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Validated All-in-One™ qPCR Primer for SCARB1(NM_005505.4) Search again
Product ID:
HQP022833
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
CD36L1, CLA-1, CLA1, HDLCQ6, HDLQTL6, SR-BI, SRB1
Gene Description:
scavenger receptor class B member 1
Target Gene Accession:
NM_005505.4(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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Gene References into function
- binding to high density lipoprotein activates endothelial nitric-oxide synthase in a ceramide-dependent manner
- SR-BI is a phagocytosis-inducing PS receptor of Sertoli cells.
- PDZK1 or other PDZ domain proteins may play an important role in regulating SR-BI cell surface expression and hence reverse cholesterol transport.
- SR-BI regulation of cholesteryl ester uptake is affected by binding to APOE in human cells
- EDL mediates both HDL binding and uptake, and the selective uptake of HDL-CE, independently of lipolysis and CLA-1.
- Testosterone up-regulates scavenger receptor BI mRNA in macrophages
- There is an association between HaeIII polymorphism of scavenger receptor class B type I gene and plasma HDL-cholesterol concentration in patients with CAD.
- basal and SR-BI-stimulated free cholesterol efflux to HDL and liposomes and SR-BI-mediated selective uptake of HDL cholesteryl ester are not affected by caveolin-1 expression
- binds and internalizes lipopolysasccharides and lipoproteins and is a orthologue of rodent SR-BI
- carriers of the minority allele, 1/2, of the scavenger receptor class B type I gene are more susceptible to the presence of saturated fatty acids in the diet because of a greater increase in LDL cholesterol
- Transcriptional activation of SR-BI is stimulated by peroxisome proliferator-activated receptor gamma and hepatocyte nuclear factor 4alpha.
- SR-BI gene variation modulates the lipid profile, particularly in type 2 diabetes, contributing to the metabolic abnormalities.
- Genetic variants in the HDL receptor, SR-B1, may be an important determinant of abnormal lipoproteins in women and may confer particular susceptibility to coronary artery disease.
- SR-B1 is required for hepatitis C virus infection of CD81-expressing hepatic cells
- CD36 and SR-BI are receptors for hypochlorite-modified low density lipoprotein
- Polymorphisms of the HDL receptor gene associated with HDL cholesterol levels in diabetic kindred
- human intestine possesses a developmental and regional SR-BI pattern of distribution
- SR-BI-facilitated diffusion is not dependent on pre-beta-high density lipoprotein interaction with human chymase
- SR-BI-mediated cholesteryl ester-selective uptake and efflux of unesterified cholesterol is regulated by HDL
- alternative spliced sr-bI (SR-BII) may influence cellular cholesterol trafficking and homeostasis in a manner that is distinct from SR-BI.
- SR-BI levels in macrophages are responsive to changes in intracellular sterol content and that these sterol-associated changes are not mediated by LXR and are unlikely to be mediated by an SREBP pathway
- plays a major role in the clearance of apoptotic cells from the thymus.
- The reciprocal inhibition of SR-BI and ABCA1 by BLT-4 and glyburide raises the possibility that these proteins may share similar or common steps in their mechanisms of lipid transport.
- Scavenger receptor BI function is not only crucial for cholesterol delivery to the liver but is also important for cholesterol efflux at the vessel wall [review].
- SR-BI is associated with membrane rafts devoid of caveolin and its expression affects intracellular lipid binding and lipid sensor proteins in HepG2 cells
- uptake of lipoprotein-associated phosphatidylcholine by the cerebrovasculature via scavenger receptor class B, type I could generate a pool of lipids
- endogenous expression of SR-BI/CLA-1 was suppressed by exposure to growth hormone or IGF-I in cultured HepG2 cells
- SR-B1 is not required for apolipoprotein A-1-mediated endothelial cholesterol efflux from vascular endothelial cells.
- analysis of uptake of individual HDL particles in living cells via the scavenger receptor class B type I
- SR-BI plays a key role in SAA metabolism through its ability to interact with and internalize SAA and SAA influences HDL cholesterol metabolism through its inhibitory effects on SR-BI-mediated selective lipid uptake
- CLA-1 functions as an endocytic SAA receptor and is involved in SAA-mediated cell signaling events associated with the immune-related and inflammatory effects of SAA
- HDL-mediated enhancement of HCVpp entry involves a complex interplay between SR-BI, HDL, and HCV envelope glycoproteins
- plausible genetic interaction between the CLA-1 exon 8 gene polymorphism and the risk of coroanry heart disease in males
- at low levels of high density lipoproteins, oxidative stress causes the relocation of eNOS away from caveolae, which turns on SR-BI-induced apoptosis and rapidly clears damaged cells to prevent further inflammatory damage to neighboring cells
- SR-BI is expressed in a cell-specific fashion in the initial & terminal steps of reverse cholesterol transport. It may be physiologically relevant and have distinct tissue-specific functions.
- SR-BI is expressed in a cell-specific fashion in the initial & terminal steps of reverse cholesterol transport. It may be physiologically relevant and have distinct tissue-specific functions.
- Serum amyloid A has a role in promoting cholesterol efflux mediated by scavenger receptor B-I
- SR-BI-mediated supply of cholesterol, the substrate for bile acid synthesis.
- only lipid-bound apoE promotes SR-BI-mediated cholesterol efflux and that the amino-terminal region of residues 1-165 of apoE is sufficient for both receptor binding and cholesterol efflux
- vitamin E intestinal absorption is, at least in part, mediated by SR-BI
- phospholipid-containing particles mediate SR-BI efflux
- The association of HCV with ApoB-containing lipoproteins may promote cellular uptake of this virus in the presence of neutralizing antibodies.
