INT199652

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Context Info
Confidence 0.54
First Reported 2006
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 3
Total Number 16
Disease Relevance 12.37
Pain Relevance 0.11

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

cytosol (Fxn) transport (Fxn) mitochondrion (Fxn)
oxidoreductase activity (Fxn) mitochondrion organization (Fxn) enzyme binding (Fxn)
Anatomy Link Frequency
blood 3
proximal 1
M cell 1
fibroblasts 1
Fxn (Mus musculus)
Pain Link Frequency Relevance Heat
Taxol 14 92.32 High High
Inflammation 14 65.36 Quite High
Bioavailability 2 55.56 Quite High
Paracetamol 28 5.00 Very Low Very Low Very Low
imagery 14 5.00 Very Low Very Low Very Low
Sicca syndrome 12 5.00 Very Low Very Low Very Low
Spinal cord 10 5.00 Very Low Very Low Very Low
peripheral neuropathy 4 5.00 Very Low Very Low Very Low
medulla 4 5.00 Very Low Very Low Very Low
Bile 4 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Ataxia 1248 100.00 Very High Very High Very High
Sprains And Strains 60 99.88 Very High Very High Very High
Disease 272 99.84 Very High Very High Very High
Targeted Disruption 52 99.36 Very High Very High Very High
Parkinson's Disease 42 98.92 Very High Very High Very High
Friedreich Ataxia 106 98.60 Very High Very High Very High
Stress 246 98.44 Very High Very High Very High
Dna Damage 226 98.04 Very High Very High Very High
Malignant Neoplastic Disease 30 96.76 Very High Very High Very High
Death 44 95.36 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
We also found interesting the effect frataxin deficiency has on ubiquitin cycle and protein degradation in both FRDA children and FRDA adults.
Negative_regulation (deficiency) of frataxin associated with ataxia
1) Confidence 0.54 Published 2010 Journal PLoS Genetics Section Body Doc Link PMC2799513 Disease Relevance 1.10 Pain Relevance 0.03
Sturm et al. [61] reported data strongly indicating that a reduction in frataxin does not affect the mitochondrial labile iron pool in human cell lines and suggests that these cells have a decreased antioxidative capacity.
Negative_regulation (reduction) of frataxin
2) Confidence 0.47 Published 2010 Journal PLoS Genetics Section Body Doc Link PMC2799513 Disease Relevance 0.87 Pain Relevance 0
These results provide insights into the nature of the disease and a working model for frataxin deficiency in humans.


