INT133602

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Context Info
Confidence 0.54
First Reported 2007
Last Reported 2010
Negated 0
Speculated 0
Reported most in Abstract
Documents 2
Total Number 5
Disease Relevance 0.38
Pain Relevance 4.02

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

signal transduction (Fadd) protein complex (Fadd) cytoplasm (Fadd)
Anatomy Link Frequency
corpus striatum 1
Fadd (Rattus norvegicus)
Pain Link Frequency Relevance Heat
cerebral cortex 2 99.28 Very High Very High Very High
Morphine 31 98.68 Very High Very High Very High
Dopamine 4 97.04 Very High Very High Very High
opiate 9 93.72 High High
agonist 6 93.44 High High
withdrawal 5 92.20 High High
antagonist 1 85.96 High High
Delta opioid receptors 1 83.44 Quite High
Cannabinoid 1 74.72 Quite High
narcan 1 72.52 Quite High
Disease Link Frequency Relevance Heat
Death 7 75.00 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Notably, the MEK inhibitor SL 327 attenuated (58%) the expression of morphine-induced psychomotor sensitization (SW 3) and fully prevented the upregulation of p-FADD, p-PEA-15 and p-Akt1 at SW 3.
Positive_regulation (upregulation) of p-FADD associated with morphine
1) Confidence 0.54 Published 2010 Journal Eur Neuropsychopharmacol Section Abstract Doc Link 19758790 Disease Relevance 0.05 Pain Relevance 0.71
The results indicate that the activation of MEK/ERK, the upregulation of p-FADD and that of the linking partners PEA-15/Akt1 have a major role in mediating the short-lasting expression of unconditioned psychomotor sensitization induced by morphine in rats.
Positive_regulation (upregulation) of p-FADD associated with morphine
2) Confidence 0.54 Published 2010 Journal Eur Neuropsychopharmacol Section Abstract Doc Link 19758790 Disease Relevance 0 Pain Relevance 0.69
Pretreatment of rats with SL 327 (a selective MEK1/2 inhibitor that blocks ERK activation) fully prevented the reduction of FADD content induced by SNC-80 in the cerebral cortex (43%) and corpus striatum (29%), demonstrating the direct involvement of ERK1/2 signaling in the regulation of FADD by the opiate agonist.
Positive_regulation (induced) of FADD in corpus striatum associated with agonist, opiate and cerebral cortex
3) Confidence 0.43 Published 2007 Journal Neuropsychopharmacology Section Abstract Doc Link 16482086 Disease Relevance 0.19 Pain Relevance 1.18
At SW 3, p-PEA-15, a FADD-ERK binding partner, was also upregulated (51%) as well as the activation of its phosphorylating Akt1 kinase (49%).
Positive_regulation (upregulated) of FADD
4) Confidence 0.42 Published 2010 Journal Eur Neuropsychopharmacol Section Abstract Doc Link 19758790 Disease Relevance 0.06 Pain Relevance 0.74
Marked concomitant increases in the content of p-FADD (48%) and the activation of MEK-ERK (46-79%) were quantified during the short-term expression of morphine sensitization (SW 3, in the absence of morphine challenge).
Positive_regulation (activation) of p-FADD associated with morphine
5) Confidence 0.36 Published 2010 Journal Eur Neuropsychopharmacol Section Abstract Doc Link 19758790 Disease Relevance 0.07 Pain Relevance 0.70

General Comments

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