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Gene Information

Gene symbol: AKR1B1

Gene name: aldo-keto reductase family 1, member B1 (aldose reductase)

HGNC ID: 381

Synonyms: AR

Related Genes

# Gene Symbol Number of hits
1 ACTN4 1 hits
2 CASP9 1 hits
3 COL1A1 1 hits
4 MAD2L2 1 hits
5 MME 1 hits
6 NOX4 1 hits
7 PLA2G1B 1 hits
8 RB1 1 hits
9 SOD1 1 hits
10 SOD2 1 hits
11 VEGFA 1 hits

Related Sentences

# PMID Sentence
1 20150532 Autoimmunity in membranous nephropathy targets aldose reductase and SOD2.
2 20150532 We detected specific anti-aldose reductase (AR) and anti-manganese superoxide dismutase (SOD2) IgG(4) in sera of patients with MN.
3 20150532 Autoimmunity in membranous nephropathy targets aldose reductase and SOD2.
4 20150532 We detected specific anti-aldose reductase (AR) and anti-manganese superoxide dismutase (SOD2) IgG(4) in sera of patients with MN.
5 20376891 Aldose reductase inhibitor ameliorates renal vascular endothelial growth factor expression in streptozotocin-induced diabetic rats.
6 23401979 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.
7 29930278 Moreover, the upregulation of aldose reductase, fibronectin, collagen III, and TGF-β1 in renal cortex of db/db mice was downregulated by epalrestat.
8 34803506 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.
9 34803506 However, the role of MAD2B in FSGS podocyte injury remains unknown.
10 34803506 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.
11 34803506 Results: The expression of MAD2B in podocytes was dramatically increased in patients with FSGS and ADR-treated mice along with podocyte cell cycle reentry.
12 34803506 By bioinformatics analysis we revealed that ATM kinase is a key upstream regulator of MAD2B.
13 34803506 Furthermore, inhibition of ATM kinase abolished MAD2B-driven cell cycle reentry and alleviated podocyte impairment in FSGS murine model.
14 34803506 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.
15 34811512 Ginsenoside Rb1 alleviates diabetic kidney podocyte injury by inhibiting aldose reductase activity.
16 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).
17 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.
18 34811512 Ginsenoside Rb1 alleviates diabetic kidney podocyte injury by inhibiting aldose reductase activity.
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).
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.
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.