INT224807

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Context Info
Confidence 0.78
First Reported 2008
Last Reported 2010
Negated 2
Speculated 0
Reported most in Body
Documents 35
Total Number 36
Disease Relevance 4.63
Pain Relevance 4.02

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

transport (Gria4) plasma membrane (Gria4)
Anatomy Link Frequency
dorsal horn 5
thalamus 3
synapses 2
spike 1
nucleus 1
Gria4 (Mus musculus)
Pain Link Frequency Relevance Heat
Glutamate receptor 88 99.92 Very High Very High Very High
Thalamus 234 99.84 Very High Very High Very High
Spinal cord 196 99.68 Very High Very High Very High
Dorsal horn 364 98.52 Very High Very High Very High
Glutamate 64 98.32 Very High Very High Very High
Pyramidal cell 84 95.76 Very High Very High Very High
GABA receptor 18 91.32 High High
long-term potentiation 56 90.72 High High
antagonist 20 90.16 High High
agonist 18 89.52 High High
Disease Link Frequency Relevance Heat
Targeted Disruption 204 100.00 Very High Very High Very High
Sprains And Strains 362 98.64 Very High Very High Very High
Absence Epilepsy 270 96.32 Very High Very High Very High
Convulsion 90 93.32 High High
Ataxia 90 85.16 High High
Cancer 52 83.28 Quite High
Infection 18 81.16 Quite High
Retina Disease 18 79.88 Quite High
Pain 56 64.40 Quite High
Congenital Anomalies 36 58.56 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Although both Gria3 and Gria4 expressed in the reticular thalamus, it has been shown previously that Gria4 encodes the predominant subunit in this critical region which, together with the cortex and thalamus form the thalamocortical circuit (4).
Gene_expression (expressed) of Gria4 in thalamus associated with thalamus
1) Confidence 0.78 Published 2008 Journal Human Molecular Genetics Section Body Doc Link PMC2405903 Disease Relevance 0.38 Pain Relevance 0.18
In the present study, we show that the spkw1 allele has a mutation in Gria4 leading to marked reduction in GluR4 protein expression, and we confirm the gene–phenotype relationship by study of Gria4 knockout mice.
Gene_expression (expression) of GluR4 associated with targeted disruption
2) Confidence 0.78 Published 2008 Journal Human Molecular Genetics Section Body Doc Link PMC2405903 Disease Relevance 0.69 Pain Relevance 0.04
To confirm the causal relationship between Gria4 deficiency and SWD, we assessed the electroencephalographic phenotype of an independent mutation of Gria4: the Gria4tm1Dgen knockout allele (expression defect data are shown in Figure 3B and C; see Materials and Methods for more details on the origin and nature of Gria4tm1Dgen).
Gene_expression (expression) of Gria4tm1Dgen associated with targeted disruption
3) Confidence 0.78 Published 2008 Journal Human Molecular Genetics Section Body Doc Link PMC2405903 Disease Relevance 0.22 Pain Relevance 0
Thus, in mice with greatly reduced Gria4 expression, the AMPA receptor composition would change in the reticular thalamus, resulting in the observed changes to AMPA receptor function.
Gene_expression (expression) of Gria4 in thalamus associated with thalamus
4) Confidence 0.78 Published 2008 Journal Human Molecular Genetics Section Body Doc Link PMC2405903 Disease Relevance 0.31 Pain Relevance 0.30
Both RNA and protein analyses confirm that full-length Gria4 expression is significantly reduced in this strain.
Gene_expression (expression) of Gria4 associated with sprains and strains
5) Confidence 0.78 Published 2008 Journal Human Molecular Genetics Section Body Doc Link PMC2405903 Disease Relevance 0.38 Pain Relevance 0.15
GluR4, in particular, is the predominant AMPA receptor expressed in the thalamic reticular nucleus, where it is expressed 3- to 4-fold higher at corticothalamic synapses than at other reticular and intrathalamic sites, making the thalamic reticular nucleus a potentially critical site of action; GluR3 is also expressed but at lower levels (21,36).
Gene_expression (expressed) of GluR4 in synapses
6) Confidence 0.78 Published 2008 Journal Human Molecular Genetics Section Body Doc Link PMC2405903 Disease Relevance 0.08 Pain Relevance 0.03
GluR4 is expressed in a small number of neocortical neurons, but is known to be highly expressed in thalamus, especially in the thalamic reticular nucleus, where it is the predominant AMPA receptor at the corticothalamic synapse, showing 3- to 4-fold higher expression than at other thalamic sites (21–24).
Gene_expression (expressed) of GluR4 in thalamus associated with thalamus
7) Confidence 0.78 Published 2008 Journal Human Molecular Genetics Section Body Doc Link PMC2405903 Disease Relevance 0.17 Pain Relevance 0.16
GluR4 is expressed in a small number of neocortical neurons, but is known to be highly expressed in thalamus, especially in the thalamic reticular nucleus, where it is the predominant AMPA receptor at the corticothalamic synapse, showing 3- to 4-fold higher expression than at other thalamic sites (21–24).
