INT179749

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Context Info
Confidence 0.34
First Reported 2004
Last Reported 2008
Negated 0
Speculated 0
Reported most in Body
Documents 3
Total Number 5
Disease Relevance 2.28
Pain Relevance 1.99

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
bridges 1
astrocytes 1
vesicles 1
central nervous system 1
SLC1A2 (Homo sapiens)
Pain Link Frequency Relevance Heat
Glutamate 298 100.00 Very High Very High Very High
cytokine 40 98.16 Very High Very High Very High
Central nervous system 67 95.08 Very High Very High Very High
Kinase C 12 94.64 High High
Inflammation 23 93.92 High High
Multiple sclerosis 38 91.64 High High
Spinal cord 45 91.20 High High
excitatory amino acid 6 61.76 Quite High
adenocard 4 47.52 Quite Low
headache 2 6.28 Low Low
Disease Link Frequency Relevance Heat
Neuromyelitis Optica 261 99.92 Very High Very High Very High
INFLAMMATION 28 93.92 High High
Demyelinating Disease 59 93.40 High High
Targeted Disruption 11 86.08 High High
Pressure And Volume Under Development 10 77.24 Quite High
Alzheimer's Dementia 2 57.92 Quite High
Fatigue 96 21.48 Low Low
Cancer 6 20.96 Low Low
Necrosis 9 20.48 Low Low
Stress 10 18.20 Low Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
The rapid down-regulation of EAAT2 and AQP4 induced by NMO-IgG in GFP-AQP4-expressing cells and colocalization of both proteins in cytoplasmic endocytotic vesicles within 10 min is consistent with a direct effect of IgG on a surface macromolecular complex.
Regulation (regulation) of EAAT2 in vesicles associated with neuromyelitis optica
1) Confidence 0.34 Published 2008 Journal The Journal of Experimental Medicine Section Body Doc Link PMC2571922 Disease Relevance 0.67 Pain Relevance 0.08
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.
Regulation (regulation) of EAAT2 in astrocytes associated with neuromyelitis optica and glutamate
2) Confidence 0.34 Published 2008 Journal The Journal of Experimental Medicine Section Body Doc Link PMC2571922 Disease Relevance 0.34 Pain Relevance 0.29
Aquaporin-4–binding autoantibodies in patients with neuromyelitis optica impair glutamate transport by down-regulating EAAT2

Neuromyelitis optica (NMO)-immunoglobulin G (IgG) is a clinically validated serum biomarker that distinguishes relapsing central nervous system (CNS) inflammatory demyelinating disorders related to NMO from multiple sclerosis.

Regulation (regulating) of EAAT2 in central nervous system associated with neuromyelitis optica, multiple sclerosis, glutamate, inflammation, central nervous system and demyelinating disease
3) Confidence 0.30 Published 2008 Journal The Journal of Experimental Medicine Section Title Doc Link PMC2571922 Disease Relevance 1.06 Pain Relevance 0.41
One mechanism of regulation of GLT-1 is related to formation of cysteine bridges.
Regulation (regulation) of GLT-1 in bridges
4) Confidence 0.08 Published 2004 Journal J Neuroinflammation Section Body Doc Link PMC533886 Disease Relevance 0.13 Pain Relevance 0.54
A large number of factors have been shown to affect the activity and expression of the glutamate transporters GLT-1 and GLAST.
Regulation (affect) of GLT-1 associated with glutamate
5) Confidence 0.07 Published 2004 Journal J Neuroinflammation Section Body Doc Link PMC533886 Disease Relevance 0.09 Pain Relevance 0.66

General Comments

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