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Validated All-in-One™ qPCR Primer for AKR1C3(NM_003739.5) Search again
Product ID:
HQP021385
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
DD3, DDX, HA1753, HAKRB, HAKRe, HSD17B5, PGFS, hluPGFS
Gene Description:
aldo-keto reductase family 1 member C3
Target Gene Accession:
NM_003739.5(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 reduction of prostaglandin (PG) D2, PGH2 and phenanthrenequinone (PQ), and the oxidation of 9alpha,11beta-PGF2 to PGD2. It may play an important role in the pathogenesis of allergic diseases such as asthma, and may also have a role in controlling cell growth and/or differentiation. This gene shares high sequence identity with three other gene members and is clustered with those three genes at chromosome 10p15-p14. [provided by RefSeq].
Gene References into function
- Glaucomatous optic nerve head astrocytes express a higher level of 3 alpha-HSD isoform AKR1C3 and its mRNA than normal astrocytes.
- expression and activity of type 5 17beta-hydroxysteroid dehydrogenase and type 3 3alpha-hydroxysteroid dehydrogenase in female subcutaneous tissue and omental adipose tissue and in preadipocytes
- On the basis of crystal structures, a detailed catalytic mechanism of prostaglandin F synthase is proposed and compared to that of AKR1C1 and AKR1C3.
- Overexpression of hPGFS is associated with primary squamous cell carcinoma of the head and neck and tumour cell lines derived from respiratory and digestive organs
- 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.
- Single nucleotide polymorphism may play a role in the pathogenesis of lung cancer in this population, particularly among heavily exposed women.
- enzyme distribution differs between normal and hormonal dependent malignancies of the breast and prostate
- Members of the Sp family of transcription factors play an important role in regulating constitutive and stimulated expression of the HSD17B5 gene in H295R cells.
- AKR1C3 protects the mineralocorticoid receptor from activation by deoxycorticosterone in mineralocorticoid target cells of the kidney and colon.
- The expression of AKR1C1 and AKR1C3 in endometrial cancer will govern the ratio of P:E2.
- Based on model structures & inhibition, catalytic mechanism of PGH2 9,11-endoperoxide reductase of PGFS is proposed.Formation of PGF(2alpha) from PGH2 may involve hydride transfer from bound NADPH to PGH2 endoperoxide without specific amino acid residues
- Type 5 17beta-HSD (AKR1C3) differs significantly from the type 1 enzyme by possessing a spacious and flexible steroid-binding site.
- Elevated expression of AKR1C3 is highly associated with prostate carcinoma
- Glu77Gly AKR1C3 polymorphism is associated with lower testosterone levels in serum.
- report the clinical history, endocrine evaluation and molecular genetics of a prepubertal girl affected by 17beta-HSD3 deficiency, in whom an erroneous diagnosis of androgen insensitivity syndrome was made
- analysis of human type 5 17beta-hydroxysteroid dehydrogenase conformation and binding to inhibitors
- HSD17B5 single nucleotide polymorphisms predicted to have functional effects do not appear to be a risk factor for precocious pubarche in girls from Barcelona, despite these girls being at high risk of developing androgen excess in adulthood
- 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.
- Polymorphisms in the HSD17B5 gene are not associated with risk of polycystic ovary syndrome or elevated testosterone levels.
- The maternal methylenetetrahydrofolate reductase A1298C polymorphism was found to be an effect modifier of the maternal intron 4 polymorphism of the AKR1C3 gene and the childhood leukemia risk.
- Among gene transcripts elevated in depressed episodes were prostaglandin D synthetase (PTGDS) and prostaglandin D2 11-ketoreductase (AKR1C3), both involved in hibernation. We hypothesized them to account for some of the rapid cycling symptoms.
- A strong immunoreactivity was detected not only in classically hormone-associated tissues such as prostate and testis but also in non-hormone-associated tissues such as kidney and bladder in humans and rats.
- genetic variation in carcinogen-metabolizing genes, particularly AKR1C3, could be associated with bladder cancer risk.
- Data suggest that adipose tissue AKR1C3 expression may be affected by metabolic disease, and its levels are significantly reduced in response to diet-induced weight loss and correlate with leptin levels.
- Higher mRNA levels of enzymes synthesizing and inactivating androgens are found in differentiated adipocytes, consistent with higher androgen-processing rates in these cells.
- 17beta-HSD type 5 was expressed in 56% of breast cancer specimens. decrease in 17beta-HSD type 5 expressions in breast cancer may play a role in the development &/or progression of cancer by modifying the intratumoral levels of estrogens & androgens.