Gene_expression (expressed) of GluR4 in neurons associated with thalamus
8) Confidence 0.78 Published 2008 Journal Human Molecular Genetics Section Body Doc Link PMC2405903 Disease Relevance 0.17 Pain Relevance 0.16
During each experiment, a Gria4spkw1/+/Gria4spkw1/spkw1 pair of (FeJ×HeJ)F1×HeJ backcross mice (?
Gene_expression (pair) of Gria4spkw1
9) Confidence 0.68 Published 2008 Journal Human Molecular Genetics Section Body Doc Link PMC2405903 Disease Relevance 0 Pain Relevance 0
GluR4, in particular, is the predominant AMPA receptor expressed in the thalamic reticular nucleus, where it is expressed 3- to 4-fold higher at corticothalamic synapses than at other reticular and intrathalamic sites, making the thalamic reticular nucleus a potentially critical site of action; GluR3 is also expressed but at lower levels (21,36).
Gene_expression (expressed) of GluR4 in synapses
10) Confidence 0.68 Published 2008 Journal Human Molecular Genetics Section Body Doc Link PMC2405903 Disease Relevance 0.08 Pain Relevance 0.04
During each experiment, a Gria4spkw1/+/Gria4spkw1/spkw1 pair of (FeJ×HeJ)F1×HeJ backcross mice (?
Gene_expression (pair) of spkw1
11) Confidence 0.68 Published 2008 Journal Human Molecular Genetics Section Body Doc Link PMC2405903 Disease Relevance 0 Pain Relevance 0
In the present study, we show that the spkw1 allele has a mutation in Gria4 leading to marked reduction in GluR4 protein expression, and we confirm the gene–phenotype relationship by study of Gria4 knockout mice.
Gene_expression (allele) of spkw1 associated with targeted disruption
12) Confidence 0.68 Published 2008 Journal Human Molecular Genetics Section Body Doc Link PMC2405903 Disease Relevance 0.71 Pain Relevance 0.04
During each experiment, a Gria4spkw1/+/Gria4spkw1/spkw1 pair of (FeJ×HeJ)F1×HeJ backcross mice (?
Gene_expression (pair) of Gria4spkw1
13) Confidence 0.68 Published 2008 Journal Human Molecular Genetics Section Body Doc Link PMC2405903 Disease Relevance 0 Pain Relevance 0
The time course of AMPA-receptor-dependent synaptic responses are largely determined by receptor desensitization, with GluR4-containing receptors, highly expressed in thalamic reticular nucleus (21), having the fastest desensitization rate (25,26).
Gene_expression (expressed) of GluR4 in nucleus
14) Confidence 0.60 Published 2008 Journal Human Molecular Genetics Section Body Doc Link PMC2405903 Disease Relevance 0.20 Pain Relevance 0.07
This overall effect is especially due to a decrease in the number of brief, large-amplitude events (Fig. 5C1–C3), consistent with altered GluR4 receptor expression.
Gene_expression (expression) of GluR4 receptor
15) Confidence 0.60 Published 2008 Journal Human Molecular Genetics Section Body Doc Link PMC2405903 Disease Relevance 0 Pain Relevance 0.07
This phenotype, caused by retroelement insertion in intron 15 of the gene encoding GluR4 (Gria4), disrupting gene expression, represents the first naturally occuring functional variant of the Gria4 gene.
Gene_expression (expression) of Gria4
16) Confidence 0.60 Published 2008 Journal Human Molecular Genetics Section Body Doc Link PMC2405903 Disease Relevance 0.27 Pain Relevance 0.16
Together these data show that a genetic deficiency in Gria4, whether reduction (Gria4spkw1 allele) or complete lack (Gria4tm1Dgen allele), is associated with a high frequency of SWD, modeling absence epilepsy.
Gene_expression (allele) of Gria4spkw1 associated with absence epilepsy
17) Confidence 0.59 Published 2008 Journal Human Molecular Genetics Section Body Doc Link PMC2405903 Disease Relevance 0.10 Pain Relevance 0
From each section, 400 pan-AMPAr-labelled puncta were selected (100 each from laminae I, IIo, IIi and III) and these were then examined to determine whether they were immunoreactive with the GluR1, GluR3 or GluR4 antibodies.
Gene_expression (antibodies) of GluR4
18) Confidence 0.40 Published 2008 Journal Mol Pain Section Body Doc Link PMC2248168 Disease Relevance 0 Pain Relevance 0.08
However, the rabbit GluR4 C-terminal antibody (GluR4-C) that was used in this study gave a different pattern of labelling to that previously observed in the dorsal horn with a guinea-pig antibody against the N-terminus of this subunit (GluR4-N) [33].
Gene_expression (used) of GluR4 in dorsal horn associated with dorsal horn
19) Confidence 0.40 Published 2008 Journal Mol Pain Section Body Doc Link PMC2248168 Disease Relevance 0 Pain Relevance 0.15
Although puncta immunoreactive with the GluR4-C antibody were relatively infrequent in laminae I–II, those that were present were often strongly immunoreactive and arranged in rows or clusters.
Gene_expression (immunoreactive) of GluR4
20) Confidence 0.40 Published 2008 Journal Mol Pain Section Body Doc Link PMC2248168 Disease Relevance 0 Pain Relevance 0.04

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