Insights on post-translational modifications in fatty liver and fibrosis progression
C. Nageswara Raju,
Kavitha Sankaranarayanan
Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease,
Год журнала:
2025,
Номер
1871(3), С. 167659 - 167659
Опубликована: Янв. 7, 2025
Язык: Английский
Lactate-induced protein lactylation in cancer: functions, biomarkers and immunotherapy strategies
Frontiers in Immunology,
Год журнала:
2025,
Номер
15
Опубликована: Янв. 10, 2025
Lactate,
long
viewed
as
a
byproduct
of
glycolysis
and
metabolic
waste.
Initially
identified
within
the
context
yogurt
fermentation,
lactate's
role
extends
beyond
culinary
applications
to
its
significance
in
biochemical
processes.
Contemporary
research
reveals
that
lactate
functions
not
merely
terminal
product
but
also
nexus
for
initiating
physiological
pathological
responses
body.
Lysine
lactylation
(Kla),
novel
post-translational
modification
(PTM)
proteins,
has
emerged
pivotal
mechanism
by
which
exerts
regulatory
influence.
This
epigenetic
potential
alter
gene
expression
patterns,
thereby
impacting
Increasing
evidence
indicates
correlation
between
adverse
prognosis
various
malignancies.
Consequently,
this
review
article
aims
encapsulate
proteins
interact
with
lactate,
elucidate
tumorigenesis
progression,
explore
therapeutic
targets
afforded
modulation
lactylation.
The
objective
is
clarify
oncogenic
provide
strategic
framework
future
directions
burgeoning
field.
Язык: Английский
Total Saponins from Panax japonicus Reduced Lipid Deposition and Inflammation in Hepatocyte via PHD2 and Hepatic Macrophage-derived Exosomal miR-463-5p
Journal of Ethnopharmacology,
Год журнала:
2025,
Номер
unknown, С. 119376 - 119376
Опубликована: Янв. 1, 2025
Язык: Английский
Conjugated linoleic acid (CLA) reduces intestinal fatty acid uptake and chylomicron formation in HFD-fed mice associated with the inhibition of DHHC7-mediated CD36 palmitoylation and the downstream ERK pathway
Food & Function,
Год журнала:
2024,
Номер
15(9), С. 5000 - 5011
Опубликована: Янв. 1, 2024
The
anti-obesity
effect
of
conjugated
linoleic
acid
(CLA)
has
been
well
elucidated,
but
whether
CLA
affects
fat
deposition
by
regulating
intestinal
dietary
absorption
remains
largely
unknown.
Thus,
this
study
aimed
to
investigate
the
effects
on
fatty
uptake
and
chylomicron
formation
explore
possible
underlying
mechanisms.
We
found
that
supplementation
reduced
in
HFD
(high
diet)-fed
mice
accompanied
decreased
serum
TG
level,
increased
fecal
lipids
expression
ApoB48
MTTP.
Correspondingly,
c9,
t11-CLA,
not
t10,
c12-CLA
induced
reduction
content
PA
(palmitic
acid)-treated
MODE-K
cells.
In
mechanism
uptake,
t11-CLA
inhibited
binding
CD36
with
palmitoyltransferase
DHHC7,
thus
leading
decreases
palmitoylation
level
localization
cell
membrane
PA-treated
formation,
CD36/FYN/LYN
complex
activation
ERK
pathway
vivo
verification,
DHHC7-mediated
total
suppressed
jejunum
HFD-fed
mice.
Altogether,
these
data
showed
associated
inhibition
downstream
pathway.
Язык: Английский
Conjugated Linoleic Acid (CLA) Mitigates High-Fat Diet (HFD)-Induced Mammary Gland Development Impairment of Pubertal Mice via Regulating CD36 Palmitoylation and Downstream JNK–ERK Pathway
Journal of Agricultural and Food Chemistry,
Год журнала:
2025,
Номер
unknown
Опубликована: Янв. 3, 2025
Conjugated
linoleic
acid
(CLA)
is
known
for
antiobesity.
However,
the
role
of
CLA
in
regulating
high-fat
diet
(HFD)-impaired
pubertal
mammary
gland
development
remains
undefined.
Here,
female
mice
and
HC11
cells
were
treated
with
HFD
or
palmitic
(PA),
supplemented
without
CLA,
respectively.
We
found
that
prevented
impaired
exposed
to
HFD.
In
vitro,
c9,
t11-CLA,
but
not
t10,
c12-CLA,
promoted
PA-suppressed
proliferation,
accompanied
by
hindered
CD36
palmitoylation
localization
on
plasma
membrane.
Moreover,
t11-CLA
reduced
formation
CD36/Fyn/Lyn
complex
inhibited
JNK
pathway
while
activated
ERK
PA-treated
HC11.
mechanism,
activation
inhibition
abolished
t11-CLA-stimulated
proliferation
vivo
verification,
total
cell
membrane
palmitoylation,
suppressed
CD36/FYN/LYN
complex,
HFD-fed
mice.
conclusion,
mitigated
HFD-impaired
via
downstream
JNK–ERK
pathway.
