INT112873

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Context Info
Confidence 0.76
First Reported 2003
Last Reported 2010
Negated 2
Speculated 0
Reported most in Body
Documents 28
Total Number 28
Disease Relevance 2.88
Pain Relevance 5.94

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

oxidoreductase activity (Glyr1) nucleus (Glyr1) DNA binding (Glyr1)
cellular_component (Glyr1)
Anatomy Link Frequency
neurons 4
telencephalon 1
spinal cord 1
inner nuclear layer 1
brain 1
Glyr1 (Mus musculus)
Pain Link Frequency Relevance Heat
gABA 480 100.00 Very High Very High Very High
Neurotransmitter 476 100.00 Very High Very High Very High
GABA receptor 71 99.76 Very High Very High Very High
antagonist 123 99.34 Very High Very High Very High
IPN 17 98.84 Very High Very High Very High
Spinal cord 939 98.80 Very High Very High Very High
Dorsal horn 313 98.32 Very High Very High Very High
Hippocampus 100 96.60 Very High Very High Very High
medulla 122 94.68 High High
Cannabinoid receptor 90 94.08 High High
Disease Link Frequency Relevance Heat
Death 19 99.92 Very High Very High Very High
Inflammatory Pain 17 98.84 Very High Very High Very High
Targeted Disruption 48 97.72 Very High Very High Very High
Sleep Disorders 14 97.64 Very High Very High Very High
Muscle Hypertonia 14 96.52 Very High Very High Very High
Lung Cancer 14 92.96 High High
Post-traumatic Stress Disorder 1 92.80 High High
Ganglion Cysts 140 90.52 High High
Nociception 69 88.72 High High
Pain 79 83.44 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Chloride uptake into brain synaptoneurosomes from knock-in mice revealed decreased responses to maximally effective glycine concentrations, although wild-type levels of GlyR expression were observed using 3H-strychnine binding and immunoblotting.
Gene_expression (expression) of GlyR in brain associated with targeted disruption
1) Confidence 0.76 Published 2003 Journal J. Neurosci. Section Abstract Doc Link 12954867 Disease Relevance 0.73 Pain Relevance 0.22
We show that GlyR alpha3 is distinctly expressed in superficial layers of the spinal cord dorsal horn.
Gene_expression (expressed) of GlyR in spinal cord dorsal horn associated with dorsal horn and spinal cord
2) Confidence 0.58 Published 2004 Journal Science Section Abstract Doc Link 15131310 Disease Relevance 0.35 Pain Relevance 0.56
Considerable advantages were provided by the apparent expression of only one type of GlyR (comprised of ?
Gene_expression (expression) of GlyR
3) Confidence 0.22 Published 2010 Journal Frontiers in Molecular Neuroscience Section Body Doc Link PMC2889717 Disease Relevance 0.11 Pain Relevance 0.38
In the rat study, a greater proportion of neurons in the DDH received GlyR-mediated mIPSCs and receptor properties were similar in each region.
Gene_expression (received) of GlyR in neurons
4) Confidence 0.18 Published 2009 Journal Mol Pain Section Body Doc Link PMC2784755 Disease Relevance 0 Pain Relevance 0.24
For example, c-Fos expression differs in the SDH and DDH after blockade of tonic inhibition with specific GABAA and GlyR antagonists [21] and an unusual form of the GlyR, containing alpha 3-subunits, is confined to the SDH of the mouse spinal cord [22].
Gene_expression (containing) of GlyR in spinal cord associated with antagonist and spinal cord
5) Confidence 0.18 Published 2009 Journal Mol Pain Section Body Doc Link PMC2784755 Disease Relevance 0.12 Pain Relevance 0.66
2 GlyR subunit was higher in DDH, whereas ?
Gene_expression (subunit) of GlyR
6) Confidence 0.18 Published 2009 Journal Mol Pain Section Body Doc Link PMC2784755 Disease Relevance 0.07 Pain Relevance 0.35
The marked differences in GlyR-mediated mIPSC amplitude in SDH and DDH neurons could be attributable to specific properties of the GlyR, such as differences in single-channel conductance, number of receptors open during quantal release (No), or channel open probability (Po).
Gene_expression (properties) of GlyR in neurons
7) Confidence 0.18 Published 2009 Journal Mol Pain Section Body Doc Link PMC2784755 Disease Relevance 0 Pain Relevance 0.09
In mice, however, we have shown that GlyR properties do not change in SDH neurons after P17 [39].