- SR-BI-mediated HDL endocytosis leads to HDL resecretion facilitating cholesterol efflux
- SR-BI prevents NO-induced cytotoxicity when transected into CHO cells.
- Subjects with low SR-BI expression had lower baseline and peak E2 levels and lower number of retrieved and fertilized oocytes.
- HDL interaction with the scavenger receptor BI (SR-BI), a proposed cell entry co-factor of HCV and a receptor mediating lipid transfer with HDL, strongly reduces neutralization of HCV
- The results suggest that the increase in SR-BI -mediated cellular cholesterol efflux and antioxidant capacity in the sera of glycogen storage disease type Ia patients may contribute to protection against premature atherosclerosis.
- PI3K activation stimulates hepatic SR-BI function post-translationally by regulating the subcellular localization of SR-BI in a P13K-dependent manner.
- COX-independent effects of aspirin were able to enhance expression of SR-BI in macrophages in a post-transcriptional, PPAR-alpha independent way.
- SR-BI-independent mechanisms mediate selective cholesterol ester uptake and cholesterol removal
- SR-BI transcytosis is regulated by cholesterol and SR-BI has a stationary function on the bile canaliculus
- Scavenger receptors SR-BI and SR-BII localized mainly to the ganglion cell layer and photoreceptor outer segments; in the latter they appear to be associated with microtubules.
- HCV soluble E2 can interact with human SR-BI and SR-BII
- LDL particles are heterogeneous in their capacity to promote Cla-1-mediated cholesterol efflux. Relative to HDL(2), large buoyant LDL may constitute physiologically-relevant acceptors for cholesterol efflux via Cla-1.
- Results show that SR-B1 mRNA expression increased in response to dexamethasone in primary rat hepatocytes however, the effect was absent or inhibitory in human HepG2 cells and THP-1 macrophages due to low glucocorticoid receptor levels.
- A stable HepG2 tumor cell line was used to establish a specific CLA-1 gene expression assay in a 96-well microplate format.
- the c.1119C>T polymorphism is associated with a lower postprandial triglyceride response in the smaller, partially catabolized lipoprotein fraction
- These results indicate that the phosphatidylinositol 3-kinase/Akt/FoxO1 pathway participates in Ang II suppression of hSR-BI/CLA-1 expression and suggests that the endothelial receptor for hSR-BI/CLA-1 is downregulated by the renin-angiotensin system.
- SCARB1 SNPs influence HDL-C levels in women, particularly in those less than 50 years old.
- These results demonstrate that scavenger class B type 1 receptor (SR-B1) is essential for infection with hepatitis C virus (HCV) produced in vitro and in vivo and suggest the possible use of anti-SR-B1 antibodies as therapeutic agents.
- Our data suggest that the LDLr plays a role in regulating cholesterol delivered to the baby from the placenta.
- SCARB1 polymorphisms not only show associations with plasma levels of total and low-density lipoprotein cholesterol, respectively, but also with the risk for peripheral arterial disease
- Regulation of alternative splicing of liver scavenger receptor class B gene by estrogen.
- scavenger receptor class B, type I and the low-density lipoprotein receptor have roles in High-density lipoprotein-associated 17beta-estradiol fatty acyl ester uptake
- inhibition of hepatic SR-BI expression under high-glucose conditions may provide a mechanism for accelerated atherosclerosis in diabetics
- Bile supersaturation in cholesterol, a prerequisite for gallstone formation, may originate from a hepatic scavenger receptor class B type I (SR-BI)-mediated pathway.
- These results demonstrate the first evidence that the ligand activity of the advanced glycation end-products (AGE)-proteins to the scavenger receptors and its pharmacokinetic properties depend on their rate of modification by AGEs.
- in women, SR-BI-mediated cellular free cholesterol efflux was significantly correlated with plasma HDL-C, whereas this relationship was not observed in men.
- SR-BI plays a crucial role in mediating the first steps of hepatitis C virus-dendritic cell interaction and represents a cell surface receptor for HCV entry into dendritic cells.
- oxPC(CD36) prevent binding to SR-BI of its physiological ligand, high density lipoprotein, because of the close proximity of the binding sites for these two ligands on SR-BI
- SR-BI expression leveles were not regulated by bile acids in this study
- Established a mouse model to study human reverse cholesterol transport by expressing CLA-1, human PDZK1, and human apoA-I gene.
- RPE cells preferentially take up xanthophylls versus carotene by a process that appears to be entirely SR-BI-dependent for ZEA & partly so for beta-C. This mechanism may explain, in part, preferential accumulation of xanthophylls in macula of the retina.
- This study provides new insights into the mechanism of SR-B splicing.
- No associations between fasting glucose, hemoglobin A(1c), plasma lipids, or oxLDL and the expression of ABCG1, ABCA1, or SR-BI were found in diabetic patients.
- the present data show that lycopene absorption is, at least in part, mediated by SR-BI but not by Niemann-Pick disease type C1, in human intestinal cells and mice.
- Silencing of liver SR-BI expression in mice and inhibition of SR-BI activity in human hepatocytes reduced infection by Plasmodium.
- SR-BI significantly boosts hepatocyte permissiveness to Plasmodium entry and promotes parasite development.
- mutation of E2 at position 451 alters the relationship between particle density and infectivity, disrupts coreceptor dependence, and increases virion sensitivity to receptor mimics and neutralizing antibodies
- we propose endothelial SR-BI as a key molecule by which statins exhibit pleiotropic or anti-inflammatory actions.
- SRBI also plays an essential role in HCV entry into primary human hepatocytes.
- SR-BI, although an important cell surface molecule for HCV infection, its presence is insufficient for HCV entry.
- Hepatitis C infections can be blocked by specific antibodies against scavenger receptor class B type I in a dose-dependent manner.