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TSH regulates pendrin membrane abundance and enhances iodide efflux in thyroid cells.
[pendred syndrome]
Thyroid
hormones
are
essential
for
normal
development
and
metabolism
.
Their
synthesis
requires
transport
of
iodide
into
thyroid
follicles
.
The
mechanisms
involving
the
apical
efflux
of
iodide
into
the
follicular
lumen
are
poorly
elucidated
.
The
discovery
of
mutations
in
the
SLC
26
A
4
gene
in
patients
with
Pendred
syndrome
(
congenital
deafness
,
goiter
,
and
defective
iodide
organification
)
suggested
a
possible
role
for
the
encoded
protein
,
pendrin
,
as
an
apical
iodide
transporter
.
We
determined
whether
TSH
regulates
pendrin
abundance
at
the
plasma
membrane
and
whether
this
influences
iodide
efflux
.
Results
of
immunoblot
and
immunofluorescence
experiments
reveal
that
TSH
and
forskolin
rapidly
increase
pendrin
abundance
at
the
plasma
membrane
through
the
protein
kinase
A
pathway
in
PCCL-
3
rat
thyroid
cells
.
The
increase
in
pendrin
membrane
abundance
correlates
with
a
decrease
in
intracellular
iodide
as
determined
by
measuring
intracellular
(
125
)
iodide
and
can
be
inhibited
by
specific
blocking
of
pendrin
.
Elimination
of
the
putative
protein
kinase
A
phosphorylation
site
T
717
A
results
in
a
diminished
translocation
to
the
membrane
in
response
to
forskolin
.
These
results
demonstrate
that
pendrin
translocates
to
the
membrane
in
response
to
TSH
and
suggest
that
it
may
have
a
physiological
role
in
apical
iodide
transport
and
thyroid
hormone
synthesis
.
Diseases
Validation
Diseases presenting
"defective iodide organification"
symptom
pendred syndrome
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