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Context Info
Confidence 0.17
First Reported 2009
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 2
Total Number 2
Disease Relevance 2.19
Pain Relevance 0.33

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

mitochondrion (POLG2) DNA binding (POLG2) nucleotidyltransferase activity (POLG2)
cytoplasm (POLG2)
POLG2 (Homo sapiens)
Pain Link Frequency Relevance Heat
peripheral neuropathy 10 99.38 Very High Very High Very High
neuralgia 1 85.96 High High
adenocard 1 76.72 Quite High
Sciatic nerve 1 76.48 Quite High
Spinal cord 2 74.96 Quite High
Multiple sclerosis 10 5.00 Very Low Very Low Very Low
Migraine 4 5.00 Very Low Very Low Very Low
Inflammation 4 5.00 Very Low Very Low Very Low
Potency 4 5.00 Very Low Very Low Very Low
headache 3 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Peripheral Neuropathy 10 99.38 Very High Very High Very High
Muscle Disease 15 98.92 Very High Very High Very High
Lactic Acidosis 1 98.72 Very High Very High Very High
Toxicity 3 97.10 Very High Very High Very High
Arrhythmia Under Development 1 87.40 High High
Hypesthesia 1 86.48 High High
Neuralgia 1 85.96 High High
Disorders Of Creatine Metabolism 8 83.08 Quite High
Disease 22 82.08 Quite High
Syndrome 6 78.00 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Over the past decade, a growing number of nuclear genetic defects have been identified that disrupt mitochondrial function either by a reduction in mtDNA copy number, and/or the accumulation of secondary mtDNA deletions: POLG1, POLG2, PEO1, SLC25A4, TYMP, DGUOK, TK2, SUCLA2, SUCLG1, MPV17 and RRM2B (Hudson and Chinnery, 2006; Chinnery and Zeviani, 2008; Copeland, 2008).
Negative_regulation (reduction) of POLG2
1) Confidence 0.17 Published 2010 Journal Brain Section Body Doc Link PMC2842512 Disease Relevance 0.63 Pain Relevance 0.07
Other nucleoside analogues, such as fialuridine, have been associated with mitochondrial toxicity leading to distortions of cell energy metabolism with subsequent lactic acidosis, myopathy, peripheral neuropathy and hepatic steatosis through inhibition of the mitochondrial DNA polymerase gamma.30,31 Preclinical studies in animals did not demonstrate any mitochondrial toxicity with telbivudine27 and thus far, there is no clinical evidence that this is the mechanism underlying the observed myopathies in clinical trials.
Negative_regulation (inhibition) of mitochondrial DNA polymerase gamma associated with toxicity, lactic acidosis, muscle disease and peripheral neuropathy
2) Confidence 0.05 Published 2009 Journal Therapeutics and Clinical Risk Management Section Body Doc Link PMC2762437 Disease Relevance 1.56 Pain Relevance 0.26

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