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rs121912436
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0.100 |
GeneticVariation |
BEFREE |
Our results showed that urate treatment provided neuroprotective effects as confirmed by enhanced survival, attenuated motor impairments, reduced oxidative damage and increased antioxidant defense in hSOD1-G85R-expressing Drosophila models of ALS.
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30690059 |
2019 |
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rs121912436
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|
0.100 |
GeneticVariation |
BEFREE |
This study aimed to evaluate the antioxidant and neuroprotective effects of LA in ALS cell and Drosophila models with mutant G85R and G93A hSOD1 genes.
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29842900 |
2018 |
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rs121912436
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0.100 |
GeneticVariation |
BEFREE |
Exploring the cause of aggregation and reduced Zn binding affinity by G85R mutation in SOD1 rendering amyotrophic lateral sclerosis.
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28321933 |
2017 |
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rs121912436
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0.100 |
GeneticVariation |
BEFREE |
As pioglitazone increases body weight through a direct inhibition of the hypothalamic melanocortin system, we studied hypothalamic neurons producing proopiomelanocortin (POMC) and the endogenous melanocortin inhibitor agouti-related peptide (AGRP), in mice expressing amyotrophic lateral sclerosis-linked mutant SOD1(G86R).
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26984187 |
2016 |
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rs121912436
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0.100 |
GeneticVariation |
BEFREE |
To elucidate this role, we bred MIF-deficient mice with SOD1(G85R) mice, which express a dismutase-inactive mutant of SOD1 and are considered a model of familial ALS.
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27551074 |
2016 |
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rs121912436
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0.100 |
GeneticVariation |
BEFREE |
Glucosylceramide synthase (GCS), the enzyme responsible for GlcCer biosynthesis, was up-regulated in muscle of SOD1(G86R) mice and ALS patients, and in muscle of wild-type mice after surgically induced denervation.
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26483191 |
2015 |
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rs121912436
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0.100 |
GeneticVariation |
BEFREE |
The differential effects of astrocyte G85R versus G37R knockdown on MN death demonstrate SOD1 mutation-specific effects on ALS pathogenesis; these differences may be a result of the different dismutase activities of the two mutants.
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20962037 |
2011 |
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rs121912436
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0.100 |
GeneticVariation |
BEFREE |
We have previously shown that several familial ALS-linked copper-zinc superoxide dismutase (SOD1) mutants (A4V, G85R, and G93A) interacted and colocalized with the retrograde dynein-dynactin motor complex in cultured cells and affected tissues of ALS mice.
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20510358 |
2010 |
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rs121912436
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0.100 |
GeneticVariation |
BEFREE |
This work characterizes the properties of wild-type (WT) mouse motoneurons in the second postnatal week and compares these at the same age and in the same conditions to those of two different SOD1 mutant lines used as models of human amyotrophic lateral sclerosis (ALS), the SOD1(G93A) low expressor line and SOD1(G85R) line, to describe any changes in the functional properties of mutant motoneurons (Mns) that may be related to the pathogenesis of human ALS.
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19828728 |
2009 |
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rs121912436
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0.100 |
GeneticVariation |
BEFREE |
A major set of gene regulations in G86R muscles resembled those of surgically denervated muscles, but many others appeared specific to the ALS condition.
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18000159 |
2008 |
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rs121912436
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0.100 |
GeneticVariation |
BEFREE |
We have previously shown that several familial ALS-linked copper-zinc superoxide dismutase (SOD1) mutants (A4V, G85R, and G93A) interact and co-localize with the dynein-dynactin complex in cultured cells and affected tissues of ALS mice.
|
18515363 |
2008 |
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rs121912436
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0.100 |
GeneticVariation |
BEFREE |
We studied the expression of mitochondrial uncoupling proteins (UCPs), key regulators of mitochondrial functions, in tissues from a mouse model of ALS (SOD1 G86R transgenic mice) and from muscular biopsies of human sporadic ALS.
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14500553 |
2003 |
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rs121912436
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0.100 |
GeneticVariation |
BEFREE |
One, caused by a G86R mutation in the superoxide dismutase-1 (SOD-1) gene associated with familial ALS, has been subjected to extensive quantitative analyses in the spinal cord.
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10578106 |
2000 |