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Human Polyclonal AKR1B1 Primary Antibody für 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
Human Monoclonal AKR1B1 Primary Antibody für 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 für IF, IHC (p) - ABIN389205
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
Show all 3 Pubmed References
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 (zeige AKR1B10 Antikörper) (low) and AKR1B1 (high) showed a better prognostic stratification of CRC (zeige CALR Antikörper) patients independent of confounding factors.
Data show that cells with higher levels of aldo-keto reductases AKR1B1 and/or AKR1B10 (zeige AKR1B10 Antikörper) (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.
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).
Result indicate that the differential scanning fluorimetry (DSF) method is useful for enzyme inhibitor drug screening for the AKR superfamily, including AKR1B10 (zeige AKR1B10 Antikörper) and a structurally similar isoform AKR1B1.
The hyperosmotic AR gene expression was dependent on activation of metalloproteinases, autocrine/paracrine TGF-beta (zeige TGFB1 Antikörper) signaling, activation of p38 MAPK (zeige MAPK14 Antikörper), ERK1/2, and PI3K (zeige PIK3CA Antikörper) signal transduction pathways, and the transcriptional activity of NFAT5 (zeige NFAT5 Antikörper).
Aberrant DNA methylation (zeige HELLS Antikörper) of AKR1B1 could be potential screening markers of colorectal cancer.
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 (zeige TP53 Antikörper).
Data indicate that inhibition of AR alleviates the MCD (zeige MLYCD Antikörper) diet-induced liver inflammation and fibrosis in db/db (zeige LEPR Antikörper) mice, probably through dampening CYP2E1 (zeige CYP2E1 Antikörper) mediated-oxidative stress and ameliorating the expression of pro-inflammatory cytokines.
FMHM suppressed the activity of AR-dependent phospholipase C (zeige PLC Antikörper)/protein kinase C (zeige PKC Antikörper) signaling, which further resulted in downstream inactivation of the IkappaB kinase (zeige CHUK Antikörper)/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-induced Smad-independent and PI3K/AKT/GSK3beta-dependent pathway.
BGG-mediated inhibition of aldose reductase prevented LPS (zeige TLR4 Antikörper)-induced activation of JNK (zeige MAPK8 Antikörper).
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
a Y48F/H110F double mutant of AKR1B3 completely lost PGDS (zeige PTGDS Antikörper) activity and showed only 2.9% of PGFS (zeige AKR1C3 Antikörper) activity
Sequential catalysis of Aldr1 by glutathione S-transferase P (zeige GSTP1 Antikörper) and glutaredoxin (zeige GRX1 Antikörper) may be a general redox switching mechanism that regulates the reduction of protein sulfenic acids to cysteines regulates the reduction of protein sulfenic acids to cysteines
L-idose is the best alternative to D-glucose in studies on aldose reductase.
prostaglandin F synthase (zeige AKR1C3 Antikörper) activity of human and bovine aldo-keto reductases
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
, aldo-keto reductase family 1, member B1 (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