rs762060740
|
|
|
0.100 |
GeneticVariation |
BEFREE |
Altogether these findings indicate that G93A-SOD1 expression results in an exacerbated pattern of neuroinflammation and suggest that C/EBPβ is a candidate to regulate the expression of potentially neurotoxic genes in microglial cells in ALS.
|
22015310 |
2012 |
rs762060740
|
|
|
0.100 |
GeneticVariation |
BEFREE |
In the present report we used the G93A transgenic mouse model of amyotrophic lateral sclerosis to develop and characterize an in vitro tool for the investigation of subtle alterations of spinal tissue prior to frank neuronal degeneration.
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16442737 |
2006 |
rs762060740
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|
|
0.100 |
GeneticVariation |
BEFREE |
In the present study, we demonstrate an age-dependent increase in Bcl-xL and Ets-2 immunoreactivity that correlates with an increase of glial fibrillary acidic protein (GFAP)-positive cells in the ventral horn of the spinal cord in both ALS transgenic mice [mutant SOD1 (G93A)] and affected humans.
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19179380 |
2009 |
rs762060740
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|
|
0.100 |
GeneticVariation |
BEFREE |
Increased number and differentiation of neural precursor cells in the brainstem of superoxide dismutase 1(G93A) (G1H) transgenic mouse model of amyotrophic lateral sclerosis.
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17439705 |
2007 |
rs762060740
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|
|
0.100 |
GeneticVariation |
BEFREE |
Mice that overexpress the human Cu,Zn superoxide dismutase-1 mutant G93A develop a delayed and progressive motor neuron disease similar to human amyotrophic lateral sclerosis (ALS).
|
16049935 |
2005 |
rs762060740
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|
|
0.100 |
GeneticVariation |
BEFREE |
Neuroprotective effects of diallyl trisulfide in SOD1-G93A transgenic mouse model of amyotrophic lateral sclerosis.
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21147075 |
2011 |
rs762060740
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|
|
0.100 |
GeneticVariation |
BEFREE |
Therefore, in the present study, we investigated the process of motor neuron degeneration as the disease progresses and to determine whether the CypA-AIF complex would play a role in inducing motor neuronal cell death in mutant superoxide dismutase 1 (SOD1)(G93A) ALS model mice.
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20553309 |
2011 |
rs762060740
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|
|
0.100 |
GeneticVariation |
BEFREE |
To assess molecular pathological effects of the anti-inflammatory peroxisome proliferator-activated receptor-gamma (PPARgamma) agonist pioglitazone in ALS, we verified changes in the population of neurons, astrocytes, and microglia in the ventral horns of spinal cord lumbar segments from the pioglitazone-treated and non-treated groups of mice carrying a transgene for G93A mutant human superoxide dismutase-1 (SOD1) (ALS mice) and non-transgenic littermates (control mice), performed immunohistochemical and immunoblot analyses of PPARgamma, active form of phosphorylated p38 mitogen-activated protein kinase (p-p38) and inhibitor of nuclear factor-kappaB (NF-kappaB)-alpha (IkappaBalpha) in the spinal cords, and compared the results between the different groups.
|
18312546 |
2008 |
rs762060740
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|
|
0.100 |
GeneticVariation |
BEFREE |
To examine the role of H63D HFE in ALS, we generated a double transgenic mouse line (SOD1/H67D) carrying the H67D HFE (homologue of human H63D) and SOD1(G93A) mutations.
|
25283820 |
2014 |
rs762060740
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|
0.100 |
GeneticVariation |
BEFREE |
We determined the expression of Wnt3a, β-catenin, and Cyclin D1 in the adult spinal cord of SOD1(G93A) ALS transgenic mice at different stages by RT-PCR, Western blot, and immunofluorescence labeling techniques.
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22426476 |
2012 |
rs762060740
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|
|
0.100 |
GeneticVariation |
BEFREE |
We transplanted human bone marrow mesenchymal stem cells (hMSCs) into the lumbar spinal cord of asymptomatic SOD1(G93A) mice, an experimental model of ALS. hMSCs were found in the spinal cord 10 weeks after, sometimes close to motoneurons and were rarely GFAP- or MAP2-positive.
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18586098 |
2008 |