INT281874

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Context Info
Confidence 0.32
First Reported 2009
Last Reported 2009
Negated 0
Speculated 0
Reported most in Body
Documents 1
Total Number 7
Disease Relevance 3.67
Pain Relevance 0.23

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
astrocytes 1
Aco1 (Mus musculus)
Pain Link Frequency Relevance Heat
midbrain 126 89.40 High High
ischemia 7 76.16 Quite High
addiction 7 69.80 Quite High
Substantia nigra 7 25.60 Quite Low
Inflammation 7 5.00 Very Low Very Low Very Low
Pain 7 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Death 413 98.52 Very High Very High Very High
Stress 84 98.12 Very High Very High Very High
Drug Induced Neurotoxicity 56 96.04 Very High Very High Very High
Parkinson's Disease 77 94.48 High High
Aging 7 82.12 Quite High
Toxicity 28 79.40 Quite High
Disease 63 78.48 Quite High
Neurodegenerative Disease 28 78.04 Quite High
Alzheimer's Dementia 7 76.92 Quite High
Cv General 4 Under Development 7 76.16 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
In eukaryotes, two isozymes of aconitase exist; one localized to the matrix of the mitochondria and the other in the cytosol (also known as iron regulatory protein 1).
Localization (localized) of aconitase
1) Confidence 0.32 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2738973 Disease Relevance 0.12 Pain Relevance 0
The goal of this study was to test the hypothesis that oxidative inactivation of m-aconitase and consequent release of the Fenton reactants H2O2 and Fe2+ contributes to neuronal death.
Localization (release) of m-aconitase in neuronal associated with death
2) Confidence 0.32 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2738973 Disease Relevance 0.72 Pain Relevance 0.09
In summary, since catalase can only attenuate cell death when m-aconitase is overexpressed, this suggests 1) that the excess H2O2 from m-aconitase inactivation is being released from astrocytes and injuring neighboring neurons and 2) that removal of astrocyte-derived extracellular H2O2 can prevent death.
Localization (released) of from m-aconitase in astrocytes associated with death
3) Confidence 0.32 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2738973 Disease Relevance 0.68 Pain Relevance 0
Collectively, these studies demonstrate that m-aconitase is a sensitive target of ROS generated in cells and tissue.
Localization (target) of m-aconitase
4) Confidence 0.30 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2738973 Disease Relevance 1.36 Pain Relevance 0.04
Evidence of .OH formation in cell free systems, presumably via the release of Fenton reactants by oxidative inactivation of m-aconitase was provided by Vasquez-Vivar et al. (2000).
Localization (release) of m-aconitase
5) Confidence 0.28 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2738973 Disease Relevance 0.33 Pain Relevance 0
Similar to the observed increases in H2O2 in m-aconitase overexpressing cells, Fe2+ was increased to greater levels in AdAcon compared to AdGFP transduced cells suggesting that both H2O2 and Fe2+ can be released from oxidatively inactivated m-aconitase.


Localization (released) of m-aconitase
6) Confidence 0.28 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2738973 Disease Relevance 0 Pain Relevance 0.10
Release of redox-active iron (Fe2+) from aconitase and other hydro-lyases has been previously reported in cell-free systems [7], [9].
Localization (Release) of aconitase
7) Confidence 0.28 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2738973 Disease Relevance 0.46 Pain Relevance 0

General Comments

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