INT67037

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Context Info
Confidence 0.78
First Reported 1996
Last Reported 2010
Negated 2
Speculated 5
Reported most in Body
Documents 121
Total Number 126
Disease Relevance 59.32
Pain Relevance 7.99

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
muscles 16
liver 13
motor neurons 7
brain 4
blood 4
Sod1 (Mus musculus)
Sod1 - G93A (8)
Pain Link Frequency Relevance Heat
Spinal cord 433 99.92 Very High Very High Very High
Sciatic nerve 33 99.92 Very High Very High Very High
tolerance 410 99.28 Very High Very High Very High
Neuropathic pain 21 98.48 Very High Very High Very High
Inflammation 409 97.96 Very High Very High Very High
medulla 47 97.20 Very High Very High Very High
agonist 42 97.12 Very High Very High Very High
Central nervous system 112 96.16 Very High Very High Very High
long-term potentiation 6 95.36 Very High Very High Very High
cerebral cortex 11 94.56 High High
Disease Link Frequency Relevance Heat
Motor Neuron Diseases 1178 100.00 Very High Very High Very High
Targeted Disruption 941 100.00 Very High Very High Very High
Toxicity 305 99.98 Very High Very High Very High
Disease 1052 99.92 Very High Very High Very High
Insulin Resistance 780 99.90 Very High Very High Very High
Death 386 99.60 Very High Very High Very High
Impaired Glucose Tolerance 370 99.60 Very High Very High Very High
Skin Cancer 14 99.60 Very High Very High Very High
Injury 168 99.52 Very High Very High Very High
Frailty 37 99.48 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
The aim of this study was to examine the role of SOD1 overexpression in peripheral nerve regeneration and neuropathic pain-related behavior in mice.
Spec (examine) Gene_expression (overexpression) of SOD1 in peripheral nerve associated with neuropathic pain
1) Confidence 0.78 Published 2006 Journal J. Neurosci. Res. Section Abstract Doc Link 16862565 Disease Relevance 1.09 Pain Relevance 0.52
Taken together, our findings suggest that SOD1 overexpression is deleterious for nerve regeneration processes and aggravates neuropathic pain-like state in mice.
Gene_expression (overexpression) of SOD1 in nerve associated with neuropathic pain
2) Confidence 0.78 Published 2006 Journal J. Neurosci. Res. Section Abstract Doc Link 16862565 Disease Relevance 1.12 Pain Relevance 0.41
The results (Figure 2) confirm that expression of the mutated SOD1 protein is maintained in muscles transplanted from B6.SOD1 animals into wild-type animals.
Gene_expression (expression) of SOD1 protein in muscles
3) Confidence 0.77 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2842435 Disease Relevance 0.12 Pain Relevance 0
The observation that transplanted wild-type muscles do not inhibit the occurrence of muscle denervation in B6.SOD1 mice provides increased confidence that expression of the G93A SOD1 mutation in muscle is not necessary for the appearance of muscle denervation or the motor neuron disease phenotype.
Gene_expression (expression) of SOD1 (G93A) in muscles associated with motor neuron diseases
4) Confidence 0.77 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2842435 Disease Relevance 0.32 Pain Relevance 0
Previous studies have shown that expression of the mutated SOD1G93A gene solely in neurons does not cause motor neuron disease [2].
Gene_expression (expression) of SOD1G93A in motor neuron associated with motor neuron diseases
5) Confidence 0.77 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2842435 Disease Relevance 0.58 Pain Relevance 0.03
Conversely, when the motor neuron-Schwann cell combination does not express the mutant SOD1G93A protein, motor terminal degeneration does not proceed despite the presence of muscle that does express the mutant enzyme.
Neg (not) Gene_expression (express) of SOD1G93A in muscle
6) Confidence 0.77 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2842435 Disease Relevance 0.08 Pain Relevance 0
In order to confirm this in the present study, we performed Western analysis of SOD1 expression in MG muscle from an B6.SOD1 donor that had been transplanted into a wild-type host 2 months earlier.
Gene_expression (expression) of SOD1 in muscle
7) Confidence 0.77 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2842435 Disease Relevance 0.06 Pain Relevance 0
Previously, Lino et al [2] showed that expression of the mutant SOD1G93A protein in neurons alone (including motor neurons) was not sufficient to cause or greatly attenuate the motor neuron disease phenotype.
Gene_expression (expression) of SOD1G93A in motor neurons associated with motor neuron diseases
8) Confidence 0.77 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2842435 Disease Relevance 0.10 Pain Relevance 0
Here we examine whether this degeneration depends on expression of mutant SOD1 in muscle fibers.