Gene_expression (properties) of GlyR in neurons
8) Confidence 0.18 Published 2009 Journal Mol Pain Section Body Doc Link PMC2784755 Disease Relevance 0 Pain Relevance 0.06
Real-time PCR using SYBR Green PCR Mastermix (PE Applied Biosystems, UK) and an ABI prism 7500 sequence detection system (PE Applied Biosystems, UK) was performed to assess the expression of the GlyR subunit genes (?
Gene_expression (expression) of GlyR
9) Confidence 0.16 Published 2009 Journal Mol Pain Section Body Doc Link PMC2784755 Disease Relevance 0 Pain Relevance 0.11
Our qPCR data for GlyR subunits show that the balance of GlyR-subunit expression differs in SDH and DDH.
Gene_expression (expression) of GlyR
10) Confidence 0.16 Published 2009 Journal Mol Pain Section Body Doc Link PMC2784755 Disease Relevance 0 Pain Relevance 0.29
One potential explanation for the slower kinetics of SDH versus DDH GlyRs in mouse is the existence of a distinctly expressed type of GlyR, containing ?
Gene_expression (expressed) of GlyR
11) Confidence 0.16 Published 2009 Journal Mol Pain Section Body Doc Link PMC2784755 Disease Relevance 0.07 Pain Relevance 0
Thus, future experiments are needed to determine why the kinetics of GlyR channels in the SDH and DDH differ.
Gene_expression (channels) of GlyR
12) Confidence 0.15 Published 2009 Journal Mol Pain Section Body Doc Link PMC2784755 Disease Relevance 0.08 Pain Relevance 0.18
One-way ANOVA's compared gene expression data for all GlyR- and GABAAR subunits in the SDH and DDH.
Gene_expression (expression) of GlyR
13) Confidence 0.14 Published 2009 Journal Mol Pain Section Body Doc Link PMC2784755 Disease Relevance 0 Pain Relevance 0
The amount of postsynaptic neurotransmitter receptor protein, such as NMDAR or GlyR, was not reduced (Table 1), which argues against a possible lack of postsynaptic sensitivity.
Gene_expression (amount) of GlyR associated with neurotransmitter
14) Confidence 0.12 Published 2008 Journal Neural Develop Section Body Doc Link PMC2576228 Disease Relevance 0 Pain Relevance 0.13
GlyR is differentially expressed in OFF cone bipolar cells, but not ON cone bipolar cells.
Neg (not) Gene_expression (expressed) of GlyR
15) Confidence 0.05 Published 2010 Journal Frontiers in Molecular Neuroscience Section Body Doc Link PMC2866564 Disease Relevance 0.09 Pain Relevance 0.23
To fully prove the existence of a nonsynaptic glycine signaling system endogenous glycine release must be demonstrated in addition to expression of functional GlyR (Scain et al., 2010).It must also be noted that the studies in support of nonsynaptic glycine signaling are limited due to the pharmacological tools used in the studies.
Gene_expression (expression) of GlyR
16) Confidence 0.05 Published 2010 Journal Frontiers in Molecular Neuroscience Section Body Doc Link PMC2866564 Disease Relevance 0 Pain Relevance 0.22
subunit of GlyR is first expressed at E14 in both the telencephalon of the brain and the ventral and dorsal horns of the spinal cord.
Gene_expression (expressed) of GlyR in telencephalon associated with spinal cord
17) Confidence 0.05 Published 2010 Journal Frontiers in Molecular Neuroscience Section Body Doc Link PMC2866564 Disease Relevance 0 Pain Relevance 0.32
The postnatal rat retina shows GlyR expression in the neuroblastic layer, while GlyR in the adult is only observed in the inner nuclear layer (INL) (Sassoe-Pognetto and Wassle, 1997).
Gene_expression (expression) of GlyR in inner nuclear layer
18) Confidence 0.05 Published 2010 Journal Frontiers in Molecular Neuroscience Section Body Doc Link PMC2866564 Disease Relevance 0.06 Pain Relevance 0.29
Differential expression of GlyR subunits over the course of development (namely ?
Gene_expression (expression) of GlyR
19) Confidence 0.05 Published 2010 Journal Frontiers in Molecular Neuroscience Section Body Doc Link PMC2866564 Disease Relevance 0.28 Pain Relevance 0.14
Overexpression of GlyR subunit ?
Gene_expression (Overexpression) of GlyR
20) Confidence 0.05 Published 2010 Journal Frontiers in Molecular Neuroscience Section Body Doc Link PMC2866564 Disease Relevance 0.09 Pain Relevance 0.07

General Comments

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