Mechanisms of Hepatitis B Virus cccDNA and Minichromosome Formation and HBV Gene Transcription
Viruses,
Год журнала:
2024,
Номер
16(4), С. 609 - 609
Опубликована: Апрель 15, 2024
Hepatitis
B
virus
(HBV)
is
the
etiologic
agent
of
chronic
hepatitis
B,
which
puts
at
least
300
million
patients
risk
developing
fibrosis,
cirrhosis,
and
hepatocellular
carcinoma.
HBV
a
partially
double-stranded
DNA
Язык: Английский
RNA Modification in Metabolism
MedComm,
Год журнала:
2025,
Номер
6(3)
Опубликована: Март 1, 2025
ABSTRACT
Epigenetic
regulation
in
disease
development
has
been
witnessed
within
this
decade.
RNA
methylation
is
the
predominant
form
of
epigenetic
regulation,
and
most
prevalent
modification
N6‐methyladenosine
(m
6
A).
Recently,
emerged
as
a
potential
target
for
treatment.
posttranscriptional
gene
expression
that
involved
both
physiological
pathological
processes.
Evidence
suggests
m
A
significantly
affects
metabolism,
its
abnormal
changes
have
observed
variety
diseases.
Metabolic
diseases
are
series
caused
by
metabolic
processes
body,
common
include
diabetes
mellitus,
obesity,
nonalcoholic
fatty
liver
disease,
etc.;
although
pathogenesis
these
differs
from
each
other
to
current
understanding,
recent
studies
suggested
pivotal
role
modulating
diseases,
A‐based
drug
on
agenda.
This
paper
reviewed
understanding
hoping
provide
systematic
information
those
area.
Язык: Английский
Liver-specific Mettl14 deletion induces nuclear heterotypia and dysregulates RNA export machinery
bioRxiv (Cold Spring Harbor Laboratory),
Год журнала:
2024,
Номер
unknown
Опубликована: Июнь 17, 2024
Abstract
Modification
of
RNA
with
N
6
-methyladenosine
(m
A)
has
gained
attention
in
recent
years
as
a
general
mechanism
gene
regulation.
In
the
liver,
m
A,
along
its
associated
machinery,
been
studied
potential
biomarker
disease
and
cancer,
impacts
on
metabolism,
cell
cycle
regulation,
pro-cancer
state
signaling.
However
these
observational
data
have
yet
to
be
causally
examined
vivo.
For
example,
neither
perturbation
key
A
writers
Mettl3
Mettl14
,
nor
readers
Ythdf1
Ythdf2
thoroughly
mechanistically
characterized
vivo
they
vitro
.
To
understand
functions
machineries,
we
developed
mouse
models
found
that
deleting
led
progressive
liver
injury
by
nuclear
heterotypia,
changes
mRNA
splicing,
processing
export
leading
increases
surveillance
recycling.
Язык: Английский