CHMP4C promotes pancreatic cancer progression by inhibiting necroptosis via the RIPK1/RIPK3/MLKL pathway
Journal of Advanced Research,
Год журнала:
2025,
Номер
unknown
Опубликована: Янв. 1, 2025
Язык: Английский
Adamantane-Quinoxalone Hybrids: Precision Chemotypes and Their Molecular Mechanisms in Acute Myeloid Leukemia
Journal of Medicinal Chemistry,
Год журнала:
2025,
Номер
unknown
Опубликована: Март 31, 2025
Acute
myeloid
leukemia
(AML)
is
an
aggressive
blood
cancer
with
a
poor
prognosis,
especially
when
diagnosed
late.
Around
10–15%
of
cases
involve
the
specific
chromosomal
abnormality
t(8;21),
which
drives
uncontrolled
cell
proliferation
and
contributes
to
disease
onset.
Despite
advances
in
AML
research
treatment
protocols,
outcomes
for
t(8;21)
remain
stagnant,
as
patients
receive
standard,
nonspecific
chemotherapies.
This
one-size-fits-all
approach
targets
both
cancerous
healthy
cells,
leading
unwanted
toxicity
highlighting
urgent
need
targeted
therapies.
In
this
study,
we
present
precision
chemotype
based
on
quinoxalone-tethered
adamantane
framework
developed
via
metal-
light-free
protocol.
The
compound
selectively
inhibits
induces
death
by
disrupting
growth
metabolic
pathways,
demonstrated
through
bioassays,
RNA
sequencing,
proteomic
analysis.
Notably,
it
spares
other
leukemic
solid
underscoring
its
specificity
potential
therapy
AML.
Язык: Английский
An insight into the therapeutic impact of quinoxaline derivatives: Recent advances in biological activities (2020–2024)
Aly M. Waseem,
Ranya Mohammed Elmagzoub,
Mervat Mohammed Mazhar Abdelgadir
и другие.
Results in Chemistry,
Год журнала:
2024,
Номер
unknown, С. 101989 - 101989
Опубликована: Дек. 1, 2024
Язык: Английский
Metal-free internal nucleophile-triggered domino route for synthesis of fused quinoxaline [1,4]-diazepine hybrids and the evaluation of their DNA binding properties
Bioorganic Chemistry,
Год журнала:
2024,
Номер
151, С. 107694 - 107694
Опубликована: Авг. 5, 2024
Язык: Английский
Porcine parvovirus infection induces necroptosis of porcine placental trophoblast cells via a ZBP1-mediated pathway
Ning Xu,
Qian Du,
Yijiao Cheng
и другие.
Research Square (Research Square),
Год журнала:
2024,
Номер
unknown
Опубликована: Май 22, 2024
Abstract
Porcine
parvovirus
(PPV)
infection
induces
germ
cell
death,
leading
to
reproductive
disorders
in
first-pregnant
sows.
placental
trophoblast
cells
(PTCs)
are
the
major
target
of
PPV,
and
we
have
previously
found
that
PPV
leads
death
PTCs
by
a
non-apoptotic
process,
which
may
be
related
pathogenicity.
The
Z-nucleic
acid-binding
protein
1
(ZBP1)
is
often
activated
after
virus
invasion
mediates
subsequent
death.
Here,
induced
ZBP1-mediated
necroptosis
porcine
presence
apoptosis
inhibitor,
AC-DEVD-CHO.
ZBP1
expression
was
upregulated
during
infection,
knockout
or
RNA
interference
significantly
reduced
its
along
with
PPV-induced
necroptosis.
We
discovered
RIPK3
MLKL,
but
not
Caspase-8,
were
involved
downstream
signaling
infection;
phosphorylation
levels
MLKL
enhanced,
Caspase-8
cleaved.
infection-induced
PTCs.
did
affect
upregulation
expression,
blocked
activation
MLKL.
infection.
UV-inactivated
less
than
non-irradiated
PPV.
A
strain
mutation
translation
initiation
codon
still
able
induce
through
ZBP1/RIPK3/MLKL
pathway.
These
results
provide
new
insights
into
pathogenic
mechanism
suggest
viral
DNA-dependent
Язык: Английский
Porcine parvovirus infection induces necroptosis of porcine placental trophoblast cells via a ZBP1-mediated pathway
Ning Xu,
Qian Du,
Yijiao Cheng
и другие.
Veterinary Research,
Год журнала:
2024,
Номер
55(1)
Опубликована: Ноя. 29, 2024
Abstract
Porcine
parvovirus
(PPV)
infection
induces
germ
cell
death,
leading
to
reproductive
disorders
in
first-pregnant
sows.
placental
trophoblast
cells
(PTCs)
are
the
major
target
of
PPV,
and
we
have
previously
found
that
PPV
leads
death
PTCs
by
a
non-apoptotic
process,
which
may
be
related
pathogenicity.
The
Z-nucleic
acid-binding
protein
1
(ZBP1)
is
often
activated
after
virus
invasion
mediates
subsequent
death.
Here,
induced
ZBP1-mediated
necroptosis
porcine
presence
apoptosis
inhibitor,
AC-DEVD-CHO.
ZBP1
expression
was
upregulated
during
infection,
knockout
or
RNA
interference
significantly
reduced
its
along
with
PPV-induced
necroptosis.
We
discovered
RIPK3
MLKL,
but
not
Caspase-8,
were
involved
downstream
signaling
infection;
phosphorylation
levels
MLKL
enhanced,
Caspase-8
cleaved.
infection-induced
PTCs.
did
affect
upregulation
expression,
blocked
activation
MLKL.
infection.
UV-inactivated
less
than
non-irradiated
PPV.
A
strain
mutation
translation
initiation
codon
still
able
induce
through
ZBP1/RIPK3/MLKL
pathway.
These
results
provide
new
insights
into
pathogenic
mechanism
suggest
viral
DNA-dependent
Язык: Английский