INT91900

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Context Info
Confidence 0.77
First Reported 2000
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 12
Total Number 12
Disease Relevance 6.62
Pain Relevance 1.51

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

mitochondrion (Sod1) aging (Sod1) peroxisome (Sod1)
intracellular (Sod1) protein complex (Sod1) cytoplasm (Sod1)
Anatomy Link Frequency
neurons 2
motoneurons 2
liver 1
cerebral cortex 1
alveolar macrophages 1
Sod1 (Mus musculus)
Pain Link Frequency Relevance Heat
cerebral cortex 3 99.68 Very High Very High Very High
Root ganglion neuron 1 98.56 Very High Very High Very High
Opioid 2 97.04 Very High Very High Very High
Morphine 6 86.48 High High
antinociception 4 85.76 High High
Spinal cord 50 85.04 High High
tail-flick 1 83.76 Quite High
Inflammation 255 82.00 Quite High
tolerance 16 80.88 Quite High
addiction 2 79.76 Quite High
Disease Link Frequency Relevance Heat
Motor Neuron Diseases 196 99.96 Very High Very High Very High
Nicotine Addiction 98 99.20 Very High Very High Very High
Ganglion Cysts 2 98.36 Very High Very High Very High
Death 91 98.16 Very High Very High Very High
Parkinson's Disease 26 97.90 Very High Very High Very High
Apoptosis 27 97.68 Very High Very High Very High
Disease 198 97.60 Very High Very High Very High
Stress 80 91.60 High High
Syndrome 1 91.52 High High
Targeted Disruption 75 91.48 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
How mutant SOD1 causes MVISE is not known but could be associated with SOD1 localization.
Localization (localization) of SOD1
1) Confidence 0.77 Published 2003 Journal BMC Neurosci Section Body Doc Link PMC169170 Disease Relevance 0.13 Pain Relevance 0
Mutant SOD1 has been localized in the mitochondria binding bcl2, the cells primary anti-apoptotic protein [8,9].
Localization (localized) of SOD1 associated with apoptosis
2) Confidence 0.76 Published 2006 Journal BMC Neurosci Section Body Doc Link PMC1488864 Disease Relevance 1.52 Pain Relevance 0.04
Third, cytochrome c colocalizes with SOD1 in small vacuoles.
Localization (colocalizes) of SOD1
3) Confidence 0.72 Published 2003 Journal BMC Neurosci Section Body Doc Link PMC169170 Disease Relevance 0.09 Pain Relevance 0
Research investigating interactions between cytoplasmic dynein and mutant SOD1 includes reports of co-localization of dynein components and mutant SOD1 in ALS mouse models [17], the interaction of mutant SOD1 proteins with cytoplasmic dynein [18] and perturbation of transport of mitochondria in motor neurons from SOD1G93A mice [19].
Localization (localization) of SOD1 in motor neurons associated with motor neuron diseases
4) Confidence 0.68 Published 2008 Journal Genome Biol Section Body Doc Link PMC2397497 Disease Relevance 0.46 Pain Relevance 0
The mechanism whereby mutant SOD1 causes mitochondrial damage has not been determined, but recent evidence shows that mutant SOD1 is imported into mitochondria [21,25,26], and this mitochondrial localization may cause direct damage to mitochondria and induce cell death [27].
Localization (imported) of SOD1 associated with death
5) Confidence 0.68 Published 2003 Journal BMC Neurosci Section Body Doc Link PMC169170 Disease Relevance 0.62 Pain Relevance 0
As a result of the mitochondrial and cytosolic location of SOD1 in liver (7), overexpression of SOD1 theoretically reduces both mitochondria and cytosolic superoxide.
Localization (location) of SOD1 in liver
6) Confidence 0.64 Published 2008 Journal Diabetes Section Body Doc Link PMC2494675 Disease Relevance 0.18 Pain Relevance 0.03
25–35 solution (Xu et al., 2008); (2) QUE prevents PC12 cell death caused by increased intracellular reactive oxygen species and calcium (Wang et al., 2005); and (3) QUE attenuates the CPZ-induced decrease in the activity of SOD1 in the cerebral cortex of mice (Zhang et al., 2008).
Localization (decrease) of SOD1 in cerebral cortex associated with cerebral cortex and death
7) Confidence 0.51 Published 2010 Journal Frontiers in Behavioral Neuroscience Section Body Doc Link PMC2842101 Disease Relevance 0.37 Pain Relevance 0.09
More significantly, our observations expand a role for mitochondrial dysfunction in the death of ALS motoneurons, which is otherwise mainly understood as a consequence of mitochondrial recruitment of mutant SOD1 in FALS [1], and which was even ruled out for SALS by one study [22].
Localization (recruitment) of SOD1 in motoneurons associated with parkinson's disease, motor neuron diseases and death
8) Confidence 0.49 Published 2007 Journal BMC Genomics Section Body Doc Link PMC1796866 Disease Relevance 0.96 Pain Relevance 0
Nevertheless, several studies have suggested that SOD1 mutations in neurons alone are insufficient to cause ALS and that dysfunction in support glia may contribute to disease development and progression [129-132].
Localization (cause) of SOD1 in neurons associated with disease and motor neuron diseases
9) Confidence 0.46 Published 2009 Journal Mol Neurodegener Section Body Doc Link PMC2784760 Disease Relevance 1.10 Pain Relevance 0.19
Vesicular Zn2+, released in the brain and from small dorsal root ganglion neurons, interacts with opioid as well as N-methyl-D-aspartate (NMDA) receptors.
Localization (released) of Zn2 in neurons associated with ganglion cysts, root ganglion neuron and opioid
10) Confidence 0.41 Published 2000 Journal Eur. J. Pharmacol. Section Abstract Doc Link 11068022 Disease Relevance 0.10 Pain Relevance 1.03
These effects were inhibitable by antioxidants including N-acetylcysteine, ascorbic acid, quercetin or overexpression of SOD1, deletion of CCR2, or by inhibition of MAPK p42/44 or p38 (Nishi et al 2005; Guest et al 2006; Hayasaki et al 2006; Huang et al 2006; Loke et al 2006).
Localization (deletion) of SOD1
11) Confidence 0.32 Published 2007 Journal International Journal of Chronic Obstructive Pulmonary Disease Section Body Doc Link PMC2695202 Disease Relevance 0.59 Pain Relevance 0.11
The activities of CuZnSOD, glutathione-S-transferase and glutathione peroxidase (GP) are all decreased in alveolar macrophages from elderly smokers (Gilks et al 1998).
Localization (glutathione-S-transferase) of CuZnSOD in alveolar macrophages associated with nicotine addiction
12) Confidence 0.32 Published 2007 Journal International Journal of Chronic Obstructive Pulmonary Disease Section Body Doc Link PMC2695202 Disease Relevance 0.52 Pain Relevance 0.03

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