How tetraspanin-mediated cell entry of SARS-CoV-2 can dysregulate the shedding of the ACE2 receptor by ADAM17.
Biochem Biophys Res Commun
; 593: 52-56, 2022 02 19.
Article
in English
| MEDLINE | ID: covidwho-1633160
ABSTRACT
COVID-19, the respiratory infection caused by the novel coronavirus SARS-CoV-2, presents a clinical picture consistent with the dysregulation of many of the pathways mediated by the metalloprotease ADAM17. ADAM17 is a sheddase that plays a key role in the modulation of ACE2, the receptor which also functions as the point of attachment leading to cell entry by the virus. This work investigates the possibility that ADAM17 dysregulation and attachment of the SARS-CoV-2 virion to the ACE2 receptor are linked events, with the latter causing the former. Tetraspanins, the transmembrane proteins that function as scaffolds for the construction of viral entry platforms, are mooted as key components in this connection.
Keywords
Full text:
Available
Collection:
International databases
Database:
MEDLINE
Main subject:
Receptors, Virus
/
Virus Internalization
/
Tetraspanin 29
/
ADAM17 Protein
/
Angiotensin-Converting Enzyme 2
/
SARS-CoV-2
Type of study:
Observational study
/
Prognostic study
Limits:
Humans
Language:
English
Journal:
Biochem Biophys Res Commun
Year:
2022
Document Type:
Article
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