The Pro-Inflammatory Chemokines CXCL9, CXCL10 and CXCL11 Are Upregulated Following SARS-CoV-2 Infection in an AKT-Dependent Manner
Article
[키워드] ACE2
acute lung injury
acute respiratory distress
acute respiratory syndrome
AKT
ALI
ARDS
Betacoronavirus
Calu-3
Cell
characterized
chemokine
chemokines CXCL9
contribute
contributing to
coronavirus
Coronavirus disease 2019
COVID-19
CXCL10
CXCL11
CXCL9
cytokine
Cytokine storm
cytokines IL-6
develop
elevated
enzyme
epithelial cell
feature
Gene Expression
GSK690693
hACE2 mice
human lung
hyperinflammation
IFN-γ
IL-6
immunostimulatory
include
increase in
increases in
infected with SARS-CoV-2
inflammatory state
inhibitor
kinase
lung
mechanical ventilation
mice
overexpression
pandemic
pathway
positive individual
pro-inflammatory
pulmonary complication
reduced
reducing
responsible
RNA virus
Sample
SARS-CoV-2
SARS-CoV-2 infected cells
SARS-COV-2 infection
SARS-CoV-2 pathogenesis
severe COVID-19
Signaling
signaling pathway
significantly
small molecule inhibitor
syndrome
target
TNFα
transcript
Transcription
transgenic
Treatment
upregulation
were used
[DOI] 10.3390/v13061062 PMC 바로가기 [Article Type] Article
[DOI] 10.3390/v13061062 PMC 바로가기 [Article Type] Article