Frontiers in Oncology,
Journal Year:
2019,
Volume and Issue:
9
Published: June 11, 2019
DNA
methylation
is
a
major
epigenetic
process
that
regulates
chromatin
structure
which
causes
transcriptional
activation
or
repression
of
genes
in
context-dependent
manner.
In
general,
takes
place
when
methyl
groups
are
added
to
the
appropriate
bases
on
genome
by
action
"writer"
molecules
known
as
methyltransferases.
How
these
marks
read
and
interpreted
into
different
functionalities
represents
one
main
mechanisms
through
switched
"ON"
"OFF"
typically
involves
types
"reader"
proteins
can
recognize
bind
methylated
regions.
A
tightly
balanced
regulation
exists
between
"writers"
"readers"
order
mediate
normal
cellular
functions.
However,
alterations
pattern
typical
hallmark
cancer
alters
way
written,
disease
states.
This
unique
characteristic
has
identified
them
attractive
therapeutic
targets.
this
review,
we
describe
current
state
knowledge
classes
thus
far
along
with
their
biological
functions,
how
they
dysregulated
cancer,
discuss
various
anti-cancer
therapies
currently
being
developed
evaluated
for
targeting
proteins.
Science,
Journal Year:
2018,
Volume and Issue:
361(6409), P. 1336 - 1340
Published: Sept. 28, 2018
The
classical
model
of
cytosine
DNA
methylation
(the
presence
5-methylcytosine,
5mC)
regulation
depicts
this
covalent
modification
as
a
stable
repressive
regulator
promoter
activity.
However,
whole-genome
analysis
5mC
reveals
widespread
tissue-
and
cell
type–specific
patterns
pervasive
dynamics
during
mammalian
development.
Here
we
review
recent
findings
that
delineate
functions
in
developmental
stages
diverse
genomic
compartments
well
discuss
the
molecular
mechanisms
connect
transcriptional
5mC.
Beyond
newly
appreciated
dynamics,
regulatory
roles
for
have
been
suggested
new
biological
contexts,
such
learning
memory
or
aging.
use
single-cell
measurement
techniques
precise
editing
tools
will
enable
functional
analyses
gene
expression,
clarifying
its
role
various
processes.
Essays in Biochemistry,
Journal Year:
2019,
Volume and Issue:
63(6), P. 727 - 741
Published: Nov. 22, 2019
Abstract
Dynamic
binding
of
transcription
factors
(TFs)
to
regulatory
elements
controls
transcriptional
states
throughout
organism
development.
Epigenetics
modifications,
such
as
DNA
methylation
mostly
within
cytosine-guanine
dinucleotides
(CpGs),
have
the
potential
modulate
TF
DNA.
Although
has
long
been
thought
repress
binding,
a
more
recent
model
proposes
that
can
also
inhibit
methylation.
Here,
we
review
possible
scenarios
by
which
and
affect
each
other.
Further
in
vivo
experiments
will
be
required
generalize
these
models.
Science Advances,
Journal Year:
2021,
Volume and Issue:
7(1)
Published: Jan. 1, 2021
Despite
past
extensive
studies,
the
mechanisms
underlying
pulmonary
fibrosis
(PF)
still
remain
poorly
understood.
Here,
we
demonstrated
that
lungs
originating
from
different
types
of
patients
with
PF,
including
coronavirus
disease
2019,
systemic
sclerosis-associated
interstitial
lung
disease,
and
idiopathic
mice
following
bleomycin
(BLM)-induced
PF
are
characterized
by
altered
methyl-CpG-binding
domain
2
(MBD2)
expression
in
macrophages.
Depletion
Mbd2
macrophages
protected
against
BLM-induced
PF.
deficiency
significantly
attenuated
transforming
growth
factor-β1
(TGF-β1)
production
reduced
M2
macrophage
accumulation
BLM
induction.
Mechanistically,
selectively
bound
to
Ship
promoter
macrophages,
which
it
repressed
enhanced
PI3K/Akt
signaling
promote
program.
Therefore,
intratracheal
administration
liposomes
loaded
siRNA
injuries
fibrosis.
