INT179753

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Context Info
Confidence 0.59
First Reported 2004
Last Reported 2010
Negated 1
Speculated 1
Reported most in Body
Documents 28
Total Number 29
Disease Relevance 13.72
Pain Relevance 8.71

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
astrocytes 8
plasma 7
spinal cord 3
glial cell 1
cerebellum 1
SLC1A2 (Homo sapiens)
Pain Link Frequency Relevance Heat
Glutamate 1603 100.00 Very High Very High Very High
Central nervous system 493 100.00 Very High Very High Very High
excitatory amino acid 46 100.00 Very High Very High Very High
Spinal cord 345 99.82 Very High Very High Very High
Kinase C 30 98.96 Very High Very High Very High
Inflammation 166 98.40 Very High Very High Very High
addiction 23 97.80 Very High Very High Very High
Inflammatory response 28 97.68 Very High Very High Very High
cytokine 100 97.20 Very High Very High Very High
Glutamate receptor 107 96.44 Very High Very High Very High
Disease Link Frequency Relevance Heat
Neuromyelitis Optica 2001 99.92 Very High Very High Very High
Demyelinating Disease 380 99.36 Very High Very High Very High
INFLAMMATION 194 98.40 Very High Very High Very High
Autism 314 98.04 Very High Very High Very High
Targeted Disruption 74 97.38 Very High Very High Very High
Aging 1 96.96 Very High Very High Very High
Toxicity 121 96.00 Very High Very High Very High
Stress 34 95.36 Very High Very High Very High
Autoimmune Disease 69 94.20 High High
Attention Deficit Hyperactivity Disorder 31 92.88 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Those cells express both EAAT1 and EAAT2, but are devoid of AQP4 (Fig. 3).
Gene_expression (express) of EAAT2
1) Confidence 0.59 Published 2008 Journal The Journal of Experimental Medicine Section Body Doc Link PMC2571922 Disease Relevance 0.71 Pain Relevance 0.07
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).
Gene_expression (express) of EAAT2 in astrocyte associated with neuromyelitis optica, glutamate and excitatory amino acid
2) Confidence 0.59 Published 2008 Journal The Journal of Experimental Medicine Section Body Doc Link PMC2571922 Disease Relevance 1.33 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).
Gene_expression (expression) of EAAT2 in astrocyte associated with neuromyelitis optica, glutamate and excitatory amino acid
3) Confidence 0.59 Published 2008 Journal The Journal of Experimental Medicine Section Body Doc Link PMC2571922 Disease Relevance 1.11 Pain Relevance 0.42
A report that EAAT2 expression (Western blot and RT-PCR) is reduced in AQP4-null astrocytes (8) prompted us to evaluate glutamate toxicity as a potential outcome of IgG-induced AQP4 modulation.
Gene_expression (expression) of EAAT2 in astrocytes associated with toxicity and glutamate
4) Confidence 0.59 Published 2008 Journal The Journal of Experimental Medicine Section Body Doc Link PMC2571922 Disease Relevance 0.96 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.
Gene_expression (expression) of EAAT2 in astrocyte associated with targeted disruption, neuromyelitis optica, glutamate and spinal cord
5) Confidence 0.59 Published 2008 Journal The Journal of Experimental Medicine Section Body Doc Link PMC2571922 Disease Relevance 0.96 Pain Relevance 0.37
NMO spinal cord tissue of normal appearance expresses normal levels of APQ4 and EAAT2 and lacks evidence of complement deposition (Fig. 5 B).
Gene_expression (expresses) of EAAT2 in spinal cord associated with neuromyelitis optica and spinal cord
6) Confidence 0.59 Published 2008 Journal The Journal of Experimental Medicine Section Body Doc Link PMC2571922 Disease Relevance 0.58 Pain Relevance 0.37
We excluded the possibility that NMO serum might contain EAAT2-specific IgG in addition to AQP4 IgG, by testing the effect of NMO serum on plasma membrane expression of EAAT2 in HEK-293 cells transfected with AQP5-GFP (Fig. 4 C).
Gene_expression (expression) of EAAT2 in plasma associated with neuromyelitis optica
7) Confidence 0.59 Published 2008 Journal The Journal of Experimental Medicine Section Body Doc Link PMC2571922 Disease Relevance 0.72 Pain Relevance 0.06
EAAT2 accounts for >90% of glutamate uptake in the CNS (9), is critical for clearing glutamate from excitatory synapses, and is expressed selectively in astrocytes.
Gene_expression (expressed) of EAAT2 in astrocytes associated with glutamate and central nervous system
