INT265157

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Context Info
Confidence 0.23
First Reported 2007
Last Reported 2007
Negated 0
Speculated 0
Reported most in Body
Documents 1
Total Number 7
Disease Relevance 0
Pain Relevance 1.91

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

cytoskeleton (Marcks) cytoplasm (Marcks)
Anatomy Link Frequency
neurons 4
Marcks (Rattus norvegicus)
Pain Link Frequency Relevance Heat
agonist 147 99.84 Very High Very High Very High
Kinase C 546 99.64 Very High Very High Very High
tetrodotoxin 98 53.20 Quite High
Glutamate 42 5.00 Very Low Very Low Very Low
nMDA receptor 28 5.00 Very Low Very Low Very Low
Glutamate receptor 21 5.00 Very Low Very Low Very Low
imagery 21 5.00 Very Low Very Low Very Low
Action potential 14 5.00 Very Low Very Low Very Low
Hippocampus 14 5.00 Very Low Very Low Very Low
GABAergic 14 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Nash(non-alcoholic Steatohepatitis) 84 5.00 Very Low Very Low Very Low
Cognitive Disorder 7 5.00 Very Low Very Low Very Low
Aging 7 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
These data suggest that agonist-driven eGFP-MARCKS translocation is mediated through PKC activation in hippocampal neurons.
Positive_regulation (mediated) of Localization (translocation) of eGFP-MARCKS in neurons associated with kinase c and agonist
1) Confidence 0.23 Published 2007 Journal Journal of Neurochemistry Section Body Doc Link PMC2658029 Disease Relevance 0 Pain Relevance 0.25
To determine whether PKC or Ca2+/CaM were responsible for M1 mACh receptor-mediated MARCKS translocation the following protocol was used.
Positive_regulation (mediated) of Localization (translocation) of MARCKS associated with kinase c
2) Confidence 0.23 Published 2007 Journal Journal of Neurochemistry Section Body Doc Link PMC2658029 Disease Relevance 0 Pain Relevance 0.27
mol/L) stimulated a rapid increase in eGFP-MARCKS translocation to the cytoplasm, which returned to baseline following picrotoxin removal (Fig. 6).
Positive_regulation (increase) of Localization (translocation) of eGFP-MARCKS
3) Confidence 0.23 Published 2007 Journal Journal of Neurochemistry Section Body Doc Link PMC2658029 Disease Relevance 0 Pain Relevance 0.23
Comparison of S1 and S2 responses indicated that MCh-stimulated eGFP-MARCKS translocation was almost completely inhibited following staurosporine treatment (Fig. 5c and d), while W7 and W5 treatments were without effect (Fig. 5d).
Positive_regulation (stimulated) of Localization (translocation) of eGFP-MARCKS
4) Confidence 0.23 Published 2007 Journal Journal of Neurochemistry Section Body Doc Link PMC2658029 Disease Relevance 0 Pain Relevance 0.29
Addition of staurosporine and W7 together almost completely inhibited picrotoxin-stimulated eGFP-MARCKS translocation (Fig. 6e and f).
Positive_regulation (stimulated) of Localization (translocation) of eGFP-MARCKS
5) Confidence 0.23 Published 2007 Journal Journal of Neurochemistry Section Body Doc Link PMC2658029 Disease Relevance 0 Pain Relevance 0.29
To determine whether synaptic activity alone could promote eGFP-MARCKS translocation, neurons were incubated with picrotoxin in the absence of agonist for 2 min.
Positive_regulation (promote) of Localization (translocation) of eGFP-MARCKS in neurons associated with agonist
6) Confidence 0.23 Published 2007 Journal Journal of Neurochemistry Section Body Doc Link PMC2658029 Disease Relevance 0 Pain Relevance 0.24
These data indicate that the picrotoxin-mediated eGFP-MARCKS translocation occurs through both PKC- and Ca2+/CaM-dependent mechanisms.


Positive_regulation (mediated) of Localization (translocation) of eGFP-MARCKS associated with kinase c
7) Confidence 0.20 Published 2007 Journal Journal of Neurochemistry Section Body Doc Link PMC2658029 Disease Relevance 0 Pain Relevance 0.33

General Comments

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