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Context Info
Confidence 0.51
First Reported 2001
Last Reported 2006
Negated 0
Speculated 0
Reported most in Abstract
Documents 2
Total Number 3
Disease Relevance 1.25
Pain Relevance 0.26

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
outflow 1
ACO1 (Homo sapiens)
Pain Link Frequency Relevance Heat
Analgesic 2 85.16 High High
anesthesia 1 68.24 Quite High
imagery 1 64.40 Quite High
Glutamate 2 25.00 Low Low
Disease Link Frequency Relevance Heat
Poisoning 12 98.84 Very High Very High Very High
Adrenoleukodystrophy 3 95.00 High High
Toxicity 2 88.16 High High
Death 2 86.16 High High
Muscle Hypotonia 1 74.24 Quite High
Convulsion 1 72.64 Quite High
Ocular Toxicity (including Many Sub-types) 2 70.48 Quite High
Disease 1 58.16 Quite High
Neurological Disease 1 49.76 Quite Low
Cognitive Disorder 1 47.28 Quite Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Antidotal therapy for FA intoxication has been aimed at preventing fluorocitrate synthesis and aconitase blockade in mitochondria, and at providing citrate outflow from this organelle.
Negative_regulation (blockade) of aconitase in outflow associated with poisoning
1) Confidence 0.51 Published 2006 Journal J Appl Toxicol Section Abstract Doc Link 16252258 Disease Relevance 0.58 Pain Relevance 0.09
Fluoroacetate (FA; CH2FCOOR) is highly toxic towards humans and other mammals through inhibition of the enzyme aconitase in the tricarboxylic acid cycle, caused by 'lethal synthesis' of an isomer of fluorocitrate (FC).
Negative_regulation (inhibition) of aconitase
2) Confidence 0.44 Published 2006 Journal J Appl Toxicol Section Abstract Doc Link 16252258 Disease Relevance 0.21 Pain Relevance 0.08
The disorders of peroxisomal beta-oxidation, which have been well characterised at the molecular level, include defects of acyl-CoA oxidase, defects of the D-bifunctional protein (D-BP) (including specific defects of its enoyl-CoA hydratase and D-3-hydroxyacyl-CoA dehydrogenase components), defects of the very-long-chain fatty acid (VLCFA)-CoA importer [X-linked adrenoleukodystrophy (ALD)] and alpha-methylacyl-CoA racemase deficiency.
Negative_regulation (defects) of hydratase associated with adrenoleukodystrophy
3) Confidence 0.00 Published 2001 Journal Biochem. Soc. Trans. Section Abstract Doc Link 11356171 Disease Relevance 0.46 Pain Relevance 0.10

General Comments

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