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Structure of ALR1 in ternary complex with NADPH and 3,5-dichlorosalicylic acid is reported as well as the implications for inhibitor binding and selectivity.
L-idose is the best alternative to D-glucose in studies on aldose reductase.
prostaglandin F synthase (show AKR1C3 ELISA Kits) activity of human and bovine aldo-keto reductases
Aldehyde reductase exerts a protective effect against carbon tetrachloride-induced hepatic steatosis by replenishing ascorbic acid via its antioxidative properties.
Aldose reductase acts as a switch which can regulate microglia by polarizing cells after spinal cord injury.
Aldose reductase contributes to diabetes-mediated mitochondrial dysfunction and damage through the activation of p53 (show TP53 ELISA Kits).
Data indicate that inhibition of AR alleviates the MCD (show MLYCD ELISA Kits) diet-induced liver inflammation and fibrosis in db/db (show LEPR ELISA Kits) mice, probably through dampening CYP2E1 (show CYP2E1 ELISA Kits) mediated-oxidative stress and ameliorating the expression of pro-inflammatory cytokines.
FMHM suppressed the activity of AR-dependent phospholipase C (show PLC ELISA Kits)/protein kinase C (show PKC ELISA Kits) signaling, which further resulted in downstream inactivation of the IkappaB kinase (show CHUK ELISA Kits)/IkappaB/nuclear factor-kappa B inflammatory pathway.
Allergen-induced airway remodeling is mediated by AR and its inhibition blocks the progression of remodeling via inhibiting TGFbeta1 (show TGFB1 ELISA Kits)-induced Smad (show SMAD1 ELISA Kits)-independent and PI3K/AKT (show AKT1 ELISA Kits)/GSK3beta (show GSK3b ELISA Kits)-dependent pathway.
BGG-mediated inhibition of aldose reductase prevented LPS (show TLR4 ELISA Kits)-induced activation of JNK (show MAPK8 ELISA Kits).
The crystal structure of AKR1a4 in its apo (show C9orf3 ELISA Kits) form at high resolution.
crystal of AKR1B3 was tetragonal, belonging to space group P4(1)2(1)2 or P4(3)2(1)2, with unit-cell parameters a = b = 107.62, c = 120.76 A
the role of AKR1B3 in regulating advanced glycosylation end products and advanced lipoxidation end products
AKR1B1 as a key modulator of tumor aggressiveness and suggests that pharmacologic inhibition of AKR1B1 has the potential to become a valuable therapeutic strategy for Basal-like breast cancer (BLBC).
Result indicate that the differential scanning fluorimetry (DSF) method is useful for enzyme inhibitor drug screening for the AKR superfamily, including AKR1B10 (show AKR1B10 ELISA Kits) and a structurally similar isoform AKR1B1.
The hyperosmotic AR gene expression was dependent on activation of metalloproteinases, autocrine/paracrine TGF-beta (show TGFB1 ELISA Kits) signaling, activation of p38 MAPK (show MAPK14 ELISA Kits), ERK1/2 (show MAPK1/3 ELISA Kits), and PI3K (show PIK3CA ELISA Kits) signal transduction pathways, and the transcriptional activity of NFAT5 (show NFAT5 ELISA Kits).
Aberrant DNA methylation (show HELLS ELISA Kits) of AKR1B1 could be potential screening markers of colorectal cancer.
-106T allele of AKR1B1 C-106T polymorphism may be associated with increased risk for essential hypertension in Chinese Han population.
These findings suggest a statistically significant association of AKR1B1 -106C>T polymorphism with retinopathy in North Indian patients
ALR (show GFER ELISA Kits) C(-106)T polymorphism was not associated with an increased risk of Diabetic Retinopathy; subgroup analysis showed a genetic association between ALR (show GFER ELISA Kits) C(-106)T polymorphism and the risk of Diabetic Retinopathy of type 1 Diabetes but not Diabetic Retinopathy of type 2 Diabetes(Meta-Analysis)
Higher expression of PLA2G2A (show PLA2G2A ELISA Kits), PTGS2 (show PTGS2 ELISA Kits), AKR1B1, AKR1C3 (show AKR1C3 ELISA Kits) and ABCC4 (show ABCC4 ELISA Kits) was seen in 22-B endometriosis cells.
Data conclude that AKR1B1 and TM6SF1 may serve as candidate methylation biomarkers for early breast cancer detection.
This gene encodes a member of the aldo/keto reductase superfamily, which consists of more than 40 known enzymes and proteins. This member catalyzes the reduction of a number of aldehydes, including the aldehyde form of glucose, and is thereby implicated in the development of diabetic complications by catalyzing the reduction of glucose to sorbitol. Multiple pseudogenes have been identified for this gene. The nomenclature system used by the HUGO Gene Nomenclature Committee to define human aldo-keto reductase family members is known to differ from that used by the Mouse Genome Informatics database.
aldo-keto reductase family 1, member B1-like
, aldose reductase
, aldo-keto reductase family 1, member B1 (aldose reductase)
, alcohol dehydrogenase
, alcohol dehydrogenase [NADP(+)]
, aldehyde reductase
, aldo-keto reductase family 1 member A1
, aldo-keto reductase family 1, member A4 (aldehyde reductase)
, 3-DG-reducing enzyme
, Lii5-2 CTCL tumor antigen
, aldehyde reductase 1
, aldo-keto reductase family 1 member B1
, low Km aldose reductase
, 20-alpha-hydroxysteroid dehydrogenase
, Aldehyde reductase 1 (low Km aldose reductase) (5.8 kb PstI fragment, probably the functional gene)
, aldo-keto reductase family 1, member B4 (aldose reductase)