Gene_expression (expression) of SOD1 in muscle fibers
9) Confidence 0.77 Published 2010 Journal PLoS ONE Section Abstract Doc Link PMC2842435 Disease Relevance 0.35 Pain Relevance 0
However, when motor neuron-Schwann cell combinations are present in wild-type muscles transplanted into B6.SOD1 mice and both cell types likely express the SOD1G93A mutation, nerve terminal degeneration proceeds in a manner indistinguishable from the contralateral, control side.
Gene_expression (express) of SOD1G93A in nerve
10) Confidence 0.77 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2842435 Disease Relevance 0.09 Pain Relevance 0
Using behavioral tests, Miller et al [15] reached a similar conclusion after reducing expression of mutant protein in muscles of mice that ubiquitously express SOD1G93A.
Gene_expression (express) of SOD1G93A in muscles
11) Confidence 0.77 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2842435 Disease Relevance 0.36 Pain Relevance 0
This and other evidence suggest that toxic interactions between motor neurons and other cells all of which express the mutant SOD1 protein may be important for disease progression [3]–[5].
Gene_expression (express) of SOD1 protein in motor neurons associated with disease progression
12) Confidence 0.77 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2842435 Disease Relevance 0.66 Pain Relevance 0.04
The SOD1G93A transgenic mouse is a common model for studying motor neuron disease and ubiquitously expresses one (G93A) of many SOD1 protein mutations known to occur in about 20% of human cases of inherited motor neuron disease [1].
Gene_expression (expresses) of SOD1 protein in motor neuron associated with targeted disruption and motor neuron diseases
13) Confidence 0.77 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2842435 Disease Relevance 0.50 Pain Relevance 0
It is possible that expression of mutant SOD1G93A in TSCs and myelinating Schwann cells alone or in combination with motor neurons may be necessary for motor terminal degeneration.
Gene_expression (expression) of SOD1G93A in Schwann cells
14) Confidence 0.77 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2842435 Disease Relevance 0.06 Pain Relevance 0.04
Control studies demonstrated that muscles transplanted from SOD1G93A mice continued to express mutant SOD1 protein.
Gene_expression (express) of SOD1 protein in muscles
15) Confidence 0.77 Published 2010 Journal PLoS ONE Section Abstract Doc Link PMC2842435 Disease Relevance 0.41 Pain Relevance 0
Another explanation for the nearly complete innervation of B6.SOD1 MG transplants by wild-type motor neurons is that the regenerated fibers in transplants do not express the mutant SOD1 protein.
Neg (not) Gene_expression (express) of SOD1 protein in motor neurons
16) Confidence 0.77 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2842435 Disease Relevance 0 Pain Relevance 0
If such transgenic fibers exist, however, then the basis of the toxicity must involve features other than expression of the mutant B6.SOD1G93A protein since fibers that did regenerate in transplants but did not cause motor terminal degeneration expressed the mutant protein.
Gene_expression (expression) of SOD1G93A associated with targeted disruption and toxicity
17) Confidence 0.77 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2842435 Disease Relevance 0.52 Pain Relevance 0
Sciatic nerves of SOD1-overexpressing and FVB/N wild type-mice were transected and immediately resutured.
Gene_expression (overexpressing) of SOD1-overexpressing in Sciatic nerves associated with sciatic nerve
18) Confidence 0.67 Published 2006 Journal J. Neurosci. Res. Section Abstract Doc Link 16862565 Disease Relevance 1.07 Pain Relevance 0.51
We found markedly worse sciatic function index outcome as well as more significant atrophy of denervated muscles in SOD1-overexpressing animals compared with wild type.
Gene_expression (overexpressing) of SOD1-overexpressing in muscles associated with frailty
19) Confidence 0.67 Published 2006 Journal J. Neurosci. Res. Section Abstract Doc Link 16862565 Disease Relevance 1.24 Pain Relevance 0.51
Hindlimb muscles were transplanted between wild-type and SOD1G93A transgenic mice and the innervation status of neuromuscular junctions (NMJs) was examined after 2 months.
Gene_expression (transplanted) of SOD1G93A in NMJs associated with targeted disruption
20) Confidence 0.67 Published 2010 Journal PLoS ONE Section Abstract Doc Link PMC2842435 Disease Relevance 0.36 Pain Relevance 0

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