INT139928

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Context Info
Confidence 0.37
First Reported 2006
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 6
Total Number 6
Disease Relevance 1.19
Pain Relevance 0.84

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

transport (Kcnma1) endoplasmic reticulum (Kcnma1) plasma membrane (Kcnma1)
transmembrane transport (Kcnma1)
Kcnma1 (Mus musculus)
Pain Link Frequency Relevance Heat
tetrodotoxin 7 99.76 Very High Very High Very High
Calcium channel 5 96.96 Very High Very High Very High
ischemia 42 95.96 Very High Very High Very High
Glutamate 12 87.00 High High
Action potential 21 86.12 High High
nMDA receptor 13 80.88 Quite High
potassium channel 7 71.84 Quite High
Neurotransmitter 7 69.32 Quite High
addiction 1 68.44 Quite High
isoflurane 2 41.52 Quite Low
Disease Link Frequency Relevance Heat
Repression 134 100.00 Very High Very High Very High
Cv General 4 Under Development 2 95.96 Very High Very High Very High
Emergencies 1 91.76 High High
Stroke 11 83.04 Quite High
Death 23 77.60 Quite High
Brain Hemorrhage 9 62.16 Quite High
Cv Unclassified Under Development 35 55.84 Quite High
Drug Induced Neurotoxicity 2 14.72 Low Low
Middle Cerebral Artery Infarction 15 5.00 Very Low Very Low Very Low
Infarction 13 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
We hypothesized that loss of robust circadian rhythmicity in Kcnma1?
Negative_regulation (loss) of Kcnma1
1) Confidence 0.37 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2586654 Disease Relevance 0 Pain Relevance 0
Pretreatment with blockers of calcium-activated potassium currents (I(KCa)) reproduced this shift and blocked subsequent cadmium-induced changes, suggesting cadmium changes latency indirectly by blocking I(KCa).
Negative_regulation (blocking) of KCa
2) Confidence 0.23 Published 2006 Journal J. Neurosci. Section Abstract Doc Link 17108170 Disease Relevance 0 Pain Relevance 0.51
To confirm that the reduction in maxi-K current observed in cells expressing the triple mutant is due to the altered interaction between the maxi-K channel and cav-1, we immunoprecipitated the maxi-K proteins from isolated lipid rafts (as indicated by a box in Figure 4).
Negative_regulation (reduction) of maxi-K
3) Confidence 0.15 Published 2009 Journal Reprod Biol Endocrinol Section Body Doc Link PMC2785819 Disease Relevance 0 Pain Relevance 0
We have now for the first time tested this hypothesis directly by selective suppression of BK channel activity, using BK?
Negative_regulation (suppression) of BK channel
4) Confidence 0.05 Published 2010 Journal PLoS ONE Section Body Doc Link PMC3012709 Disease Relevance 0.65 Pain Relevance 0.28
We showed previously that the splicing repression of the BK channel STREX exon is mediated by a CaRRE (CACAUNRUUAU) located in the 3?
Negative_regulation (repression) of BK channel associated with repression
5) Confidence 0.01 Published 2007 Journal PLoS Biology Section Body Doc Link PMC1790950 Disease Relevance 0.38 Pain Relevance 0
We previously showed that the repression of the BK channel STREX exon after depolarization requires calcium ion influx through L-type calcium channels and a downstream Ca++/calmodulin-dependent protein kinase (CaMK) [23].
Negative_regulation (repression) of BK channel associated with calcium channel and repression
6) Confidence 0.01 Published 2007 Journal PLoS Biology Section Body Doc Link PMC1790950 Disease Relevance 0.16 Pain Relevance 0.05

General Comments

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