Cells,
Год журнала:
2024,
Номер
13(24), С. 2115 - 2115
Опубликована: Дек. 20, 2024
The
mammalian
Apolipoprotein-L
families
(APOLs)
contain
several
isoforms
of
membrane-interacting
proteins,
some
which
are
involved
in
the
control
membrane
dynamics
(traffic,
fission
and
fusion).
Specifically,
human
APOL1
APOL3
appear
to
remodeling
linked
pathogen
infection.
Through
its
association
with
Non-Muscular
Myosin-2A
(NM2A),
controls
Golgi-derived
trafficking
vesicles
carrying
lipid
scramblase
Autophagy-9A
(ATG9A).
These
deliver
together
phosphatidylinositol-4-kinase-B
(PI4KB)
activated
Stimulator
Interferon
Genes
(STING)
mitochondrion-endoplasmic
reticulum
(ER)
contact
sites
(MERCSs)
for
induction
completion
mitophagy
apoptosis.
direct
interactions
PI4KB
activity
controllers
(Neuronal
Calcium
Sensor-1,
or
NCS1,
Calneuron-1,
CALN1,
ADP-Ribosylation
Factor-1,
ARF1),
PI(4)P
synthesis.
is
required
different
processes
infection-induced
inflammation:
(i)
STING
activation
at
Golgi
subsequent
lysosomal
degradation
inflammation
termination;
(ii)
mitochondrion
MERCSs
apoptosis;
(iii)
phagolysosome
formation
antigen
processing.
In
addition,
governs
mitophagosome
fusion
endolysosomes
completion,
APOL3-like
murine
APOL7C
phagosome
permeabilization
cross-presentation
dendritic
cells.
Similarly,
can
induce
intracellular
bacterial
membranes,
a
role
also
be
proposed
endothelial
APOLd1
adipocyte
mAPOL6,
promote
angiogenesis
adipogenesis,
respectively,
under
inflammatory
conditions.
Thus,
APOL
play
distinct
roles
associated
inflammation.
Cell Communication and Signaling,
Год журнала:
2025,
Номер
23(1)
Опубликована: Апрель 7, 2025
The
cGAS-STING
signaling
pathway
serves
as
a
critical
link
between
DNA
sensing
and
innate
immunity,
has
tremendous
potential
to
improve
anti-tumor
immunity
by
generating
type
I
interferons.
However,
STING
agonists
have
shown
decreasing
biotherapeutic
efficacy
in
clinical
trials.
Tumor
metabolism,
characterized
aberrant
nutrient
utilization
energy
production,
is
fundamental
hallmark
of
tumorigenesis.
And
modulating
metabolic
pathways
tumor
cells
been
discovered
therapeutic
strategy
for
tumors.
As
research
concerning
progressed,
emerging
evidence
highlights
its
role
reprogramming,
independent
immune
function,
indicating
targets
activation
cancers.
In
this
review,
we
delve
into
the
interplay
multiple
pathways.
We
also
synthesize
current
knowledge
on
antitumor
functions
STING,
within
microenvironment
(TME)
that
could
be
exploited
activation.
This
review
necessity
future
dissect
complex
interactions
with
various
cancer
types,
emphasizing
personalized
strategies
based
profiling.
Cells,
Год журнала:
2024,
Номер
13(20), С. 1738 - 1738
Опубликована: Окт. 20, 2024
Apolipoprotein-L1
(APOL1)
is
a
membrane-interacting
protein
induced
by
inflammation,
which
confers
human
resistance
to
infection
African
trypanosomes.
APOL1
kills
Trypanosoma
brucei
through
induction
of
apoptotic-like
parasite
death,
but
two
T.
clones
acquired
APOL1,
allowing
them
cause
sleeping
sickness.
An
C-terminal
sequence
alteration,
such
as
occurs
in
natural
West
variants
G1
and
G2,
restored
these
clones.
However,
unfolding
or
G2
mutations
enhances
hydrophobicity,
resulting
kidney
podocyte
dysfunctions
affecting
renal
filtration.
The
mechanism
involved
debated.
ability
generate
ion
pores
trypanosome
intracellular
membranes
synthetic
was
provided
an
explanation.
transmembrane
insertion
strictly
depends
on
acidic
conditions,
cytopathology
mainly
results
from
secreted
activity
the
plasma
membrane,
under
non-acidic
conditions.
