ABSTRACT
Background
Adenosine
deaminase
action
on
RNA
1
(ADAR1)
can
convert
the
adenosine
in
double‐stranded
(dsRNA)
molecules
into
inosine
a
process
known
as
A‐to‐I
editing.
ADAR1
regulates
gene
expression
output
by
interacting
with
and
other
proteins;
plays
important
roles
development,
including
growth;
is
linked
to
innate
immunity,
tumors,
central
nervous
system
(CNS)
diseases.
Results
In
recent
years,
role
of
tumors
has
been
widely
discussed,
but
its
CNS
diseases
not
reviewed.
It
worth
noting
that
studies
have
shown
great
potential
treatment
neurodegenerative
diseases,
mechanisms
are
still
unclear.
Therefore,
it
necessary
elaborate
Conclusions
Here,
we
focus
effects
such
Aicardi–AicardiGoutières
syndrome,
Alzheimer's
disease,
Parkinson's
glioblastoma,
epilepsy,
amyotrophic
lateral
sclerosis,
autism.
We
also
evaluate
impact
ADAR1‐based
strategies
these
particular
development
new
technologies
microRNAs,
nanotechnology,
editing,
stem
cell
therapy.
hope
provide
directions
insights
for
future
editing
technology
brain
science
Experimental & Molecular Medicine,
Journal Year:
2024,
Volume and Issue:
56(6), P. 1250 - 1262
Published: June 14, 2024
Alu
elements
are
highly
abundant
primate-specific
short
interspersed
nuclear
that
account
for
~10%
of
the
human
genome.
Due
to
their
preferential
location
in
gene-rich
regions,
especially
introns
and
3'
UTRs,
can
exert
regulatory
effects
on
expression
both
host
neighboring
genes.
When
two
with
inverse
orientations
positioned
close
proximity,
transcription
results
generation
distinct
double-stranded
RNAs
(dsRNAs),
known
as
inverted
repeats
(IRAlus).
IRAlus
key
immunogenic
self-dsRNAs
post-transcriptional
cis-regulatory
play
a
role
circular
RNA
biogenesis,
well
transport
stability.
Recently,
dsRNAs
have
emerged
regulators
activators
Z-DNA-binding
proteins.
The
formation
activity
be
modulated
through
editing
interactions
RNA-binding
proteins,
misregulation
has
been
implicated
several
immune-associated
disorders.
In
this
review,
we
summarize
emerging
functions
dsRNAs,
mechanisms
governing
activity,
relevance
pathogenesis
diseases.
Cell & Bioscience,
Journal Year:
2024,
Volume and Issue:
14(1)
Published: March 16, 2024
Abstract
With
the
advancement
of
sequencing
technologies
and
bioinformatics,
over
than
170
different
RNA
modifications
have
been
identified.
However,
only
a
few
these
can
lead
to
base
pair
changes,
which
are
called
editing.
editing
is
ubiquitous
modification
in
mammalian
transcriptomes
an
important
co/posttranscriptional
that
plays
crucial
role
various
cellular
processes.
There
two
main
types
events:
adenosine
inosine
(A-to-I)
editing,
catalyzed
by
ADARs
on
double-stranded
or
ADATs
tRNA,
cytosine
uridine
(C-to-U)
APOBECs.
This
article
provides
overview
structure,
function,
applications
enzymes.
We
discuss
structural
characteristics
three
enzyme
families
their
catalytic
mechanisms
also
explain
biological
particularly
innate
immunity,
cancer
biogenesis,
antiviral
activity.
Additionally,
this
describes
tools
for
manipulating
correct
disease-causing
mutations,
as
well
potential
enzymes
field
biotechnology
therapy.
Trends in Cell Biology,
Journal Year:
2024,
Volume and Issue:
unknown
Published: July 1, 2024
Adenosine
deaminase
acting
on
RNA
1
(ADAR1)
converts
adenosine
to
inosine
in
double-stranded
(dsRNA)
molecules,
a
process
known
as
A-to-I
editing.
ADAR1
deficiency
humans
and
mice
results
profound
inflammatory
diseases
characterised
by
the
spontaneous
induction
of
innate
immunity.
In
cells
lacking
ADAR1,
unedited
RNAs
activate
sensors.
These
include
melanoma
differentiation-associated
gene
5
(MDA5)
that
induces
expression
cytokines,
particularly
type
I
interferons
(IFNs),
protein
kinase
R
(PKR),
oligoadenylate
synthase
(OAS),
Z-DNA/RNA
binding
(ZBP1).
Immunogenic
'defused'
may
transcripts
from
repetitive
elements
other
long
duplex
RNAs.
Here,
we
review
these
recent
fundamental
discoveries
discuss
implications
for
human
diseases.
Some
tumours
depend
escape
immune
surveillance,
opening
possibility
unleashing
anticancer
therapies
with
inhibitors.
Cell Reports,
Journal Year:
2024,
Volume and Issue:
43(8), P. 114618 - 114618
Published: Aug. 1, 2024
Adar
null
mutant
mouse
embryos
die
with
aberrant
double-stranded
RNA
(dsRNA)-driven
interferon
induction,
and
Mavs
double
mutants,
in
which
induction
is
prevented,
soon
after
birth.
Protein
kinase
R
(Pkr)
aberrantly
activated
pup
intestines
before
death,
intestinal
crypt
cells
die,
villi
are
lost.
Eifak2
triple
mice
rescue
all
defects
have
long-term
survival.
Adenosine
deaminase
acting
on
1
(ADAR1)
PKR
co-immunoprecipitate
from
cells,
suggesting
inhibition
by
direct
interaction.
AlphaFold
studies
an
inhibitory
dsRNA
binding
domain
(dsRBD)-kinase
interaction
ADAR1
dsRBD3-PKR
provide
a
testable
model
of
the
inhibition.
Wild-type
or
editing-inactive
human
expressed
A549
inhibits
activation
endogenous
PKR.
required
for,
but
not
sufficient
Mutating
contact
prevents
co-immunoprecipitation,
activity,
co-localization
cells.
ABSTRACT
Background
Adenosine
deaminase
action
on
RNA
1
(ADAR1)
can
convert
the
adenosine
in
double‐stranded
(dsRNA)
molecules
into
inosine
a
process
known
as
A‐to‐I
editing.
ADAR1
regulates
gene
expression
output
by
interacting
with
and
other
proteins;
plays
important
roles
development,
including
growth;
is
linked
to
innate
immunity,
tumors,
central
nervous
system
(CNS)
diseases.
Results
In
recent
years,
role
of
tumors
has
been
widely
discussed,
but
its
CNS
diseases
not
reviewed.
It
worth
noting
that
studies
have
shown
great
potential
treatment
neurodegenerative
diseases,
mechanisms
are
still
unclear.
Therefore,
it
necessary
elaborate
Conclusions
Here,
we
focus
effects
such
Aicardi–AicardiGoutières
syndrome,
Alzheimer's
disease,
Parkinson's
glioblastoma,
epilepsy,
amyotrophic
lateral
sclerosis,
autism.
We
also
evaluate
impact
ADAR1‐based
strategies
these
particular
development
new
technologies
microRNAs,
nanotechnology,
editing,
stem
cell
therapy.
hope
provide
directions
insights
for
future
editing
technology
brain
science
