INT135998

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Context Info
Confidence 0.72
First Reported 2006
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 18
Total Number 18
Disease Relevance 3.14
Pain Relevance 5.15

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

transport (Gria2) endoplasmic reticulum (Gria2) plasma membrane (Gria2)
protein complex (Gria2)
Anatomy Link Frequency
plasma 1
horizontal cells 1
neurons 1
spine 1
brain 1
Gria2 (Mus musculus)
Pain Link Frequency Relevance Heat
nMDA receptor 140 100.00 Very High Very High Very High
Glutamate receptor 91 100.00 Very High Very High Very High
Glutamate 87 100.00 Very High Very High Very High
Spinal sensitization 6 99.76 Very High Very High Very High
Calcium channel 4 99.74 Very High Very High Very High
Kinase C 108 99.24 Very High Very High Very High
Central nervous system 67 99.04 Very High Very High Very High
cocaine 36 98.48 Very High Very High Very High
Hippocampus 125 96.68 Very High Very High Very High
Thalamus 1 96.08 Very High Very High Very High
Disease Link Frequency Relevance Heat
Nociception 158 99.08 Very High Very High Very High
Anxiety Disorder 116 97.48 Very High Very High Very High
Targeted Disruption 111 97.24 Very High Very High Very High
Neuropathic Pain 29 95.16 Very High Very High Very High
Hyperalgesia 30 92.68 High High
Inflammatory Pain 65 92.12 High High
Congenital Anomalies 12 88.24 High High
INFLAMMATION 64 83.20 Quite High
Pain 96 78.84 Quite High
Stress 25 62.84 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
We found that deletion of GluR2 was more effective at blocking initial learning in context A than subsequent learning in context B (significant context x genotype interaction (F (1, 47) ?
Localization (deletion) of GluR2
1) Confidence 0.72 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2947514 Disease Relevance 0.10 Pain Relevance 0.07
This phosphorylation of GluR2 on Serine880 may further impede the affinity of GluR2 for GRIP, release GluR2 from GRIP-GluR2 complex and finally lead to the internalization of GluR2 subunits.
Localization (release) of GluR2
2) Confidence 0.71 Published 2010 Journal Mol Pain Section Body Doc Link PMC2823608 Disease Relevance 0.33 Pain Relevance 0.21
The translocation of AMPA receptors from the cytosol to the plasma membrane also requires the involvement of Stargazin.
Localization (translocation) of AMPA in plasma
3) Confidence 0.62 Published 2010 Journal Mol Pain Section Body Doc Link PMC2823608 Disease Relevance 0 Pain Relevance 0.17
PKC phosphorylates GluR2 at Serine880 to release GluR2 from GRIP and to promote the internalization of GluR2 [36].
Localization (release) of GluR2 associated with kinase c
4) Confidence 0.62 Published 2010 Journal Mol Pain Section Body Doc Link PMC2823608 Disease Relevance 0.30 Pain Relevance 0.54
It suggests a significant membrane translocation of GluR1-containing AMPA receptors to a spinal nociceptive synapse during acute noxious stimulation [27].
Localization (translocation) of AMPA in synapse associated with nociception
5) Confidence 0.62 Published 2010 Journal Mol Pain Section Body Doc Link PMC2823608 Disease Relevance 0.51 Pain Relevance 0.63
It has been found that phosphorylation of GluR2 at Serine880 by PKC reduces the affinity of GluR2 for GRIP, thus, released GluR2 from GRIP and promotes the internalization of GluR2 [36].
Localization (released) of GluR2 associated with kinase c
6) Confidence 0.62 Published 2010 Journal Mol Pain Section Body Doc Link PMC2823608 Disease Relevance 0.36 Pain Relevance 0.30
In the CNS, GluR1 and GluR2 subunits are ubiquitously expressed and are present in most AMPA receptors in the adult mammalian CNS.
Localization (receptors) of AMPA associated with central nervous system
7) Confidence 0.58 Published 2010 Journal Mol Pain Section Body Doc Link PMC2823608 Disease Relevance 0 Pain Relevance 0.33
Addictive drugs trigger AMPA receptor redistribution
Localization (redistribution) of AMPA
8) Confidence 0.50 Published 2010 Journal PLoS ONE Section Body Doc Link PMC3013137 Disease Relevance 0 Pain Relevance 0.63