8) Confidence 0.52 Published 2008 Journal The Journal of Experimental Medicine Section Body Doc Link PMC2571922 Disease Relevance 1.05 Pain Relevance 0.44
EAAT2 and EAAT1 are enriched in separate microdomains of the astrocytic plasma membrane (18, 19); EAAT2 is enriched in regions that highly express AQP4 (18).
Gene_expression (enriched) of EAAT2 in plasma
9) Confidence 0.51 Published 2008 Journal The Journal of Experimental Medicine Section Body Doc Link PMC2571922 Disease Relevance 0.50 Pain Relevance 0.08
AQP4 and EAAT2 coimmunoprecipitate
Gene_expression (coimmunoprecipitate) of EAAT2
10) Confidence 0.51 Published 2008 Journal The Journal of Experimental Medicine Section Body Doc Link PMC2571922 Disease Relevance 0.51 Pain Relevance 0.08
NMO spinal cord lesions lack both AQP4 and EAAT2
Neg (lack) Gene_expression (lack) of EAAT2 in spinal cord associated with neuromyelitis optica and spinal cord
11) Confidence 0.51 Published 2008 Journal The Journal of Experimental Medicine Section Body Doc Link PMC2571922 Disease Relevance 0.50 Pain Relevance 0.35
EAAT2 and EAAT1 are enriched in separate microdomains of the astrocytic plasma membrane (18, 19); EAAT2 is enriched in regions that highly express AQP4 (18).
Gene_expression (enriched) of EAAT2 in plasma
12) Confidence 0.51 Published 2008 Journal The Journal of Experimental Medicine Section Body Doc Link PMC2571922 Disease Relevance 0.44 Pain Relevance 0.08
Commercial antibodies (AQP4, EAAT1, EAAT2, or GFP; 2 ?
Gene_expression (antibodies) of EAAT2
13) Confidence 0.51 Published 2008 Journal The Journal of Experimental Medicine Section Body Doc Link PMC2571922 Disease Relevance 0.10 Pain Relevance 0.13
NMO spinal cord tissue of normal appearance expresses normal levels of APQ4 and EAAT2 and lacks evidence of complement deposition (Fig. 5 B).
Gene_expression (levels) of EAAT2 in spinal cord associated with neuromyelitis optica and spinal cord
14) Confidence 0.46 Published 2008 Journal The Journal of Experimental Medicine Section Body Doc Link PMC2571922 Disease Relevance 0.57 Pain Relevance 0.36
Expression of EAAT2 protein on the surface of cells expressing AQP might be increased through upregulated mRNA translation or, alternatively, through a posttranslational modification increasing EAAT2 protein stability or trafficking to the plasma membrane.
Gene_expression (Expression) of EAAT2 in plasma
15) Confidence 0.46 Published 2008 Journal The Journal of Experimental Medicine Section Body Doc Link PMC2571922 Disease Relevance 0.15 Pain Relevance 0.10
We conclude that restriction of EAAT2 expression to the plasma membrane of astrocytes is determined by dependence on astrocytic AQP expression.
Gene_expression (expression) of EAAT2 in plasma associated with addiction
16) Confidence 0.46 Published 2008 Journal The Journal of Experimental Medicine Section Body Doc Link PMC2571922 Disease Relevance 0.08 Pain Relevance 0.18
These complementary observations accord with reports that EAAT2 protein expression is restricted to astrocytes, despite ubiquitous expression of EAAT2 mRNA (11).
Gene_expression (expression) of EAAT2 in astrocytes
17) Confidence 0.46 Published 2008 Journal The Journal of Experimental Medicine Section Body Doc Link PMC2571922 Disease Relevance 0.08 Pain Relevance 0.14
Our finding that both are depleted from plasma membranes of cultured astrocytes exposed to NMO-IgG is consistent with the notion that EAAT2 expression depends on AQP4 expression.
Gene_expression (expression) of EAAT2 in plasma associated with neuromyelitis optica
18) Confidence 0.46 Published 2008 Journal The Journal of Experimental Medicine Section Body Doc Link PMC2571922 Disease Relevance 0.26 Pain Relevance 0.09
In cells grown for 7 d in astrocyte differentiation medium, plasma membrane expression of both AQP4 and EAAT2 is enhanced (Fig. 2, B and C).
Gene_expression (expression) of EAAT2 in plasma
19) Confidence 0.46 Published 2008 Journal The Journal of Experimental Medicine Section Body Doc Link PMC2571922 Disease Relevance 0.33 Pain Relevance 0.14
These complementary observations accord with reports that EAAT2 protein expression is restricted to astrocytes, despite ubiquitous expression of EAAT2 mRNA (11).
Gene_expression (expression) of EAAT2 mRNA in astrocytes
20) Confidence 0.46 Published 2008 Journal The Journal of Experimental Medicine Section Body Doc Link PMC2571922 Disease Relevance 0.08 Pain Relevance 0.15

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