INT331130

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Context Info
Confidence 0.48
First Reported 2010
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 1
Total Number 6
Disease Relevance 4.93
Pain Relevance 0

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) mitochondrion (FXN) mitochondrion organization (FXN)
enzyme binding (FXN) cytoplasm (FXN)
FXN (Homo sapiens)
Pain Link Frequency Relevance Heat
Lasting pain 6 5.00 Very Low Very Low Very Low
fibrosis 6 5.00 Very Low Very Low Very Low
Inflammation 6 5.00 Very Low Very Low Very Low
Inflammatory response 6 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Ataxia 138 99.54 Very High Very High Very High
Targeted Disruption 78 98.60 Very High Very High Very High
Disease 78 97.82 Very High Very High Very High
Neurodegenerative Disease 18 97.12 Very High Very High Very High
Diabetes Mellitus 6 94.08 High High
Hypertrophic Cardiomyopathy 6 93.20 High High
Embryonic Lethality 18 92.16 High High
Cold Sores 108 88.76 High High
Stress 24 80.12 Quite High
Thrombocytopenia 6 57.00 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Friedreich's ataxia (FA) is the most common form of autosomal recessive ataxia and it is caused by a decrease in the levels of frataxin, a mitochondrial protein encoded by the nuclear FRDA (FXN) gene [172].
Negative_regulation (decrease) of frataxin associated with ataxia
1) Confidence 0.48 Published 2010 Journal Journal of Biomedicine and Biotechnology Section Body Doc Link PMC2938438 Disease Relevance 0.85 Pain Relevance 0
Some knock-in mice bearing the human gene with an expansion mutation surprisingly failed to develop any clinical phenotype, despite the significant reduction in frataxin levels to 25%–36% the wild-type levels [184].
Negative_regulation (reduction) of frataxin associated with targeted disruption
2) Confidence 0.42 Published 2010 Journal Journal of Biomedicine and Biotechnology Section Body Doc Link PMC2938438 Disease Relevance 1.29 Pain Relevance 0
Previous reports of transgenic mice indeed support the use of the frataxin genomic locus to correct frataxin deficiency in vivo.
Negative_regulation (deficiency) of frataxin associated with targeted disruption
3) Confidence 0.36 Published 2010 Journal Journal of Biomedicine and Biotechnology Section Body Doc Link PMC2938438 Disease Relevance 0.54 Pain Relevance 0
These results constitute the first “proof of principle” that neurological function can be recovered through a gene therapy approach aimed at correcting frataxin deficiency.
Negative_regulation (deficiency) of frataxin
4) Confidence 0.31 Published 2010 Journal Journal of Biomedicine and Biotechnology Section Body Doc Link PMC2938438 Disease Relevance 0.56 Pain Relevance 0
Friedreich's ataxia (FA) is the most common form of autosomal recessive ataxia and it is caused by a decrease in the levels of frataxin, a mitochondrial protein encoded by the nuclear FRDA (FXN) gene [172].
Negative_regulation (decrease) of FXN associated with ataxia
5) Confidence 0.31 Published 2010 Journal Journal of Biomedicine and Biotechnology Section Body Doc Link PMC2938438 Disease Relevance 0.87 Pain Relevance 0
The most common cause of the disease is an expansion of the GAA triplet within the first intron of the FRDA gene, which has a dramatic effect in reducing mRNA levels and consequently frataxin protein levels [173].
Negative_regulation (reducing) of frataxin associated with disease
6) Confidence 0.31 Published 2010 Journal Journal of Biomedicine and Biotechnology Section Body Doc Link PMC2938438 Disease Relevance 0.81 Pain Relevance 0

General Comments

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