INT117799

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Context Info
Confidence 0.46
First Reported 2004
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 4
Total Number 9
Disease Relevance 0.42
Pain Relevance 1.98

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 2
inner nuclear layer 1
photoreceptor cells 1
forebrain 1
Glyr1 (Mus musculus)
Pain Link Frequency Relevance Heat
antagonist 30 98.64 Very High Very High Very High
antiepileptic Drug 6 98.12 Very High Very High Very High
gABA 170 95.24 Very High Very High Very High
Neurotransmitter 180 95.04 Very High Very High Very High
Hippocampus 42 94.64 High High
agonist 30 92.28 High High
Ventral tegmentum 18 90.96 High High
midbrain 48 90.48 High High
Thalamus 36 89.96 High High
Spinal cord 302 83.76 Quite High
Disease Link Frequency Relevance Heat
Death 6 88.44 High High
Ganglion Cysts 60 72.96 Quite High
Spasticity 6 67.04 Quite High
Pain 18 5.00 Very Low Very Low Very Low
Targeted Disruption 12 5.00 Very Low Very Low Very Low
Nociception 12 5.00 Very Low Very Low Very Low
Sleep Disorders 6 5.00 Very Low Very Low Very Low
Lung Cancer 6 5.00 Very Low Very Low Very Low
Depression 6 5.00 Very Low Very Low Very Low
Muscle Hypertonia 6 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Although potentiation of the inhibitory glycine receptor (GlyR) may contribute to the mechanism of action of antiepileptic drugs (AEDs), the effects of AEDs on GlyRs have not been investigated in detail in forebrain neurons.
Positive_regulation (potentiation) of GlyR in forebrain associated with antiepileptic drug
1) Confidence 0.46 Published 2004 Journal Epilepsy Res. Section Abstract Doc Link 15066672 Disease Relevance 0 Pain Relevance 0.31
This is not surprising, since the information contained in data at only one (saturating) concentration cannot give a unique solution for all the rate constants in a model as complex as that needed to describe GlyR activation.
Positive_regulation (activation) of GlyR
2) Confidence 0.11 Published 2007 Journal The Journal of Physiology Section Body Doc Link PMC2075563 Disease Relevance 0 Pain Relevance 0.03
We have recently reported a detailed mechanism for GlyR activation based on the analysis of cell-attached recordings of recombinant channels expressed in HEK cells (Beato et al. 2002, 2004; Burzomato et al. 2004).
Positive_regulation (activation) of GlyR
3) Confidence 0.08 Published 2007 Journal The Journal of Physiology Section Body Doc Link PMC2075563 Disease Relevance 0 Pain Relevance 0.05
Experiments using the GlyR antagonist strychnine and L-type Ca+2 blockers on spinal neurons suggest that GlyR activation leads to Ca+2 transients that in turn cause accumulation of the anchoring protein Gephyrin and GlyR.
Positive_regulation (accumulation) of GlyR in neurons associated with antagonist
4) Confidence 0.04 Published 2010 Journal Frontiers in Molecular Neuroscience Section Body Doc Link PMC2866564 Disease Relevance 0 Pain Relevance 0.43
Experiments using the GlyR antagonist strychnine and L-type Ca+2 blockers on spinal neurons suggest that GlyR activation leads to Ca+2 transients that in turn cause accumulation of the anchoring protein Gephyrin and GlyR.
Positive_regulation (activation) of GlyR in neurons associated with antagonist
5) Confidence 0.04 Published 2010 Journal Frontiers in Molecular Neuroscience Section Body Doc Link PMC2866564 Disease Relevance 0 Pain Relevance 0.47
Taurine's ability to directly induce rod photoreceptor cells regardless of mitotic state via GlyR activation remains untested.
Positive_regulation (activation) of GlyR in photoreceptor cells
6) Confidence 0.03 Published 2010 Journal Frontiers in Molecular Neuroscience Section Body Doc Link PMC2866564 Disease Relevance 0.28 Pain Relevance 0.04
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).
Positive_regulation (observed) of GlyR in inner nuclear layer
7) Confidence 0.03 Published 2010 Journal Frontiers in Molecular Neuroscience Section Body Doc Link PMC2866564 Disease Relevance 0.07 Pain Relevance 0.28
Although no detailed immunohistochemistry or in situ hybridization studies have been conducted for GlyR?
Positive_regulation (conducted) of GlyR
8) Confidence 0.03 Published 2010 Journal Frontiers in Molecular Neuroscience Section Body Doc Link PMC2866564 Disease Relevance 0.06 Pain Relevance 0.03
-alanine and taurine uptake inhibitor guanidinoethanesulfonic acid indicated that the modulation of these transporters could regulate tonic GlyR activation.
Positive_regulation (activation) of GlyR
9) Confidence 0.03 Published 2010 Journal Frontiers in Molecular Neuroscience Section Body Doc Link PMC2866564 Disease Relevance 0 Pain Relevance 0.34

General Comments

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