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PMID |
Sentence |
1 |
20150532
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Autoimmunity in membranous nephropathy targets aldose reductase and SOD2.
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2 |
20150532
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We detected specific anti-aldose reductase (AR) and anti-manganese superoxide dismutase (SOD2) IgG(4) in sera of patients with MN.
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3 |
20150532
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Autoimmunity in membranous nephropathy targets aldose reductase and SOD2.
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4 |
20150532
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We detected specific anti-aldose reductase (AR) and anti-manganese superoxide dismutase (SOD2) IgG(4) in sera of patients with MN.
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5 |
20376891
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Aldose reductase inhibitor ameliorates renal vascular endothelial growth factor expression in streptozotocin-induced diabetic rats.
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6 |
23401979
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In recent years, first human podocyte autoantigens, responsible for autoantibodies and in situ immune complexes formation, were discovered: neutral endopeptidase, m-type phospholipase A2 receptor, superoxide-dismutase 2, aldose-reductase, alpha-enolase.
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7 |
29930278
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Moreover, the upregulation of aldose reductase, fibronectin, collagen III, and TGF-β1 in renal cortex of db/db mice was downregulated by epalrestat.
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8 |
34803506
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Mitotic arrest deficient 2-like protein 2 (MAD2B), an inhibitor of anaphase-promoting complex (APC)/cyclosome, precisely controls the metaphase to anaphase transition and ordered cell cycle progression.
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9 |
34803506
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However, the role of MAD2B in FSGS podocyte injury remains unknown.
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10 |
34803506
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Additionally, KU-55933, a specific inhibitor of ataxia-telangiectasia mutated (ATM) was utilized in vivo and in vitro to explore the role of ATM in regulating MAD2B.
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11 |
34803506
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Results: The expression of MAD2B in podocytes was dramatically increased in patients with FSGS and ADR-treated mice along with podocyte cell cycle reentry.
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12 |
34803506
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By bioinformatics analysis we revealed that ATM kinase is a key upstream regulator of MAD2B.
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13 |
34803506
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Furthermore, inhibition of ATM kinase abolished MAD2B-driven cell cycle reentry and alleviated podocyte impairment in FSGS murine model.
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14 |
34803506
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In vitro studies by site-directed mutagenesis and immunoprecipitation we revealed ATM phosphorylated MAD2B and consequently hampered the ubiquitination of MAD2B in a phosphorylation-dependent manner.
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15 |
34811512
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Ginsenoside Rb1 alleviates diabetic kidney podocyte injury by inhibiting aldose reductase activity.
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16 |
34811512
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Furthermore, Rb1 treatment reversed high glucose-induced increases in Cyto c, Caspase 9 and mitochondrial regulatory protein NOX4, but did not affect the upregulated expression of aldose reductase (AR).
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17 |
34811512
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We compared the effects of Rb1 with eparestat, a known aldose reductase inhibitor, in high glucose-treated podocytes, and found that both alleviated high glucose-induced cell apoptosis and mitochondrial damage, and Rb1 was more effective in inhibiting apoptosis.
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18 |
34811512
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Ginsenoside Rb1 alleviates diabetic kidney podocyte injury by inhibiting aldose reductase activity.
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19 |
34811512
|
Furthermore, Rb1 treatment reversed high glucose-induced increases in Cyto c, Caspase 9 and mitochondrial regulatory protein NOX4, but did not affect the upregulated expression of aldose reductase (AR).
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20 |
34811512
|
We compared the effects of Rb1 with eparestat, a known aldose reductase inhibitor, in high glucose-treated podocytes, and found that both alleviated high glucose-induced cell apoptosis and mitochondrial damage, and Rb1 was more effective in inhibiting apoptosis.
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21 |
34811512
|
Ginsenoside Rb1 alleviates diabetic kidney podocyte injury by inhibiting aldose reductase activity.
|
22 |
34811512
|
Furthermore, Rb1 treatment reversed high glucose-induced increases in Cyto c, Caspase 9 and mitochondrial regulatory protein NOX4, but did not affect the upregulated expression of aldose reductase (AR).
|
23 |
34811512
|
We compared the effects of Rb1 with eparestat, a known aldose reductase inhibitor, in high glucose-treated podocytes, and found that both alleviated high glucose-induced cell apoptosis and mitochondrial damage, and Rb1 was more effective in inhibiting apoptosis.
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