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diagnostics
AKR1B10 may have a potential role as a tumor marker
nutrition
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pretreatment of sugarcane bagasse hydrolysate to eliminate toxic compounds unsuitable for use as growth medium in xylitol production. optimization of adsorption time, type odf acid used, concentration and charcoal leads to a high ratio of xylose reductase, EC1.1.1.21, to xylitol dehydrogenase, EC1.1.1.9, of 4.5
synthesis
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homochiral 3-hydroxy-4-substituted beta-lactams serve as precursors to the corresponding alpah-hydroxy-beta-amino acids, the enzyme might be useful insynthesis of these key components of many biologically and therapeutically important compounds
biotechnology
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use of enzyme in production of xylitol from bagasse hydrolysate, enzyme activity is higher in medium containing acetic acid than in control medium
biotechnology
ALDRXV4 gene from Xerophyta viscosa is a potential candidate for developing stress-tolerant crop plants
drug development
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homochiral 3-hydroxy-4-substituted beta-lactams serve as precursors to the corresponding alpah-hydroxy-beta-amino acids, the enzyme might be useful insynthesis of these key components of many biologically and therapeutically important compounds
drug development
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the enzyme is a target for inhibitor design, enzyme inhibition has considerable potential for the treatment of diabetes, without increased risk of hypoglycemia
drug development
the enzyme may be a potential drug target or vaccine candidate for schistosomes
drug development
development of reductase inhibitors as drugs counteracting the onset of diabetic complications
drug development
development of reductase inhibitors as drugs counteracting the onset of diabetic complications
medicine
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enzyme protein levels and activity decrease progressively during heart failure upon rapid left ventricular pacing, such as myocardial capacity to detoxify lipid-peroxidation derived aldehydes
medicine
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inhibition of enzyme by tolrestat or sorbinil prevents apotosis and activation of calpase-3, attenuation of TNF-alpha and hyperglykemia-induced activation of protein kinase C, but does not prevent the activation of transkription factor NK-kappaB and protein kinase C by phorbol ester, enzyme is an obligatory mediator of the apoptotic events upstream of protein kinase C
medicine
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inhibition of enzyme by zolrestat attenuates apoptosis in sorbitol-treated cells. Hyperosmolarity-induced cell death requires induction of enzyme as well as a decrease in intracellular glutathione levels
medicine
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inhibition of enzyme inhibits vascular smooth muscle cell growth upon injuries via a decrease in activity of transcription factor NF-kappaB
medicine
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inhibition of enzyme prevents TNF-alpha-induced increase in Bax and Bak and the downregulation of Bcl-2, inhibition abrogates Ap-1 DNA binding activity and prevents the activation of caspase-3, JNK, and p38 MAPK in cells stimulated by TNFalpha
medicine
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myocardial enzyme activity is increased during ischemia, partially due to activation by nitric oxide, enzyme inhibition increases glycolysis and glucose oxidation
medicine
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pharmacological inhibition of enzyme significantly reduces ischemic injury and improves functional recovery in enzyme transgenic mice
medicine
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inhibition of AR may assist in the chemotherapy of malignant tumors by suppressing the rapid growth of cancer cells
medicine
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inhibition of AR may be a significant therapeutic approach in preventing bacterial endotoxin-induced sepsis and tissue damage
medicine
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in streptozotocin-diabetic mice, aldose reductase inhibitor treatment or genetic deficiency of aldose reductase result in significant dephosphorylation of both peroxisome proliferator-activated receptor alpha and ERK1/2
medicine
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inhibition of enzyme in neural stem cells exposed to high glucose concentration results in decrease of oxidative stress, restoration of cell viability and proliferation, and reduction of apoptotic cell death. Inhibition attenuates the down-regulation of glucose transporter 1 expression
medicine
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inhibition/antisense abolition of aldose reductase inhibits the tumor necrosis factor alpha-induced synthesis of prostaglandin E2 and the activity of cyclooxygenase. Inhibition of aldose reductase prevents tumor necrosis factor alpha-induced activation of protein kinase C and NF-kappaB which results in the abrogation of Cox-2 mRNA and protein expression
medicine
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treatment with the nitric oxide synthase inhibitor, N-nitro-L-arginine methyl ester prevented ischemia-induced aldose reductase activation and myocardial sorbitol accumulation in rat hearts subjected to global ischemia ex vivo or coronary ligation in situ, whereas inhibition of inducible nitric oxide synthase and neuronal nitric oxide synthase have no effect. Activation of aldose reductase in the ischemic heart is abolished by pretreatment with peroxynitrite scavengers hesperetin or 5,10,15,20-tetrakis-[4-sulfonatophenyl]-porphyrinato-iron [III]
medicine
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ALR2 is a critical target to prevent and control diabetic complications through the inhibition of its activity
medicine
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inhibition of aldose reductase may represent a useful strategy for treating vascular inflammation associated with diabetes
medicine
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levels of ALR2 activity as well as sorbitol in erythrocytes may have value as a quantitative trait to establish a risk profile for development of diabetic retinopathy, type 2 diabetic patients with diabetic retinopathy show significantly higher specific activity of ALR2 as compared to type 2 diabetic patients without diabetic retinopathy
medicine
aldose reductase ALR2 is a target enzyme for the treatment of diabetic complications
medicine
the enzyme may be a potential drug target or vaccine candidate for schistosomes
medicine
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fidarestat decreases doxorubicin-induced upregulation of CD11b in THP-1 monocytes. Fidarestat attenuates doxorubicin-induced upregulation of IL-6, IL-1bta, and Nos2 in murine bone-marrow derived macrophages. Fidarestat also attenuates doxorubicin-induced activation and infiltration of multiple subsets of inflammatory immune cells identified by expression of markers CD11b+, CD11b+F4/80+, Ly6C+CCR2high, and Ly6C+CD11b+ in the mouse spleen and liver. Upregulation of markers of mitochondrial biogenesis PGC-1alpha, COX IV, TFAM, and phosphorylation of AMPKalpha1 (Ser485) is observed in THP-1 cells and livers of mice treated with doxorubicin in combination with fidarestat
medicine
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mice devoid of AKR1B3 and exposed to acute occlusion of the left anterior descending coronary artery display reduced infarct size and improved functional recovery at 48 hours compared to wild-type mice. The cardioprotection observed in AKR1B3 null mice is linked to acute activation of the beta-catenin pathway and consequent activation of mesenchymal markers and genes linked to fibrotic remodeling. The increased activity of the beta-catenin pathway at 48 hours of recovery is not observed at 28 days post-infarction. In ex vivo studies, inhibition of beta-catenin blocks the cardioprotection observed in AKR1B3 null mice hearts