Negative_regulation (deficiency) of frataxin associated with disease
3) Confidence 0.40 Published 2010 Journal PLoS Genetics Section Body Doc Link PMC2799513 Disease Relevance 0.94 Pain Relevance 0
Moreover, evidence consistent with nuclear DNA (nDNA) damage is demonstrated by decreasing the levels of frataxin in a RAD52 (854976) double-strand break repair deficient yeast strain, which results in rapid G2/M cell cycle arrest [16].
Negative_regulation (decreasing) of frataxin in M cell associated with sprains and strains
4) Confidence 0.40 Published 2010 Journal PLoS Genetics Section Body Doc Link PMC2799513 Disease Relevance 0.68 Pain Relevance 0
Many of the key pathways observed by transcription profiling were downregulated, and we believe these data suggest that patients with prolonged frataxin deficiency undergo a systemic survival response to chronic genotoxic stress and consequent DNA damage detectable in blood.
Negative_regulation (deficiency) of frataxin in blood associated with dna damage
5) Confidence 0.40 Published 2010 Journal PLoS Genetics Section Abstract Doc Link PMC2799513 Disease Relevance 0.97 Pain Relevance 0
These data – the 23 gene sets associated to a genotoxic stress response and the direct biological evidence of mtDNA and nDNA damage in the blood – result in a working model of the disease, where repressed levels of frataxin create a vicious cycle of mitochondrial dysfunction (probably due to ISC biosynthesis impairment), decreased oxidative phosphorylation, and increased reactive oxygen species production and genotoxic stress (Figure 5).
Negative_regulation (repressed) of frataxin in blood associated with parkinson's disease, dna damage and disease
6) Confidence 0.40 Published 2010 Journal PLoS Genetics Section Body Doc Link PMC2799513 Disease Relevance 0.65 Pain Relevance 0
The authors conclude that frataxin deficiency leads to heme deficiency.
Negative_regulation (deficiency) of frataxin
7) Confidence 0.40 Published 2010 Journal PLoS Genetics Section Body Doc Link PMC2799513 Disease Relevance 0.64 Pain Relevance 0
A decrease in frataxin may also increase reactive oxygen species (ROS) produced by increases in bioavailable iron [5], [7]–[10] and the lack of iron detoxification [11].
Negative_regulation (decrease) of frataxin
8) Confidence 0.40 Published 2010 Journal PLoS Genetics Section Body Doc Link PMC2799513 Disease Relevance 0.64 Pain Relevance 0
The disease is caused by a defect in the frataxin gene, which is involved in iron homeostasis and likely protects against reactive oxygen species.
Negative_regulation (defect) of frataxin associated with disease
9) Confidence 0.40 Published 2010 Journal PLoS Genetics Section Abstract Doc Link PMC2799513 Disease Relevance 0.92 Pain Relevance 0
Other gene sets consist of mostly downregulated genes in response to bleomycin, MMS, ultraviolet B (UVB), and ultraviolet C (UVC) radiation, which were also downregulated in the FRDA dataset (denoted by the negative GSA scores) (Table 1).
Negative_regulation (downregulated) of FRDA associated with ataxia
10) Confidence 0.40 Published 2010 Journal PLoS Genetics Section Body Doc Link PMC2799513 Disease Relevance 0.45 Pain Relevance 0.05
Karthikeyan et al. [16] also demonstrate how yeast strains with reduced frataxin accumulate mitochondrial iron and generate reactive hydroxyl radicals, which damage cell membranes, proteins, and mitochondrial DNA, resulting in the decreased capacity for ATP synthesis through impaired oxidative phosphorylation.
Negative_regulation (reduced) of frataxin associated with sprains and strains
11) Confidence 0.40 Published 2010 Journal PLoS Genetics Section Body Doc Link PMC2799513 Disease Relevance 0.67 Pain Relevance 0
Furthermore, Chantrel-Groussard et al. [9] found that reduced frataxin does not induce superoxide dismutases nor the import iron machinery by endogenous oxidative stress in FRDA fibroblasts compared to controls.
Negative_regulation (reduced) of frataxin in fibroblasts associated with stress and ataxia
12) Confidence 0.35 Published 2010 Journal PLoS Genetics Section Body Doc Link PMC2799513 Disease Relevance 1.24 Pain Relevance 0
A majority of genes, 899, were downregulated in FRDA compared with control, while 471 genes were upregulated.
Negative_regulation (downregulated) of FRDA associated with ataxia
13) Confidence 0.35 Published 2010 Journal PLoS Genetics Section Body Doc Link PMC2799513 Disease Relevance 0.52 Pain Relevance 0
Therefore, we believe the DNA damage in the blood of the Friedreich's ataxia patient is a secondary event to the primary one of frataxin depletion and neurodegeneration.
Negative_regulation (depletion) of frataxin in blood associated with ataxia
14) Confidence 0.35 Published 2010 Journal PLoS Genetics Section Body Doc Link PMC2799513 Disease Relevance 0.62 Pain Relevance 0
The above mentioned studies suggest that iron accumulation is a distal consequence of an earlier, proximal consequence of frataxin deficiency.
Negative_regulation (deficiency) of frataxin in proximal
15) Confidence 0.28 Published 2006 Journal Orphanet J Rare Dis Section Body Doc Link PMC1664553 Disease Relevance 0.38 Pain Relevance 0
However, it has been shown that the deficiency of frataxin in a new mouse knock-out model of Friedreich ataxia does not cause oxidative stress [143].
Negative_regulation (deficiency) of frataxin associated with stress, friedreich ataxia and targeted disruption
16) Confidence 0.24 Published 2006 Journal Orphanet J Rare Dis Section Body Doc Link PMC1664553 Disease Relevance 1.07 Pain Relevance 0.03

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