General Information:

Id: 11,827 (click here to show other Interactions for entry)
Diseases: COVID-19
Homo sapiens
Reference: Hoffmann M et al.(2020) SARS-CoV-2 Cell Entry Depends on ACE2 and TMPRSS2 and Is Blocked by a Clinically Proven Protease Inhibitor Cell 181: 271-280.e8 [PMID: 32142651]

Interaction Information:

Comment The spike (S) protein of coronaviruses facilitates viral entry into target cells. Entry depends on binding of the surface unit, S1, of the S protein to a cellular receptor, which facilitates viral attachment to the surface of target cells. In addition, entry requires S protein priming by cellular proteases, which entails S protein cleavage at the S1/S2 and the S2’ site and allows fusion of viral and cellular membranes, a process driven by the S2 subunit. The goal of this study was to obtain insights into how SARS-2-S facilitates viral entry into target cells and how this process can be blocked. Directed expression of human and bat (Rhinolophus alcyone) ACE2 but not human DPP4, the entry receptor used by MERS-CoV, or human APN, the entry receptor used by HCoV-229E, allowed SARS-2-S- and SARS-S-driven entry into otherwise non-susceptible BHK-21 cells. Moreover, anti-serum raised against human ACE2 blocked SARS-S- andSARS-2-S- but not VSV-G- or MERS-S-driven entry. Finally, authentic SARS-CoV-2 infected BHK-21 cells transfected to express ACE2 cells but not parental BHK-21 cells with high efficiency, indicating that SARS-2-S, like SARS-S, uses ACE2 for cellular entry.
Formal Description
Interaction-ID: 116824


SARS-CoV-2 S protein

interacts (colocalizes) with



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