International Immunopharmacology,
Journal Year:
2024,
Volume and Issue:
136, P. 112367 - 112367
Published: May 31, 2024
SLC25A19
is
a
mitochondrial
thiamine
pyrophosphate
(TPP)
carrier
that
mediates
TPP
entry
into
the
mitochondria.
has
been
recognized
to
play
crucial
role
in
many
metabolic
diseases,
but
its
cancer
not
clearly
reported.
Based
on
clinical
data
from
The
Cancer
Genome
Atlas
(TCGA),
following
parameters
were
analyzed
among
HCC
patients:
expression,
enrichment
analyses,
immune
infiltration,
ferroptosis
and
prognosis
analyses.
In
vitro,
high
expression
was
validated
by
qRT-PCR
Immunohistochemistry.
Subsequently,
series
of
cell
function
experiments,
including
CCK8,
EdU,
clone
formation,
trans-well
scratch
assays,
conducted
illustrate
effect
growth
metastasis
cells.
Meanwhile,
indicators
related
also
detected.
SCL25A19
highly
expressed
predicts
poor
prognosis.
Elevated
patients
markedly
associated
with
T
stage,
pathological
status
(PS),
tumor
(TS),
histologic
grade
(HG),
AFP.
Our
results
indicate
generally
good
predictive
diagnostic
ability.
gene
analyses
showed
significantly
correlated
fatty
acid
metabolism,
marker
genes.
vitro
experiments
have
confirmed
silencing
can
inhibit
proliferation
migration
ability
cells
induce
HCC.
conclusion,
these
findings
novel
prognostic
biomarker
invasion
HCC,
it
an
excellent
candidate
for
therapeutic
target
against
Science,
Journal Year:
2022,
Volume and Issue:
378(6617), P. 317 - 322
Published: Oct. 20, 2022
In
the
mitochondrial
outer
membrane,
α-helical
transmembrane
proteins
play
critical
roles
in
cytoplasmic-mitochondrial
communication.
Using
genome-wide
CRISPR
screens,
we
identified
carrier
homolog
2
(MTCH2),
and
its
paralog
MTCH1,
showed
that
it
is
required
for
insertion
of
biophysically
diverse
tail-anchored
(TA),
signal-anchored,
multipass
proteins,
but
not
membrane
β-barrel
proteins.
Purified
MTCH2
was
sufficient
to
mediate
into
reconstituted
proteoliposomes.
Functional
mutational
studies
suggested
has
evolved
from
a
solute
transporter.
uses
membrane-embedded
hydrophilic
residues
function
as
gatekeeper
controlling
mislocalization
TAs
endoplasmic
reticulum
modulating
sensitivity
leukemia
cells
apoptosis.
Our
identification
an
insertase
provides
mechanistic
explanation
phenotypes
disease
states
associated
with
dysfunction.
Science,
Journal Year:
2023,
Volume and Issue:
382(6672), P. 820 - 828
Published: Nov. 2, 2023
Mitochondria
must
maintain
adequate
amounts
of
metabolites
for
protective
and
biosynthetic
functions.
However,
how
mitochondria
sense
the
abundance
regulate
metabolic
homeostasis
is
not
well
understood.
In
this
work,
we
focused
on
glutathione
(GSH),
a
critical
redox
metabolite
in
mitochondria,
identified
feedback
mechanism
that
controls
its
through
mitochondrial
GSH
transporter,
SLC25A39.
Under
physiological
conditions,
SLC25A39
rapidly
degraded
by
protease
AFG3L2.
Depletion
dissociates
AFG3L2
from
SLC25A39,
causing
compensatory
increase
uptake.
Genetic
proteomic
analyses
putative
iron-sulfur
cluster
matrix-facing
loop
as
essential
regulation,
coupling
iron
to
import.
Altogether,
our
work
revealed
paradigm
autoregulatory
control
organelles.
Circulation Research,
Journal Year:
2024,
Volume and Issue:
135(2), P. 372 - 396
Published: July 4, 2024
Despite
clinical
and
scientific
advancements,
heart
failure
is
the
major
cause
of
morbidity
mortality
worldwide.
Both
mitochondrial
dysfunction
inflammation
contribute
to
development
progression
failure.
Although
crucial
reparative
healing
following
acute
cardiomyocyte
injury,
chronic
damages
heart,
impairs
function,
decreases
cardiac
output.
Mitochondria,
which
comprise
one
third
volume,
may
prove
a
potential
therapeutic
target
for
Known
primarily
energy
production,
mitochondria
are
also
involved
in
other
processes
including
calcium
homeostasis
regulation
cellular
apoptosis.
Mitochondrial
function
closely
related
morphology,
alters
through
dynamics,
thus
ensuring
that
needs
cell
met.
However,
failure,
changes
substrate
use
lead
impaired
myocyte
function.
This
review
discusses
cristae
role
contact
site
organizing
system
complex
ultrastructure
changes.
Additionally,
this
covers
mitochondria-endoplasmic
reticulum
sites,
communication
via
nanotunnels,
altered
metabolite
production
during
We
highlight
these
often-neglected
factors
promising
targets
