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Validated All-in-One™ qPCR Primer for AKR1C1(NM_001353.5) Search again
Product ID:
HQP117879
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
2-ALPHA-HSD, 20-ALPHA-HSD, C9, DD1, DD1/DD2, DDH, DDH1, H-37, HAKRC, HBAB, MBAB
Gene Description:
aldo-keto reductase family 1 member C1
Target Gene Accession:
NM_001353.5(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. These enzymes catalyze the conversion of aldehydes and ketones to their corresponding alcohols by utilizing NADH and/or NADPH as cofactors. The enzymes display overlapping but distinct substrate specificity. This enzyme catalyzes the reaction of progesterone to the inactive form 20-alpha-hydroxy-progesterone.
Gene References into function
- Expression of dihydrodiol dehydrogenase in the resected stage I non-small cell lung cancer
- Reduction of dihydrodiol dehydrogenase expression is associated with resected hepatocellular carcinoma
- progesterone itself contributes to the regulation of local progesterone concentration through 20alpha-HSD levels in endometrial stromal cells at peri-implantation periods.
- X ray diffraction and site-directed mutagenesis: identification of an alternative binding site for C21-steroids
- Glaucomatous optic nerve head astrocytes express a higher level of 3 alpha-HSD isoform AKR1C1 and its mRNA than normal astrocytes.
- Expression of SRD5A1 (5alphaR1) and SRD5A2 (5alphaR2) is elevated, and expression of AKR1C1 (20alpha-HSO), AKR1C2 (3alpha-HSO3) and AKR1C3 (3alpha-HSO2) is reduced in tumorous as compared to normal breast tissue.
- Loss of AKR1C1 and AKR1C2 in breast cancer results in decreased progesterone catabolism, which, in combination with increased PR expression, may augment progesterone signaling by its nuclear receptors.
- mRNA abundance and activity of AKR1C enzymes in abdominal adipose tissue are positive correlates of adiposity in women. Increased progesterone and/or dihydrotestosterone reduction in abdominal adipose tissue may impact fat cell metabolism.
- The expression of AKR1C1 and AKR1C3 in endometrial cancer will govern the ratio of P:E2.
- DDH may play important roles in tumor progression of squamous cell carcinoma via induction of apoptosis- and drug-resistance
- Activity of AKR1C1 in overall oracin reduction was one order of magnitude higher compared to AKR1C2 and 1C4.
- Carbonyl reductase-1 (CBR1), microsomal prostaglandin E synthase-1 and 2 (mPGES-1, mPGES-2), cytosolic prostaglandin E synthase (cPGES), aldoketoreductase (AKR1C1) and prostaglandin F synthase (AKR1C3) were all expressed in hair follicles.
- Carbonyl reductase-1 (CBR1), microsomal prostaglandin E synthase-1 and 2 (mPGES-1, mPGES-2), cytosolic prostaglandin E synthase (cPGES), the aldoketoreductase AKR1C1 and the prostaglandin F synthase AKR1C3 were all expressed in hair follicles.
- Overexpression of AKR1C1 counteracted the S-phase accumulation of cells and apoptosis caused by MTX treatment. This suggests a role of AKR1C1 in cell proliferation.
- Incubations of normal human bronchial epithelial cells with individual heavy metals showed that the upregulation of AKR1C1 and AKR1C2 was predominantly caused by lead.