INT131897

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Context Info
Confidence 0.70
First Reported 2005
Last Reported 2010
Negated 0
Speculated 0
Reported most in Abstract
Documents 7
Total Number 7
Disease Relevance 4.75
Pain Relevance 2.80

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 (Kcna6)
Anatomy Link Frequency
brain 2
neurons 1
Kcna6 (Rattus norvegicus)
Pain Link Frequency Relevance Heat
ischemia 38 99.84 Very High Very High Very High
addiction 4 99.50 Very High Very High Very High
Glutamate 20 99.46 Very High Very High Very High
cerebral cortex 2 89.84 High High
Action potential 17 87.88 High High
hyperexcitability 12 87.48 High High
Neuronal excitability 12 87.12 High High
Central nervous system 36 86.24 High High
sodium channel 4 83.84 Quite High
Pyramidal cell 10 70.04 Quite High
Disease Link Frequency Relevance Heat
Cv Unclassified Under Development 38 99.84 Very High Very High Very High
Hypoxia 14 99.16 Very High Very High Very High
Channelopathies 1 86.08 High High
Acquired Immune Deficiency Syndrome Or Hiv Infection 83 84.88 Quite High
Stroke 9 77.52 Quite High
Convulsion 4 75.00 Quite High
Generalized Anxiety Disorder 18 48.16 Quite Low
Apoptosis 4 45.28 Quite Low
Death 12 32.24 Quite Low
Infection 34 30.40 Quite Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Hypoxia/ischemia in rat brain induced a dramatic dephosphorylation of Kv2.1 and the translocation of surface Kv2.1 from clusters to a uniform localization.
Phosphorylation (dephosphorylation) of Kv2 in brain associated with hypoxia and ischemia
1) Confidence 0.70 Published 2005 Journal J. Neurosci. Section Abstract Doc Link 16319318 Disease Relevance 1.08 Pain Relevance 0.52
In cultured rat hippocampal neurons, chemical ischemia (CI) elicited a similar dephosphorylation and translocation of Kv2.1.
Phosphorylation (dephosphorylation) of Kv2 in neurons associated with ischemia
2) Confidence 0.54 Published 2005 Journal J. Neurosci. Section Abstract Doc Link 16319318 Disease Relevance 1.07 Pain Relevance 0.56
These events were reversible and were mediated by Ca2+ release from intracellular stores and calcineurin-mediated Kv2.1 dephosphorylation.
Phosphorylation (dephosphorylation) of Kv2
3) Confidence 0.47 Published 2005 Journal J. Neurosci. Section Abstract Doc Link 16319318 Disease Relevance 1.03 Pain Relevance 0.58
Hypoxia/ischemia in rat brain induced a dramatic dephosphorylation of Kv2.1 and the translocation of surface Kv2.1 from clusters to a uniform localization.
Phosphorylation (dephosphorylation) of Kv2 in brain associated with hypoxia and ischemia
4) Confidence 0.47 Published 2005 Journal J. Neurosci. Section Abstract Doc Link 16319318 Disease Relevance 1.09 Pain Relevance 0.53
Given that multiple phosphorylation sites within the Kv2.1 C-terminus influence the voltage-dependence of activation [26], the phosphorylation of AIS-localized Kv2.1 provides a mechanism to regulate axonal excitability.


Phosphorylation (phosphorylation) of Kv2 associated with addiction
5) Confidence 0.43 Published 2008 Journal BMC Neurosci Section Body Doc Link PMC2592246 Disease Relevance 0 Pain Relevance 0.32
Glutamate or carbachol treatments induce both Kv2.1 dephosphorylation and declustering [7-9].
Phosphorylation (dephosphorylation) of Kv2 associated with glutamate
6) Confidence 0.38 Published 2008 Journal BMC Neurosci Section Body Doc Link PMC2592246 Disease Relevance 0.14 Pain Relevance 0.13
Glutamate produces a Ca2+-dependent dephosphorylation of Kv2.1 channels, which disrupts channel clusters and increases mean open channel probability and conductance (Murakoshi et al. 1997; Misonou et al. 2004).
Phosphorylation (dephosphorylation) of Kv2 associated with glutamate
7) Confidence 0.17 Published 2010 Journal J Neuroimmune Pharmacol Section Body Doc Link PMC2914283 Disease Relevance 0.33 Pain Relevance 0.17

General Comments

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