Last update 01 Nov 2024

SCARB1

Last update 01 Nov 2024

Basic Info

Synonyms

CD36, CD36 and LIMPII analogous 1, CD36 antigen (collagen type I receptor, thrombospondin receptor)-like 1

+ [10]

Introduction

Receptor for different ligands such as phospholipids, cholesterol ester, lipoproteins, phosphatidylserine and apoptotic cells (PubMed:12016218, PubMed:12519372, PubMed:21226579). Receptor for HDL, mediating selective uptake of cholesteryl ether and HDL-dependent cholesterol efflux (PubMed:26965621). Also facilitates the flux of free and esterified cholesterol between the cell surface and apoB-containing lipoproteins and modified lipoproteins, although less efficiently than HDL. May be involved in the phagocytosis of apoptotic cells, via its phosphatidylserine binding activity (PubMed:12016218). (Microbial infection) Acts as a receptor for hepatitis C virus in hepatocytes and appears to facilitate its cell entry (PubMed:12356718, PubMed:12913001, PubMed:18000990). Binding between SCARB1 and the hepatitis C virus glycoprotein E2 is independent of the genotype of the viral isolate (PubMed:12356718). (Microbial infection) Mediates uptake of M.fortuitum, E.coli and S.aureus. (Microbial infection) Facilitates the entry of human coronavirus SARS-CoV-2 by acting as an entry cofactor through HDL binding.

Drugs associated with SCARB1

CER-001

Target

APOA1 x SCARB1

Mechanism

APOA1 stimulants [+1]

Active Org.

Academic Medical Center University of Amsterdam [+2]

Originator Org.

Cerenis Therapeutics, Inc.

Active Indication

Sepsis [+5]

Inactive Indication

Acrocallosal Syndrome [+8]

Drug Highest PhasePhase 2

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

ML279

Target

SCARB1

Mechanism

SCARB1 inhibitors

Active Org.

The Broad Institute, Inc.

Originator Org.

The Broad Institute, Inc.

Active Indication

Cardiovascular Diseases

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

ML278

Target

SCARB1

Mechanism

SCARB1 inhibitors

Active Org.

One Cambridge Center Trust

Originator Org.

One Cambridge Center Trust

Active Indication

Hepatitis C

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

Clinical Trials associated with SCARB1

EUCTR2020-004202-60-IT / Not yet recruitingPhase 2

A RAndomized pilot study comparing short-term CER-001 infusions at different doses to prevent Sepsis-induced acute kidney injury - RACERS STUDY

Start Date13 Jan 2021

Sponsor / Collaborator-

EUCTR2015-003713-23-FR / Not yet recruitingPhase 3

PHASE III, MULTI-CENTER, RANDOMIZED, 48 WEEKS, DOUBLE-BLIND, PARALLEL-GROUP, PLACEBO-CONTROLLED STUDY TO EVALUATE EFFICACY AND SAFETY OF CER-001 ON VESSEL WALL AREA IN PATIENTS WITH GENETICALLY DEFINED FAMILIAL PRIMARY HYPOALPHALIPOPROTEINEMIA AND RECEIVING BACKGROUND OPTIMIZED LIPID THERAPY - TANGO

Start Date09 Feb 2017

Sponsor / Collaborator-

NCT02697136 / TerminatedPhase 3

Phase 3, Multicenter, Randomized, 48 Week, Double Blind, Parallel Group, Placebo Controlled Study to Evaluate Efficacy and Safety of CER-001 on Vessel Wall Area in Patients With Genetically Defined Familial Primary Hypoalphalipoproteinemia

The purpose of this study is to assess the impact of 29 intravenous infusions of CER-001 vs. placebo, given at weekly (9 infusions) and biweekly (20 infusions) intervals on carotid vessel wall area as measured by 3TMRI, when administered to patients with familial primary hypoalphalipoproteinemia with proven CVD and appropriate background lipid-lowering therapy.

Start Date01 Dec 2015

Sponsor / Collaborator

Cerenis Therapeutics, Inc.

100 Clinical Results associated with SCARB1

100 Translational Medicine associated with SCARB1

0 Patents (Medical) associated with SCARB1

2,509

Literatures (Medical) associated with SCARB1

01 Jan 2025·Comparative Biochemistry and Physiology Part B: Biochemistry and Molecular Biology

Comparative analysis of Scarb1 and Cd36 in grass carp (Ctenopharyngodon idellus): Implications for DHA uptake

