SCARB1 Membrane Protein Introduction

Introduction of SCARB1

Scavenger receptor class B member 1 (SCARB1), encoded by the SCARB1 gene, is also known as SRB1, SR-BI or CD36. SCARB1 is identified as a member of the Class B family of Scavenger Receptor proteins. The structure of SCARB1 is predicted to contain two transmembrane domains, one intracellular N- and C-termini and an extracellular loop with a large extracellular domain (ECD) where there are six cysteine (Cys) residues involved in disulfide bond formation, and those intramolecular disulfide bonds appear to maintain the receptor in a conformation integral to its cholesterol transport functions. SCARB1 is expressed in numerous cell types/tissues, including the liver and adrenal.

Function of SCARB1 Membrane Protein

SCARB1 is a receptor for high-density lipoprotein (HDL), and it promotes selective HDL-cholesteryl ester (HDL-CE) hepatic uptake, playing a critical role in lipoprotein metabolism. It has been reported that SCARB1 plays a key role in reverse cholesterol transport, promoting the hepatic selective uptake of cholesterol and facilitating the secretion of cholesterol into bile. Additionally, SCARB1 can also promote the elimination of excess body cholesterol via biliary cholesterol secretion. SCARB1 is also shown to play a significant role in macrophage cholesterol flux that may partly account for its effects on atherogenesis. SCARB1 can interact with several molecules to activate different pathways. For instance, HDL/SCARB1 interaction activates the PI3K and Erk1/2 pathways; PDZK1/SCARB1 interaction activates eNOS and endothelial cell migration; Src/SCARB1 interaction activates MAPK, p38, JNK, FAK, and GTPases.

Fig.1 Hepatic SR-BI: Selective Uptake of HDL Lipids Regulates HDL Function. (Linton, 2017)

Application of SCARB1 Membrane Protein in Literature

1. Muthuramu I., et al. Hepatocyte-Specific SR-BI Gene Transfer Corrects Cardiac Dysfunction in Scarb1-Deficient Mice and Improves Pressure Overload-Induced Cardiomyopathy. Arterioscler Thromb Vasc Biol. 2018, 38(9): 2028-2040. PubMed ID: 29976771
   
   

   This article shows that detrimental effects of SR-BI deficiency on cardiac structure and function can be nullified by hepatocyte-specific SR-BI transfer, which restores HDL metabolism.

2. Xu G.H., et al. Up-regulation of SR-BI promotes progression and serves as a prognostic biomarker in clear cell renal cell carcinoma. BMC Cancer. 2018, 18(1): 88. PubMed ID: 29357836
   
   

   This article indicates that the inhibition of SR-BI attenuates the tumorous behaviors of clear cell renal cell carcinoma (ccRCC), expression of metastasis and AKT pathway-related proteins, suggesting SR-BI may serve as a potential prognostic biomarker and therapeutic target for ccRCC.

3. Ren K., et al. Quercetin induces the selective uptake of HDL-cholesterol via promoting SR-BI expression and the activation of the PPARgamma/LXRalpha pathway. Food Funct. 2018, 9(1): 624-635. PubMed ID: 29292466
   
   

   This study suggests that quercetin-induced up-regulation of SR-BI and subsequent lipid uptake in hepatocytes might contribute to its beneficial effects on cholesterol homeostasis and atherogenesis.

4. Fung K.Y., et al. SR-BI Mediated Transcytosis of HDL in Brain Microvascular Endothelial Cells Is Independent of Caveolin, Clathrin, and PDZK1. Front Physiol. 2017, 8: 841. PubMed ID: 29163190
   
   

   This article indicates that SR-BI-mediated transcytosis in brain microvascular endothelial cells is distinct from uptake and signaling pathways described for this receptor in other cell types.

5. Kinslechner K., et al. Malignant Phenotypes in Metastatic Melanoma are Governed by SR-BI and its Association with Glycosylation and STAT5 Activation. Mol Cancer Res. 2018, 16(1): 135-146. PubMed ID: 28974560
   
   

   This report indicates that high SR-BI expression in melanoma is linked with increased cellular glycosylation and hence is essential for a metastasis-specific expression signature.

SCARB1 Preparation Options

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Reference

1. Linton M F, et al. (2017). SR-BI: A Multifunctional Receptor in Cholesterol Homeostasis and Atherosclerosis. Trends Endocrinol Metab. 28: 461-472.

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