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Last update 23 Jan 2025

SCARB1

Last update 23 Jan 2025

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

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

ML312

Target

SCARB1

Mechanism

SCARB1 inhibitors

Active Org.

The Broad Institute, Inc.

Originator Org.

The Broad Institute, Inc.

Active Indication-

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

NCT01560468

/ TerminatedPhase 1IIT

Phase I Study of Hepatitis C Virus (HCV) Entry Inhibitor (ITX 5061) in Liver Transplant Recipients With HCV Infection

This study will test the safety and tolerability of HCV Entry Inhibitor ITX 5061 in Liver Transplant Recipients with Hepatitis C infection. The investigators hypothesize that ITX 5061 oral monotherapy will be safe in adults during and after liver transplantation and that therapy will also inhibit HCV infection of newly transplanted livers in adults with prior HCV infection.

Start Date01 Mar 2012

Sponsor / Collaborator

iTherX Pharmaceuticals, Inc.

NCT01292824

/ CompletedPhase 1IIT

Phase I Study of Hepatitis C Virus (HCV) Entry Inhibitor (ITX 5061) in Liver Transplant Recipients With HCV Infection

This is a phase I pilot study to determine the safety and preliminary efficacy of a novel hepatitis C virus (HCV) entry inhibitor (ITX 5061) in patients with HCV infection undergoing liver transplantation.

Start Date01 Feb 2011

Sponsor / Collaborator

University of Birmingham

[+2]

NCT01165359

/ CompletedPhase 1IIT

A Randomized, Double-Blind, Phase 1b Study to Assess the Safety and Activity of the HCV Entry Inhibitor ITX 5061 in Treatment-Naive HCV Mono-Infected Adults

Hepatitis C (HCV) is a disease that affects the liver. ITX 5061 is a new medication that is being tested to treat HCV. This study will evaluate the safety of ITX 5061 and examine different doses of the medication to evaluate which dose is the most effective at lowering the amount of HCV in the blood.

Start Date01 Sep 2010

Sponsor / Collaborator

National Institute of Allergy & Infectious Diseases

100 Clinical Results associated with SCARB1

100 Translational Medicine associated with SCARB1

0 Patents (Medical) associated with SCARB1

2,579

Literatures (Medical) associated with SCARB1

01 Jan 2025·Ecotoxicology and Environmental Safety

Cyclopiazonic acid suppresses the function of Leydig cells in prepubertal male rats by disrupting mitofusin 1-mediated mitochondrial function

Article

Author: Zhu, He ; Yu, Yang ; Li, Xiaoheng ; Zhu, Yang ; Ge, Ren-Shan ; Li, Xingwang ; Zhu, Qiqi ; Wang, Yiyan ; Lin, Hang ; Sang, Jianmin ; Su, Ming ; Li, Huitao

This research investigated the impact of cyclopiazonic acid (CPA), a mycotoxin, on the function of progenitor Leydig cells (PLCs) in prepubertal male rats, focusing on its potential disruption of mitochondrial integrity through mitofusin 1 (MFN1) modulation. In vivo, Sprague Dawley rats received CPA (0.2, 1, 5 mg/kg/day) via gavage from postnatal days 21-28 to evaluate PLC function and mitochondrial morphology using serum hormone levels, histology, qPCR, and Western blot analyses. In vitro, rat R2C cells were treated with CPA (0.1, 1, 10 μM) alone or in combination with 100 μM leflunomide to assess PLC development through testosterone measurements, Western blotting, flow cytometry, and Mito-Tracker Green Staining. The findings from in vivo experiments showed that CPA reduced serum testosterone and progesterone levels at 1 mg/kg/day. The qPCR and Western blotting analyses revealed significant alterations in the expression of genes and proteins pertinent to PLC function, such as Scarb1, Star, Cyp11a1, and Cyp17a1. Immunofluorescence staining further revealed a reduction in MFN1 expression following exposure to CPA. In vitro experiments corroborated these observations, demonstrating that CPA induced mitochondrial fragmentation by downregulating SIRT1, PGC1-α, MFN1, and OPA1, increase reactive oxygen species, and inhibit testosterone synthesis in R2C cells. The administration of leflunomide was shown to mitigate the detrimental effects of CPA on PLCs. In conclusion, this research sheds new light on the deleterious effects of CPA on the reproductive development of prepubertal males.

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.

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