INT179744

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Context Info
Confidence 0.45
First Reported 2004
Last Reported 2009
Negated 0
Speculated 0
Reported most in Body
Documents 16
Total Number 16
Disease Relevance 12.32
Pain Relevance 6.14

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 (SLC1A2) transmembrane transport (SLC1A2)
Anatomy Link Frequency
spinal cord 3
astrocyte 3
neuronal 2
gray matter 2
plasma 1
SLC1A2 (Homo sapiens)
Pain Link Frequency Relevance Heat
excitatory amino acid 27 100.00 Very High Very High Very High
Spinal cord 205 99.84 Very High Very High Very High
Glutamate 842 99.70 Very High Very High Very High
Central nervous system 278 98.08 Very High Very High Very High
Multiple sclerosis 118 97.92 Very High Very High Very High
Inflammatory response 15 97.28 Very High Very High Very High
Neuronal excitability 2 97.00 Very High Very High Very High
Glutamate receptor 58 89.84 High High
nMDA receptor 3 86.88 High High
Inflammation 96 85.92 High High
Disease Link Frequency Relevance Heat
Neuromyelitis Optica 1131 99.58 Very High Very High Very High
Targeted Disruption 44 99.50 Very High Very High Very High
Stress 12 98.24 Very High Very High Very High
Demyelinating Disease 209 97.92 Very High Very High Very High
Motor Neuron Diseases 190 97.84 Very High Very High Very High
INFLAMMATION 111 96.92 Very High Very High Very High
Death 7 95.28 Very High Very High Very High
Hepatic Encephalopathy 2 95.16 Very High Very High Very High
Autoimmune Disease 40 93.80 High High
Pressure And Volume Under Development 30 85.20 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Marked reduction of EAAT2 in AQP4-deficient regions of NMO patient spinal cord lesions supports our immunocytochemical and immunoprecipitation data.
Negative_regulation (reduction) of EAAT2 in spinal cord associated with neuromyelitis optica and spinal cord
1) Confidence 0.45 Published 2008 Journal The Journal of Experimental Medicine Section Abstract Doc Link PMC2571922 Disease Relevance 0.96 Pain Relevance 0.40
Without complement, astrocytic membranes remain intact, but AQP4 is endocytosed with concomitant loss of Na+-dependent glutamate transport and loss of the excitatory amino acid transporter 2 (EAAT2) .
Negative_regulation (loss) of EAAT2 associated with glutamate and excitatory amino acid
2) Confidence 0.45 Published 2008 Journal The Journal of Experimental Medicine Section Abstract Doc Link PMC2571922 Disease Relevance 1.05 Pain Relevance 0.44
Without complement, astrocytic membranes remain intact, but AQP4 is endocytosed with concomitant loss of Na+-dependent glutamate transport and loss of the excitatory amino acid transporter 2 (EAAT2) .
Negative_regulation (loss) of excitatory amino acid transporter 2 associated with glutamate and excitatory amino acid
3) Confidence 0.45 Published 2008 Journal The Journal of Experimental Medicine Section Abstract Doc Link PMC2571922 Disease Relevance 1.05 Pain Relevance 0.44
NMO patient sera did not appreciably affect EAAT1 expression in these cells (Fig. 4 D), in contrast to EAAT2 loss from the plasma membrane.
Negative_regulation (loss) of EAAT2 in plasma associated with neuromyelitis optica
4) Confidence 0.45 Published 2008 Journal The Journal of Experimental Medicine Section Body Doc Link PMC2571922 Disease Relevance 0.69 Pain Relevance 0.08
EAAT2 loss may partially account for the destructive involvement of spinal cord gray matter which is characteristic of NMO.
Negative_regulation (loss) of EAAT2 in gray matter associated with neuromyelitis optica and spinal cord
5) Confidence 0.45 Published 2008 Journal The Journal of Experimental Medicine Section Body Doc Link PMC2571922 Disease Relevance 0.86 Pain Relevance 0.54
The marked loss of EAAT2 described in this report parallels loss of AQP4 in lesioned NMO spinal cord tissue and contrasts with the increases in EAAT2 and AQP4 reported in both active and chronic MS lesions (20).
Negative_regulation (loss) of EAAT2 in spinal cord associated with neuromyelitis optica, multiple sclerosis and spinal cord
6) Confidence 0.39 Published 2008 Journal The Journal of Experimental Medicine Section Body Doc Link PMC2571922 Disease Relevance 1.02 Pain Relevance 0.60
In this study, we demonstrate that: (a) when active complement is present, binding of NMO-IgG to AQP4 in astrocyte membranes causes membrane lesioning; (b) in the absence of complement, NMO-IgG causes antigen-specific removal of AQP4 from astrocytic membranes with reduction of Na+-dependent glutamate transport and loss of surface EAAT2; (c) transgenic expression of AQP4 in nonastrocytic cells, and physiological up-regulation of AQP4 in differentiating astrocytes, induces surface EAAT2 expression; (d) AQP4 and EAAT2 exist in astrocytic membranes as a macromolecular complex; and (e) regions of AQP4 loss in NMO spinal cord lesions are deficient in EAAT2.
Negative_regulation (deficient) of EAAT2 in astrocyte associated with targeted disruption, neuromyelitis optica, glutamate and spinal cord
7) Confidence 0.33 Published 2008 Journal The Journal of Experimental Medicine Section Body Doc Link PMC2571922 Disease Relevance 0.95 Pain Relevance 0.29
However, serum containing NMO-IgG induced rapid surface down-regulation of both GFP-AQP4 and EAAT2 (Fig. 4 A).
Negative_regulation (down-regulation) of EAAT2 associated with neuromyelitis optica
8) Confidence 0.33 Published 2008 Journal The Journal of Experimental Medicine Section Body Doc Link PMC2571922 Disease Relevance 0.63 Pain Relevance 0.17
NMO spinal cord lesions lack both AQP4 and EAAT2
Negative_regulation (lack) of EAAT2 in spinal cord associated with neuromyelitis optica and spinal cord
9) Confidence 0.33 Published 2008 Journal The Journal of Experimental Medicine Section Body Doc Link PMC2571922 Disease Relevance 0.50 Pain Relevance 0.35
Lesioned NMO spinal cord gray matter contrasts to normal appearing gray matter by exhibiting markedly reduced EAAT2, in addition to AQP4 loss and deposition of complement activation products (Fig. 5 B).
Negative_regulation (reduced) of EAAT2 in gray matter associated with neuromyelitis optica and spinal cord
10) Confidence 0.33 Published 2008 Journal The Journal of Experimental Medicine Section Body Doc Link PMC2571922 Disease Relevance 0.69 Pain Relevance 0.44
Together, these findings are consistent with absence of EAAT2 staining being a biological phenomenon within the NMO lesion.
Negative_regulation (absence) of EAAT2 associated with neuromyelitis optica
11) Confidence 0.32 Published 2008 Journal The Journal of Experimental Medicine Section Body Doc Link PMC2571922 Disease Relevance 0.77 Pain Relevance 0.47
A recent report that astrocytes lacking AQP4 express a reduced level of the astrocytic Na+-dependent excitatory amino acid transporter 2 (EAAT2; homologue of rodent GLT-1 [8]) led us to hypothesize that if NMO-IgG altered the expression of EAAT2 in astrocyte membranes, this might impair glutamate homeostasis (6).
Negative_regulation (reduced) of excitatory amino acid transporter 2 in astrocyte associated with neuromyelitis optica, glutamate and excitatory amino acid
12) Confidence 0.29 Published 2008 Journal The Journal of Experimental Medicine Section Body Doc Link PMC2571922 Disease Relevance 1.32 Pain Relevance 0.46
Our immunohistochemical analysis of nonpathologic human CNS tissue (both cortical and spinal cord) reveal that EAAT2, but not EAAT1, normally colocalizes with AQP4 in gray matter astrocytes (Fig. 5 A) and that EAAT2 is most enriched in spinal cord gray matter (Fig. 5 B, top).
Negative_regulation (enriched) of EAAT2 in astrocytes associated with central nervous system and spinal cord
13) Confidence 0.28 Published 2008 Journal The Journal of Experimental Medicine Section Body Doc Link PMC2571922 Disease Relevance 0.40 Pain Relevance 0.35
This elevation has been attributed to the loss of the glial cell excitatory amino acid transporter EAAT2 [103].

