INT250283

Context Info Confidence 0.53 First Reported 2008 Last Reported 2010 Negated 0 Speculated 0 Reported most in Body Documents 5 Total Number 6 Disease Relevance 3.22 Pain Relevance 2.29

plasma membrane (SLC1A2) transmembrane transport (SLC1A2)

Anatomy Link Frequency plasma 1 spinal cord 1 cerebellum 1 white matter 1 SLC1A2 (Homo sapiens)

Pain Link Frequency Relevance Heat Spinal cord 60 99.38 anesthesia 4 98.60 Glutamate 258 98.56 Multiple sclerosis 32 98.16 addiction 4 98.04 Central nervous system 84 93.28 nMDA receptor 50 88.28 amygdala 116 84.24 Inflammation 28 76.80 Glutamate receptor 26 73.60

Disease Link Frequency Relevance Heat Autism 628 99.68 Neuromyelitis Optica 348 99.14 Demyelinating Disease 60 98.16 Autoimmune Disease 12 96.64 Aging 2 96.12 Targeted Disruption 12 89.04 Toxicity 32 80.84 INFLAMMATION 32 76.80 Disease Progression 4 64.96 Neurodegenerative Disease 12 61.80

Sentences Mentioned In

Key:

Protein

Mutation

Event

Anatomy

Negation

Speculation

Pain term

Disease term

The marked loss of EAAT2 described in this report parallels loss of AQP4 in lesioned NMO spinal cord tissue and contrasts with the increases in EAAT2 and AQP4 reported in both active and chronic MS lesions (20).

Positive_regulation (increases) of EAAT2 in spinal cord associated with neuromyelitis optica, multiple sclerosis and spinal cord

1) Confidence 0.53 Published 2008 Journal The Journal of Experimental Medicine Section Body Doc Link PMC2571922 Disease Relevance 1.03 Pain Relevance 0.61

For example, it might be feasible to ameliorate tissue damage in both gray and white matter if therapeutic upregulation of EAAT2 can be achieved in patients whose neurological dysfunction is attributable to AQP4 autoimmunity.

Positive_regulation (upregulation) of EAAT2 in white matter associated with anesthesia and autoimmune disease

2) Confidence 0.46 Published 2008 Journal The Journal of Experimental Medicine Section Body Doc Link PMC2571922 Disease Relevance 1.09 Pain Relevance 0.43

We did not detect EAAT2 in GFP vector-transfected cells (Fig. 3 B), but EAAT2 was strikingly upregulated in the plasma membrane of cells transgenically expressing either AQP4 or AQP5 (Fig. 3 B).

Positive_regulation (upregulated) of EAAT2 in plasma

3) Confidence 0.35 Published 2008 Journal The Journal of Experimental Medicine Section Body Doc Link PMC2571922 Disease Relevance 0.26 Pain Relevance 0.12

We confirmed that upregulated EAAT2 protein in GFP-AQP4 transfected cells was functional by demonstrating that GFP-AQP4 cells imported two- to threefold more glutamate via the Na+-dependent pathway relative to GFP vector cells (P < 0.0002; Fig. 3 F).

Positive_regulation (upregulated) of EAAT2 associated with glutamate

4) Confidence 0.35 Published 2008 Journal The Journal of Experimental Medicine Section Body Doc Link PMC2571922 Disease Relevance 0.07 Pain Relevance 0.23

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 EAAT 2 in cerebellum associated with autism

5) Confidence 0.04 Published 2010 Journal Frontiers in Human Neuroscience Section Body Doc Link PMC3010743 Disease Relevance 0.38 Pain Relevance 0.43

Since the protein level and activity of glutamate transporters are controlled by the extracellular glutamate concentration or by activity-dependent mechanisms (Levy et al., 1995), increased EAAT 1 and EAAT 2 protein levels may be due to increased extracellular glutamate concentrations in autism.

Positive_regulation (increased) of EAAT 2 associated with glutamate and autism

6) Confidence 0.02 Published 2010 Journal Frontiers in Human Neuroscience Section Body Doc Link PMC3010743 Disease Relevance 0.37 Pain Relevance 0.48

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