Notch
signalling
activity
regulates
hematopoiesis
in
Drosophila
and
vertebrates
alike.
Parasitoid
wasp
infestation
of
larvae,
however,
requires
a
timely
downregulation
to
allow
the
formation
encapsulation-active
blood
cells.
Here
we
show
that
CSL
transcription
factor
Suppressor
Hairless
[Su(H)]
is
phosphorylated
at
Serine
269
response
parasitoid
infestation.
As
this
phosphorylation
interferes
with
DNA-binding
Su(H),
it
reversibly
precludes
its
activity.
Accordingly,
phospho-deficient
Su(H)
S269A
mutants
are
immune
compromised.
A
screen
for
kinases
involved
identified
Pkc53E,
required
normal
as
well
response.
Genetic
molecular
interactions
support
specificity
Su(H)-Pkc53E
relationship.
Moreover,
phorbol
ester
treatment
inhibits
vivo
human
cell
culture.
We
conclude
Pkc53E
targets
during
parasitic
infestation,
thereby
remodeling
population
egg
encapsulation.
Notch
signaling
activity
regulates
hematopoiesis
in
Drosophila
and
vertebrates
alike.
Parasitoid
wasp
infestation
of
larvae,
however,
requires
a
rapid
downregulation
to
allow
the
formation
encapsulation-active
blood
cells.
Here
we
show
that
CSL
transcription
factor
Suppressor
Hairless
[Su(H)]
is
phosphorylated
at
Serine
269
response
parasitoid
infestation.
As
this
phosphorylation
interferes
with
DNA-binding
Su(H),
it
reversibly
inhibits
activity.
Accordingly,
phospho-deficient
Su(H)
S269A
mutants
are
immune
compromised.
A
screen
for
kinases
involved
identified
Pkc53E,
required
normal
as
well
response.
Genetic
molecular
interactions
support
specificity
Su(H)-Pkc53E
relationship.
Moreover,
phorbol
ester
treatment
vivo
human
cell
culture.
We
conclude
Pkc53E
targets
during
parasitic
infestation,
inducing
activity,
thereby
remodeling
population
egg
encapsulation.
Stem Cells International,
Journal Year:
2023,
Volume and Issue:
2023, P. 1 - 13
Published: Nov. 9, 2023
Background.
Poor
graft
function
(PGF)
is
a
life-threatening
complication
following
hematopoietic
stem
cell
transplantation
(HSCT).
Current
therapies,
such
as
CD34+
infusion,
have
shown
limited
effectiveness.
Conversely,
mesenchymal
cells
(MSCs)
show
potential
in
addressing
PGF.
Adipose-derived
(ADSCs)
effectively
support
long-term
proliferation.
Therefore,
this
study
aimed
to
investigate
the
mechanisms
underlying
provided
by
ADSCs.
Methods.
ADSCs
were
isolated
from
mice
and
subsequently
identified.
In
vitro
experiments
involved
coculturing
feeders
with
Lin-Sca-1+c-kit+
(LSK)
for
2
5
weeks.
The
number
of
LSK
was
quantified
after
coculture.
Scanning
electron
microscopy
utilized
observe
interaction
between
cells.
Hes-1
expression
assessed
using
western
blot
real-time
quantitative
PCR.
An
γ-secretase
inhibitor
(GSI)
used
confirm
involvement
Jagged-1/Notch-1/Hes-1
pathway
expansion.
Additionally,
Jagged-1
knocked
down
demonstrate
its
significance
ADSC-mediated
support.
vivo
conducted
through
infusion
LSK,
+
fibroblasts,
ADSCs,
respectively.
Mouse
survival,
platelet
count,
leukocyte
hemoglobin
levels
monitored.
Results.
showed
high-Jagged-1
promoted
There
direct
After
coculture,
increased
Moreover,
GSI-reduced
proliferation
expression.
Knockdown
attenuated
ADSCs-mediated
promotion
Furthermore,
facilitated
recovery
survival
NOD/SCID
mice.
Conclusion.
both
may
be
mediated,
at
least
part,
Jagged-1/Notch-1
signaling
pathway.
These
findings
provide
valuable
insights
into
implications
improving
treatment
PGF
HSCT.
Medicine,
Journal Year:
2023,
Volume and Issue:
102(48), P. e36237 - e36237
Published: Dec. 1, 2023
In-depth
studies
on
the
mechanisms
of
pathogenesis
sepsis
and
diagnostic
biomarkers
in
early
stages
may
be
key
to
developing
individualized
effective
treatment
strategies.
This
study
aimed
identify
sepsis-related
hub
genes
evaluate
their
reliability.
The
gene
expression
profiles
GSE4607
GSE131761
were
obtained
from
Gene
Expression
Omnibus.
Differentially
co-expressed
between
control
groups
screened.
Single-sample
set
enrichment
analysis
variation
performed
investigate
biological
functions
genes.
A
receiver
operating
characteristic
curve
was
used
value.
Datasets
GSE154918
GSE185263
as
external
validation
datasets
verify
reliability
Four
differentially
genes,
FAM89A,
FFAR3,
G0S2,
FGF13,
extracted
using
a
weighted
co-expression
network
differential
methods.
These
4
upregulated
group
distinct
those
controls.
Moreover,
curves
exhibited
considerable
value
discriminating
septic
blood
samples
non-septic
group.
consistency
these
externally
validated.
analyses
indicated
that
significantly
correlated
with
regulation
immunity
metabolism
sepsis.
identified
FGF13
help
elucidate
molecular
underlying
drive
introduction
new
advance
diagnosis
treatment.
Notch
signalling
activity
regulates
hematopoiesis
in
Drosophila
and
vertebrates
alike.
Parasitoid
wasp
infestation
of
larvae,
however,
requires
a
timely
downregulation
to
allow
the
formation
encapsulation-active
blood
cells.
Here
we
show
that
CSL
transcription
factor
Suppressor
Hairless
[Su(H)]
is
phosphorylated
at
Serine
269
response
parasitoid
infestation.
As
this
phosphorylation
interferes
with
DNA-binding
Su(H),
it
reversibly
precludes
its
activity.
Accordingly,
phospho-deficient
Su(H)
S269A
mutants
are
immune
compromised.
A
screen
for
kinases
involved
identified
Pkc53E,
required
normal
as
well
response.
Genetic
molecular
interactions
support
specificity
Su(H)-Pkc53E
relationship.
Moreover,
phorbol
ester
treatment
inhibits
vivo
human
cell
culture.
We
conclude
Pkc53E
targets
during
parasitic
infestation,
thereby
remodeling
population
egg
encapsulation.