Article

The polyunsaturated fatty acid docosahexaenoic acid (DHA) significantly influences fish growth and lipid metabolism. Nevertheless, the specific mechanism by which DHA is transported and exerts its effects remains unclear. Scavenger receptor class B type I (SCARB1) is essential for maintaining cellular cholesterol levels and regulating the immune system in mammals, as well as facilitating the uptake of fatty acids (FAs). Another class B scavenger receptor, cluster-determinant 36 (CD36), is involved in promoting the uptake and transport of long-chain fatty acids. However, the molecular characteristics of the grass carp scarb1 gene have not yet been reported, and the potential role of Scarb1 and Cd36 in mediating DHA transport and metabolism remains uncertain. This study aimed to investigate the effects of Scarb1 and Cd36 on DHA transport. Initially, grass carp scarb1-1 and scarb1-2 were cloned. Predictions were made regarding their structural characteristics, including number and presence of transmembrane domains and glycosylation sites. Furthermore, gene structure analysis revealed that scarb1-1 has two additional exons in the 3'-region compared to scarb1-2. The multiple sequence alignment indicated that Scarb1 exhibits conserved motifs and amino acid residues across vertebrates. mRNA expression of scarb1-1 was the highest in the intestine, while scarb1-2 was highest expressed in adipose tissue, with both having lower expression levels in muscle tissue. Scarb1-1 was primarily localized on the cell membrane, whereas Scarb1-2 was found in both the cell membrane and cytoplasm. After overexpression of grass carp Scarb1-1, Scarb1-2, and Cd36 in HEK 293 T cells, DHA incubation showed that only Cd36 significantly increased cellular DHA relative content, suggesting a potential role of Cd36 in DHA transport. These findings will serve as a basis for further research on fatty acid transport in fish.

01 Jan 2025·Theriogenology

Paternal trans fatty acid and vitamin E diet affect the expression pattern of androgen signaling pathway genes in the testis of rat offspring

Article

Author: Shams, Amir Abbas ; Alizadeh, AliReza ; Karoii, Danial Hashemi ; Vesali, Samira ; Shahhoseini, Maryam ; Vesal, Soheil

Numerous studies have shown that an improper diet in parents has a negative impact on offspring's health. Furthermore, the negative effects of trans fatty acids (TFA) in maternal diets on fertility and health and their impact on future generations have been documented. However, there is limited research on the negative effects of TFA in paternal diets on male children. The current work used qRT-PCR to investigate the effects of trans fatty acids and vitamin E in the paternal diet on the expression pattern of androgen signaling pathway genes such as STAR, CYP11a1, HSD3B, SRD5a2, and SCARB1 in offspring testes. In this experiment, parental rats were randomly separated into four groups, each with ten father rats, and were fed for eight weeks (60 days) as follows. 1: Standard diet group plus liquid sunflower oil (control). 2: Standard diet group containing trans fatty acids (CTH). 3: The regular diet group received 2.5 times the recommended quantity of vitamin E supplement. 4: Standard diet group with vitamin E and trans fatty acid supplementation (ETH). The testis tissue samples from 35 offspring were then used. Following RNA extraction from tissues and cDNA synthesis, quantitative real-time PCR was used to evaluate the expression levels of androgen signaling pathway genes such as STAR, CYP11A1, HSD3B, SCARB1, and SRD5A2. Our findings showed that the expression of CYP11A1 was considerably reduced in the progeny of paternal rats given ETH compared to the CTH group. The expression levels of the STAR gene were significantly lower in the progeny of paternal rats administered TFA, ETH, and vitamin E compared to the controls. Although the CTH group had lower SCARB1 expression than the other groups, the difference was not statistically significant. Paternal vitamin E consumption substantially affected SRD5A2 expression when compared to offspring of paternal rats fed vitamin E + trans fatty acid or those fed a conventional diet containing trans fatty acid. Furthermore, the vitamin E group showed a statistically significant increase in HSD3B expression compared to the other groups. Bioinformatics analyses, such as protein-protein interaction networks and gene ontology term enrichment, revealed that these genes play roles in lipid biosynthesis, hormone metabolism, male sex differentiation, reproductive development, and steroid biosynthesis. Our data indicate that paternal trans fatty acid consumption influences the expression of particular androgen signaling pathway genes in offspring testis, with vitamin E potentially mitigating some of these effects.

01 Dec 2024·Theriogenology

Sirtuin 1-mediated autophagy regulates testosterone synthesis in Leydig cells of piglets

Article

Author: Abouelfetouh, Mahmoud M ; Yu, Lingyun ; He, Yijing ; Ju, Shiqiang ; Li, Qiao ; Zhang, Yanyan ; Zhou, Zhenlei ; Abouelfetouh, Mahmoud M. ; Liu, Chengyin

Testosterone is secreted by Leydig cells (LCs), which play an important physiological role in preserving male secondary sex characteristics, protecting male reproductive function, and establishing the blood-testis barrier. Studies have shown that autophagy is particularly active in LCs; however, its involvement in testosterone synthesis in porcine LCs has not been fully explored. Therefore, this experiment aimed to investigate the influence of autophagy on testosterone secretion in porcine LCs and its potential regulatory mechanism. Our results demonstrated that both testicular autophagy and serum testosterone levels increased in piglets during postnatal development from 4 to 18 weeks. In addition, autophagy was found to degrade the Na⁺/H⁺ exchange regulatory factor 2 (NHERF2), leading to the up-regulation of scavenger receptor class B type 1 (SRB1). This process resulted in increased cholesterol intake and enhanced testosterone production. The observable level of sirtuin 1 (SIRT1) was directly proportional to the level of autophagy. In vitro investigations have shown that SIRT1 can affect the level of autophagy, cholesterol uptake as well as testosterone release. In conclusion, testosterone synthesis during pig development is regulated by SIRT1. SIRT1 mediates the degradation of NHERF2 through autophagy, thereby weakening its negative regulatory effect on the high-density lipoprotein receptor SRB1 in Leydig cells. This process increases cholesterol uptake and enhances testosterone synthesis.

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SCARB1

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