INT293464

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Context Info
Confidence 0.80
First Reported 2010
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 1
Total Number 7
Disease Relevance 0
Pain Relevance 0.16

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

transmembrane transport (Kcnh1)
Anatomy Link Frequency
synapses 2
neuronal 1
plasma 1
neurons 1
Kcnh1 (Rattus norvegicus)
Pain Link Frequency Relevance Heat
Neuronal excitability 21 97.20 Very High Very High Very High
Pyramidal cell 7 92.08 High High
Hippocampus 7 54.32 Quite High
tetrodotoxin 7 15.60 Low Low
Action potential 21 5.00 Very Low Very Low Very Low
imagery 14 5.00 Very Low Very Low Very Low
hyperexcitability 7 5.00 Very Low Very Low Very Low
repetitive firing 7 5.00 Very Low Very Low Very Low
potassium channel 7 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Infection 14 29.88 Quite Low
Neurological Disease 7 5.00 Very Low Very Low Very Low
Channelopathies 7 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
In-depth characterization of the axodendritic-distribution of gold particles revealed that Eag1 predominantly localized to the presynaptic terminal including both, the plasma membrane and intracellular components (Fig. 1D).
Localization (localized) of Eag1 in plasma
1) Confidence 0.80 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2810327 Disease Relevance 0 Pain Relevance 0.07
We found that disruption of F-actin (by Latrunculin A, 3 µM, 1 hour; [12]) or microtubules (by Nocodazole, 10 µM, 1 hour; [12]) reduced the number of Eag1 channels inside synaptic terminals as assessed by colocalization of Eag1 with the presynaptic marker synaptophysin (Mander coefficients?
Localization (colocalization) of Eag1
2) Confidence 0.75 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2810327 Disease Relevance 0 Pain Relevance 0
In accordance with these results, our SPT studies revealed that both treatments significantly reduced the synaptic dwell time of Eag1 (0.52±0.04 s, n?
Localization (time) of Eag1
3) Confidence 0.75 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2810327 Disease Relevance 0 Pain Relevance 0
In conclusion, our data demonstrate that mAb62 is able to detect endogenous Eag1 in rat hippocampal neurons and, therefore, serves as a tool for performing SPT studies.


Localization (detect) of Eag1 in neurons
4) Confidence 0.75 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2810327 Disease Relevance 0 Pain Relevance 0.04
This result is of high interest as it strongly suggests that changes in the mobility of Eag1 might be of physiological relevance for the role of Eag1 channels in neuronal excitability.
Localization (mobility) of Eag1 in neuronal associated with neuronal excitability
5) Confidence 0.75 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2810327 Disease Relevance 0 Pain Relevance 0.05
Eag1 did not only slow-down, but got also transiently stabilized inside synapses.
Localization (slow) of Eag1 in synapses
6) Confidence 0.75 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2810327 Disease Relevance 0 Pain Relevance 0
Eag1 did not only slow-down, but got also transiently stabilized inside synapses.
Localization (stabilized) of Eag1 in synapses
7) Confidence 0.75 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2810327 Disease Relevance 0 Pain Relevance 0

General Comments

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