INT120201

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Context Info
Confidence 0.35
First Reported 2004
Last Reported 2010
Negated 1
Speculated 0
Reported most in Body
Documents 54
Total Number 54
Disease Relevance 26.29
Pain Relevance 2.95

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
neurons 8
astrocytes 4
midbrain 4
neuronal 3
brain 1
Aco1 (Mus musculus)
Pain Link Frequency Relevance Heat
midbrain 846 99.86 Very High Very High Very High
addiction 53 99.36 Very High Very High Very High
Pain 56 98.32 Very High Very High Very High
cytokine 2 87.08 High High
Inflammation 54 86.68 High High
ischemia 47 83.56 Quite High
Substantia nigra 47 81.52 Quite High
Mechanotransduction 15 78.96 Quite High
Abeta 4 77.84 Quite High
Paracetamol 2 66.24 Quite High
Disease Link Frequency Relevance Heat
Death 2773 99.92 Very High Very High Very High
Parkinson's Disease 517 99.24 Very High Very High Very High
Alzheimer's Dementia 50 98.92 Very High Very High Very High
Pain 59 98.32 Very High Very High Very High
Drug Induced Neurotoxicity 376 98.04 Very High Very High Very High
Disease 440 97.64 Very High Very High Very High
Shock 4 97.48 Very High Very High Very High
Stress 570 95.56 Very High Very High Very High
Infection 47 94.52 High High
Iron Overload 1 93.16 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Transduction with AdAcon increases aconitase expression and activity in primary midbrain cultures
Gene_expression (expression) of aconitase in midbrain associated with midbrain
1) Confidence 0.35 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2738973 Disease Relevance 0.22 Pain Relevance 0.08
We proceeded to test whether increasing m-aconitase expression would exacerbate the release of Fenton reactants following oxidative inactivation.
Gene_expression (expression) of m-aconitase
2) Confidence 0.31 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2738973 Disease Relevance 0.06 Pain Relevance 0.11
The exacerbation of Fe2+ and H2O2 production in m-aconitase overexpressing cells suggests its role as their source.
Gene_expression (overexpressing) of m-aconitase
3) Confidence 0.31 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2738973 Disease Relevance 0.38 Pain Relevance 0
Cultures were transduced with an adenoviral construct expressing rat m-aconitase cDNA containing a green fluorescent protein (GFP) reporter (AdAcon).
Gene_expression (expressing) of m-aconitase
4) Confidence 0.31 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2738973 Disease Relevance 0.49 Pain Relevance 0.17
To confirm the mechanism of H2O2 and Fe2+ in the death of cells overexpressing m-aconitase, we asked whether cell death could be prevented by their pharmacological removal using catalase and HBED respectively.
Gene_expression (overexpressing) of m-aconitase associated with death
5) Confidence 0.31 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2738973 Disease Relevance 1.02 Pain Relevance 0.05
Exacerbation of PQ2+-induced H2O2 production observed in m-aconitase overexpressing cultures presumably originates from the latter source due to increased m-aconitase available for inactivation by O2.?
Gene_expression (overexpressing) of m-aconitase
6) Confidence 0.31 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2738973 Disease Relevance 0.37 Pain Relevance 0
Fenton reaction) in cells expressing basal levels of m-aconitase, extracellular H2O2 was also mediating cell death in m-aconitase overexpressing cultures.
Gene_expression (overexpressing) of m-aconitase associated with death
7) Confidence 0.31 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2738973 Disease Relevance 0.77 Pain Relevance 0
Overexpression of m-aconitase was achieved by transducing cells with an adenoviral construct expressing m-aconitase cDNA and a GFP reporter (AdAcon) or with an adenoviral construct only expressing GFP (AdGFP) to control for viral-mediated effects.
Gene_expression (Overexpression) of m-aconitase
8) Confidence 0.31 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2738973 Disease Relevance 0.18 Pain Relevance 0.04
More importantly, neurons from AdAcon transduced cultures revealed greater damage than AdGFP transduced cells at 500 ┬ÁM PQ2+ supporting that m-aconitase overexpression exacerbates neuronal death upon oxidative inactivation.
Gene_expression (overexpression) of m-aconitase in neurons associated with death
