Journal of Biochemical and Molecular Toxicology,
Journal Year:
2024,
Volume and Issue:
38(7)
Published: July 1, 2024
Glioma
is
a
central
nervous
system
(CNS)
malignant
tumor
with
high
heterogeneity
and
mortality,
which
severely
threatens
the
health
of
patients.
The
overall
survival
glioma
patients
relatively
short
it
critical
to
identify
new
molecular
targets
for
developing
effective
treatment
strategies.
UBE2K
ubiquitin
conjugating
enzyme
oncogenic
function
in
several
tumors.
However,
whether
participates
gliomas
remains
unknown.
Herein,
cells,
was
found
highly
expressed
U87
U251
cells.
Subsequently,
cells
were
transfected
si-UBE2K
silence
UBE2K,
si-NC
transfection
as
negative
control.
In
both
cell
viability
sharply
reduced
by
transfecting
48
72
h.
Markedly
decreased
colony
number,
number
migrated
invaded
declined
relative
wound
healing
rate
observed
Moreover,
Bcl-2
level
markedly
reduced,
while
Bax
cleaved-caspase-3
levels
increased
after
transfection.
Furthermore,
p62
signally
declined,
Beclin-1
LC-3
II/I
greatly
facilitating
effect
on
apoptosis
autophagy
abolished
coculture
3-MA,
an
inhibitor
autophagy.
Collectively,
facilitated
vitro
growth
possibly
inhibiting
autophagy-related
apoptosis,
might
be
promising
target
treating
glioma.
The Journal of Cell Biology,
Journal Year:
2024,
Volume and Issue:
223(5)
Published: March 22, 2024
Ubiquitin
regulates
various
cellular
functions
by
posttranslationally
modifying
substrates
with
diverse
ubiquitin
codes.
Recent
discoveries
of
new
chain
topologies,
types
bonds,
and
non-protein
have
substantially
expanded
the
complexity
code.
Here,
we
describe
system
covering
basic
principles
recent
related
to
mechanisms,
technologies,
biological
importance.
Life Science Alliance,
Journal Year:
2024,
Volume and Issue:
7(8), P. e202402740 - e202402740
Published: May 21, 2024
The
ubiquitin
(Ub)
code
denotes
the
complex
Ub
architectures,
including
chains
of
different
lengths,
linkage
types,
and
combinations,
which
enable
ubiquitination
to
control
a
wide
range
protein
fates.
Although
many
linkage-specific
interactors
have
been
described,
how
are
able
decode
more
architectures
is
not
fully
understood.
We
conducted
interactor
screen,
in
humans
yeast,
using
varying
as
well
homotypic
heterotypic
branched
two
most
abundant
types-lysine
48-linked
(K48)
lysine
63-linked
(K63)
Ub.
identified
some
first
K48/K63-linked
branch-specific
interactors,
histone
ADP-ribosyltransferase
PARP10/ARTD10,
E3
ligase
UBR4,
huntingtin-interacting
HIP1.
Furthermore,
we
revealed
importance
chain
length
by
identifying
with
preference
for
Ub3
over
Ub2
chains,
Ub-directed
endoprotease
DDI2,
autophagy
receptor
CCDC50,
p97
adaptor
FAF1.
Crucially,
compared
datasets
collected
common
deubiquitinase
inhibitors-chloroacetamide
N-ethylmaleimide.
This
inhibitor-dependent
highlighting
inhibitor
consideration
during
pulldown
studies.
dataset
key
resource
understanding
read.
Cellular and Molecular Life Sciences,
Journal Year:
2024,
Volume and Issue:
81(1)
Published: July 30, 2024
Sepsis
is
a
life-threatening
organ
dysfunction
caused
by
dysregulated
host
response
to
infection.
The
inflammatory
cytokine
storm
causes
systemic
damage,
especially
acute
lung
injury
in
sepsis.
In
this
study,
we
found
that
the
expression
of
S-phase
kinase-associated
protein
2
(Skp2)
was
significantly
decreased
sepsis-induced
(ALI).
activated
MEK/ERK
pathway
and
inhibited
Skp2
pulmonary
epithelium,
resulting
reduction
K48
ubiquitination
solute
carrier
family
3
member
(SLC3A2),
thereby
impairing
its
membrane
localization
cystine/glutamate
exchange
function.
Consequently,
intracellular
redox
reactions
induced
ferroptosis
epithelial
cells,
leading
injury.
Finally,
demonstrated
intravenous
administration
mRNA-encapsulating
lipid
nanoparticles
(LNPs)
epithelium
alleviated
septic
mice.
Taken
together,
these
data
provide
an
innovative
understanding
underlying
mechanisms
ALI
promising
therapeutic
strategy
for
The Journal of Biochemistry,
Journal Year:
2022,
Volume and Issue:
171(4), P. 361 - 366
Published: Jan. 10, 2022
Abstract
Protein
ubiquitylation
regulates
numerous
pathways,
and
the
diverse
information
encoded
by
various
forms
of
is
known
as
ubiquitin
code.
Recent
studies
revealed
that
branched
chains
are
abundant
in
mammalian
cells
regulate
important
pathways.
They
include
proteasomal
degradation
misfolded
disease-causing
proteins,
regulation
NF-κB
signalling
apoptotic
cell
fate
decisions.
Targeted
protein
through
chemical
degraders
emerged
a
transformative
therapeutic
paradigm
aimed
at
inducing
disappearance
unwanted
cellular
proteins.
To
further
improve
efficacy
target
expand
its
applications,
understanding
molecular
mechanism
degraders’
action
from
view
code
biology
required.
In
this
review,
I
discuss
roles
biological
pathways
chemically
induced
targeted
focusing
on
codes
we
have
characterized.
Frontiers in Molecular Biosciences,
Journal Year:
2023,
Volume and Issue:
10
Published: Feb. 8, 2023
Huntington’s
disease
(HD)
is
a
neurodegenerative
disorder
caused
by
CAG
repeat
expansion
in
the
N-terminus
of
HTT
gene.
The
translates
into
polyglutamine
mutant
(mHTT)
protein,
resulting
intracellular
aggregation
and
neurotoxicity.
Lowering
mHTT
protein
reducing
synthesis
or
improving
degradation
would
delay
prevent
onset
HD,
ubiquitin-proteasome
system
(UPS)
could
be
an
important
pathway
to
clear
proteins
prior
aggregation.
UPS
not
impaired
proteasomes
can
degrade
entirely
when
targeted
for
degradation.
However,
differently
ubiquitinated
compared
wild-type
(wtHTT),
suggesting
that
polyQ
affects
interaction
with
(de)
ubiquitinating
enzymes
subsequent
targeting
soluble
associated
several
ubiquitin-modifying
enzymes,
various
have
been
identified
are
linked
disease,
either
turnover
affecting
overall
homeostasis.
Here
we
describe
their
potential
mechanism
action
toward
improved
towards
proteostasis
machinery.
