INT137332

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Context Info
Confidence 0.70
First Reported 2003
Last Reported 2010
Negated 3
Speculated 4
Reported most in Body
Documents 41
Total Number 45
Disease Relevance 19.80
Pain Relevance 4.69

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 16
muscle 8
blood 6
neuronal 4
muscle fibers 2
Sod1 (Mus musculus)
Sod1 - G93A (3)
Pain Link Frequency Relevance Heat
Sciatic nerve 13 99.92 Very High Very High Very High
tolerance 244 99.28 Very High Very High Very High
Neuropathic pain 16 98.48 Very High Very High Very High
Inflammation 322 97.96 Very High Very High Very High
Central nervous system 44 96.16 Very High Very High Very High
long-term potentiation 4 95.36 Very High Very High Very High
cytokine 210 94.00 High High
Spinal cord 71 91.24 High High
ketamine 9 83.48 Quite High
medulla 20 82.72 Quite High
Disease Link Frequency Relevance Heat
Targeted Disruption 171 100.00 Very High Very High Very High
Insulin Resistance 464 99.90 Very High Very High Very High
Motor Neuron Diseases 166 99.88 Very High Very High Very High
Impaired Glucose Tolerance 220 99.60 Very High Very High Very High
Skin Cancer 14 99.60 Very High Very High Very High
Frailty 13 99.48 Very High Very High Very High
Cognitive Disorder 49 99.40 Very High Very High Very High
Neurodegenerative Disease 76 99.24 Very High Very High Very High
Stress 215 98.72 Very High Very High Very High
Neuropathic Pain 16 98.48 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Taken together, our findings suggest that SOD1 overexpression is deleterious for nerve regeneration processes and aggravates neuropathic pain-like state in mice.
Positive_regulation (overexpression) of Gene_expression (overexpression) of SOD1 in nerve associated with neuropathic pain
1) Confidence 0.70 Published 2006 Journal J. Neurosci. Res. Section Abstract Doc Link 16862565 Disease Relevance 1.12 Pain Relevance 0.41
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) Positive_regulation (overexpression) of Spec (examine) Gene_expression (overexpression) of SOD1 in peripheral nerve associated with neuropathic pain
2) Confidence 0.70 Published 2006 Journal J. Neurosci. Res. Section Abstract Doc Link 16862565 Disease Relevance 1.09 Pain Relevance 0.52
Therefore, the overexpression of SOD1 may augment the phosphphorylation of Foxo1 by the reduction of phosphatase activity.
Positive_regulation (overexpression) of Gene_expression (overexpression) of SOD1
3) Confidence 0.60 Published 2008 Journal Diabetes Section Body Doc Link PMC2494675 Disease Relevance 0.07 Pain Relevance 0.03
Hepatic overexpression of SOD1 was associated with reduced level of superoxide in liver to a level comparable with that in db/m mice (Fig. 1B).
Positive_regulation (overexpression) of Gene_expression (overexpression) of SOD1 in liver
4) Confidence 0.60 Published 2008 Journal Diabetes Section Body Doc Link PMC2494675 Disease Relevance 0.07 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.
Positive_regulation (overexpression) of Gene_expression (overexpression) of SOD1 in liver
5) Confidence 0.60 Published 2008 Journal Diabetes Section Body Doc Link PMC2494675 Disease Relevance 0.14 Pain Relevance 0.03
expression was markedly suppressed by SOD1 overexpression, and this seemed to be a key molecular mechanism in the inhibition of gluconeogenesis.
Positive_regulation (overexpression) of Gene_expression (overexpression) of SOD1
6) Confidence 0.60 Published 2008 Journal Diabetes Section Body Doc Link PMC2494675 Disease Relevance 0.38 Pain Relevance 0.09
In the present study, overexpression of SOD1 suppressed the expression of gluconeogenic genes.
Positive_regulation (overexpression) of Gene_expression (overexpression) of SOD1
7) Confidence 0.60 Published 2008 Journal Diabetes Section Body Doc Link PMC2494675 Disease Relevance 0.56 Pain Relevance 0
Overexpression of SOD1 reduced phosphorylation of CREB (Fig. 5).
Positive_regulation (Overexpression) of Gene_expression (Overexpression) of SOD1
8) Confidence 0.60 Published 2008 Journal Diabetes Section Body Doc Link PMC2494675 Disease Relevance 0.09 Pain Relevance 0.03
Overexpression of SOD1 reduces phosphorylation of CREB.
Positive_regulation (Overexpression) of Gene_expression (Overexpression) of SOD1
9) Confidence 0.60 Published 2008 Journal Diabetes Section Body Doc Link PMC2494675 Disease Relevance 0.10 Pain Relevance 0.03
To elucidate the effect of the reduction of hepatic ROS on glucose metabolism, we investigated the effect of SOD1 overexpression in liver on blood glucose level in db/db mice.
Spec (investigated) Positive_regulation (overexpression) of Gene_expression (overexpression) of SOD1 in liver
10) Confidence 0.60 Published 2008 Journal Diabetes Section Body Doc Link PMC2494675 Disease Relevance 0.28 Pain Relevance 0.03
In the present study, we used overexpression of SOD1 as a strategy to reduce ROS levels in the liver.
Positive_regulation (overexpression) of Gene_expression (overexpression) of SOD1 in liver
11) Confidence 0.60 Published 2008 Journal Diabetes Section Body Doc Link PMC2494675 Disease Relevance 0.12 Pain Relevance 0
We found that treatment of db/db mice with AdSOD2 reduced blood glucose level and ameliorated glucose tolerance and that the effect was almost similar to overexpression of AdSOD1 (N.
Positive_regulation (overexpression) of Gene_expression (overexpression) of AdSOD1 in blood associated with tolerance and impaired glucose tolerance
12) Confidence 0.52 Published 2008 Journal Diabetes Section Body Doc Link PMC2494675 Disease Relevance 0.32 Pain Relevance 0.05
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.
Positive_regulation (overexpressing) of Gene_expression (overexpressing) of SOD1-overexpressing in muscles associated with frailty
13) Confidence 0.50 Published 2006 Journal J. Neurosci. Res. Section Abstract Doc Link 16862565 Disease Relevance 1.24 Pain Relevance 0.51
Sciatic nerves of SOD1-overexpressing and FVB/N wild type-mice were transected and immediately resutured.
Positive_regulation (overexpressing) of Gene_expression (overexpressing) of SOD1-overexpressing in Sciatic nerves associated with sciatic nerve
14) Confidence 0.50 Published 2006 Journal J. Neurosci. Res. Section Abstract Doc Link 16862565 Disease Relevance 1.07 Pain Relevance 0.51
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.
Positive_regulation (necessary) of Gene_expression (expression) of SOD1G93A in Schwann cells
15) Confidence 0.50 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2842435 Disease Relevance 0.06 Pain Relevance 0.07
Here we examine whether this degeneration depends on expression of mutant SOD1 in muscle fibers.


