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SCARB1 knockdown decreases MITF expression and extracellular vesicle release in melanoma cells.
miR-24 accelerates atherogenesis by repressing SR-BI-mediated selective lipid uptake from HDL-C.
This study concluded that CD81 and SCARB1 SNPs may serve as powerful predictor factors for treatment responses in CHC patients, and this effect is correlated with serum lipoprotein and FBS levels.
High-density lipoprotein increases expression of SR-B1 in placental cells but also reduces uptake of transthyretin-thyroid hormone through the SR-B1 transporter.
Findings showed that the expression of hSR-B1 was significantly reduced on the surface of platelets from CAD patients with atherosclerotic disease, as compared with healthy controls (6/8% vs. 13/6%) (P < 0,001).
Results provide strong evidence for the association of rs10846744, which resides within an enhancer region, with Lp-PLA2 activity and evidence from a number of large genetic studies for association with cardiovascular disease events.
Results demonstrate that SR-BI is a highly expressed receptor in human metastatic melanoma and is crucial for the maintenance of the metastatic phenotype.
The data obtained showed that not only cigarette, but also the other environmental stressors reduced SR-B1 expression in epidermal cutaneous tissues and that this effect might be involved in impaired wound healing.
Findings suggested that polymorphism rs5888 had negative association with coronary heart disease, especially in male. [review]
We demonstrate that 4F and Cl/NO2-HDL act on scavenger receptor type I (SR-B1) using human aorta endothelial cells (HAEC) and SR-B1 ((-/-)) mouse aortic endothelial cells.
Our results demonstrate that SR-BI functions as an oncogene and promotes progression of clear cell renal cell carcinoma (ccRCC). SR-BI may serve as a potential prognostic biomarker and therapeutic target for ccRCC.
SCARB1 gene polymorphisms may serve as a potential predictor of treatment responses in chronic hepatitis C patients receiving interferon-based therapy
The S112F single amino acid mutation in SR-BI inhibited the infectivity of hepatitis C virus derived from cell culture in a cell culture model by downregulating the expression of the SR-BI protein.
The cell surface receptor SR-BI (scavenger receptor class B member 1), is essential for hepatitis C virus (HCV) entry into hepatocytes. Variations in the gene coding this receptor influence infectivity and viral load. We analyzed these variations to gain a better understanding of inter-individual differences over the course of HCV infection.
The SCARB1AA genotype decreased cardiovascular risk and carrying GA genotype and G allele increased the risk of CAD. AA genotype carriers had higher levels of big-sized HDL subfraction.
These findings provide new insights into the role of SR-B1 in cellular cholesterol homeostasis and suggest molecular links between SR-B1-dependent lipid sensing and cell cholesterol and lipid droplet dynamics
Liposomes modified with both apolipoproteins A-I and E were internalized in HepG2 cells in FBS-depleted culture medium at the same levels as unmodified liposomes in FBS-containing culture medium, which indicates that apolipoproteins A-I and E were the major serum components involved in liposomal binding to SR-B1 or LDLR (or both).
Here we show that inhibition of SR-B1 reduced cell survival, migration and invasion, and cholesterol content in NB cell lines. Additionally analysis of SR-B1 levels in NB patient biopsies using the R2: Genomics Analysis and Visualization Platform showed that high SR-B1 expression correlated with decreased overall and event-free survival.
the cigarette smoke (CS)-induced loss of SRB1 induced an alteration of sebocytes lipid content, also demonstrated by cholesterol quantification in SRB1 siRNA experiments. In conclusion, exposure to CS, induced SRB1 post-translational modifications in sebocytes and this might affect sebocytes/skin functionality
This study was to characterize the protein markers of dysfunctional high density lipoproteins in SR-BI deficient (SR-BI(-/-)) mice.
Data implicate receptor type B-1 (SCARB1) expression by myeloid-derived suppressor cells (MDSC) as a target for therapy.
Rosuvastatin protected SR-B1(-/-)/apoE(-/-) mice against atherosclerosis and platelet accumulation in coronary arteries and attenuated myocardial fibrosis and cardiomegaly, despite increased plasma total cholesterol.
Raising apoA1 to supraphysiological levels can dramatically protect against doxorubicin-induced cardiotoxicity via a pathway that is mediated by SR-B1 and involves Akt1/2 activation in cardiomyocytes.
our results suggest the involvement of SR-BI in the maternal provision of embryonic vitamin E to the mouse embryo during neural tube closure.
Results suggested that SR-BI deficiency promoted ApoM expression, but the increased ApoM might be independent from high density lipoprotein-mediated cholesterol uptake in hepatocytes.
These findings uncover a novel role for SR-B1 as a contributor to the capture of specific odorants in the nasal cavity of mammals.
In summary, the authors identified NAP1L1 as a novel binding partner of hepatitis c virus NS3 and found that the protease domain of NS3 is responsible for interactions with NAP1L1. They demonstrated the functional role of NAP1L1 in hepatitis c virus entry through regulating the protein expression of SR-B1.
SR-BI-triggered autophagy promoted co-elimination of apoptotic immune cells and dead bacteria but barely influenced bacterial sequestration and survival or inflammasome activation, thus exclusively counteracting damage inflicted by immune responses.
Overexpression of miR-24 inhibited SR-B1 expression by directly targeting SR-B1 3' UTR and repressed high density lipoprotein uptake and steroidogenesis in steroidogenic cells.
These data suggest that a moderate amount of alcohol plays a novel role in reverse cholesterol transport, mainly mediated by PPARgamma and SR-B1.
To investigate the pharmacokinetics (PKs) and pharmacodynamics (PDs) for ION-353382, an antisense oligonucleotide (ASO) targeting scavenger receptor class B type I (SRB1) mRNA, using alpha-2-macroglobulin (A2M), murinoglobulin double-knockout (DKO), and wild-type mice
Rutaecarpine was identified to be a candidate that protected ApoE(-/-) mice from developing atherosclerosis through preferentially promoting activities of ABCA1 and SR-BI within RCT.
SR-B1 is a silica receptor associated with canonical inflammasome activation.
Our results suggest that LPA-enhanced foam cell formation is mediated by LPA1/3 -AKT 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 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.
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 but not ABCA1.
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)