Identification of oligopeptides from severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) non structural protein 8 (NSP8) and their similarities with type 1 angiotensin II receptor key sites

Autor: Ammar Achour
Jazyk: angličtina
Rok vydání: 2021
Předmět:
0301 basic medicine
ACE-2
angiotensin-converting enzyme 2
SARS-CoV-2
severe severe acute respiratory syndrome coronavirus 2
NSP8
Angiotensin receptor
AT1R
angiotensin II type 1 receptor
G protein
Short Communication
Cellular homeostasis
RM1-950
a.a
amino acids
Viral Nonstructural Proteins
AT1R
Receptor
Angiotensin
Type 1
Cpp
cell penetrating peptide
03 medical and health sciences
0302 clinical medicine
Mediator
Desensitization (telecommunications)
Sarscov-2
Humans
Amino Acid Sequence
Receptor
Covid 19
Coronavirus disease 2019
Pharmacology
Ang II
angiotensin II
Coronavirus RNA-Dependent RNA Polymerase
SARS-CoV-2
Chemistry
COVID-19
similarity Angiotensin II
General Medicine
Angiotensin II
NSP8
non structural protein 8
Cell biology
ORF1ab
open reading frame 1ab
030104 developmental biology
030220 oncology & carcinogenesis
peptides
Phosphorylation
LPS
lipopolysaccharides
Therapeutics. Pharmacology
Oligopeptides
Zdroj: Biomedicine & Pharmacotherapy
Biomedicine & Pharmacotherapy, Vol 141, Iss, Pp 111722-(2021)
ISSN: 1950-6007
0753-3322
Popis: Coronavirus disease 2019 is associated with clinical symptoms including severe inflammatory syndrome and a higher expression of angiotensin II. As a pro-inflammatory mediator, the physiologic effects of angiotensin II are mediated by a G-protein coupled receptor, termed AT1R. Following binding, AT1R initiates the process of signal desensitization necessary to maintain cellular homeostasis. At the cellular level, this function occurs via the G protein-dependent signaling and the phosphorylation. We describe amino acids similarities between SARS COV-2 nonstructural protein (NSP8) which is associated with intracellular membranes and AT1R key sites. Since abnormal activation of AT1R receptor leads to a number of physiological disorders, we hypothesize that SARS COV-2 might further interfere with the angiotensin II receptor functions.
Databáze: OpenAIRE
Externí odkaz: