INT17246

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Context Info
Confidence 0.56
First Reported 1991
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 16
Total Number 16
Disease Relevance 9.69
Pain Relevance 0.79

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

mitochondrion (POLG) cell death (POLG) aging (POLG)
DNA binding (POLG) nucleotidyltransferase activity (POLG) DNA metabolic process (POLG)
Anatomy Link Frequency
embryo 3
bars 1
gastrulation 1
visual system 1
gonad 1
POLG (Homo sapiens)
Pain Link Frequency Relevance Heat
Pain 60 98.48 Very High Very High Very High
imagery 60 95.92 Very High Very High Very High
withdrawal 1 86.76 High High
adenocard 1 76.72 Quite High
peripheral neuropathy 9 75.00 Quite High
Neuropathic pain 13 74.72 Quite High
Pain score 3 47.36 Quite Low
Peripheral nervous system 1 44.00 Quite Low
Action potential 12 5.00 Very Low Very Low Very Low
Pain scale 11 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Helminth Infection 828 99.36 Very High Very High Very High
Lifespan 216 99.32 Very High Very High Very High
Parkinson's Disease 79 99.22 Very High Very High Very High
Death 36 99.00 Very High Very High Very High
Neuropathic Pain 47 98.34 Very High Very High Very High
Fatigue 14 96.20 Very High Very High Very High
Myalgia 13 95.84 Very High Very High Very High
Frailty 4 95.48 Very High Very High Very High
Sprains And Strains 144 95.12 Very High Very High Very High
Disseminated Intravascular Coagulation 36 94.48 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Homozygous disruption of the mouse POLG gene leads to embryonic death at late gastrulation and before early organogenesis (7).
Negative_regulation (disruption) of POLG in gastrulation associated with death
1) Confidence 0.56 Published 2009 Journal Nucleic Acids Research Section Body Doc Link PMC2665216 Disease Relevance 0.84 Pain Relevance 0.06
Quantitative PCR analysis confirmed that the polg-1 transcripts are extremely reduced in adult homozygous deletion mutants (Figure 1A).
Negative_regulation (reduced) of polg-1
2) Confidence 0.56 Published 2009 Journal Nucleic Acids Research Section Body Doc Link PMC2665216 Disease Relevance 0.17 Pain Relevance 0
Surprisingly, loss of polg-1 that resulted in animals having 25 times lower mtDNA levels than normal, did not affect the embryonic and larval development of C. elegans.
Negative_regulation (loss) of polg-1
3) Confidence 0.49 Published 2009 Journal Nucleic Acids Research Section Body Doc Link PMC2665216 Disease Relevance 0.53 Pain Relevance 0
However, previous RNAi-based genome-wide screening analysis did not reveal any phenotypes caused by downregulation of the polg-1 gene (16–18).
Negative_regulation (downregulation) of polg-1
4) Confidence 0.49 Published 2009 Journal Nucleic Acids Research Section Body Doc Link PMC2665216 Disease Relevance 0.58 Pain Relevance 0
Polg-1 deficiency causes severe mtDNA depletion, but not a developmental arrest
Negative_regulation (deficiency) of Polg-1
5) Confidence 0.41 Published 2009 Journal Nucleic Acids Research Section Body Doc Link PMC2665216 Disease Relevance 0.28 Pain Relevance 0.09
Flies deficient in POLG activity (tam mutants) are weak and uncoordinated and grow significantly slower than wild-type flies, with noticeable defects in the development of the adult visual system (6).
Negative_regulation (deficient) of POLG in visual system
6) Confidence 0.41 Published 2009 Journal Nucleic Acids Research Section Body Doc Link PMC2665216 Disease Relevance 1.03 Pain Relevance 0.08
This was even more apparent from the results of gonad-less polg-1 deficient animals polg-1(ok1548), glp-4(bn2) that had 4–5 times lower mtDNA copy number than gonad-less glp-4(bn2) mutants at adult day 4.
Negative_regulation (deficient) of polg-1 in gonad
7) Confidence 0.41 Published 2009 Journal Nucleic Acids Research Section Body Doc Link PMC2665216 Disease Relevance 0.20 Pain Relevance 0
(D) mtDNA copy number in polg-1(ok1548), HIS-72::mCherry (black bars) and HIS-72::mCherry (squared bars) animals.
Negative_regulation (number) of polg-1 in bars
8) Confidence 0.41 Published 2009 Journal Nucleic Acids Research Section Body Doc Link PMC2665216 Disease Relevance 0.76 Pain Relevance 0
Our work also provides evidence that the mtDNA copy number is an essential limiting factor for C. elegans development and that a high maternal contribution of both, mtDNA and POLG-1 in the embryo ensures a normal development, even in the absence of polg-1 gene.
Negative_regulation (absence) of polg-1 in embryo
9) Confidence 0.41 Published 2009 Journal Nucleic Acids Research Section Body Doc Link PMC2665216 Disease Relevance 0.05 Pain Relevance 0
Figure 4.Embryonic development of polg-1(ok1548) progeny.
Negative_regulation (development) of polg-1
10) Confidence 0.41 Published 2009 Journal Nucleic Acids Research Section Body Doc Link PMC2665216 Disease Relevance 0.08 Pain Relevance 0
Our work also provides evidence that the mtDNA copy number is an essential limiting factor for C. elegans development and that a high maternal contribution of both, mtDNA and POLG-1 in the embryo ensures a normal development, even in the absence of polg-1 gene.
Negative_regulation (contribution) of POLG-1 in embryo
11) Confidence 0.41 Published 2009 Journal Nucleic Acids Research Section Body Doc Link PMC2665216 Disease Relevance 0.06 Pain Relevance 0
Ultimately, mtDNA depletion in polg-1 deficient animals precluded them from producing viable offspring, even if they produced a handful of embryos that arrested very early in development.
Negative_regulation (depletion) of polg-1 in embryos
12) Confidence 0.36 Published 2009 Journal Nucleic Acids Research Section Body Doc Link PMC2665216 Disease Relevance 0.36 Pain Relevance 0
In vitro, NRTIs inhibit the gamma-DNA polymerase, responsible for replication of mtDNA, and cause mtDNA dysfunction.
Negative_regulation (inhibit) of gamma-DNA polymerase
13) Confidence 0.30 Published 2001 Journal J. Peripher. Nerv. Syst. Section Abstract Doc Link 11293802 Disease Relevance 1.56 Pain Relevance 0.14
It is likely that mitochondrial dysfunction, probably resulting from drug-induced inhibition of the mitochondrial DNA polymerase, is implicated in the pathogenesis of this complication of zidovudine therapy.
Negative_regulation (inhibition) of mitochondrial DNA polymerase associated with parkinson's disease
14) Confidence 0.25 Published 1991 Journal Ann. Neurol. Section Abstract Doc Link 1892364 Disease Relevance 0.46 Pain Relevance 0.12
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 POLG1
15) Confidence 0.17 Published 2010 Journal Brain Section Body Doc Link PMC2842512 Disease Relevance 0.62 Pain Relevance 0.07
The pathogenesis of ATN is thought to reflect the selective ability of the dideoxynucleoside analogues to inhibit gamma DNA polymerase, reduce mitochondrial DNA content, and lead to mitochondrial dysfunction [8].
Negative_regulation (inhibit) of gamma DNA polymerase associated with parkinson's disease and neuropathic pain
16) Confidence 0.06 Published 2007 Journal PLoS ONE Section Body Doc Link PMC1919427 Disease Relevance 2.12 Pain Relevance 0.22

General Comments

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