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Ligation of beta4 integrins activates PKB/Akt and ERK1/2 by distinct pathways-relevance of the keratin filament.
[epidermolysis bullosa simplex]
In
normal
epithelial
cells
hemidesmosomes
mediate
stable
adhesion
to
the
underlying
basement
membrane
.
In
carcinoma
cells
a
functional
and
spatial
dissociation
of
the
hemidesmosomal
complex
is
observed
stimulating
the
hypothesis
that
the
beta
4
integrin
may
trigger
essential
signalling
cascades
determining
cell
fate
.
In
the
present
study
we
dissected
the
signalling
pathways
giving
rise
to
PKB
/
Akt
and
ERK
1
/
2
activation
in
response
to
beta
4
ligation
by
3
E
1
.
It
was
found
that
the
activation
of
PKB
/
Akt
is
sensitive
towards
alterations
of
the
keratin
filament
as
demonstrated
by
using
KEB
-
7
cells
that
carry
a
keratin
mutation
typical
for
epidermolysis
bullosa
simplex
.
Similar
results
were
achieved
by
chemically
induced
keratin
aggregations
.
Of
note
,
the
signalling
to
ERK
1
/
2
was
not
affected
.
ERK
1
/
2
activation
utilizes
an
EGF
-R
transactivation
mechanism
as
shown
by
dominant-negative
expression
experiments
and
also
by
treatment
with
a
specific
inhibitor
(
AG
1478
)
.
Downstream
from
the
EGF
-R
the
activation
of
ERK
1
/
2
takes
the
prototypical
signalling
cascade
via
Shc
,
Ras
and
Raf-
1
as
demonstrated
by
dominant-negative
expression
experiments
.
Taken
together
our
data
define
a
new
model
of
beta
4
-
dependent
PKB
/
Akt
and
ERK
1
/
2
activation
demonstrating
the
keratin
filament
as
a
structure
necessary
in
signal
transmission
.
Diseases
Validation
Diseases presenting
"the signalling to erk1"
symptom
epidermolysis bullosa simplex
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