INT161371

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Context Info
Confidence 0.61
First Reported 2006
Last Reported 2010
Negated 0
Speculated 1
Reported most in Body
Documents 7
Total Number 8
Disease Relevance 2.44
Pain Relevance 1.58

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

cell proliferation (Glul) mitochondrion (Glul) lyase activity (Glul)
Golgi apparatus (Glul) intracellular (Glul) protein complex (Glul)
Anatomy Link Frequency
glial cells 3
brain 2
neurons 1
synaptic vesicles 1
central nervous system 1
Glul (Mus musculus)
Pain Link Frequency Relevance Heat
Glutamate 36 100.00 Very High Very High Very High
gABA 50 99.92 Very High Very High Very High
primary afferent fibers 1 97.68 Very High Very High Very High
Central nervous system 15 96.44 Very High Very High Very High
Neurotransmitter 10 95.84 Very High Very High Very High
GABAergic 15 86.72 High High
Pain 1 77.20 Quite High
Thermal hyperalgesia 1 75.00 Quite High
Pain threshold 1 70.32 Quite High
IPN 1 60.56 Quite High
Disease Link Frequency Relevance Heat
Generalized Anxiety Disorder 5 99.92 Very High Very High Very High
Brain Injury 10 99.64 Very High Very High Very High
Nociception 7 98.68 Very High Very High Very High
Cognitive Disorder 1 87.80 High High
Targeted Disruption 50 84.24 Quite High
Convulsion 1 81.52 Quite High
Stab Wounds 15 81.12 Quite High
Injury 55 80.24 Quite High
Anxiety Disorder 3 80.00 Quite High
Pain 2 77.20 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
For Müller glial cells, these known genes included retinaldehyde binding protein 1 (Rlbp1; Bunt-Milam and Saari, 1983) and glutamate-ammonia ligase (Glul; Riepe and Norenburg, 1977).


Gene_expression (included) of glutamate-ammonia ligase in glial cells associated with glutamate
1) Confidence 0.61 Published 2008 Journal The Journal of Comparative Neurology Section Body Doc Link PMC2665264 Disease Relevance 0 Pain Relevance 0.05
Double-labeling experiments in dissociated retinal cells were conducted by using probes against novel bipolar cell-enriched genes and antibodies against calbindin (Calb), a protein expressed abundantly in horizontal cells and weakly in a subset of amacrine cells (Hamano et al., 1990; Elshatory et al., 2007), and Glul, a Müller glial cell marker (Riepe and Norenburg, 1977), to determine whether the novel molecular markers are found in these cell types.
Gene_expression (expressed) of Glul in glial cell
2) Confidence 0.53 Published 2008 Journal The Journal of Comparative Neurology Section Body Doc Link PMC2665264 Disease Relevance 0.18 Pain Relevance 0
For Müller glial cells, these known genes included retinaldehyde binding protein 1 (Rlbp1; Bunt-Milam and Saari, 1983) and glutamate-ammonia ligase (Glul; Riepe and Norenburg, 1977).


Gene_expression (included) of Glul in glial cells associated with glutamate
3) Confidence 0.53 Published 2008 Journal The Journal of Comparative Neurology Section Body Doc Link PMC2665264 Disease Relevance 0 Pain Relevance 0.08
The anti-Glul antibody was produced from mice immunized with glutamine ammonia ligase purified from sheep brain, and staining of adult retinal sections revealed a pattern of immunoreactivity that was similar to previous observations (see Supplementary Fig. 3; Rhee et al., 2007).
Gene_expression (produced) of Glul in brain
4) Confidence 0.47 Published 2008 Journal The Journal of Comparative Neurology Section Body Doc Link PMC2665264 Disease Relevance 0 Pain Relevance 0
To assess the functional state of astrocytes after traumatic brain injury, we analyzed the expression of two glutamate transporters, glutamate aspartate transporter (GLAST) and glutamate transporter-1 (GLT-1/EAAT2), the glutamate transaminase, glutamine synthetase (GS) and the calcium regulatory protein S-100B.
Spec (analyzed) Gene_expression (expression) of glutamine synthetase in brain associated with glutamate and brain injury
5) Confidence 0.34 Published 2006 Journal J Neuroinflammation Section Body Doc Link PMC1533808 Disease Relevance 0.66 Pain Relevance 0.24
Gamma-aminobutyric acid, which is synthesized by two isoforms of glutamate decarboxylase (GAD), inhibits the transfer of nociceptive signals from primary afferent fibers to the central nervous system.
Gene_expression (synthesized) of glutamate decarboxylase in central nervous system associated with nociception, glutamate, generalized anxiety disorder, primary afferent fibers and central nervous system
6) Confidence 0.31 Published 2009 Journal J. Pharmacol. Exp. Ther. Section Abstract Doc Link 19571163 Disease Relevance 0.71 Pain Relevance 0.50
Not only for neurons, but M6a was also weakly expressed in processes of Müller glia cells, which are evident from the co-expression of M6a with Müller glia marker, glutamine synthetase (Figure 1D).
Gene_expression (expression) of glutamine synthetase in neurons
7) Confidence 0.18 Published 2008 Journal Molecular Vision Section Body Doc Link PMC2529470 Disease Relevance 0.13 Pain Relevance 0.05
GABA is synthesized from glutamic acid by glutamate decarboxylase (GAD) [1] and is accumulated into synaptic vesicles by the vesicular GABA transporter (VGAT) [2,3].
Gene_expression (synthesized) of glutamate decarboxylase in synaptic vesicles associated with glutamate, gaba and generalized anxiety disorder
8) Confidence 0.14 Published 2010 Journal Mol Brain Section Body Doc Link PMC3023674 Disease Relevance 0.75 Pain Relevance 0.67

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