Dysregulation
of
CD4+
T
cell
differentiation
is
linked
to
autoimmune
diseases.
Metabolic
reprogramming
from
oxidative
phosphorylation
glycolysis
and
accumulation
lactate
are
involved
in
this
process.
However,
the
underlying
mechanisms
remain
unclear.
Our
study
showed
that
lactate-derived
lactylation
regulated
differentiation.
Lactylation
levels
cells
increased
with
progression
experimental
uveitis
(EAU).
Inhibition
suppressed
TH17
attenuated
EAU
inflammation.
The
global
lactylome
revealed
landscape
lactylated
sites
proteins
normal
mice.
Specifically,
hyperlactylation
Ikzf1
at
Lys164
promoted
by
directly
modulating
expression
TH17-related
genes,
including
Runx1,
Tlr4,
interleukin-2
(IL-2),
IL-4.
Delactylation
impaired
These
findings
exemplify
how
regulates
site
specificity
protein
promote
implicate
as
a
potential
therapeutic
target
for
Journal of Experimental & Clinical Cancer Research,
Год журнала:
2022,
Номер
41(1)
Опубликована: Апрель 15, 2022
Metabolites
are
intermediate
products
of
cellular
metabolism
catalysed
by
various
enzymes.
Metabolic
remodelling,
as
a
biochemical
fingerprint
cancer
cells,
causes
abnormal
metabolite
accumulation.
These
metabolites
mainly
generate
energy
or
serve
signal
transduction
mediators
via
noncovalent
interactions.
After
the
development
highly
sensitive
mass
spectrometry
technology,
were
shown
to
covalently
modify
proteins
forms
lysine
acylation,
including
acetylation,
crotonylation,
lactylation,
succinylation,
propionylation,
butyrylation,
malonylation,
glutarylation,
2-hydroxyisobutyrylation
and
β-hydroxybutyrylation.
modifications
can
regulate
gene
expression
intracellular
signalling
pathways,
highlighting
extensive
roles
metabolites.
Lysine
acetylation
is
not
discussed
in
detail
this
review
since
it
has
been
broadly
investigated.
We
focus
on
nine
aforementioned
novel
acylations
beyond
which
be
classified
into
two
categories:
histone
nonhistone
acylations.
summarize
characteristics
common
functions
these
acylation
types
and,
most
importantly,
provide
glimpse
their
fine-tuned
control
tumorigenesis
potential
value
tumour
diagnosis,
monitoring
therapy.
Frontiers in Oncology,
Год журнала:
2022,
Номер
12
Опубликована: Июнь 22, 2022
Aldehyde
dehydrogenases
1
family
member
A1(ALDH1A1)
gene
codes
a
cytoplasmic
enzyme
and
shows
vital
physiological
pathophysiological
functions
in
many
areas.
ALDH1A1
plays
important
roles
various
diseases,
especially
cancers.
We
reviewed
summarized
representative
correlative
studies
found
that
could
induce
cancers
via
the
maintenance
of
cancer
stem
cell
properties,
modification
metabolism,
promotion
DNA
repair.
expression
is
regulated
by
several
epigenetic
processes.
also
acted
as
tumor
suppressor
certain
The
detoxification
often
causes
chemotherapy
failure.
Currently,
ALDH1A1-targeted
therapy
widely
used
treatment,
but
mechanism
which
regulates
development
not
fully
understood.
This
review
will
provide
insight
into
status
research
new
viewpoint
for
therapy.
Genes & Diseases,
Год журнала:
2022,
Номер
11(1), С. 218 - 233
Опубликована: Дек. 28, 2022
Ribonucleotide
reductase
M2
(RRM2)
is
a
small
subunit
in
ribonucleotide
reductases,
which
participate
nucleotide
metabolism
and
catalyze
the
conversion
of
nucleotides
to
deoxynucleotides,
maintaining
dNTP
pools
for
DNA
biosynthesis,
repair,
replication.
RRM2
performs
critical
role
malignant
biological
behaviors
cancers.
The
structure,
regulation,
function
its
inhibitors
were
discussed.
gene
can
produce
two
transcripts
encoding
same
ORF.
expression
regulated
at
multiple
levels
during
processes
from
transcription
translation.
Moreover,
this
associated
with
resistance,
cell
death,
tumor
immunity.
In
order
develop
design
RRM2,
appropriate
strategies
be
adopted
based
on
different
mechanisms.
Thus,
greater
appreciation
characteristics
benefit
understanding
tumorigenesis,
resistance
cancer,
microenvironment.
RRM2-targeted
therapy
will
more
attention
future
therapeutic
approaches
enhancement
treatment
effects
amelioration
dismal
prognosis.
Dysregulation
of
CD4+
T
cell
differentiation
is
linked
to
autoimmune
diseases.
Metabolic
reprogramming
from
oxidative
phosphorylation
glycolysis
and
accumulation
lactate
are
involved
in
this
process.
However,
the
underlying
mechanisms
remain
unclear.
Our
study
showed
that
lactate-derived
lactylation
regulated
differentiation.
Lactylation
levels
cells
increased
with
progression
experimental
uveitis
(EAU).
Inhibition
suppressed
TH17
attenuated
EAU
inflammation.
The
global
lactylome
revealed
landscape
lactylated
sites
proteins
normal
mice.
Specifically,
hyperlactylation
Ikzf1
at
Lys164
promoted
by
directly
modulating
expression
TH17-related
genes,
including
Runx1,
Tlr4,
interleukin-2
(IL-2),
IL-4.
Delactylation
impaired
These
findings
exemplify
how
regulates
site
specificity
protein
promote
implicate
as
a
potential
therapeutic
target
for