These
data
suggested
potential
application
ameliorating
obesity-impaired
development.
Язык: Английский
TaoHeChengQi Decotion Alleviate Chronic renal failure via Regulation of PHD2/UCP1 and RIPK3/AKT/TGF-β Pathway
Phytomedicine,
Год журнала:
2025,
Номер
141, С. 156548 - 156548
Опубликована: Март 13, 2025
Язык: Английский
PHD1-3 oxygen sensors in vivo—lessons learned from gene deletions
Pflügers Archiv - European Journal of Physiology,
Год журнала:
2024,
Номер
476(9), С. 1307 - 1337
Опубликована: Март 21, 2024
Oxygen
sensors
enable
cells
to
adapt
limited
oxygen
availability
(hypoxia),
affecting
various
cellular
and
tissue
responses.
Prolyl-4-hydroxylase
domain
1-3
(PHD1-3;
also
called
Egln1-3,
HIF-P4H
1-3,
HIF-PH
1-3)
proteins
belong
the
Fe
Язык: Английский
The P124A mutation of SRP14 alters its migration on SDS-PAGE without impacting its function
Acta Biochimica et Biophysica Sinica,
Год журнала:
2024,
Номер
56(2), С. 315 - 322
Опубликована: Янв. 15, 2024
SRP14
is
a
crucial
protein
subunit
of
the
signal
recognition
particle
(SRP),
ribonucleoprotein
complex
essential
for
co-translational
translocation
to
endoplasmic
reticulum.
During
our
investigation
expression
across
diverse
cell
lines,
we
observe
variations
in
its
migration
on
sodium
dodecyl
sulfate-polyacrylamide
gel
electrophoresis
(SDS-PAGE),
with
some
cells
exhibiting
slower
and
others
migrating
faster.
However,
cause
this
phenomenon
remains
elusive.
Our
research
rules
out
alternative
splicing
as
and,
instead,
identifies
presence
P124A
mutation
(SRP14
Язык: Английский
MitoMAMMAL: a genome scale model of mammalian mitochondria predicts cardiac and BAT metabolism
bioRxiv (Cold Spring Harbor Laboratory),
Год журнала:
2024,
Номер
unknown
Опубликована: Июль 26, 2024
Abstract
Mitochondria
perform
several
essential
functions
in
order
to
maintain
cellular
homeostasis
and
mitochondrial
metabolism
is
inherently
flexible
allow
correct
function
a
wide
range
of
tissues.
Dysregulated
can
therefore
affect
different
tissues
ways
which
presents
experimental
challenges
understanding
the
pathology
diseases.
System-level
metabolic
modelling
useful
gaining
in-depth
insights
into
tissue-specific
metabolism,
yet
despite
mouse
being
common
model
organism
used
research,
there
currently
no
specific
available.
In
this
work,
building
upon
similarity
between
human
we
have
created
mitoMammal,
genome-scale
that
contains
gene-product
reaction
rules.
MitoMammal
able
metabolism.
To
demonstrate
feature,
using
an
adapted
E-Flux2
algorithm,
first
integrated
proteomic
data
extracted
from
mitochondria
isolated
cardiomyocytes
brown
adipocyte
tissue.
We
then
transcriptomic
vitro
differentiated
adipose
cells
modelled
context
flux
balance
analysis.
all
three
simulations,
mitoMammal
made
mostly
accurate,
some
novel
predictions
relating
energy
adipocytes.
This
demonstrates
its
usefulness
research
cardiac
disease
diabetes
both
contexts.
Язык: Английский
MitoMAMMAL: a genome scale model of mammalian mitochondria predicts cardiac and BAT metabolism
Bioinformatics Advances,
Год журнала:
2024,
Номер
5(1)
Опубликована: Ноя. 5, 2024
Abstract
Motivation
Mitochondria
are
essential
for
cellular
metabolism
and
inherently
flexible
to
allow
correct
function
in
a
wide
range
of
tissues.
Consequently,
dysregulated
mitochondrial
affects
different
tissues
ways
leading
challenges
understanding
the
pathology
diseases.
System-level
metabolic
modelling
is
useful
studying
tissue-specific
metabolism,
yet
despite
mouse
being
common
model
organism
research,
no
specific
currently
available.
Results
Building
upon
similarity
between
human
we
present
mitoMammal,
genome-scale
that
contains
gene-product
reaction
rules.
MitoMammal
able
metabolism.
To
demonstrate
this,
using
an
adapted
E-Flux
algorithm,
integrated
proteomic
data
from
mitochondria
isolated
cardiomyocytes
brown
adipocyte
tissue,
as
well
transcriptomic
vitro
differentiated
adipocytes
modelled
context
flux
balance
analysis.
In
all
three
simulations,
mitoMammal
made
mostly
accurate,
some
novel
predictions
relating
energy
adipocytes.
This
demonstrates
its
usefulness
research
cardiac
disease
diabetes
both
contexts.
Availability
implementation
The
Jupyter
Notebook
available
at:
https://gitlab.com/habermann_lab/mitomammal.
Язык: Английский