INT243533

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Context Info
Confidence 0.35
First Reported 2008
Last Reported 2008
Negated 0
Speculated 0
Reported most in Body
Documents 1
Total Number 5
Disease Relevance 3.93
Pain Relevance 0.92

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

nucleus (SOX10) DNA binding (SOX10) cytoplasm (SOX10)
Anatomy Link Frequency
dendrite 1
synapse 1
temporal lobe 1
SOX10 (Homo sapiens)
Pain Link Frequency Relevance Heat
Glutamate receptor 25 99.60 Very High Very High Very High
Neurotransmitter 15 97.24 Very High Very High Very High
antagonist 10 97.16 Very High Very High Very High
Glutamate 70 95.76 Very High Very High Very High
excitatory amino acid 15 94.60 High High
Hippocampus 75 82.36 Quite High
nMDA receptor 30 75.36 Quite High
agonist 20 74.16 Quite High
ischemia 5 74.08 Quite High
Central nervous system 40 65.04 Quite High
Disease Link Frequency Relevance Heat
Epilepsy 25 99.98 Very High Very High Very High
Toxicity 145 99.96 Very High Very High Very High
Drug Induced Neurotoxicity 40 99.96 Very High Very High Very High
Brain Disease 25 99.16 Very High Very High Very High
Injury 110 97.12 Very High Very High Very High
Partial Seizures 5 93.40 High High
Poisoning 115 91.76 High High
Frailty 35 89.60 High High
Cognitive Disorder 25 89.24 High High
Convulsion 50 88.68 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Current evidence on DOM induced neurotoxicity supports the view that the main cause of neurotoxicity is the activation of GluRs and the release of endogenous glutamate leading to a cascade of events mediating cell and tissue injury (Figure 8).
Positive_regulation (induced) of DOM associated with glutamate, drug induced neurotoxicity and injury
1) Confidence 0.35 Published 2008 Journal Marine Drugs Section Body Doc Link PMC2525487 Disease Relevance 0.86 Pain Relevance 0.18
It was suggested that temporal lobe epilepsy following DOM exposure might develop after a "silent period" of one year.
Positive_regulation (following) of DOM in temporal lobe associated with epilepsy
2) Confidence 0.35 Published 2008 Journal Marine Drugs Section Body Doc Link PMC2525487 Disease Relevance 1.37 Pain Relevance 0.03
The demonstration that GluRs are targeted and anchored at excitatory synapses through a network of scaffolding proteins concentrated at the tip of the post-synaptic dendritic spine region [192], and that the dendrite has been identified as a preferential target for DOM toxicity opens the possibility that these proteins may also be involved in DOM cell injury.


Positive_regulation (target) of DOM in dendrite associated with toxicity and injury
3) Confidence 0.35 Published 2008 Journal Marine Drugs Section Body Doc Link PMC2525487 Disease Relevance 0.86 Pain Relevance 0.27
DOM induces excitotoxicity by an integrative action on ionotropic GluRs [iGluRs] at both sides of the synapse for which it has high affinity, preferentially the KA subtype, coupled with an effect that prevents the channel from rapid desensitization [48,59–79].
Positive_regulation (induces) of DOM in synapse
4) Confidence 0.32 Published 2008 Journal Marine Drugs Section Body Doc Link PMC2525487 Disease Relevance 0.37 Pain Relevance 0.31
On the other hand a significantly increases DOM toxicity was associated with the neurotrophin NT3 and the H1 receptor antagonist terfenadine in vitro exposure [230, 232].


Positive_regulation (increases) of DOM associated with toxicity and antagonist
5) Confidence 0.32 Published 2008 Journal Marine Drugs Section Body Doc Link PMC2525487 Disease Relevance 0.48 Pain Relevance 0.14

General Comments

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