Spec (whether) Positive_regulation (depends) of Gene_expression (expression) of SOD1 in muscle fibers
16) Confidence 0.50 Published 2010 Journal PLoS ONE Section Abstract Doc Link PMC2842435 Disease Relevance 0.35 Pain Relevance 0
The elevated expression of MnSOD, Cu/ZnSOD, reactive oxygen species (ROS), and reduction in glutathione, indicate altered redox balance upon LPS, A?
Positive_regulation (upon) of Gene_expression (expression) of Cu/ZnSOD
17) Confidence 0.49 Published 2005 Journal J Neuroinflammation Section Body Doc Link PMC1262754 Disease Relevance 0.37 Pain Relevance 0.26
The elevated expression of MnSOD, Cu/ZnSOD, reactive oxygen species (ROS), and reduction in glutathione, indicate altered redox balance upon LPS, A?
Positive_regulation (elevated) of Gene_expression (expression) of Cu/ZnSOD
18) Confidence 0.49 Published 2005 Journal J Neuroinflammation Section Body Doc Link PMC1262754 Disease Relevance 0.37 Pain Relevance 0.26
Within three minutes of adding DHB, the rate of ATP production showed a statistically significant increase compared to disease controls (198 ± 7 vs. 125 ± 9 RLU/100 s/mg protein, p < 0.001) (Figure 3B), thus confirming that DHB promotes ATP production in G93A-SOD1 transgenic mice.
Positive_regulation (promotes) of Gene_expression (production) of G93A-SOD1 (G93A) associated with targeted disruption and disease
19) Confidence 0.47 Published 2006 Journal BMC Neurosci Section Body Doc Link PMC1488864 Disease Relevance 0.34 Pain Relevance 0
One goal of the present study was to test the hypothesis that expression of the mutant SOD1G93A protein in muscle is necessary for the appearance of motor terminal degeneration.
Positive_regulation (necessary) of Gene_expression (expression) of SOD1G93A in muscle
20) Confidence 0.46 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2842435 Disease Relevance 0.14 Pain Relevance 0.05

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