INT135644

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Context Info
Confidence 0.19
First Reported 2006
Last Reported 2009
Negated 0
Speculated 0
Reported most in Body
Documents 2
Total Number 3
Disease Relevance 2.60
Pain Relevance 0.22

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

cytosol (Aco1) mitochondrion (Aco1) lyase activity (Aco1)
Golgi apparatus (Aco1) endoplasmic reticulum (Aco1) RNA binding (Aco1)
Anatomy Link Frequency
neuronal 1
Aco1 (Mus musculus)
Pain Link Frequency Relevance Heat
ischemia 2 93.52 High High
abdominal pain 1 78.72 Quite High
hyperexcitability 1 71.04 Quite High
midbrain 36 60.00 Quite High
Inflammation 2 5.00 Very Low Very Low Very Low
Pain 2 5.00 Very Low Very Low Very Low
addiction 2 5.00 Very Low Very Low Very Low
Substantia nigra 2 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Aging 2 99.48 Very High Very High Very High
Toxicity 8 96.76 Very High Very High Very High
Parkinson's Disease 22 96.40 Very High Very High Very High
Alzheimer's Dementia 2 94.28 High High
Cv General 4 Under Development 2 93.52 High High
Death 118 91.32 High High
Stress 24 91.12 High High
Epilepsy 2 84.96 Quite High
Ataxia 2 83.84 Quite High
Supranuclear Palsy 2 83.00 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Our data demonstrate that oxidative inactivation of m-aconitase results in the formation of Fenton reactants in neuronal cells which provides evidence for the pathogenic mechanism in which m-aconitase not only serves as a target but also as a source of oxidants.
m-aconitase Binding (target) of in neuronal
1) Confidence 0.19 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2738973 Disease Relevance 0.56 Pain Relevance 0
Aconitase has been widely recognized as a sensitive and relatively specific target of ROS, particularly O2.?.
Aconitase Binding (recognized) of
2) Confidence 0.15 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2738973 Disease Relevance 1.58 Pain Relevance 0.10
The toxic effects of SFAC are caused by fluorocitrate action, a toxic metabolite, which has a competitive action with aconitase enzyme, leading to citrate accumulation and resulting in interference in energy production by Krebs cycle blockade.
aconitase enzyme Binding (action) of
3) Confidence 0.03 Published 2006 Journal Hum Exp Toxicol Section Abstract Doc Link 16696292 Disease Relevance 0.46 Pain Relevance 0.11

General Comments

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