3.

Negative_regulation (loss) of EAAT2 in glial cell associated with excitatory amino acid
14) Confidence 0.16 Published 2009 Journal Orphanet J Rare Dis Section Body Doc Link PMC2656493 Disease Relevance 1.09 Pain Relevance 0.27
This conclusion is further supported by studies demonstrating that inhibition of GLT-1 could facilitate hippocampal neurotransmission [37] and lead to increased neuronal excitability, as seen in for example hepatic encephalopathy [38].
Negative_regulation (inhibition) of GLT-1 in neuronal associated with neuronal excitability and hepatic encephalopathy
15) Confidence 0.08 Published 2004 Journal J Neuroinflammation Section Body Doc Link PMC533886 Disease Relevance 0.25 Pain Relevance 0.22
Even more convincing for the role of astroglia in keeping the [Glu]ec low, it has been demonstrated with knockout techniques in rats that loss of GLT-1 or GLAST produces elevated [Glu]ec and neurodegeneration characteristic of excitotoxicity, while the loss of neuronal glutamate transporter does not elevate [Glu]ec [15].


Negative_regulation (loss) of GLT-1 in neuronal associated with targeted disruption and glutamate
16) Confidence 0.07 Published 2004 Journal J Neuroinflammation Section Body Doc Link PMC533886 Disease Relevance 0.10 Pain Relevance 0.62

General Comments

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