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SCARB1 gene variants are associated with a new lipid phenotype, characterized by high levels of both HDL (show HSD11B1 Proteins) cholesterol and Lp(a (show APOA Proteins)). SCARB1 exonic variants often result in diminished function of translated SR-B1 via reduced binding/intracellular transport of Lp(a (show APOA Proteins)).
Data suggest that activation of SR-BI by APOAI down-regulates sphingosine 1-phosphate/S1PR2 (show S1PR2 Proteins)-mediated inflammation in vascular endothelial cells by activating the PI3K (show PIK3CA Proteins)/Akt (show AKT1 Proteins) signaling pathway; oxidized-LDL does the opposite. (APOA1 (show APOA1 Proteins) = apolipoprotein A-I (show APOA1 Proteins); SR-BI/SCARB1 = scavenger receptor class B type I; S1PR2 (show S1PR2 Proteins) = sphingosine 1-phosphate receptor 2 (show S1PR2 Proteins); PI3K (show PIK3CA Proteins) = phosphatidylinositol 3-kinase; Akt (show AKT1 Proteins) = proto-oncogene c-akt (show AKT1 Proteins))
Sustained virologic response was significantly associated with SCARB1 rs10846744 in chronic hepatitis C patients, treated with pegylated interferon-alpha (show IFNA Proteins) and ribavirin.
Model recombinant HDL (show HSD11B1 Proteins) (rHDL) particles formed in vitro with S1P (show MBTPS1 Proteins) incorporated into the particle initiated the internalization of S1PR1 (show S1PR1 Proteins), whereas rHDL without supplemented S1P (show MBTPS1 Proteins) did not, suggesting that S1P (show MBTPS1 Proteins) transported in HDL (show HSD11B1 Proteins) can selectively activate S1PR1 (show S1PR1 Proteins).
Data implicate that scavenger receptor class B member 1 (SR-B1) as a target in chronic lymphocytic leukemia (CLL) and high-density lipoproteins nanoparticles (HDL (show HSD11B1 Proteins) NPs (show NPS Proteins)) as targeted monotherapy for CLL.
SCARB1 gene polymorphisms may contribute to genetic susceptibility to coronary heart disease. C allele of rs10846744 and the C allele of rs2278986 may serve as risk and protective factors for CHD (show CHDH Proteins), respectively.
VEGF-A (show VEGFA Proteins) was found to be a prerequisite for the localization of scavenger receptor BI in the plasma membrane of endothelial cells and is a regulatory factor of transendothelial transport of HDL (show HSD11B1 Proteins) but not LDL.
our findings implied that scavenger receptor class B type 1 might serve as a diagnostic and independent prognostic biomarker in clear cell renal cell carcinoma (show MOK Proteins).
data support an SR-B1 nibbling mechanism that is similar to that of streptococcal serum opacity factor, which also selectively removes CE and releases apoAI, leaving an apoAII (show APOA2 Proteins)-rich remnant.
Using mass spectrometry and site directed mutagenesis, a new Sp1 (show PSG1 Proteins) phosphorylation site Ser702 was defined to be associated with Sp1 (show PSG1 Proteins)-HDAC1 (show HDAC1 Proteins) interaction and may be important in SR-BI activation, shedding light on the knowledge of delicate mechanism of hepatic HDL (show HSD11B1 Proteins) receptor SR-BI gene modulation by LDL.
Our results suggest that LPA-enhanced foam cell formation is mediated by LPA1 (show LPAR1 Proteins)/3 -AKT (show AKT1 Proteins) activation and subsequent SRBI expression.
Results show the first high-resolution structure of the C-terminal transmembrane domain of SR-BI. This region of SR-BI harbors a leucine zipper dimerization motif, which when mutated impairs the ability of the receptor to bind HDL (show HSD11B1 Proteins) and mediate cholesterol delivery.
Carboxy-terminal deletion of SR-BI reduced receptor levels in liver and steroidogenic tissues (adrenal cortex, ovary, testicular Leydig cells) and induced hypercholesterolemia.
Loss of ScarB1 is associated with Coronary Atherosclerosis and Ischemic Heart Disease in Low-density Lipoprotein Receptor (show LDLR Proteins) Knockout Mice when fed the modified western-type diet.
We showed here that SR-BI deficiency led to increased atherogenesis with features of advanced fibroatheroma and expansive arterial remodeling in LDL-R KO mice fed an atherogenic diet.
The seven intron CGIs are methylated differentially in Y1 cells, mouse Leydig tumor cells, ovarian granulosa cells, and mouse liver hepa 1-6 cells; experiments raised the possibility that DNA methylation (show HELLS Proteins) participates in hormonal regulation of SR-BI expression in a tissue-specific manner.
SR-B1, the HDL (show HSD11B1 Proteins) receptor, is expressed abundantly in liver sinusoidal endothelial cells and marginally in hepatocytes.
SR-B1 and targeted HDL (show HSD11B1 Proteins) NPs (show NPS Proteins) provide a fundamental advance in studying cholesterol-dependent cellular uptake mechanisms.
Studied the role of SR-BI in endothelial cells using several novel transgenic mouse models expressing SR-BI in endothelium of mice with normal C57Bl6/N, apoE (show APOE Proteins)-KO, or Scarb1-KO backgrounds.
Luteinization causes upregulation of SR-BI expression, its posttranslational maturation by glycosylation, and insertion into luteal cell membranes.
Aortic endothelial cells transcytose high-density lipoproteins by mechanisms that involve either SR-BI or ABCG1 (show ABCG1 Proteins) but not ABCA1 (show ABCA1 Proteins).
The protein encoded by this gene is a plasma membrane receptor for high density lipoprotein cholesterol (HDL). The encoded protein mediates cholesterol transfer to and from HDL. In addition, this protein is a receptor for hepatitis C virus glycoprotein E2. Two transcript variants encoding different isoforms have been found for this gene.
scavenger receptor class B member 1
, scavenger receptor class B, member 1
, scavenger receptor class B type I
, high density lipoprotein receptor SR-BI
, CD36 and LIMPII analogous 1
, CD36 antigen (collagen type I receptor, thrombospondin receptor)-like 1
, scavenger receptor class B type III
, HDL QTL 1
, scavenger receptor class B1
, CD36 antigen (collagen type I receptor thrombospondin receptor)-like 1 (scavanger receptor class B type 1)
, scavanger receptor class B type 1
, CD36 antigen (collagen type I receptor, thrombospondin receptor-like 1)