INT102586

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Context Info
Confidence 0.42
First Reported 2002
Last Reported 2003
Negated 0
Speculated 0
Reported most in Title
Documents 2
Total Number 2
Disease Relevance 0.68
Pain Relevance 0.50

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

transport (Kcnj8) mitochondrion (Kcnj8)
Anatomy Link Frequency
Mouse 1
pore 1
Kcnj8 (Mus musculus)
Pain Link Frequency Relevance Heat
Angina 5 99.92 Very High Very High Very High
Inward rectifier potassium channel 1 98.04 Very High Very High Very High
potassium channel 1 79.44 Quite High
Disease Link Frequency Relevance Heat
Variant Angina Pectoris 2 99.92 Very High Very High Very High
Angina 2 99.38 Very High Very High Very High
Sudden Death 1 87.24 High High
Cv General 2 Under Development 1 84.60 Quite High
Increased Venous Pressure Under Development 1 77.04 Quite High
Death 1 71.56 Quite High
Cv General 3 Under Development 1 64.36 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
A mouse model of human variant (vasospastic) angina has been recently obtained by disruption of Kir6.1/Kcnj8, a gene coding for a small pore-forming inward rectifier potassium channel.
Negative_regulation (disruption) of Kir6 in pore associated with angina and inward rectifier potassium channel
1) Confidence 0.42 Published 2003 Journal Int. J. Mol. Med. Section Abstract Doc Link 12964027 Disease Relevance 0.19 Pain Relevance 0.28
Mouse model of Prinzmetal angina by disruption of the inward rectifier Kir6.1.
Negative_regulation (disruption) of Kir6 in Mouse associated with angina and variant angina pectoris
2) Confidence 0.38 Published 2002 Journal Nat. Med. Section Title Doc Link 11984590 Disease Relevance 0.48 Pain Relevance 0.22

General Comments

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