INT250250

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Context Info
Confidence 0.37
First Reported 2008
Last Reported 2008
Negated 0
Speculated 0
Reported most in Body
Documents 1
Total Number 1
Disease Relevance 1.10
Pain Relevance 0.39

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 (AQP4, SLC1A2) transmembrane transport (AQP4, SLC1A2) transport (AQP4)
cytoplasm (AQP4)
Anatomy Link Frequency
astrocyte 3
AQP4 (Homo sapiens)
SLC1A2 (Homo sapiens)
Pain Link Frequency Relevance Heat
Glutamate 54 98.94 Very High Very High Very High
Spinal cord 15 95.36 Very High Very High Very High
Central nervous system 21 81.40 Quite High
Glutamate receptor 4 75.68 Quite High
excitatory amino acid 2 66.04 Quite High
Inflammatory response 1 60.64 Quite High
Multiple sclerosis 8 23.68 Low Low
Inflammation 7 5.00 Very Low Very Low Very Low
Demyelination 2 5.00 Very Low Very Low Very Low
anesthesia 1 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Targeted Disruption 3 99.98 Very High Very High Very High
Neuromyelitis Optica 87 96.70 Very High Very High Very High
INFLAMMATION 8 60.28 Quite High
Autoimmune Disease 3 57.16 Quite High
Demyelinating Disease 15 23.68 Low Low
Toxicity 5 5.00 Very Low Very Low Very Low
Neurodegenerative Disease 3 5.00 Very Low Very Low Very Low
Pressure And Volume Under Development 2 5.00 Very Low Very Low Very Low
Necrosis 1 5.00 Very Low Very Low Very Low
Disease Progression 1 5.00 Very Low Very Low Very Low

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.
Gene_expression (expression) of AQP4 in astrocyte Positive_regulation (induces) of Gene_expression (expression) of EAAT2 in astrocyte associated with targeted disruption, neuromyelitis optica, glutamate and spinal cord
1) Confidence 0.37 Published 2008 Journal The Journal of Experimental Medicine Section Body Doc Link PMC2571922 Disease Relevance 1.10 Pain Relevance 0.39

General Comments

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