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Context Info
Confidence 0.05
First Reported 2008
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 9
Total Number 11
Disease Relevance 12.75
Pain Relevance 3.52

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

transport (AQP4) plasma membrane (AQP4) transmembrane transport (AQP4)
cytoplasm (AQP4)
Anatomy Mention Frequency
astrocytes 3
plasma 1
M-1 1
AQP4 (Homo sapiens)
nmo (Drosophila melanogaster)
Pain Term Frequency Confidence Heat
Glutamate 432 98.16 Very High Very High Very High
Multiple sclerosis 106 98.00 Very High Very High Very High
Spinal cord 123 96.92 Very High Very High Very High
Central nervous system 180 94.40 High High
Demyelination 37 87.44 High High
Glutamate receptor 32 86.84 High High
excitatory amino acid 16 83.12 Quite High
Neuritis 33 79.24 Quite High
Inflammation 59 78.88 Quite High
Inflammatory response 8 71.80 Quite High
Disease Term Frequency Confidence Heat
Neuromyelitis Optica 978 100.00 Very High Very High Very High
Demyelinating Disease 198 98.00 Very High Very High Very High
Disease 42 96.84 Very High Very High Very High
Neurological Disease 27 94.44 High High
Systemic Lupus Erythematosus 45 93.80 High High
Targeted Disruption 24 90.32 High High
Pressure And Volume Under Development 16 86.08 High High
Necrosis 8 85.04 High High
Optic Neuritis 30 79.24 Quite High
INFLAMMATION 67 78.88 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
The potential pathogenic sequelae we demonstrate in this study for NMO-IgG binding to AQP4-rich membranes in primary astrocytes are both competing and cooperative.
AQP4 Binding (binding) of NMO-IgG in astrocytes associated with neuromyelitis optica
1) Confidence 0.05 Published 2008 Journal The Journal of Experimental Medicine Section Body Doc Link PMC2571922 Disease Relevance 0.94 Pain Relevance 0.61
Binding of NMO-IgG to the extracellular domain of AQP4 reversibly down-regulates its plasma membrane expression (6).
AQP4 Binding (Binding) of NMO-IgG in plasma associated with neuromyelitis optica
2) Confidence 0.05 Published 2008 Journal The Journal of Experimental Medicine Section Body Doc Link PMC2571922 Disease Relevance 1.53 Pain Relevance 0.31
Thus, binding of NMO-IgG to astrocytic AQP4 initiates several potentially neuropathogenic mechanisms: complement activation, AQP4 and EAAT2 down-regulation, and disruption of glutamate homeostasis.



AQP4 Binding (binding) of NMO-IgG associated with neuromyelitis optica and glutamate
3) Confidence 0.04 Published 2008 Journal The Journal of Experimental Medicine Section Abstract Doc Link PMC2571922 Disease Relevance 0.81 Pain Relevance 0.39
Our observations in primary astrocytes, type 2 differentiated CG-4 cells, and transfected nonneural HEK-293 cells indicate that the interaction of NMO-IgG with AQP4 induces at least three possible outcomes, each potentially pathogenic: (a) complement activation, (b) down-regulation of AQP4, and (c) coupled down-regulation of the EAAT2 glutamate transporter.
AQP4 Binding (interaction) of NMO-IgG in astrocytes associated with neuromyelitis optica and glutamate
4) Confidence 0.04 Published 2008 Journal The Journal of Experimental Medicine Section Body Doc Link PMC2571922 Disease Relevance 0.22 Pain Relevance 0.23
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.
AQP4 Binding (binding) of NMO-IgG in astrocyte associated with targeted disruption, neuromyelitis optica, glutamate and spinal cord
5) Confidence 0.04 Published 2008 Journal The Journal of Experimental Medicine Section Body Doc Link PMC2571922 Disease Relevance 0.99 Pain Relevance 0.45
Thus, binding of NMO-IgG to astrocytic AQP4 initiates several potentially neuropathogenic mechanisms: complement activation, AQP4 and EAAT2 down-regulation, and disruption of glutamate homeostasis.



AQP4 Binding (binding) of NMO-IgG associated with neuromyelitis optica and glutamate
6) Confidence 0.04 Published 2008 Journal The Journal of Experimental Medicine Section Abstract Doc Link PMC2571922 Disease Relevance 0.81 Pain Relevance 0.40
In the presence of active complement, binding of NMO-IgG to surface AQP4 initiated robust complement activation and rapid loss of the target cell membrane's integrity.
AQP4 Binding (binding) of NMO-IgG associated with neuromyelitis optica
7) Confidence 0.04 Published 2008 Journal The Journal of Experimental Medicine Section Body Doc Link PMC2571922 Disease Relevance 1.56 Pain Relevance 0.35
Our results suggest M-23 AQP4 as initial and major target antigen for antibody binding in definite and high risk NMO patients, whereas Abs to M-1 AQP4 are predominantly developed with increasing disease duration and severity.
AQP4 Binding (binding) of NMO in M-1 associated with neuromyelitis optica and disease
8) Confidence 0.03 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2864757 Disease Relevance 1.13 Pain Relevance 0.13
However, the advent of serological testing for AQP4-IgG has revealed that NMO and its inaugural forms are more common than previously recognized.
AQP4 Binding (recognized) of NMO associated with neuromyelitis optica
9) Confidence 0.03 Published 2008 Journal The Journal of Experimental Medicine Section Body Doc Link PMC2571922 Disease Relevance 1.71 Pain Relevance 0.49
NMO-Ig Abs resulted in different staining patterns when binding to full length AQP4 in contrast to the M-23 AQP4 isoform.
AQP4 Binding (binding) of NMO associated with neuromyelitis optica
10) Confidence 0.03 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2864757 Disease Relevance 1.22 Pain Relevance 0.06
Our study confirms weaker binding of NMO-IgG to full length AQP4, resulting in a lower sensitivity for clinically definite NMO (70%) and high risk NMO (39%) patients, besides also the M-23 IgG seropositive patient with SLE associated myelitis was negative for full length AQP4-IgG.
AQP4 Binding (binding) of NMO associated with neuromyelitis optica, demyelinating disease and systemic lupus erythematosus
11) Confidence 0.02 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2864757 Disease Relevance 1.84 Pain Relevance 0.11

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