INT179756

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Context Info
Confidence 0.38
First Reported 2004
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 8
Total Number 8
Disease Relevance 2.95
Pain Relevance 3.06

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
plasma 4
astrocyte 2
cerebellum 2
SLC1A2 (Homo sapiens)
Pain Link Frequency Relevance Heat
Glutamate 441 100.00 Very High Very High Very High
Kinase C 18 98.96 Very High Very High Very High
adenocard 6 95.76 Very High Very High Very High
Spinal cord 60 95.36 Very High Very High Very High
nMDA receptor 28 89.12 High High
cytokine 60 88.92 High High
Locus ceruleus 6 82.16 Quite High
agonist 5 80.12 Quite High
Multiple sclerosis 53 78.96 Quite High
Central nervous system 90 76.84 Quite High
Disease Link Frequency Relevance Heat
Neuromyelitis Optica 348 99.72 Very High Very High Very High
Autism 314 99.68 Very High Very High Very High
Targeted Disruption 15 97.70 Very High Very High Very High
Aging 1 96.96 Very High Very High Very High
Attention Deficit Hyperactivity Disorder 23 92.88 High High
Disease 30 90.96 High High
Cognitive Disorder 64 89.28 High High
Fatigue 144 86.00 High High
Demyelinating Disease 81 78.96 Quite High
Immunodeficiency 6 58.08 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
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.
Positive_regulation (induces) of Gene_expression (expression) of EAAT2 in astrocyte associated with targeted disruption, neuromyelitis optica, glutamate and spinal cord
1) Confidence 0.38 Published 2008 Journal The Journal of Experimental Medicine Section Body Doc Link PMC2571922 Disease Relevance 0.97 Pain Relevance 0.37
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.
Positive_regulation (increased) of Gene_expression (Expression) of EAAT2 in plasma
2) Confidence 0.35 Published 2008 Journal The Journal of Experimental Medicine Section Body Doc Link PMC2571922 Disease Relevance 0.15 Pain Relevance 0.10
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.
Positive_regulation (depends) of Gene_expression (expression) of EAAT2 in plasma associated with neuromyelitis optica
3) Confidence 0.35 Published 2008 Journal The Journal of Experimental Medicine Section Body Doc Link PMC2571922 Disease Relevance 0.26 Pain Relevance 0.09
EAAT2 expression is up-regulated when AQP4 protein expression is induced in nonneural cells
Positive_regulation (up-regulated) of Gene_expression (expression) of EAAT2
4) Confidence 0.35 Published 2008 Journal The Journal of Experimental Medicine Section Body Doc Link PMC2571922 Disease Relevance 0.27 Pain Relevance 0.14
The synthesis of GLT-1 has been shown to be stimulated by factors acting via receptor tyrosine kinases and pathways dependent on phosphatidylinositol-3-kinase (PI3K) and the nuclear transcription factor NF?
Positive_regulation (on) of Gene_expression (synthesis) of GLT-1
5) Confidence 0.09 Published 2004 Journal J Neuroinflammation Section Body Doc Link PMC533886 Disease Relevance 0.08 Pain Relevance 0.65
The synthesis of GLT-1 has been shown to be stimulated by factors acting via receptor tyrosine kinases and pathways dependent on phosphatidylinositol-3-kinase (PI3K) and the nuclear transcription factor NF?
Positive_regulation (via) of Gene_expression (synthesis) of GLT-1
6) Confidence 0.09 Published 2004 Journal J Neuroinflammation Section Body Doc Link PMC533886 Disease Relevance 0.08 Pain Relevance 0.62
GLT-1 glutamate transporter-1

[Glu]ec extracellular glutamate concentration

Positive_regulation (glutamate transporter) of Gene_expression (glutamate transporter) of GLT-1 associated with glutamate
7) Confidence 0.08 Published 2004 Journal J Neuroinflammation Section Body Doc Link PMC533886 Disease Relevance 0.78 Pain Relevance 0.66
Furthermore, both the mRNA and protein levels of EAAT 1 and EAAT 2 were found to be significantly increased in the autistic cerebellum (Purcell et al., 2001).
Positive_regulation (increased) of Gene_expression (levels) of EAAT 2 in cerebellum associated with autism
8) Confidence 0.06 Published 2010 Journal Frontiers in Human Neuroscience Section Body Doc Link PMC3010743 Disease Relevance 0.39 Pain Relevance 0.43

General Comments

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