9) Confidence 0.31 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2738973 Disease Relevance 0.32 Pain Relevance 0
Co-labeling studies identified astrocytes as the predominant cell type expressing transduced m-aconitase although neurons were identified as the primary cell type dying.
Gene_expression (expressing) of m-aconitase in neurons
10) Confidence 0.31 Published 2009 Journal PLoS ONE Section Abstract Doc Link PMC2738973 Disease Relevance 0.70 Pain Relevance 0
This became apparent by the difference in number of MAP2+ neurons between cultures expressing basal levels of m-aconitase and those overexpressing the enzyme as well as by lack of damage to astrocytic morphology.
Gene_expression (expressing) of m-aconitase in neurons
11) Confidence 0.31 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2738973 Disease Relevance 0.63 Pain Relevance 0.08
To confirm the role of m-aconitase as a source of Fenton reagents and death, we overexpressed m-aconitase using an adenoviral construct thereby increasing the target available for inactivation by ROS.
Gene_expression (overexpressed) of m-aconitase associated with death
12) Confidence 0.31 Published 2009 Journal PLoS ONE Section Abstract Doc Link PMC2738973 Disease Relevance 0.69 Pain Relevance 0
M-aconitase was overexpressed in mature primary midbrain cultures using an adenoviral vector.
Gene_expression (overexpressed) of M-aconitase in midbrain associated with midbrain
13) Confidence 0.31 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2738973 Disease Relevance 0.43 Pain Relevance 0.19
Oxidative inactivation of m-aconitase overexpressing cultures resulted in exacerbation of H2O2 production, Fe2+ accumulation and increased neuronal death.
Gene_expression (overexpressing) of m-aconitase in neuronal associated with death
14) Confidence 0.31 Published 2009 Journal PLoS ONE Section Abstract Doc Link PMC2738973 Disease Relevance 0.71 Pain Relevance 0
Although astrocytes were the predominant cell type to overexpress m-aconitase, the neuronal population was more susceptible to death compared to astrocytes.
Gene_expression (overexpress) of m-aconitase in neuronal associated with death
15) Confidence 0.31 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2738973 Disease Relevance 0.57 Pain Relevance 0.07
To confirm the role of m-aconitase versus other cellular proteins in the production of Fe2+ and H2O2, we specifically overexpressed m-aconitase.
Gene_expression (overexpressed) of m-aconitase
16) Confidence 0.31 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2738973 Disease Relevance 0.17 Pain Relevance 0.07
However, in m-aconitase overexpressing cells, either catalase or HBED was sufficient to significantly inhibit cell death (Fig. 7).
Gene_expression (overexpressing) of m-aconitase associated with death
17) Confidence 0.31 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2738973 Disease Relevance 0.96 Pain Relevance 0.06
Co-localization of GFP fluorescence with MAP2 and GFAP performed 24 hrs after transduction with AdAcon, revealed the expression of m-aconitase largely in GFAP positive cells, suggesting that m-aconitase was predominately overexpressed in astrocytes (Fig. 8a,b).
Gene_expression (expression) of m-aconitase in astrocytes
18) Confidence 0.31 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2738973 Disease Relevance 0.48 Pain Relevance 0.05
Increased cell death in m-aconitase overexpressing cultures was attenuated by addition of catalase and/or a cell permeable iron chelator suggesting that neuronal death occurred in part via astrocyte-derived H2O2.


Gene_expression (overexpressing) of m-aconitase in astrocyte associated with death
19) Confidence 0.31 Published 2009 Journal PLoS ONE Section Abstract Doc Link PMC2738973 Disease Relevance 0.71 Pain Relevance 0
The use of cell impermeable extracellular catalase not only provided a sink for ROS generated within cellular compartments, but revealed a key role of astrocyte-derived extracellular H2O2 in the death of neurons in m-aconitase overexpressing cultures.
Gene_expression (overexpressing) of m-aconitase in neurons associated with death
20) Confidence 0.31 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2738973 Disease Relevance 0.66 Pain Relevance 0

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