INT35017

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Context Info
Confidence 0.59
First Reported 1987
Last Reported 2009
Negated 0
Speculated 0
Reported most in Abstract
Documents 5
Total Number 5
Disease Relevance 0.24
Pain Relevance 3.22

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

Golgi apparatus (Syn1) ligase activity (Syn1)
Anatomy Link Frequency
external 2
Syn1 (Rattus norvegicus)
Pain Link Frequency Relevance Heat
agonist 5 99.78 Very High Very High Very High
Neurotransmitter 2 99.74 Very High Very High Very High
opiate 16 99.62 Very High Very High Very High
Glutamate 6 99.16 Very High Very High Very High
antagonist 7 98.00 Very High Very High Very High
Morphine 5 96.16 Very High Very High Very High
Spinal cord 3 95.68 Very High Very High Very High
dorsal root ganglion 2 94.40 High High
tetrodotoxin 3 91.64 High High
amygdala 1 89.36 High High
Disease Link Frequency Relevance Heat
Ganglion Cysts 2 94.40 High High
Opiate Addiction 1 66.04 Quite High
Depression 44 23.72 Low Low
Drug Induced Neurotoxicity 8 5.00 Very Low Very Low Very Low
INFLAMMATION 7 5.00 Very Low Very Low Very Low
Kernicterus 7 5.00 Very Low Very Low Very Low
Li-fraumeni Syndrome 6 5.00 Very Low Very Low Very Low
Cognitive Disorder 4 5.00 Very Low Very Low Very Low
Jaundice 4 5.00 Very Low Very Low Very Low
Death 3 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Since opiates were shown to attenuate neurotransmitter release and reduce synapsin I phosphorylation, it is suggested that the increase in synapsin I levels would lead to the requirement of higher amounts of opiate agonists to obtain the opiate physiological effects.
Negative_regulation (reduce) of Phosphorylation (phosphorylation) of synapsin I associated with neurotransmitter, agonist and opiate
1) Confidence 0.59 Published 1995 Journal Brain Res. Mol. Brain Res. Section Abstract Doc Link 8750825 Disease Relevance 0.07 Pain Relevance 1.42
Moreover, the PTZ-stimulated synapsin I phosphorylation was reversed by addition of EGTA sufficient to chelate all external free Ca2+.
Negative_regulation (reversed) of Phosphorylation (phosphorylation) of synapsin I in external
2) Confidence 0.57 Published 1987 Journal Biochem. Pharmacol. Section Abstract Doc Link 3107572 Disease Relevance 0 Pain Relevance 0.22
We have previously shown that acute kappa-opiate agonist treatment reduces phosphorylation of synapsin I stimulated by depolarizing agents (such as 60 mM KCl).
Negative_regulation (reduces) of Phosphorylation (phosphorylation) of synapsin I associated with agonist and opiate
3) Confidence 0.43 Published 1993 Journal J. Neurochem. Section Abstract Doc Link 8436965 Disease Relevance 0.17 Pain Relevance 1.04
The calmodulin antagonists N-(6-aminohexyl)-5-chloro-1-naphthalenesulfonamide (W-7, strongly) and N-(6-aminohexyl)-1-naphthalenesulfonamide (W-5, weakly) reduced the PTZ-stimulatory effect on synapsin I phosphorylation by about 75 and 15%, respectively, whereas these antagonists had essentially no effect on PTZ-stimulated synaptosomal accumulation of Ca2+.
Negative_regulation (reduced) of Phosphorylation (phosphorylation) of synapsin I associated with antagonist
4) Confidence 0.42 Published 1987 Journal Biochem. Pharmacol. Section Abstract Doc Link 3107572 Disease Relevance 0 Pain Relevance 0.26
Regarding possible mechanisms by which UCB inhibits glutamate release, one possibility may involve the inhibition of synapsin I phosphorylation [43], which plays an important role in neurotransmitter release process [44].
Negative_regulation (inhibition) of Phosphorylation (phosphorylation) of synapsin I associated with neurotransmitter and glutamate
5) Confidence 0.09 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2690688 Disease Relevance 0 Pain Relevance 0.28

General Comments

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