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Validated All-in-One™ qPCR Primer for SREBF2(NM_004599.3) Search again
Product ID:
HQP017705
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
SREBP-2, SREBP2, bHLHd2
Gene Description:
sterol regulatory element binding transcription factor 2
Target Gene Accession:
NM_004599.3(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 ubiquitously expressed transcription factor that controls cholesterol homeostasis by stimulating transcription of sterol-regulated genes. The encoded protein contains a basic helix-loop-helix-leucine zipper (bHLH-Zip) domain.
Gene References into function
- a common variation in the SREBP-2 gene is related with early-stage carotid atherosclerosis in subjects with a risk of cardiovascular events without detectable change in plasma lipid levels
- Transport from endoplasmic reticulum to Golgi apparatus is sterol regulated and requires co-expression of SCAP and Insigs.
- Sterol regulatory element-binding protein-2 interacts with hepatocyte nuclear factor-4 to enhance sterol isomerase gene expression in hepatocytes
- Simvastatin increased nuclear factors, notably sterol regulatory element-binding protein-2, capable of binding to the paraoxonase promoter.
- results show the crystal structure of importin-beta complexed with the active form of SREBP-2
- The lipogenic effect of SREBP2(N) in liver cells was suppressed by ATF6(N).
- activation of Erk-MAPK pathways by hormones such as insulin might be related to a novel regulatory principle of SREBP-2
- High levels of SREBP-2 protein is associted with during prostate cancer progression to androgen independence
- nSREBPs are essential for high levels of lipid synthesis in the liver and indicate that Insig's modulate nSREBP levels by binding and retaining SCAP in the ER.
- SREBP2 down-regulates ATP-binding cassette transporter A1 in vascular endothelial cells
- EC nuclei showed strong SREBP staining in human atherosclerotic lesions, suggesting a role for SREBP. Endothelial cholesterol depletion & SREBP activation play a role in inflammatory processes in which phospholipid oxidation products accumulate.
- the SREBP-2 polymorphism is related to elevated concentrations of serum TC and LDL-C in hypercholesterolemic subjects
- the opposite regulation of hepatic lipase expression by fatty acids and statins is mediated via SREBP, possibly through interaction with upstream stimulatory factors
- SREBP-2 homodimers and heterodimers localize in the nucleus and activate transcription.
- Variants of SREBF2 might be genetic factors involved in the pathogenesis of vascular dementia.
- Phagocytosis triggered the proteolytic activation of SREBP-1a and SREBP-2; upon overexpression of these proteins, phagocytosis-induced transcription and lipid synthesis were blocked; SREBPs are essential regulators of membrane biogenesis
- Active SREBP-2 also induced expression of the CASP-2 gene and the caspase-2 protein and increased the cholesterol and triacylglycerol cellular content.
- SREBP2 modulates brain palmitoyl-coa hydrolase gene transcription.
- A possible gene-gene interaction between the genes encoding SREBP-2 and SCAP that modulate plasma lipids in a strictly gender-specific fashion.
- Low density lipoproteins stimulate LRP1 transcription and decrease SREBP-2 active form which negatively regulates LRP1 transcription
- The role of SREBP-2 in the regulation of ABCA1 transcription via generation of oxysterol ligands for liver X receptor is reported.
- Modulation of human Niemann-Pick disease, type C1 protein expression and promoter activity by cholesterol in a =sterol regulatory element binding protein-2 dependent mechanism.
- CYP4F2 transcription and that CYP4F2 induction by statins is mediated by SREBP-2.
- SREBP transcription factors play an important role in disturbed lipid metabolism in renal failure.
- The SREBP-2-595A isoform was associated with an increased risk of early-onset myocardial infarction in U.S. men.
- Endoplasmic reticulum stress causes the activation of sterol regulatory element binding protein-2.
- SREBP-2 can transcriptionally activate proprotein convertase subtilisin/kexin type 9 (PCSK9) via the sterol-regulatory element (SRE) in its proximal promoter region in HepG2 cells.
- novel mechanism for flavonoid-induced cytoprotection in SH-SY5Y cells involving SREBP-2-mediated sterol synthesis that decreases lipid peroxidation by maintaining membrane integrity in the presence of oxidative stress.
- Transport of LDL-derived cholesterol from late endosomes/lysosomes to the sterol-regulatory pool is regulated by the NPC1 protein and promotes feedback inhibition of the SREBP pathway.
- Real-time RT-PCR analyses confirmed that exercise-induced muscle damage led to a rapid (3 h) increase in sterol response element binding protein 2 (SREBP-2).
- growth factors inhibit sumoylation of SREBPs through their phosphorylation, thus avoiding the recruitment of an HDAC3 corepressor complex and stimulating the lipid uptake and synthesis required for cell growth.
- Results suggest that AKAP12A may activate SREBP-2 by increasing cholesterol efflux, and is a novel regulator of cellular cholesterol metabolism.
- This study is the first report to evaluate the association between SREBP-2 gene polymorphisms and the susceptibility of avascular necrosis in the Korean population.
- that down regulation of Srebf2 may be the triggering factor for down regulation of the cholesterol biosynthesis pathway
- The cholesterol contant of endoplasmic reticulum exceeds 5% of total endoplasmic reticulum lipids (molar basis), sterol regulatory element binding transcription factor 2 transport is abruptly blocked.
- The individuals carrying the G allele of SREBP-2 have more favorable lipid profiles than those carrying the C allele in Han but not in Hei Yi Zhuang.