Journal of Neuroscience,
Journal Year:
2015,
Volume and Issue:
35(41), P. 13836 - 13842
Published: Oct. 14, 2015
The
mammalian
target
of
rapamycin
(mTOR)
is
a
central
regulator
diverse
array
cellular
processes,
including
cell
growth,
proliferation,
autophagy,
translation,
and
actin
polymerization.
Components
the
mTOR
cascade
are
present
at
synapses
influence
synaptic
plasticity
spine
morphogenesis.
A
prevailing
view
that
study
its
role
in
autism
spectrum
disorders
(ASDs)
will
elucidate
molecular
mechanisms
by
which
regulates
neuronal
function
under
physiological
pathological
conditions.
Although
many
ASDs
arise
as
result
mutations
genes
with
multiple
functions,
they
appear
to
converge
on
common
biological
pathways
give
rise
autism-relevant
behaviors.
Dysregulation
signaling
has
been
identified
phenotypic
feature
fragile
X
syndrome,
tuberous
sclerosis
complex
1
2,
neurofibromatosis
1,
phosphatase
tensin
homolog,
potentially
Rett
syndrome.
Below
summary
topics
covered
symposium
presents
dysregulation
unifying
theme
subset
ASDs.
Molecular and Cellular Biology,
Journal Year:
2018,
Volume and Issue:
38(12)
Published: April 3, 2018
Translation
is
a
key
step
in
the
regulation
of
gene
expression
and
one
most
energy-consuming
processes
cell.
In
response
to
various
stimuli,
multiple
signaling
pathways
converge
on
translational
machinery
regulate
its
function.
To
date,
roles
phosphoinositide
3-kinase
(PI3K)/AKT
mitogen-activated
protein
kinase
(MAPK)
translation
are
among
best
understood.
Both
engage
mechanistic
target
rapamycin
(mTOR)
variety
components
machinery.
While
these
synthesis
homeostasis,
their
dysregulation
results
aberrant
leading
human
diseases,
including
diabetes,
neurological
disorders,
cancer.
Here
we
review
PI3K/AKT
MAPK
mRNA
translation.
We
also
highlight
additional
mechanisms
that
have
recently
emerged
as
regulators
apparatus.
Journal of Cellular and Molecular Medicine,
Journal Year:
2013,
Volume and Issue:
17(1), P. 12 - 29
Published: Jan. 1, 2013
Summary
The
rapid
accumulation
of
knowledge
on
apoptosis
regulation
in
the
1990s
was
followed
by
development
several
experimental
anticancer‐
and
anti‐ischaemia
(stroke
or
myocardial
infarction)
drugs.
Activation
apoptotic
pathways
removal
cellular
inhibitors
has
been
suggested
to
aid
cancer
therapy
inhibition
thought
limit
ischaemia‐induced
damage.
However,
initial
clinical
studies
apoptosis‐modulating
drugs
led
unexpected
results
different
conditions
this
may
have
due
co‐effects
non‐apoptotic
interconnected
cell
death
mechanisms
‘yin‐yang’
role
autophagy
survival
versus
death.
In
review,
we
extend
analysis
beyond
apoptosis.
Upon
introduction
molecular
governing
necrosis
(also
called
necroptosis
programmed
necrosis),
focus
character
signals
shared
processes
involving
mitochondria
(
e.g
.
mitophagy
mitoptosis)
playing
prominent
roles
multiple
Bcl2‐family
members
p53).
We
also
briefly
highlight
stress‐induced
senescence
that
plays
a
not
only
organismal
ageing
but
offers
novel
anticancer
strategies.
Finally,
illustrate
forms
settings
while
discussing
irradiation‐induced
mitotic
catastrophe.
signalling
are
discussed
their
relation
biology
treatment
approaches.
Science Signaling,
Journal Year:
2019,
Volume and Issue:
12(585)
Published: June 11, 2019
AMP-activated
protein
kinase
(AMPK)
senses
energetic
stress
and,
in
turn,
promotes
catabolic
and
suppresses
anabolic
metabolism
coordinately
to
restore
energy
balance.
We
found
that
a
diverse
array
of
AMPK
activators
increased
mTOR
complex
2
(mTORC2)
signaling
an
AMPK-dependent
manner
cultured
cells.
Activation
with
the
type
diabetes
drug
metformin
(GlucoPhage)
also
mTORC2
liver
vivo
primary
hepatocytes
manner.
AMPK-mediated
activation
did
not
result
from
suppression
mTORC1
thus
reduced
negative
feedback
on
PI3K
flux.
Rather,
associated
directly
phosphorylated
(mTOR
rictor).
As
determined
by
two-stage
vitro
assay,
phosphorylation
recombinant
was
sufficient
increase
catalytic
activity
toward
Akt.
Hence,
components
downstream
signaling.
Functionally,
inactivation
AMPK,
mTORC2,
Akt
apoptosis
during
acute
stress.
By
showing
activates
cell
survival,
these
data
provide
potential
mechanism
for
how
paradoxically
tumorigenesis
certain
contexts
despite
its
tumor-suppressive
function
through
inhibition
growth-promoting
mTORC1.
Collectively,
unveil
as
target
AMPK-mTORC2
axis
promoter
survival
Annual Review of Neuroscience,
Journal Year:
2018,
Volume and Issue:
41(1), P. 1 - 23
Published: Feb. 28, 2018
The
mechanistic
target
of
rapamycin
(mTOR)
is
an
important
signaling
hub
that
integrates
environmental
information
regarding
energy
availability
and
stimulates
anabolic
molecular
processes
cell
growth.
Abnormalities
in
this
pathway
have
been
identified
several
syndromes
which
autism
spectrum
disorder
(ASD)
highly
prevalent.
Several
studies
investigated
mTOR
developmental
neuronal
that,
when
dysregulated,
could
contribute
to
the
development
ASD.
Although
many
potential
mechanisms
still
remain
be
fully
understood,
these
associations
are
great
interest
because
clinical
inhibitors.
Clinical
trials
evaluating
efficacy
inhibitors
improve
neurodevelopmental
outcomes
initiated.
Molecules,
Journal Year:
2021,
Volume and Issue:
26(7), P. 2029 - 2029
Published: April 2, 2021
Flavonoids
represent
an
important
group
of
bioactive
compounds
derived
from
plant-based
foods
and
beverages
with
known
biological
activity
in
cells.
From
the
modulation
inflammation
to
inhibition
cell
proliferation,
flavonoids
have
been
described
as
therapeutic
adjuvants
against
several
diseases,
including
diabetes,
arteriosclerosis,
neurological
disorders,
cancer.
Cancer
is
a
complex
multifactor
disease
that
has
studied
for
years
however,
its
prevention
still
one
best
efficient
factors
impacting
epidemiology
disease.
In
molecular
cellular
context,
some
mechanisms
underlying
oncogenesis
progression
are
understood,
hallmarks
this
text,
we
review
signaling
pathways,
inflammation,
immunity,
redox
metabolism,
growth,
autophagy,
apoptosis,
cycle,
analyze
action
The
current
literature
provides
enough
evidence
supporting
may
be
cancer
therapy,
highlighting
importance
healthy
balanced
diets
prevent
onset