RT-PCR primers used in this study are as follows: GluR2 forward, 5'-CCATGAAAGTGGGAGGTAACTTG-3'; GluR2 reverse, 5'-AAGCCCCTGCTCGTTCAGT-3'; ADAR2 forward, 5'-TGTAAGCACGCGCTGTACTGT-3'; ADAR2 reverse, 5'-GACTCGTGGTATGTGGTAGGCTTAG-3'; ?
Localization (reverse) of GluR2
9) Confidence 0.40 Published 2010 Journal Mol Neurodegener Section Body Doc Link PMC3006372 Disease Relevance 0 Pain Relevance 0
RT-PCR primers used in this study are as follows: GluR2 forward, 5'-CCATGAAAGTGGGAGGTAACTTG-3'; GluR2 reverse, 5'-AAGCCCCTGCTCGTTCAGT-3'; ADAR2 forward, 5'-TGTAAGCACGCGCTGTACTGT-3'; ADAR2 reverse, 5'-GACTCGTGGTATGTGGTAGGCTTAG-3'; ?
Localization (reverse) of GluR2
10) Confidence 0.40 Published 2010 Journal Mol Neurodegener Section Body Doc Link PMC3006372 Disease Relevance 0 Pain Relevance 0
The absence of Neto1 had no effect on the overall abundance of NR1, NR2A, NR2B, PSD-95, GluR2, VAMP2, or GABAAR1 proteins (Figure 6L) in whole brain extracts, or of NR1, NR2A, NR2B, or PSD-95 in crude synaptosomes (Figure 6M).
Localization (abundance) of GluR2 in brain
11) Confidence 0.37 Published 2009 Journal PLoS Biology Section Body Doc Link PMC2652390 Disease Relevance 0.17 Pain Relevance 0.05
These data show that intracellular calcium in horizontal cells is regulated by voltage-dependent L- and N-type calcium channels, ionotropic AMPA and kainate receptors, and release of calcium from internal stores after activation of ryanodine receptors.
Localization (release) of AMPA in horizontal cells associated with calcium channel
12) Confidence 0.33 Published 2006 Journal J. Neurophysiol. Section Abstract Doc Link 16738216 Disease Relevance 0 Pain Relevance 0.42
In contrast, no significant differences were observed in the abundance of PSD-95, NR1, NR2B, or GluR2 between Neto-1 null versus wild-type mice (Figure 9A and 9B).
Localization (abundance) of GluR2
13) Confidence 0.31 Published 2009 Journal PLoS Biology Section Body Doc Link PMC2652390 Disease Relevance 0.06 Pain Relevance 0.03
The enhanced amplitude of EPSCs by octopamine in Ap oa1 mice may be due to increased function of postsynaptic AMPA receptor or presynaptic glutamate release.
Localization (release) of AMPA associated with glutamate
14) Confidence 0.13 Published 2008 Journal Mol Pain Section Body Doc Link PMC2570662 Disease Relevance 0.43 Pain Relevance 0.23
Enhancement of 4-7.5 Hz or slow 1-4 Hz oscillations may occur through AMPA receptor insertion or phosphorylation of networks which are being triggered by a common source (e.g. hippocampus or thalamus).
Localization (insertion) of AMPA receptor in hippocampus associated with thalamus and hippocampus
15) Confidence 0.09 Published 2010 Journal Mol Brain Section Body Doc Link PMC2888801 Disease Relevance 0.49 Pain Relevance 0.31
On the other hand, these inhibitors did not cause any effects on AMPA and NMDA receptor-mediated EPSCs in CaMKIV transgenic mice (Fig. 3 and 4), suggesting that the inhibition of synaptic potentiation by protein synthesis inhibitors was not due to a functional modification of AMPA and NMDA receptors.
Localization (modification) of AMPA associated with targeted disruption and nmda receptor
16) Confidence 0.01 Published 2010 Journal Mol Brain Section Body Doc Link PMC2949850 Disease Relevance 0.38 Pain Relevance 0.62
Predictions made from focally stimulated NMDA EPSCs for unidentified lamina I and II neurons in neonatal rats indicated that synapses co-expressing AMPA and NMDA receptors have both NR2A and NR2B subunits while silent synapses have mainly NR2A subunits [24].
Localization (receptors) of AMPA in neurons associated with nmda receptor
17) Confidence 0.00 Published 2010 Journal Mol Pain Section Body Doc Link PMC2879240 Disease Relevance 0 Pain Relevance 0.48
Furthermore, AMPA and NMDA-type glutamate receptors (AMPARs and NMDARs, respectively) that are colocalized on individual spine heads interact to produce two kinetically and mechanistically distinct phases of synaptically evoked Ca influx.
Localization (colocalized) of AMPA in spine associated with glutamate receptor
18) Confidence 0.00 Published 2009 Journal PLoS Biology Section Abstract Doc Link PMC2734993 Disease Relevance 0 Pain Relevance 0.13

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