INT85946

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Context Info
Confidence 0.61
First Reported 1998
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 10
Total Number 10
Disease Relevance 1.23
Pain Relevance 5.09

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

endoplasmic reticulum (Gria2) plasma membrane (Gria2) protein complex (Gria2)
Anatomy Link Frequency
Shanks 1
spinal cord 1
dopamine neurons 1
anterior pituitary 1
Gria2 (Rattus norvegicus)
Pain Link Frequency Relevance Heat
Glutamate receptor 28 100.00 Very High Very High Very High
Spinal cord 6 100.00 Very High Very High Very High
Ventral tegmentum 102 99.84 Very High Very High Very High
Dopamine 77 99.68 Very High Very High Very High
substance P 17 99.40 Very High Very High Very High
Nucleus accumbens 22 99.20 Very High Very High Very High
tetrodotoxin 5 99.08 Very High Very High Very High
gABA 26 98.52 Very High Very High Very High
Glutamate 50 98.48 Very High Very High Very High
antagonist 70 98.28 Very High Very High Very High
Disease Link Frequency Relevance Heat
Depression 103 96.80 Very High Very High Very High
Drug Dependence 10 82.76 Quite High
Li-fraumeni Syndrome 16 68.48 Quite High
Injury 4 50.00 Quite Low
Neuropathic Pain 1 42.64 Quite Low
Adenoma 5 40.88 Quite Low
Nociception 2 40.80 Quite Low
Carpal Tunnel Syndrome 4 23.52 Low Low
Attention Deficit Hyperactivity Disorder 1 17.08 Low Low
Sprains And Strains 2 12.40 Low Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
A cobalt-quenching assay confirmed the immunocytochemical results indicating that synaptic scaling after activity blockade did not involve a change in abundance of GluR2-lacking AMPA receptors.
Localization (abundance) of GluR2
1) Confidence 0.61 Published 2009 Journal Eur. J. Neurosci. Section Abstract Doc Link 19674091 Disease Relevance 0.06 Pain Relevance 0.68
Prolonged activity blockade (1-3 days) with an AMPA receptor antagonist increased cell surface (synaptic and extrasynaptic) glutamate receptor 1 (GluR1) and GluR2 but not GluR3, as well as GluR1/2 co-localization on the cell surface and total GluR1 and GluR2 protein levels.
Localization (localization) of GluR2 associated with glutamate receptor and antagonist
2) Confidence 0.61 Published 2009 Journal Eur. J. Neurosci. Section Abstract Doc Link 19674091 Disease Relevance 0.08 Pain Relevance 0.58
Prolonged activity blockade (1-3 days) with an AMPA receptor antagonist increased cell surface (synaptic and extrasynaptic) glutamate receptor 1 (GluR1) and GluR2 but not GluR3, as well as GluR1/2 co-localization on the cell surface and total GluR1 and GluR2 protein levels.
Localization (localization) of GluR2 associated with glutamate receptor and antagonist
3) Confidence 0.58 Published 2009 Journal Eur. J. Neurosci. Section Abstract Doc Link 19674091 Disease Relevance 0.08 Pain Relevance 0.57
Here we provide the first evidence, to our knowledge, showing the localization of GluR2 in VTA dopamine neurons, instead of GABA neurons.
Localization (localization) of GluR2 in dopamine neurons associated with ventral tegmentum, gaba and dopamine
4) Confidence 0.56 Published 2010 Journal PLoS ONE Section Body Doc Link PMC3004941 Disease Relevance 0.84 Pain Relevance 1.35
GluR1 and GluR2 surface expression was also increased by tetrodotoxin alone or in combination with an N-methyl-d-aspartate receptor or AMPA receptor antagonist but not by the l-type Ca(2+) channel antagonist nifedipine.
Localization (expression) of GluR2 associated with tetrodotoxin and antagonist
5) Confidence 0.50 Published 2009 Journal Eur. J. Neurosci. Section Abstract Doc Link 19674091 Disease Relevance 0.07 Pain Relevance 0.64
Shanks et al. [23] systematically compared the structures of GluA2 tetramer that were expressed constitutively in HEK cells and GnTI(?)
Localization (tetramer) of GluA2 in Shanks
6) Confidence 0.40 Published 2010 Journal Mol Neurobiol Section Body Doc Link PMC2992128 Disease Relevance 0 Pain Relevance 0
Corticosterone increases surface mobility of GluR2
Localization (mobility) of GluR2
7) Confidence 0.35 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2659165 Disease Relevance 0 Pain Relevance 0.03
While they do report significant decreases in GluR2 and GluR3 subunits, there are no significant changes in GluR1 expression (see Supplementary Material Figure 4a; Wright et al., 2008).
Localization (decreases) of GluR2
8) Confidence 0.16 Published 2008 Journal Frontiers in Systems Neuroscience Section Body Doc Link PMC2638550 Disease Relevance 0.10 Pain Relevance 0.13
The localization of the IFN-gamma R in the spinal cord differed from that of the AMPA glutamate receptor subunits 2 and 3 and the substance P receptor (NK1).
Localization (localization) of AMPA glutamate receptor subunits 2 in spinal cord associated with glutamate receptor, substance p and spinal cord
9) Confidence 0.16 Published 1998 Journal J. Neurocytol. Section Abstract Doc Link 10640190 Disease Relevance 0 Pain Relevance 0.49
Glutamate or certain aspartate analogues have been found to stimulate PRL, GH and LH release and rat anterior pituitary cells express mRNA of glutamate receptors GluR1, GluR2, GluR3, GluR4, GluR5, GluR6, GluR7, KA1 and KA2 subunits (765).
Localization (release) of GluR2 in anterior pituitary associated with glutamate and glutamate receptor
10) Confidence 0.10 Published 2008 Journal Journal of Neuroendocrinology Section Body Doc Link PMC2229370 Disease Relevance 0 Pain Relevance 0.61

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