In
this
review,
I
argue
that
besides
inactivation
APOL3
functions
membrane
dynamics
(fission
fusion),
induce
inflammation-linked
toxicity
not
pore
formation,
disturbance
increased
interaction
with
cholesterol,
cation
channels
activity.
A
mutation
domain
(N264K)
abrogates
variant
at
expense
slightly
sensitivity
trypanosomes,
further
illustrating
continuous
mutual
adaptation
between
host
parasite.
Journal of Virology,
Год журнала:
2025,
Номер
unknown
Опубликована: Апрель 10, 2025
ABSTRACT
Flavivirus
infection
involves
extensive
remodeling
of
the
endoplasmic
reticulum
(ER),
which
is
key
to
both
replication
viral
RNA
genome
as
well
assembly
and
release
new
virions.
However,
little
known
about
how
proteins
host
factors
cooperatively
facilitate
such
a
vast
transformation
ER,
this
influences
different
steps
life
cycle.
In
study,
we
screened
for
that
were
enriched
in
close
proximity
tick-borne
encephalitis
virus
(TBEV)
protein
NS4B
found
top
candidates
coupled
trafficking
between
ER
exit
sites
(ERES)
Golgi.
We
characterized
role
ACBD3,
one
identified
proteins,
showed
it
promotes
TBEV
infection.
Depletion
ACBD3
inhibited
resulted
abnormal
leading
reduced
virion
release.
ACBD3’s
proviral
mechanism
did
not
involve
recruitment
PI4PK
previously
described
enteroviruses.
Instead,
productive
required
full-length
localizes
ER-Golgi
contact
together
with
NS4B.
propose
promote
by
coordinating
particle
The
direct
coupling
Golgi
facilitates
efficient
transport.
IMPORTANCE
Flaviviruses
like
have
significant
effects
on
human
health.
During
flavivirus
infection,
particles
enter
cells
transform
membranous
organelle
main
site
cellular
synthesis.
Although
critical
successful
details
process
are
unknown.
Here,
ACBD
ensuring
apparatus,
responsible
transporting
material
out
cell.
uses
guarantee
connection
transformed
remain
functional
so
replicated
produced
exported
from
cell
can
infect
further
cells.
Our
work
sheds
light
basic
biology
virus-induced
organelles.
ACS Infectious Diseases,
Год журнала:
2025,
Номер
unknown
Опубликована: Апрель 21, 2025
Human
oxysterol-binding
protein
(OSBP)
is
a
potentially
druggable
mediator
in
the
replication
of
broad
spectrum
positive-sense
(+)
single-stranded
RNA
(ssRNA)
viruses,
including
members
Picornaviridae,
Flaviviridae,
and
Coronaviridae.
OSBP
cytoplasmic
lipid
transporting
capable
moving
cholesterol
phosphoinositides
between
endoplasmic
reticulum
(ER)
Golgi,
ER
lysosome.
Several
structurally
diverse
antiviral
compounds
have
been
reported
to
function
through
targeting
OSBP,
natural
product
compound
OSW-1.
Our
prior
work
shows
that
transient
OSW-1
treatment
induces
reduction
levels
over
multiple
successive
cell
generations
(i.e.,
multigenerational),
with
no
apparent
cellular
toxicity,
OSW-1-induced
has
activity
against
(+)ssRNA
viruses.
This
study
extends
these
findings
establishes
vitro
pathogenic
human
rhinovirus
(HRV1B),
feline
coronavirus
peritonitis
virus
(FIPV),
229E
(HCoV-229E),
severe
acute
respiratory
syndrome
2
(SARS-CoV-2).
We
also
demonstrate
airway
epithelial
cells
alters
expression
innate
immune
mediators,
interferon
(IFN)
related
genes
IFNB1,
IFNL3,
CXCL10,
ISG15,
MX1.
Furthermore,
enhances
induction
specific
components
type
I
III
IFN
responses
triggered
by
viral
mimetic
polyinosinic-polycytidylic
acid
(Poly
IC).
In
summary,
this
further
demonstrates
importance
presents
as
potential
regulator
responses.
