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Validated All-in-One™ qPCR Primer for AKR1B1(NM_001628.3) Search again
Product ID:
HQP005861
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
ADR, ALDR1, ALR2, AR
Gene Description:
aldo-keto reductase family 1 member B
Target Gene Accession:
NM_001628.3(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
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| A | B |
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Each All-in-One™ qPCR Primer is experimentally validated to yield a single dissociation curve peak and to generate a single amplification of the correct size for the targeted gene. A cDNA Pool, containing reverse transcript products of 8 different human tissue total RNA(Liver, Testis,Muscle,Thyroid,Brain,Spleen,Stomach,Small Intestine)),was used as the qPCR validation template. qPCR was performed using 0.2 µM primer with 2XAll-in-One™ qPCR Mix (Catalog#: QP001,QP002,QP004,QP005). Reactions were incubated for 10min. at 95°C, followed by 40 cycles of 95°C for 10 sec.; 60°C, 20 sec. and 72°C, 15sec. using Bio-Rad iQ5™ Instrument. At the end of the last cycle, temperature was increased from 72 to 95°C to produce a melting curve. Panel A: Validated Result for Amplification Curve; Panel B: Validated Result for Melting Curve. |
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Summary
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. [provided by RefSeq].
Gene References into function
- X-ray structure of human aldose reductase holoenzyme in complex with statil determined at a resolution of 2.1 A
- Polymorphisms in aldose reductase is associated with those diabetic retinopathy patients who had proliferative retinopathy and maculopathy
- AKR1B1 and CTSH may be good markers for prediction of sensitivity to certain drugs
- polymorphic in diabetic nephropathy and retinopathy in type 2 diabetes
- polymorphic in diabetic nephropathy and in retinopathy in type 2 diabetes
- crystal structure analysis and molecular dynamics simulations
- expression of cAMP-regulated AKR1B1 is decreased in adrenocortical cancer.
- AR is a critical regulator of TNF-alpha-induced apoptotic signaling in endothelial cells
- The C-106T polymorphism of the aldose reductase gene may contribute to an early development of neurophysiologic deterioration in type 2 diabetic patients.
- Transgenic mice broadly overexpressing human aldose reductase show that AR plays a key role in ischemic injury and impairment of functional and metabolic recovery after ischemia.
- AR is an obligatory mediator of TNF-alpha signaling leading to an increase in the expression of adhesion molecules and increased binding of monocytes to the endothelium.
- C-106T polymorphism in the AR gene is a risk factor for development of diabetic nephropathy in type 2 diabetes in patients with poor glycaemic control
- AKR1B1 polymorphisms were strongly associated with the rate of functional decline of diabetic complications.
- AR is an obligatory mediator of growth factor-induced up-regulation of COX-2, PGE2, and growth of Caco-2 colon cancer cells.
- Two X-ray data sets for a complex of human aldose reductase (h-AR) with the inhibitor IDD 594 and the cofactor NADP(+) were collected from two different parts of the same crystal to a resolution of 0.81 A at 15 and 60 K using cold helium gas as cryogen.
- Expression of AKR1B1 was significantly decreased in PD cases.
- A novel binding site conformation has been identified in a region of ALR2 where previous complex structures suggested only low adaptability of the binding pocket.
- Aldose reductase acceleration may affect the peritoneum in nondiabetic patients undergoing peritoneal dialysis via carbonyl and oxidative stress.
- Aldose reductase gene was identified in the genome-wide loss-of-function genetic screen as putative tumor suppressor located at 7q35.
- Levels of ALR2 activity as well as sorbitol in erythrocytes may have value as a quantitative trait to be included among other markers to establish a risk profile for development of diabetic retinopathy.
- Meta-analysis study shows the correlation between the (AC)n dinucleotide repeat polymorphism at the 5' end and the occurrence of diabetic nephropathy in type 1 diabetic subjects in contrast to type 2 diabetic subjects, in which there was no association.
- oxLDL-induced upregulation of aldose reductase in human macrophages is proinflammatory in foam cells and may represent a potential link among hyperlipidemia, atherosclerosis, and diabetes mellitus.
- the binding site residues deviating between ALR1 and ALR2 influence ligand affinity in a complex interplay, presumably involving changes of dynamic properties and differences of the solvation/desolvation balance upon ligand binding
- Genetic polymorphisms of ALR2 independently predicted new onset of renal and cardiorenal end points, with the latter being largely mediated through renal disease in Chinese type 2 diabetic patients.