Nutrients,
Journal Year:
2024,
Volume and Issue:
16(15), P. 2433 - 2433
Published: July 26, 2024
Existing
research
indicates
that
different
types
of
meat
have
varying
effects
on
health
and
aging,
but
the
specific
causal
relationships
remain
unclear.
This
study
aimed
to
explore
relationship
between
intake
aging-related
phenotypes.
employed
Mendelian
randomization
(MR)
select
genetic
variants
associated
with
from
large
genomic
databases,
ensuring
independence
pleiotropy-free
nature
these
instrumental
variables
(IVs),
calculated
F-statistic
evaluate
strength
IVs.
The
validity
estimates
was
assessed
through
sensitivity
analyses
various
MR
methods
(MR-Egger,
weighted
median,
inverse-variance
(IVW),
simple
mode,
mode),
MR-Egger
regression
intercept
used
test
for
pleiotropy
bias
Cochran's
Q
heterogeneity
results.
findings
reveal
a
positive
consumers
DNA
methylation
PhenoAge
acceleration,
suggesting
increased
may
accelerate
biological
aging
process.
Specifically,
lamb
is
found
effect
mitochondrial
copy
number,
while
processed
consumption
shows
negative
telomere
length.
No
significant
were
observed
other
intake.
highlights
impact
processing
cooking
meat's
role
in
enhancing
our
understanding
how
their
preparation
affect
process,
providing
theoretical
basis
dietary
strategies
at
delaying
quality
life.
Nature Structural & Molecular Biology,
Journal Year:
2021,
Volume and Issue:
28(7), P. 594 - 603
Published: June 17, 2021
DNA
methylation
plays
a
critical
role
during
development,
particularly
in
repressing
retrotransposons.
The
mammalian
landscape
is
dependent
on
the
combined
activities
of
canonical
maintenance
enzyme
Dnmt1
and
de
novo
Dnmts,
3a
3b.
Here,
we
demonstrate
that
displays
activity
vitro
vivo
with
specific
retrotransposon
targeting.
We
used
whole-genome
bisulfite
long-read
Nanopore
sequencing
genetically
engineered
methylation-depleted
mouse
embryonic
stem
cells
to
provide
an
in-depth
assessment
quantification
this
activity.
Utilizing
additional
knockout
lines
molecular
characterization,
show
depends
Uhrf1,
its
genomic
recruitment
overlaps
regions
enrich
for
Trim28
H3K9
trimethylation.
Our
data
can
catalyze
both
context,
especially
at
retrotransposons,
where
mechanism
may
stability
long-term
repression
epigenetic
propagation
throughout
development.
Annual Review of Immunology,
Journal Year:
2024,
Volume and Issue:
42(1), P. 455 - 488
Published: Feb. 16, 2024
Ten-eleven
translocation
(TET)
proteins
are
iron-dependent
and
α-ketoglutarate-dependent
dioxygenases
that
sequentially
oxidize
the
methyl
group
of
5-methylcytosine
(5mC)
to
5-hydroxymethylcytosine
(5hmC),
5-formylcytosine
(5fC)
5-carboxylcytosine
(5caC).
All
three
epigenetic
modifications
intermediates
in
DNA
demethylation.
TET
recruited
by
transcription
factors
RNA
polymerase
II
modify
5mC
at
enhancers
gene
bodies,
thereby
regulating
expression
during
development,
cell
lineage
specification,
activation.
It
is
not
yet
clear,
however,
how
established
biochemical
activities
enzymes
oxidizing
mediating
demethylation
relate
known
association
deficiency
with
inflammation,
clonal
hematopoiesis,
cancer.
There
hints
ability
promote
proliferation
a
signal-dependent
manner
may
be
harnessed
for
cancer
immunotherapy.
In
this
review,
we
draw
upon
recent
findings
cells
immune
system
illustrate
as
well
emerging
ideas
influence
cellular
function.
Nucleic Acids Research,
Journal Year:
2020,
Volume and Issue:
49(6), P. 3020 - 3032
Published: Nov. 11, 2020
Abstract
DNA
methylation
is
essential
to
development
and
cellular
physiology
in
mammals.
