IFN-stimulated gene
[대역어] None
[용어속성] Gene
[용어속성] Gene
SARS-CoV-2 Orf6 hijacks Nup98 to block STAT nuclear import and antagonize interferon signaling
SARS-CoV-2 Orf6은 Nup98을 하이재킹하여 STAT 핵 수입을 차단하고 인터페론 신호를 길항합니다
530
[키워드] acute respiratory syndrome
acute respiratory syndrome coronavirus
addition
antagonistic
antagonize interferon signaling
Antiviral
antiviral action
antiviral response
antiviral signaling
arginine
bind
binding
C-terminal domain
causative agent
complex
coronavirus
coronavirus disease
Coronavirus disease 2019
COVID-19
Critical
Defense
disrupt
docking
Health
health problem
Host
Host immune response
host immune responses
IFN
IFN signaling
IFN-stimulated gene
IFN-stimulated genes
immune responses
impair
Infection
inhibit
interact
interferon
interferon signaling antagonism
ISGs
mechanism
methionine
NPC
nuclear
nuclear pore
nuclear translocation
Nup98
ORF6
overcome
pandemic
pathogenic virus
pathogenic viruses
Pathogens
pathway
Previous studies
previous study
Protein
Rae1
replicate
residue
respiratory
SARS-CoV
SARS-CoV-2
severe acute respiratory syndrome Coronavirus
severe acute respiratory syndrome coronavirus 2
Significance
STAT
Stat1
STAT2
STATs
the interferon
transcriptional
Vaccines
Viral
viral pathogen
viral pathogens
virus
virus
viruses
[DOI] 10.1073/pnas.2016650117 PMC 바로가기 [Article Type] 530
[DOI] 10.1073/pnas.2016650117 PMC 바로가기 [Article Type] 530
Impaired type I interferon activity and inflammatory responses in severe COVID-19 patients
Report
[키워드] Analysis
Antiviral
antiviral immunity
bacterial superinfections
Blood
cause
characterized
Cohort
coronavirus disease
Coronavirus disease 2019
COVID-19
COVID-19 patient
Critical
critical COVID-19 patient
deficiency
dendritic cell
Disease progression
disease severity
driven by
driving
elicit
engage
ENhance
epithelial
exacerbated
expressed
expression
functions
hallmark
host immune responses
IFN
IFN signaling
IFN-stimulated gene
IFN-α
IFN-β
IFN-λ
IFNs
immune
Immune cell
immunopathology
Impaired
increase
Inflammatory response
influenza infection
inhibiting
interfere
interferon
interleukin-6
ISGs
Local
lung
lung epithelium
Major
mice
morbidity
mucosal surface
Necrosis
nuclear
p53
parameter
patients
performed
Peripheral blood
phenotype
proinflammatory
proliferation
respiratory viral infections
response
responses
Science
secreted
severe COVID-19
severe COVID-19 patient
severity
Signaling
susceptibility
therapeutic
therapeutic approaches
thought
Transcription
transcriptional
Trigger
turn
Type
type I
Type I IFN
type I interferon
Type III IFN
viral infections
Viral load
viral respiratory disease
viral respiratory infections
Viral RNA
[DOI] 10.1126/science.abc6027 PMC 바로가기 [Article Type] Report
[DOI] 10.1126/science.abc6027 PMC 바로가기 [Article Type] Report
Type III interferons disrupt the lung epithelial barrier upon viral recognition
Report
[키워드] aberrant immune response
acute respiratory syndrome
airway
Antiviral
antiviral immunity
bacterial superinfections
cause
characterized
Clinical practice
contribute
coronavirus
coronavirus disease
COVID-19
COVID-19 patient
Critical
critical COVID-19 patient
dendritic cell
disrupt
driving
elicit
Endemic
engage
ENhance
epithelial
Evidence
expressed
expression
functions
IFN
IFN signaling
IFN-stimulated gene
IFN-α
IFN-β
IFN-λ
IFNs
Immune cell
immunopathology
increase
indicate
induce
Infection
influenza infection
Influenza virus
inhibiting
interfere
ISGs
Local
Lower respiratory tract
lung
lung epithelial
lung epithelium
Major
mice
morbidity
Mortality
Mounting
mucosal surface
Necrosis
p53
parameter
Pathogenesis
pathophysiological
Patient
Peripheral blood
produced
proinflammatory
proliferation
respiratory viral infections
response
responses
RNA viruses
SARS-CoV-2
Science
secreted
Severe case
severity
susceptibility
therapeutic
thought
Transcription
Trigger
turn
Type
type I
Type I IFN
Type III IFN
type III interferon
viral burden
viral infections
viral respiratory disease
viral respiratory infections
Viral RNA
viruses
[DOI] 10.1126/science.abc3545 PMC 바로가기 [Article Type] Report
[DOI] 10.1126/science.abc3545 PMC 바로가기 [Article Type] Report
GILT restricts the cellular entry mediated by the envelope glycoproteins of SARS-CoV, Ebola virus and Lassa fever virus
Article
[키워드] Antiviral
cathepsin L
cellular entry
demonstrated
Ebola virus
enveloped RNA virus
enveloped RNA viruses
expressed
expression
fibroblast
GILT
glycoprotein
IFN-stimulated gene
IFNs
immune
inhibit
inhibited
interferon
Interferon-stimulated genes (ISGs)
ISG
ISGs
Lassa fever
Lassa fever virus
lung epithelial cell
lysosomal
lysosome
Lysosomes
metabolism
Modification
Mutation
N-linked glycosylation
overexpression
Pathogenesis
reduced
required
restrict
RNA virus
SARS Coronavirus
SARS-CoV
selected
viral entry
viral envelope
viral infection
viral replication
virus
viruses
while
[DOI] 10.1080/22221751.2019.1677446 PMC 바로가기 [Article Type] Article
[DOI] 10.1080/22221751.2019.1677446 PMC 바로가기 [Article Type] Article
Dynamic Innate Immune Responses of Human Bronchial Epithelial Cells to Severe Acute Respiratory Syndrome-Associated Coronavirus Infection
Research Article
[키워드] 2B4 cell
2B4 cells
Activation
aggravate
antiviral genes
antiviral signaling
bronchial
bronchial epithelial cell
calu-3 cells
cellular
cloned
complementary
complex
coronavirus
detected
detrimental
dynamic
epithelial
epithelial cell line
event
expression
found
functional
growth
highlight
Host
Human
identify
IFN-stimulated gene
IFN-β
IFN-λ
Immune-mediated
Infected
Inflammatory cytokine
Inflammatory mediators
Inflammatory responses
Innate
interferon
interferon regulatory factor
ISGs
limit
lung epithelial cell
Lungs
nuclear
pathology
post infection
Protein
Replication
respiratory
response
resulting
SARS pathogenesis
SARS-CoV
SARS-CoV infection
secreting
severe
Signaling
Support
target
these cell
triggered
[DOI] 10.1371/journal.pone.0008729 PMC 바로가기 [Article Type] Research Article
[DOI] 10.1371/journal.pone.0008729 PMC 바로가기 [Article Type] Research Article