INT106339

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Context Info
Confidence 0.49
First Reported 2002
Last Reported 2002
Negated 0
Speculated 1
Reported most in Abstract
Documents 1
Total Number 2
Disease Relevance 0
Pain Relevance 1.12

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

cytosol (Insr) endosome (Insr) plasma membrane (Insr)
nucleus (Insr)
Insr (Rattus norvegicus)
Pain Link Frequency Relevance Heat
antagonist 6 89.04 High High
gABA 14 86.96 High High
agonist 2 84.36 Quite High
Hippocampus 6 82.52 Quite High
tetrodotoxin 2 68.16 Quite High
Central nervous system 2 55.60 Quite High
Neurotransmitter 2 51.60 Quite High

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Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
IGF-I (10 nM) inhibited K(+)- as well as veratridine-evoked ACh release from rat hippocampal slices and the effect is possibly mediated via the activation of a typical IGF-I receptor and the subsequent phosphorylation of the insulin receptor substrate-1 (IRS-1).
Spec (possibly) Positive_regulation (mediated) of Phosphorylation (phosphorylation) of insulin receptor
1) Confidence 0.49 Published 2002 Journal Neuroscience Section Abstract Doc Link 12421625 Disease Relevance 0 Pain Relevance 0.56
IGF-I (10 nM) inhibited K(+)- as well as veratridine-evoked ACh release from rat hippocampal slices and the effect is possibly mediated via the activation of a typical IGF-I receptor and the subsequent phosphorylation of the insulin receptor substrate-1 (IRS-1).
Positive_regulation (activation) of Phosphorylation (phosphorylation) of insulin receptor
2) Confidence 0.49 Published 2002 Journal Neuroscience Section Abstract Doc Link 12421625 Disease Relevance 0 Pain Relevance 0.56

General Comments

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