Together,
our
data
support
possibility
MBD2
could
be
a
viable
target
clinical
settings.
Signal Transduction and Targeted Therapy,
Journal Year:
2023,
Volume and Issue:
8(1)
Published: May 22, 2023
Abstract
Over
decades,
researchers
have
focused
on
the
epigenetic
control
of
DNA-templated
processes.
Histone
modification,
DNA
methylation,
chromatin
remodeling,
RNA
and
noncoding
RNAs
modulate
many
biological
processes
that
are
crucial
to
development
cancers.
Dysregulation
epigenome
drives
aberrant
transcriptional
programs.
A
growing
body
evidence
suggests
mechanisms
modification
dysregulated
in
human
cancers
might
be
excellent
targets
for
tumor
treatment.
Epigenetics
has
also
been
shown
influence
immunogenicity
immune
cells
involved
antitumor
responses.
Thus,
application
therapy
cancer
immunotherapy
their
combinations
may
important
implications
Here,
we
present
an
up-to-date
thorough
description
how
modifications
cell
responses
microenvironment
(TME)
epigenetics
internally
modify
TME.
Additionally,
highlight
therapeutic
potential
targeting
regulators
immunotherapy.
Harnessing
complex
interplay
between
immunology
develop
therapeutics
combine
thereof
is
challenging
but
could
yield
significant
benefits.
The
purpose
this
review
assist
understanding
impact
TME,
so
better
immunotherapies
can
developed.
Biomolecules,
Journal Year:
2021,
Volume and Issue:
11(2), P. 195 - 195
Published: Jan. 30, 2021
There
are
currently
no
validated
biomarkers
which
can
be
used
to
accurately
diagnose
Alzheimer's
disease
(AD)
or
distinguish
it
from
other
dementia-causing
neuropathologies.
Moreover,
date,
only
symptomatic
treatments
exist
for
this
progressive
neurodegenerative
disorder.
In
the
search
new,
more
reliable
and
potential
therapeutic
options,
epigenetic
modifications
have
emerged
as
important
players
in
pathogenesis
of
AD.
The
aim
article
was
provide
a
brief
overview
current
knowledge
regarding
role
epigenetics
(including
mitoepigenetics)
AD,
possibility
applying
these
advances
future
AD
therapy.
Extensive
research
has
suggested
an
DNA
methylation
hydroxymethylation,
histone
posttranslational
modifications,
non-coding
RNA
regulation
(with
emphasis
on
microRNAs)
course
development
Recent
studies
also
indicated
mitochondrial
(mtDNA)
interesting
biomarker
since
dysfunctions
mitochondria
lower
mtDNA
copy
number
been
associated
with
pathophysiology.
evidence
suggests
that
changes
successfully
detected,
not
central
nervous
system,
but
cerebrospinal
fluid
periphery,
contributing
further
their
both
targets
Nature Genetics,
Journal Year:
2022,
Volume and Issue:
54(12), P. 1895 - 1906
Published: Dec. 1, 2022
Cytosine
methylation
efficiently
silences
CpG-rich
regulatory
regions
of
genes
and
repeats
in
mammalian
genomes.
To
what
extent
this
entails
direct
inhibition
transcription
factor
(TF)
binding
versus
indirect
via
recruitment
methyl-CpG-binding
domain
(MBD)
proteins
is
unclear.
Here
we
show
that
combinatorial
genetic
deletions
all
four
with
functional
MBDs
mouse
embryonic
stem
cells,
derived
neurons
or
a
human
cell
line
do
not
reactivate
methylated
promoters.
These
do,
however,
become
activated
by
methylation-restricted
TFs
if
DNA
removed.
We
identify
several
causal
neurons,
including
ONECUT1,
which
sensitive
only
at
motif
variant.
Rampantly
upregulated
retrotransposons
methylation-free
feature
CRE
motif,
activates
them
the
absence
methylation-sensitive
CREB1.
Our
study
reveals
vivo
argues
inhibition,
rather
than
repression
tested
MBD
proteins,
prevailing
mechanism
methylation-mediated
repeats.