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Validated All-in-One™ qPCR Primer for HMGCR(NM_000859.2) Search again
Product ID:
HQP100217
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
LDLCQ3, LGMDR28, MYPLG
Gene Description:
3-hydroxy-3-methylglutaryl-CoA reductase
Target Gene Accession:
NM_000859.2(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
HMG-CoA reductase is the rate-limiting enzyme for cholesterol synthesis and is regulated via a negative feedback mechanism mediated by sterols and non-sterol metabolites derived from mevalonate, the product of the reaction catalyzed by reductase. Normally in mammalian cells this enzyme is suppressed by cholesterol derived from the internalization and degradation of low density lipoprotein (LDL) via the LDL receptor. Competitive inhibitors of the reductase induce the expression of LDL receptors in the liver, which in turn increases the catabolism of plasma LDL and lowers the plasma concentration of cholesterol, an important determinant of atherosclerosis. Alternatively spliced transcript variants encoding different isoforms have been found for this gene.
Gene References into function
- Mevastatin inhibition of HMG-CoA reductase attenuates VCAM-1 expression in umbilical vein endothelial cells, but increases E-selectin expression, after TNF-alpha induction.
- characterization of the coordinated regulation of cholesterol metabolism in human liver; regulation of its mRNA in liver
- regulation of isoprenoid/cholesterol biosynthesis in cells from mevalonate kinase-deficient patients by presence of this enzyme
- HMG-CoA inhibition with cerivastatin reduced vascular smooth muscle cells proliferation and C5b-9-induced ERK1/2 activation
- 3-hydroxy-3-methylglutaryl-CoA reductase is ubiquinated in permeabilized cells mediated by cytosolic E1 and a putative membrane-bound ubiquitin ligase
- The present study demonstrated that both SOD1 and the metal-free form of enzyme (Apo SOD1) inhibit HMG-CoA reductase gene expression in HepG2 cells, in normal human fibroblasts, and in fibroblasts of subjects affected by familiar hypercholesterolemia
- Competitive inhibitors of the reductase induce the expression of LDL receptors in the liver, which in turn increases the catabolism of plasma LDL and lowers the plasma concentration of cholesterol, an important determinant of atherosclerosis.
- data indicate that buildup of cholesterol synthesis intermediates represses the pathway selectively at HMGCR and reveal a previously unappreciated link between feedback inhibition of HMGCR and carbon flow through the cholesterol synthetic pathway.
- polymorphism of the HMGCR gene appears to be linked to both Alzheimer's risk and disease progression
- In Schwann cells neuregulin-1 increases the transcription of the 3-hydroxy-3-methylglutarylcoenzyme A reductase, the rate-limiting enzyme for cholesterol biosynthesis.
- These results suggest that the HMGCR gene may serve as a modifier gene for hypercholesterolemia in Chinese diabetic patients.
- The roles of sterol regulatory element-binding protein (SREBP)-dependent gene expression, side chain oxysterol biosynthesis, and cholesterol precursors in the short term regulation of endoplasmic reticulum cholesterol level and HMGR activity, is examined
- acute myocardial infarction from information on functional gene variants that favor inflammation or modulate cholesterol metabolism: IL6 -174 G/C, TNF -308 G/A, IL10 -1082 G/A, SERPINA3 -51 G/T, IFNG +874 T/A, HMGCR -911 C/A, and APOE epsilon2/3/4
- snp and the common haplotypes inferred from them were tested for association with plasma LDL-C and LDL-C response to simvastatin in blacks and whites. Black carriers of H7 and/or H2 had lower baseline LDL-C and significantly attenuated LDL-C response
- HIF-1alpha accumulation is able to increase level and activity of HMG-CoAR by stimulating its transcription
- a common HMGCR SNP located within intron 13 was associated with variation in the proportion of HMGCR mRNA that is alternatively spliced
- Identified variants in HMGCR that are associated with LDL-cholesterol across populations and affect alternative splicing of HMGCR exon13.
- Expression of the HMGCR gene was up-regulated by lovastatin (P < .001) but not red yeast rice in both LNCaP and LNCaP-AR cells (LNCaP human PCa cell lines).
- ACBP is a transcriptional regulator of the HMGCS1 and HMGCR genes encoding rate-limiting enzymes of cholesterol synthesis pathway.