INT319281

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Context Info
Confidence 0.69
First Reported 2010
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 1
Total Number 4
Disease Relevance 2.03
Pain Relevance 1.62

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

mitochondrion (Glud1) oxidoreductase activity (Glud1) enzyme binding (Glud1)
cellular amino acid metabolic process (Glud1) cytoplasm (Glud1)
Anatomy Link Frequency
neurons 3
glial cells 1
Glud1 (Mus musculus)
Pain Link Frequency Relevance Heat
Glutamate 468 100.00 Very High Very High Very High
Central nervous system 28 99.76 Very High Very High Very High
Hippocampus 96 76.64 Quite High
Neurotransmitter 24 65.04 Quite High
anesthesia 4 6.44 Low Low
chemokine 36 5.00 Very Low Very Low Very Low
nMDA receptor 24 5.00 Very Low Very Low Very Low
Inflammation 16 5.00 Very Low Very Low Very Low
Inflammatory response 12 5.00 Very Low Very Low Very Low
long-term potentiation 4 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Targeted Disruption 312 84.40 Quite High
Lifespan 24 80.76 Quite High
Aging 48 66.56 Quite High
Neurodegenerative Disease 24 65.52 Quite High
Embryonic Lethality 4 63.20 Quite High
Disease 52 61.68 Quite High
Attention Deficit Hyperactivity Disorder 48 55.56 Quite High
Tuberous Sclerosis 4 46.96 Quite Low
Toxicity 12 22.12 Low Low
Death 40 12.76 Low Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
This analysis revealed mechanistic insights into the types of molecular functions, neurobiological pathways and gene-gene interactions that might influence the responses of CNS neurons to increased Glud1 mitochondrial activity and of neurons and glial cells to chronic, moderate excess of synaptic Glu release.


Positive_regulation (increased) of Glud1 in neurons associated with glutamate and central nervous system
1) Confidence 0.69 Published 2010 Journal BMC Genomics Section Body Doc Link PMC2896956 Disease Relevance 0.33 Pain Relevance 0.37
To achieve excess Glu formation in neurons and increased release from synaptic terminals in these animals, the gene for the enzyme glutamate dehydrogenase 1 (Glud1) was introduced under the control of the promoter for neuron-specific enolase (Nse), thus its over-expression occurs only in neurons [14].
Positive_regulation (enzyme) of glutamate dehydrogenase 1 in neurons associated with glutamate
2) Confidence 0.50 Published 2010 Journal BMC Genomics Section Body Doc Link PMC2896956 Disease Relevance 0.68 Pain Relevance 0.44
To achieve excess Glu formation in neurons and increased release from synaptic terminals in these animals, the gene for the enzyme glutamate dehydrogenase 1 (Glud1) was introduced under the control of the promoter for neuron-specific enolase (Nse), thus its over-expression occurs only in neurons [14].
Positive_regulation (enzyme) of Glud1 in neurons associated with glutamate
3) Confidence 0.50 Published 2010 Journal BMC Genomics Section Body Doc Link PMC2896956 Disease Relevance 0.69 Pain Relevance 0.44
This analysis revealed mechanistic insights into the types of molecular functions, neurobiological pathways and gene-gene interactions that might influence the responses of CNS neurons to increased Glud1 mitochondrial activity and of neurons and glial cells to chronic, moderate excess of synaptic Glu release.


Positive_regulation (increased) of Glud1 in glial cells associated with glutamate and central nervous system
4) Confidence 0.23 Published 2010 Journal BMC Genomics Section Body Doc Link PMC2896956 Disease Relevance 0.33 Pain Relevance 0.37

General Comments

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