Research Square (Research Square),
Journal Year:
2024,
Volume and Issue:
unknown
Published: March 21, 2024
Abstract
Mitochondrial
unfolded
protein
response
(UPR
mt
)
is
triggered
through
eIF2α
phosphorylation
in
mammal.
However,
the
mechanisms
of
UPR
activation
and
influence
on
mitochondrial
translation
remain
unclear.
In
this
study,
we
confirmed
that
was
a
rapid
specific
stress
with
pharmacological
induction,
along
expression
phosphorylation,
ATF4,
CHOP.
Meanwhile,
up-regulation
some
chaperones,
cytochrome
P450
enzymes,
DDIT4
determined
by
RNA-Seq
ribosome
profiling,
essential
for
expressing
ATF4
CHOP,
then
traffics
into
nucleus
initiates
CHOP
expression.
addition,
generation
ROS
morphology
unchanged
under
GTPP
induced
.
Furthermore,
unraveled
mechanism
HRI
kinase
mediates
proteins
CRISPR-Cas9
technology
recruitment
interaction
other
proteins.
number
imports
were
inhibited
accumulation
protein.
These
findings
provide
molecular
impact
cellular
translation,
which
will
offer
novel
insights
functional
research
,
including
its
implications
human
diseases
pathobiology.
Research Square (Research Square),
Journal Year:
2024,
Volume and Issue:
unknown
Published: Oct. 17, 2024
AbstractBrucella
being
a
successful
pathogen,
employs
plethora
of
immune
evasion
mechanisms.
This
contributes
to
pathogenesis,
persistence
and
also
limits
the
efficacy
available
treatment.
Increasing
understanding
host-pathogen
interactions
suggests
that
integrating
host-directed
strategies
with
existing
anti-Brucella
treatments
could
lead
more
effective
bacterial
clearance
reduction
in
drug-resistant
strains.
SIRT2
is
nicotinamide
adenine
dinucleotide
(NAD+)-dependent
deacetylase
found
mammals.
It
can
deacetylate
various
transcription
factors
regulatory
proteins,
playing
crucial
role
pathogen
infection-induced
apoptosis.
In
this
study,
we
investigate
Brucella-induced
cell
apoptosis
using
bovine
placental
trophoblast
cells.
Our
results
indicate
B.
abortus
A19
infection
upregulates
protein
expression
significantly
induces
mitochondrial
these
Furthermore,
Inhibition
exacerbates
A19-induced
markedly
inhibits
intracellular
survival.
These
prove
pathogenesis
mechanism
action.
Abstract
Mitochondria
are
versatile
and
complex
organelles
that
can
continuously
communicate
interact
with
the
cellular
milieu.
Deregulated
communication
between
mitochondria
host
cells/organelles
has
significant
consequences
is
an
underlying
factor
of
many
pathophysiological
conditions,
including
process
aging.
During
aging,
lose
function,
mitocellular
pathways
break
down;
mitochondrial
dysfunction
interacts
dyscommunication,
forming
a
vicious
circle.
Therefore,
strategies
to
protect
function
promote
effective
increase
healthy
lifespan
longevity,
which
might
be
new
treatment
paradigm
for
age-related
disorders.
In
this
review,
we
comprehensively
discuss
signal
transduction
mechanisms
inter-
intracellular
communication,
as
well
interactions
hallmarks
This
review
emphasizes
indispensable
position
in
aging
organisms,
crucial
signaling
hubs.
addition,
also
specifically
focus
on
status
mitochondria-targeted
interventions
provide
potential
therapeutic
targets
diseases.
Graphical
Research Square (Research Square),
Journal Year:
2024,
Volume and Issue:
unknown
Published: March 21, 2024
Abstract
Mitochondrial
unfolded
protein
response
(UPR
mt
)
is
triggered
through
eIF2α
phosphorylation
in
mammal.
However,
the
mechanisms
of
UPR
activation
and
influence
on
mitochondrial
translation
remain
unclear.
In
this
study,
we
confirmed
that
was
a
rapid
specific
stress
with
pharmacological
induction,
along
expression
phosphorylation,
ATF4,
CHOP.
Meanwhile,
up-regulation
some
chaperones,
cytochrome
P450
enzymes,
DDIT4
determined
by
RNA-Seq
ribosome
profiling,
essential
for
expressing
ATF4
CHOP,
then
traffics
into
nucleus
initiates
CHOP
expression.
addition,
generation
ROS
morphology
unchanged
under
GTPP
induced
.
Furthermore,
unraveled
mechanism
HRI
kinase
mediates
proteins
CRISPR-Cas9
technology
recruitment
interaction
other
proteins.
number
imports
were
inhibited
accumulation
protein.
These
findings
provide
molecular
impact
cellular
translation,
which
will
offer
novel
insights
functional
research
,
including
its
implications
human
diseases
pathobiology.