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Human Polyclonal AKR1B1 Primary Antibody for IHC (p), ELISA - ABIN543543
Steuber, Heine, Podjarny, Klebe: Merging the binding sites of aldose and aldehyde reductase for detection of inhibitor selectivity-determining features. in Journal of molecular biology 2008
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Human Polyclonal AKR1B1 Primary Antibody for ELISA, WB - ABIN543544
Grundmann, Bohn, Obermeier, Amann: Cloning and prokaryotic expression of a biologically active human placental aldose reductase. in DNA and cell biology 1990
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Human Polyclonal AKR1B1 Primary Antibody for IF, IHC (p) - ABIN389205
Gleissner, Sanders, Nadler, Ley: Upregulation of aldose reductase during foam cell formation as possible link among diabetes, hyperlipidemia, and atherosclerosis. in Arteriosclerosis, thrombosis, and vascular biology 2008
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Human Monoclonal AKR1B1 Primary Antibody for IHC (p), ELISA - ABIN513262
Ebert, Kisiela, Wsól, Maser: Proteasome inhibitors MG-132 and bortezomib induce AKR1C1, AKR1C3, AKR1B1, and AKR1B10 in human colon cancer cell lines SW-480 and HT-29. in Chemico-biological interactions 2011
Human Polyclonal AKR1B1 Primary Antibody for IF, IHC - ABIN6713052
Zeng, Li, Dong, Wang, Ma, Jiang, Jin, Tu: Anti-neuroinflammatory efficacy of the aldose reductase inhibitor FMHM via phospholipase C/protein kinase C-dependent NF-κB and MAPK pathways. in Toxicology and applied pharmacology 2014
Human Polyclonal AKR1B1 Primary Antibody for WB - ABIN513260
Hernández-Ochoa, Robison, Contreras, Shen, Zhao, Schneider: Elevated extracellular glucose and uncontrolled type 1 diabetes enhance NFAT5 signaling and disrupt the transverse tubular network in mouse skeletal muscle. in Experimental biology and medicine (Maywood, N.J.) 2012
Mouse (Murine) Polyclonal AKR1B1 Primary Antibody for IHC, WB - ABIN3022391
Yang, Lu, Yu, Sun, Guo, Li, Guan: Quantitative Analysis of Differential Proteome Expression in Epithelial-to-Mesenchymal Transition of Bladder Epithelial Cells Using SILAC Method. in Molecules (Basel, Switzerland) 2016
Here, we show that treatment of colorectal cancer (CRC) cells with fidarestat increases the efficacy of doxorubicin (DOX)-induced death in HT-29 and SW480 cells and in nude mice xenografts. Aldose reductase inhibition also results in higher intracellular accumulation of DOX and decreases the expression of drug transporter proteins MDR1, MRP1, and ABCG2.
AKR1B1 rs759853 polymorphism had no association with diabetic retinopathy (DR) risk under all genetic models. However, after subgroup analysis by diabetes mellitus; type, the rs759853 polymorphism was a protective factor against the DR onset in patients with type 1 diabetes mellitus; Subgroup analysis by genotyping method suggested that rs759853 was significantly correlated with decreased risk of DR under dominate model
A combined gene expression signature of AKR1B10 (low) and AKR1B1 (high) showed a better prognostic stratification of CRC patients independent of confounding factors.
Data show that cells with higher levels of aldo-keto reductases AKR1B1 and/or AKR1B10 (AKR1Bs) were more sensitive to 2-deoxyglucose (2DG).
genetic association studies in population in north India: Data suggest that an SNP in promoter region of aldose reductase (C-106T) is associated with peripheral neuropathy in patients with type 2 diabetes mellitus in the population studied.
Under hyperglycemic conditions, aldose reductase (AR)-mediated sorbitol formation and associated rise in cell volume, which subsequently results in platelet hyperactivation, occur.
In the Eastern Asians with type 2 diabetes mellitus, the AR gene C-106T gene polymorphism is correlated with an increased risk of diabetic nephropathy; the Eastern Asians with the T allele of AR gene C-106T gene polymorphism might be susceptible to DN
An meta-analysis showed that aldose reductase C-106T variants appear to influence the risk for diabetic retinopathy in Chinese Han persons (meta-analysis).
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).
inhibiting AR or degrading H2O2 could protect endothelial function and maintain the antioxidant activities of uric acid.
Result indicate that the differential scanning fluorimetry (DSF) method is useful for enzyme inhibitor drug screening for the AKR superfamily, including AKR1B10 and a structurally similar isoform AKR1B1.
The hyperosmotic AR gene expression was dependent on activation of metalloproteinases, autocrine/paracrine TGF-beta signaling, activation of p38 MAPK, ERK1/2, and PI3K signal transduction pathways, and the transcriptional activity of NFAT5.
Aberrant DNA methylation 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
mRNA expression in macrophages correlates positively with M1 polarization, and depends on hyperglycemia
Meta-analysis shows that the AR rs759853 polymorphism may correlate with the susceptibility of DN. However, data do not support the association between this DNA variation and the progression of DN.
ALR C(-106)T polymorphism was not associated with an increased risk of Diabetic Retinopathy; subgroup analysis showed a genetic association between ALR 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, PTGS2, AKR1B1, AKR1C3 and ABCC4 was seen in 22-B endometriosis cells.
Data conclude that AKR1B1 and TM6SF1 may serve as candidate methylation biomarkers for early breast cancer detection.
L-idose is the best alternative to D-glucose in studies on aldose reductase.
prostaglandin F synthase activity of human and bovine aldo-keto reductases
is most likely the enzyme responsible for the production of prostaglandin f2 alpha in the bovine endometrium
crystal structure analysis and molecular dynamics simulations
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.
Lii5-2 CTCL tumor antigen
, aldehyde reductase 1
, aldo-keto reductase family 1 member B1
, aldose reductase
, low Km aldose reductase
, 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)
, 20-alpha-hydroxysteroid dehydrogenase
, aldehyde reductase
, aldo-keto reductase family 1, member B1 (aldose reductase)