INT91899

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Context Info
Confidence 0.47
First Reported 2000
Last Reported 2010
Negated 1
Speculated 0
Reported most in Body
Documents 17
Total Number 17
Disease Relevance 11.56
Pain Relevance 2.63

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
liver 1
neurons 1
brain 1
motor neurons 1
cortex 1
Sod1 (Mus musculus)
Pain Link Frequency Relevance Heat
Root ganglion neuron 1 100.00 Very High Very High Very High
Opioid 2 99.76 Very High Very High Very High
Inflammation 44 99.68 Very High Very High Very High
Spinal cord 97 95.52 Very High Very High Very High
Morphine 6 91.92 High High
antinociception 4 91.20 High High
Multiple sclerosis 6 89.80 High High
Demyelination 1 89.32 High High
tail-flick 1 89.20 High High
tolerance 5 86.32 High High
Disease Link Frequency Relevance Heat
Stress 73 100.00 Very High Very High Very High
Ganglion Cysts 2 100.00 Very High Very High Very High
Motor Neuron Diseases 246 99.98 Very High Very High Very High
Toxicity 73 99.98 Very High Very High Very High
INFLAMMATION 56 99.68 Very High Very High Very High
Cancer 246 99.54 Very High Very High Very High
Disease 279 96.88 Very High Very High Very High
Death 151 95.72 Very High Very High Very High
Metastasis 100 94.64 High High
Targeted Disruption 155 94.32 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
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].
SOD1 Binding (interactions) of in motor neurons associated with motor neuron diseases
1) Confidence 0.47 Published 2008 Journal Genome Biol Section Body Doc Link PMC2397497 Disease Relevance 0.47 Pain Relevance 0
All studies conducted on SOD1 aggregation thus far have been on the large aggregates that might be composed of long fibrils.
SOD1 Binding (aggregation) of
2) Confidence 0.46 Published 2003 Journal BMC Neurosci Section Body Doc Link PMC169170 Disease Relevance 0.71 Pain Relevance 0
The first proposes that the mutated SOD1 interacts with NO to produce peroxynitrite (ONOO-), which damages proteins by modifying tyrosine to nitrotyrosine residues [42-44].
SOD1 Neg (NO) Binding (interacts) of
3) Confidence 0.46 Published 2003 Journal BMC Neurosci Section Body Doc Link PMC169170 Disease Relevance 0.28 Pain Relevance 0
The role of mutant SOD1 aggregation, however, remains unclear.
SOD1 Binding (aggregation) of
4) Confidence 0.46 Published 2003 Journal BMC Neurosci Section Body Doc Link PMC169170 Disease Relevance 0.68 Pain Relevance 0
Some SOD1 aggregates overlap with CO1 signal while others do not (see Fig. 2A and 2B).
SOD1 Binding (aggregates) of
5) Confidence 0.34 Published 2003 Journal BMC Neurosci Section Body Doc Link PMC169170 Disease Relevance 0.15 Pain Relevance 0.03
Fridovich and colleagues first noticed the presence of SOD1 in the intermembrane space in liver mitochondria [37].
SOD1 Binding (presence) of in liver
6) Confidence 0.34 Published 2003 Journal BMC Neurosci Section Body Doc Link PMC169170 Disease Relevance 0.14 Pain Relevance 0
These changes include astrogliosis, fragmentation of Golgi apparatus, SOD1 aggregation and vacuolar degeneration [7,11-14].
SOD1 Binding (aggregation) of
7) Confidence 0.34 Published 2003 Journal BMC Neurosci Section Body Doc Link PMC169170 Disease Relevance 1.32 Pain Relevance 0.05
SOD1 aggregates are in the majority of vacuoles (Fig. 10; also see figures 2, 3, 5, 6 and 9, arrowheads).
SOD1 Binding (aggregates) of
8) Confidence 0.34 Published 2003 Journal BMC Neurosci Section Body Doc Link PMC169170 Disease Relevance 0.09 Pain Relevance 0.03
In this context, our observation that SOD1 aggregates are associated with vacuolar membrane (Figs. 2, 10) suggests that mutant SOD1 interacts with mitochondrial membrane and this interaction promotes aggregation.
SOD1 Binding (interacts) of
9) Confidence 0.34 Published 2003 Journal BMC Neurosci Section Body Doc Link PMC169170 Disease Relevance 0.47 Pain Relevance 0
These results suggest that cPLA2 plays an important role in supplying arachidonic acid to the COX-2 driven inflammatory pathway in ALS associated with SOD1 mutations.
SOD1 Binding (associated) of associated with inflammation and motor neuron diseases
10) Confidence 0.30 Published 2005 Journal J. Neurochem. Section Abstract Doc Link 15816863 Disease Relevance 1.11 Pain Relevance 0.35
Previous reports have indicated that a common mechanism of toxicity associated with the mutant form of SOD1 is the sequential activation of caspase-1 and caspase-3 [36].
SOD1 Binding (associated) of associated with toxicity
11) Confidence 0.27 Published 2010 Journal J Neuroinflammation Section Body Doc Link PMC2974667 Disease Relevance 1.21 Pain Relevance 0.50
In summary, CPZ acts on cupric enzymes, including SOD1, cytochrome oxidase, and D?
SOD1 Binding (enzymes) of
12) Confidence 0.25 Published 2010 Journal Frontiers in Behavioral Neuroscience Section Body Doc Link PMC2842101 Disease Relevance 0.51 Pain Relevance 0.11
40 and increased zinc levels in the brain without changing GFAP, SOD1, APP, C100, or NF200 levels to TgC100 mice.
SOD1 Binding (changing) of in brain
13) Confidence 0.24 Published 2010 Journal International Journal of Alzheimer's Disease Section Body Doc Link PMC2952897 Disease Relevance 0.58 Pain Relevance 0.15
Recently, Juarez et al, have shown that TM attenuates angiogenesis and tumor cell proliferation by inhibiting superoxide dismutase 1 (SOD1) [30].
superoxide dismutase 1 Binding (inhibiting) of associated with cancer
14) Confidence 0.24 Published 2010 Journal Mol Cancer Section Body Doc Link PMC2922193 Disease Relevance 1.36 Pain Relevance 0.07
Recently, Juarez et al, have shown that TM attenuates angiogenesis and tumor cell proliferation by inhibiting superoxide dismutase 1 (SOD1) [30].
SOD1 Binding (inhibiting) of associated with cancer
15) Confidence 0.24 Published 2010 Journal Mol Cancer Section Body Doc Link PMC2922193 Disease Relevance 1.36 Pain Relevance 0.07
However, several candidate compounds for ALS therapy [123] address aspects of SOD1 mutants, such as oxidative stress, impaired metal binding, and defects in protein folding, that we have also identified as affected in the motor cortex of sporadic, non-SOD1-linked patients.
SOD1 Binding (binding) of in cortex associated with stress and motor neuron diseases
16) Confidence 0.23 Published 2007 Journal BMC Genomics Section Body Doc Link PMC1796866 Disease Relevance 1.03 Pain Relevance 0.10
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.
Zn2 Binding (interacts) of in neurons associated with ganglion cysts, root ganglion neuron and opioid
17) Confidence 0.21 Published 2000 Journal Eur. J. Pharmacol. Section Abstract Doc Link 11068022 Disease Relevance 0.10 Pain Relevance 1.19

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