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ERK1/2 signaling is essential for the chemoattraction exerted by human FGF2 and human anosmin-1 on newborn rat and mouse OPCs via FGFR1.
[kallmann syndrome]
Signaling
through
fibroblast
growth
factor
receptors
(
FGFRs
)
is
essential
for
many
cellular
processes
including
proliferation
and
migration
,
as
well
as
differentiation
events
such
as
myelination
.
Anosmin-
1
is
an
extracellular
matrix
(
ECM
)
glycoprotein
that
interacts
with
the
fibroblast
growth
factor
receptor
1
(
FGFR
1
)
to
exert
its
biological
actions
through
this
receptor
,
although
the
intracellular
pathways
underlying
anosmin-
1
signaling
remain
largely
unknown
.
This
protein
is
defective
in
the
X-
linked
form
of
Kallmann
syndrome
(
KS
)
and
has
a
prominent
role
in
the
migration
of
neuronal
and
oligodendroglial
precursors
.
We
have
shown
that
anosmin-
1
exerts
a
chemotactic
effect
via
FGFR
1
on
neuronal
precursors
from
the
subventricular
zone
(
SVZ
)
and
the
essential
role
of
the
ERK
1
/
2
signaling
.
We
report
here
the
positive
chemotactic
effect
of
FGF
2
and
anosmin-
1
on
rat
and
mouse
postnatal
OPCs
via
FGFR
1
.
The
same
effect
was
observed
with
the
truncated
N-
terminal
region
of
anosmin-
1
(
A
1
Nt
)
.
The
introduction
in
anosmin-
1
of
the
missense
mutation
F
5
17
L
found
in
patients
suffering
from
KS
annulled
the
chemotactic
activity
;
however
,
the
mutant
form
carrying
the
disease-causing
mutation
E
514
K
also
found
in
KS
patients
,
behaved
as
the
wild-
type
protein
.
The
chemoattraction
exhibited
by
FGF
2
and
anosmin-
1
on
OPCs
was
blocked
by
the
mitogen-activated
protein
kinase
(
MAPK
)
inhibitor
U
0126
,
suggesting
that
the
activation
of
the
ERK
1
/
2
MAPK
signaling
pathway
following
interaction
with
the
FGFR
1
is
necessary
for
FGF
2
and
anosmin-
1
to
exert
their
chemotactic
effect
.
In
fact
,
both
proteins
were
able
to
induce
the
phosphorylation
of
the
ERK
1
/
2
kinases
after
the
activation
of
the
FGFR
1
receptor
.
Diseases
Validation
Diseases presenting
"positive chemotactic effect"
symptom
kallmann syndrome
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