology Section Body Doc Link PMC3015038 Disease Relevance 0.43 Pain Relevance 0.58
The increased potency may be related to an enhanced ability of NCX-1024 to prevent nuclear factor-kappaB activation.
Positive_regulation (enhanced) of NCX-1024 associated with potency
6) Confidence 0.30 Published 2004 Journal J. Pharmacol. Exp. Ther. Section Abstract Doc Link 15128863 Disease Relevance 0.58 Pain Relevance 0.42
In conclusion, hypoxia-reoxygenation stress increases intracellular Ca2+ content via enhanced NCX-mediated Ca2+ influx and decreased SERCA2a expression resulting in myocardial cell injury through intracellular Ca2+ overload in neonatal cardiomyocytes.
Positive_regulation (enhanced) of NCX in cardiomyocytes associated with stress, hypoxia and injury
7) Confidence 0.23 Published 2010 Journal Yonsei Medical Journal Section Body Doc Link PMC2824862 Disease Relevance 0.88 Pain Relevance 0
The Ca2+ entry across the membrane through L-type Ca2+ channels is balanced by the efflux of Ca2+ from the cell via the NCX and PMCA1.36 In the present results, the density of L-type Ca2+ channels and PMCA1 appeared to decrease, but the quantification of NCX was higher in hypoxia-reoxygenated cells, similar to the observations in various animal models of heart failure.38,39 In a study using mice with cardiac-specific ablation of NCX, Ca2+ entry via reverse-mode NCX is a major cause of intracellular Ca2+ overload.40 When hypoxia-reoxygenated cells were treated with thiopental, transcription levels of PMCA1 and NCX were restored to the level of normal cells, but there was no alteration in the level of L-type Ca2+ channel.
Positive_regulation (restored) of NCX in heart associated with hypoxia and myocardial infarction
8) Confidence 0.21 Published 2010 Journal Yonsei Medical Journal Section Body Doc Link PMC2824862 Disease Relevance 0.57 Pain Relevance 0
Decreased SERCA2a expression should alter the balance of Ca2+ homeostasis in favor of increased Ca2+ extrusion via NCX and might be expected to reduce SR Ca2+ content.
Positive_regulation (increased) of NCX
9) Confidence 0.19 Published 2008 Journal Diabetes Section Body Doc Link PMC2494698 Disease Relevance 0.50 Pain Relevance 0.07
This proteolytic inactivation of NCX could allow further accumulation of Ca2+ or delay its elimination, that ultimately results in the destruction of the neurons.
Positive_regulation (inactivation) of NCX in neurons
10) Confidence 0.06 Published 2006 Journal BMC Neurosci Section Body Doc Link PMC1526740 Disease Relevance 0.27 Pain Relevance 0.14
Whether glutamate induced Ca2+ influx and the activation of calpain observed in our neuronal cells also results in the inactivation of NCX that can be prevented by estrogen remains to be investigated.
Positive_regulation (inactivation) of NCX in neuronal associated with glutamate
11) Confidence 0.05 Published 2006 Journal BMC Neurosci Section Body Doc Link PMC1526740 Disease Relevance 0.31 Pain Relevance 0.15

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