Browse our anti-SCARB1 (SCARB1) Antibodies

Human Scavenger Receptor Class B, Member 1 (SCARB1) interaction partners

1. Results demonstrate that SR-BI is a highly expressed receptor in human metastatic melanoma and is crucial for the maintenance of the metastatic phenotype.

2. 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.

3. Findings suggested that polymorphism rs5888 had negative association with coronary heart disease, especially in male. [review]

4. 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.

5. 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.

6. SCARB1 gene polymorphisms may serve as a potential predictor of treatment responses in chronic hepatitis C patients receiving interferon-based therapy

7. 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.

8. 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.

9. 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.

10. 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.

11. 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

12. 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).

13. 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.

14. 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

15. Our analyses revealed no apparent differences in protein expression profiles of SRBs in central and peripheral regions of human donor tissues, indicating that carotenoid-binding proteins rather than transporters are likely to mediate selective accumulation of carotenoids into the macula.

16. Low SRB1 expression is associated with non-alcoholic steatohepatitis but is unchanged in hepatocellular carcinoma.

17. SCARB1 rs5888 and environmental oxidative stress have a prominent role in age-related macular degeneration(ARMD) susceptibility, early ARMD progression to advanced stage disease and even in the outcome of the disease-an area of macular lesion.

18. SCARB1 gene variants are associated with a new lipid phenotype, characterized by high levels of both HDL cholesterol and Lp(a). SCARB1 exonic variants often result in diminished function of translated SR-B1 via reduced binding/intracellular transport of Lp(a).

19. Data suggest that activation of SR-BI by APOAI down-regulates sphingosine 1-phosphate/S1PR2-mediated inflammation in vascular endothelial cells by activating the PI3K/Akt signaling pathway; oxidized-LDL does the opposite. (APOA1 = apolipoprotein A-I; SR-BI/SCARB1 = scavenger receptor class B type I; S1PR2 = sphingosine 1-phosphate receptor 2; PI3K = phosphatidylinositol 3-kinase; Akt = proto-oncogene c-akt)

20. Sustained virologic response was significantly associated with SCARB1 rs10846744 in chronic hepatitis C patients, treated with pegylated interferon-alpha and ribavirin.

Mouse (Murine) Scavenger Receptor Class B, Member 1 (SCARB1) interaction partners

1. 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.

2. 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.

3. our results suggest the involvement of SR-BI in the maternal provision of embryonic vitamin E to the mouse embryo during neural tube closure.

4. 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.

5. 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.

6. These findings uncover a novel role for SR-B1 as a contributor to the capture of specific odorants in the nasal cavity of mammals.

7. 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.

8. 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.

9. 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.

10. These data suggest that a moderate amount of alcohol plays a novel role in reverse cholesterol transport, mainly mediated by PPARgamma and SR-B1.

11. 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

12. 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.

13. SR-B1 is a silica receptor associated with canonical inflammasome activation.

14. Our results suggest that LPA-enhanced foam cell formation is mediated by LPA1/3 -AKT activation and subsequent SRBI expression.

15. 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.

16. 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.

17. Carboxy-terminal deletion of SR-BI reduced receptor levels in liver and steroidogenic tissues (adrenal cortex, ovary, testicular Leydig cells) and induced hypercholesterolemia.

18. Loss of ScarB1 is associated with Coronary Atherosclerosis and Ischemic Heart Disease in Low-density Lipoprotein Receptor Knockout Mice when fed the modified western-type diet.

19. 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.

20. 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 participates in hormonal regulation of SR-BI expression in a tissue-specific manner.

Pig (Porcine) Scavenger Receptor Class B, Member 1 (SCARB1) interaction partners

1. Luteinization causes upregulation of SR-BI expression, its posttranslational maturation by glycosylation, and insertion into luteal cell membranes.

Cow (Bovine) Scavenger Receptor Class B, Member 1 (SCARB1) interaction partners

1. Aortic endothelial cells transcytose high-density lipoproteins by mechanisms that involve either SR-BI or ABCG1 but not ABCA1.