Faulty
frequently
observed
human
diseases
like
cancer
neurological
disorders.
Molecularly,
this
epigenetic
mark
linked
other
chromatin
modifications
it
regulates
key
genomic
processes,
including
transcription
splicing.
Each
round
of
replication
generates
two
hemi-methylated
copies
the
genome.
These
must
be
converted
back
symmetrically
methylated
before
next
S-phase,
or
will
fade
away;
therefore
maintenance
essential.
Mechanistically,
modification
takes
place
during
after
replication,
occurs
within
very
dynamic
context
re-assembly.
Here,
we
review
recent
discoveries
unresolved
questions
regarding
mechanisms,
dynamics
fidelity
We
also
discuss
how
could
regulated
normal
misregulated
disease.
International Journal of Molecular Sciences,
Journal Year:
2020,
Volume and Issue:
21(15), P. 5281 - 5281
Published: July 25, 2020
The
aging
process
starts
directly
after
birth
and
lasts
for
the
entire
lifespan;
it
manifests
itself
with
a
decline
in
an
organism's
ability
to
adapt
is
linked
development
of
age-related
diseases
that
eventually
lead
premature
death.
This
review
aims
explore
how
microRNAs
(miRNAs)
are
involved
skin
functioning
aging.
Recent
evidence
has
suggested
miRNAs
regulate
all
aspects
cutaneous
biogenesis,
functionality,
It
been
noted
some
were
down-regulated
long-lived
individuals,
such
as
let-7,
miR-17,
miR-34
(known
longevity-related
miRNAs).
They
conserved
humans
presumably
promote
lifespan
prolongation;
conversely,
they
up-regulated
diseases,
like
cancers.
analysis
age-associated
revealed
increased
expression
miR-130,
miR-138,
miR-181a/b
keratinocytes
during
replicative
senescence.
These
affected
cell
proliferation
pathways
via
targeting
p63
Sirtuin
1
mRNAs.
Notably,
miR-181a
was
also
implicated
immunosenescence,
represented
by
Langerhans
cells.
Dermal
fibroblasts
expressed
levels
biomarkers
affect
telomere
maintenance
phases
cellular
life
cycle,
miR-23a-3p,
34a-5p,
miR-125a,
miR-181a-5p,
miR-221/222-3p.
Among
them,
family,
stimulated
ultraviolet
B
irradiation,
deteriorates
collagen
extracellular
matrix
due
activation
metalloproteinases
thereby
potentiates
wrinkle
formation.
In
addition
pro-aging
effects
miRNAs,
plausible
antiaging
activity
miR-146a
antagonized
UVA-induced
inhibition
suppressed
aging-related
genes
(e.g.,
p21WAF-1,
p16,
p53)
through
Smad4
noticed.
Nevertheless,
role
still
not
fully
elucidated
needs
be
further
discovered
explained.
Nucleic Acids Research,
Journal Year:
2021,
Volume and Issue:
49(11), P. 6053 - 6068
Published: April 12, 2021
Abstract
During
S
phase,
the
cooperation
between
macromolecular
complexes
regulating
DNA
synthesis,
epigenetic
information
maintenance
and
repair
is
advantageous
for
cells,
as
they
can
rapidly
detect
damage
initiate
response
(DDR).
UHRF1
a
fundamental
regulator;
its
ability
to
coordinate
methylation
histone
code
unique
across
proteomes
of
different
species.
Recently,
UHRF1’s
role
in
has
been
explored
recognized
be
important
maintaining
epigenome.
sensor
interstrand
crosslinks
determinant
switch
towards
homologous
recombination
double-strand
breaks;
loss
results
enhanced
sensitivity
damage.
These
functions
are
finely
regulated
by
specific
post-translational
modifications
mediated
SRA
domain,
which
binds
damaged
DNA,
RING
domain.
Here,
we
review
recent
studies
on
DDR
focusing
how
it
recognizes
cooperates
with
other
proteins
repair.
We
then
discuss
abilities
reading
writing
modifications,
or
interactions
ncRNAs,
could
interlace
DDR.