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Last update 08 May 2025

SCARB2

Last update 08 May 2025

Basic Info

Synonyms

85 kDa lysosomal membrane sialoglycoprotein, CD36, CD36 antigen-like 2

+ [12]

Introduction

Acts as a lysosomal receptor for glucosylceramidase (GBA1) targeting. (Microbial infection) Acts as a receptor for enterovirus 71.

Drugs associated with SCARB2

CN118027124

Patent Mining

Target

SCARB2

Mechanism-

Active Org.

Guangdong Pharmaceutical University

Originator Org.

Guangdong Pharmaceutical University

Active Indication

Neoplasms

Inactive Indication-

Drug Highest PhaseDiscovery

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with SCARB2

100 Translational Medicine associated with SCARB2

0 Patents (Medical) associated with SCARB2

405

Literatures (Medical) associated with SCARB2

01 Jan 2026·Neural Regeneration Research

Base and translation of β-glucocerebrosidase and its transporter LIMP-2 in neuropathies

Article

Author: Arnold, Philipp ; Zunke, Friederike

01 Mar 2025·Antiviral Research

Metformin inhibits EV-A71 and CVA16 infections by regulating TRIB3-SCARB2 axis and activating AMPK

Article

Author: Jiang, Jiandong ; Yang, Ge ; Li, Yuhuan ; Wang, Huiqiang ; Wu, Shuo ; Yan, Haiyan ; Cui, Boming ; Wang, Kun

Our previous study had found that cellular pseudokinase tribbles 3 (TRIB3) facilitates the infection of enterovirus A71 (EV-A71) via upregulating the protein level of EV-A71 receptor scavenger receptor class B member 2 (SCARB2). In the present study, we used metformin, which had been reported to down-regulate TRIB3 expression, to verify the potential of TRIB3 as an antiviral target. Here, we found that metformin can indeed impede the replication of EV-A71 and Coxsackievirus A16 (CVA16) through inhibiting the transcription of TRIB3 to indirectly down-regulate SCARB2 protein levels to block viral infection. Importantly, we also found that metformin can inhibit the replication of EV-A71 and CVA16 in a TRIB3-independent manner. In fact, we found that both metformin and cellular AMP-activated protein kinase (AMPK) agonist AICAR can inhibit the replication of EV-A71 and CVA16 by pharmacologically activating AMPK. Moreover, AMPK phosphorylation specific inhibitor Compound C treatment can reverse the antiviral effect of metformin, indicating that metformin can indeed play an antiviral role through regulating AMPK. More importantly, we confirmed that metformin could effectively protected mice from lethal EV-A71 infection. Metformin treatment decreased the levels of EV-A71 VP1 protein and viral RNA in the infected muscles, and improved muscle pathology. These findings suggest that TRIB3 does have potential as a target for antiviral drugs, and metformin may be a potential agent or supplement against enterovirus infection.

01 Mar 2025·Virologica Sinica

In vivo quantitative proteomic analysis of porcine alveolar macrophages in PRRSV-infected pigs

Article

Author: Hu, Fangyu ; Hu, Guangli ; Peng, Ouyang ; Huang, Yihui ; Xu, Qiuping ; Zhang, Hao ; Wei, Ying ; Cao, Yongchang ; Zou, Chuangchao ; Zeng, Siying

Porcine reproductive and respiratory syndrome (PRRS), a highly infectious immunosuppressive disease caused by porcine reproductive and respiratory syndrome virus (PRRSV), has led to significant economic losses in the global swine industry. The complexity of preventing and controlling PRRS, compounded by the limited efficacy of current vaccines, underscores the urgent need to identify antiviral targets and develop effective therapeutics against PRRSV. From the perspective of virus-host interactions, the discovery of target molecules associated with PRRSV resistance offers a promising strategy for future disease management. In this study, we conduct a comprehensive proteomic analysis using data-independent acquisition (DIA) mode to investigate the host response throughout the acute phase of PRRSV infection. This approach provides critical insights into the regulation of host antiviral and immune pathways during acute infection, advancing our theoretical understanding of PRRSV-host interactions and host gene dynamics during this critical phase. Notably, we identified SCARB2, a major lysosomal membrane protein associated with cholesterol metabolism, as a potential regulator of PRRSV replication. These findings offer novel perspectives for the prevention and control of PRRSV, contributing to the development of targeted antiviral strategies.

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SCARB2

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