INT139162

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Context Info
Confidence 0.34
First Reported 2006
Last Reported 2007
Negated 0
Speculated 2
Reported most in Body
Documents 1
Total Number 16
Disease Relevance 0
Pain Relevance 5.10

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 5
plasma 1
neurites 1
synapses 1
ovary 1
Marcks (Rattus norvegicus)
Pain Link Frequency Relevance Heat
Kinase C 1098 100.00 Very High Very High Very High
imagery 42 99.92 Very High Very High Very High
agonist 294 99.84 Very High Very High Very High
substance P 2 76.96 Quite High
Enkephalin 2 73.12 Quite High
Nucleus accumbens 8 68.88 Quite High
tetrodotoxin 196 60.52 Quite High
nMDA receptor 56 43.68 Quite Low
Substantia nigra 4 32.08 Quite Low
Action potential 28 28.80 Quite Low
Disease Link Frequency Relevance Heat
Nash(non-alcoholic Steatohepatitis) 168 49.48 Quite Low
Cognitive Disorder 14 5.00 Very Low Very Low Very Low
Aging 14 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
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).
Localization (translocation) of eGFP-MARCKS
1) Confidence 0.34 Published 2007 Journal Journal of Neurochemistry Section Body Doc Link PMC2658029 Disease Relevance 0 Pain Relevance 0.29
To determine whether PKC or Ca2+/CaM were responsible for M1 mACh receptor-mediated MARCKS translocation the following protocol was used.
Localization (translocation) of MARCKS associated with kinase c
2) Confidence 0.34 Published 2007 Journal Journal of Neurochemistry Section Body Doc Link PMC2658029 Disease Relevance 0 Pain Relevance 0.27
To determine whether synaptic activity alone could promote eGFP-MARCKS translocation, neurons were incubated with picrotoxin in the absence of agonist for 2 min.
Localization (translocation) of eGFP-MARCKS in neurons associated with agonist
3) Confidence 0.34 Published 2007 Journal Journal of Neurochemistry Section Body Doc Link PMC2658029 Disease Relevance 0 Pain Relevance 0.24
Increased synaptic activity induced by picrotoxin in the hippocampal neurons also resulted in the translocation of MARCKS and inhibitor studies implicate both a PKC and CaM regulatory component under these conditions.
Localization (translocation) of MARCKS in neurons associated with kinase c
4) Confidence 0.34 Published 2007 Journal Journal of Neurochemistry Section Body Doc Link PMC2658029 Disease Relevance 0 Pain Relevance 0.46
mol/L) stimulated a rapid increase in eGFP-MARCKS translocation to the cytoplasm, which returned to baseline following picrotoxin removal (Fig. 6).
Localization (translocation) of eGFP-MARCKS
5) Confidence 0.34 Published 2007 Journal Journal of Neurochemistry Section Body Doc Link PMC2658029 Disease Relevance 0 Pain Relevance 0.22
Addition of staurosporine and W7 together almost completely inhibited picrotoxin-stimulated eGFP-MARCKS translocation (Fig. 6e and f).
Localization (translocation) of eGFP-MARCKS
6) Confidence 0.34 Published 2007 Journal Journal of Neurochemistry Section Body Doc Link PMC2658029 Disease Relevance 0 Pain Relevance 0.29
Imaging of eGFP-MARCKS translocation was undertaken as described for the eGFP-PHPLC?
Localization (translocation) of eGFP-MARCKS associated with imagery
7) Confidence 0.34 Published 2007 Journal Journal of Neurochemistry Section Body Doc Link PMC2658029 Disease Relevance 0 Pain Relevance 0.30
These data suggest that agonist-driven eGFP-MARCKS translocation is mediated through PKC activation in hippocampal neurons.
Localization (translocation) of eGFP-MARCKS in neurons associated with kinase c and agonist
8) Confidence 0.34 Published 2007 Journal Journal of Neurochemistry Section Body Doc Link PMC2658029 Disease Relevance 0 Pain Relevance 0.25
Moreover, our studies, using the translocation of eGFP-MARCKS have provided evidence for the activation of PKC in hippocampal neurons following M1 mACh receptor stimulation under conditions of increased synaptic activity.
Localization (translocation) of eGFP-MARCKS in neurons associated with kinase c
9) Confidence 0.34 Published 2007 Journal Journal of Neurochemistry Section Body Doc Link PMC2658029 Disease Relevance 0 Pain Relevance 0.35
mol/L) produced a rapid and transient translocation of MARCKS to the cytoplasm, which quickly returned to the plasma membrane on agonist removal.
Localization (translocation) of MARCKS in plasma associated with agonist
10) Confidence 0.34 Published 2007 Journal Journal of Neurochemistry Section Body Doc Link PMC2658029 Disease Relevance 0 Pain Relevance 0.33
Indeed, MARCKS translocation in response to MCh was paralleled by a reciprocal movement of eGFP-PKC?
Localization (translocation) of MARCKS associated with kinase c
11) Confidence 0.32 Published 2007 Journal Journal of Neurochemistry Section Body Doc Link PMC2658029 Disease Relevance 0 Pain Relevance 0.46
These data indicate that the picrotoxin-mediated eGFP-MARCKS translocation occurs through both PKC- and Ca2+/CaM-dependent mechanisms.


Localization (translocation) of eGFP-MARCKS associated with kinase c
12) Confidence 0.30 Published 2007 Journal Journal of Neurochemistry Section Body Doc Link PMC2658029 Disease Relevance 0 Pain Relevance 0.33
The translocation of eGFP-MARCKS indicates that PKC activity can be stimulated in hippocampal neurons following stimulation of the M1 mACh receptor and also following picrotoxin-mediated enhancement of synaptic activity.
Localization (translocation) of eGFP-MARCKS in neurons associated with kinase c
13) Confidence 0.30 Published 2007 Journal Journal of Neurochemistry Section Body Doc Link PMC2658029 Disease Relevance 0 Pain Relevance 0.41
Here we provide evidence that the translocation of eGFP-MARCKS stimulated by MCh is predominantly dependent on PKC activity, supporting our previous studies with M3 mACh receptors both in Chinese hamster ovary cells (Bartlett et al. 2005) and in cerebellar granule cells (Young et al. 2004).
Localization (translocation) of eGFP-MARCKS in ovary associated with kinase c
14) Confidence 0.30 Published 2007 Journal Journal of Neurochemistry Section Body Doc Link PMC2658029 Disease Relevance 0 Pain Relevance 0.42
We performed in situ hybridization histochemistry on the monkey basal ganglia to investigate the mRNA localization of three protein kinase C substrates (GAP-43, MARCKS, and neurogranin), of which expression plays a role in structural changes in neurites and synapses.
Spec (investigate) Localization (localization) of MARCKS in neurites associated with kinase c
15) Confidence 0.16 Published 2006 Journal J. Comp. Neurol. Section Abstract Doc Link 17029258 Disease Relevance 0 Pain Relevance 0.23
We performed in situ hybridization histochemistry on the monkey basal ganglia to investigate the mRNA localization of three protein kinase C substrates (GAP-43, MARCKS, and neurogranin), of which expression plays a role in structural changes in neurites and synapses.
Spec (investigate) Localization (localization) of MARCKS in synapses associated with kinase c
16) Confidence 0.06 Published 2006 Journal J. Comp. Neurol. Section Abstract Doc Link 17029258 Disease Relevance 0 Pain Relevance 0.23

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