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WASp Family Verprolin-Homologous Protein-2 (WAVE2) and Wiskott-Aldrich Syndrome Protein (WASp) Engage in Distinct Downstream Signaling Interactions at the T Cell Antigen Receptor Site.
[wiskott-aldrich syndrome]
T
-
cell
antigen
receptor
(
TCR
)
engagement
has
been
shown
to
activate
pathways
leading
to
actin
cytoskeletal
polymerization
and
reorganization
,
which
are
essential
for
lymphocyte
activation
and
function
.
Several
actin
regulatory
proteins
were
implicated
in
regulating
the
actin
machinery
,
such
as
members
of
the
Wiskott
-
Aldrich
syndrome
protein
(
WASp
)
family
.
These
include
WASp
,
and
the
WASp
family
Verprolin-homologous
protein-
2
(
WAVE
2
)
.
Although
WASp
and
WAVE
2
share
several
structural
features
,
the
precise
regulatory
mechanisms
and
potential
redundancy
between
them
have
not
been
fully
characterized
.
Specifically
,
unlike
WASp
,
the
dynamic
molecular
interactions
that
regulate
WAVE
2
recruitment
to
the
cell
membrane
and
specifically
to
the
TCR
signaling-
complex
are
largely
unknown
.
Here
,
we
identify
the
molecular
mechanism
that
controls
the
recruitment
of
WAVE
2
in
comparison
to
WASp
.
Using
fluorescence
resonance
energy
transfer
(
FRET
)
and
novel
triple-color
FRET
(
3
FRET
)
technology
,
we
demonstrate
how
WAVE
2
signaling
complexes
are
dynamically
regulated
during
lymphocyte
activation
,
in
-vivo
.
We
show
that
similar
to
WASp
,
WAVE
2
recruitment
to
the
TCR
site
depends
on
protein
tyrosine
kinase
,
ZAP-
70
,
and
the
adaptors
LAT
,
SLP-
76
,
and
Nck
.
However
,
in
contrast
to
WASp
,
WAVE
2
leaves
this
signaling
complex
and
migrates
peripherally
together
with
vinculin
to
the
membrane
leading
edge
.
Our
experiments
demonstrate
that
WASp
and
WAVE
2
differ
in
their
dynamics
and
their
associated
proteins
.
Thus
,
this
study
reveals
the
differential
mechanisms
regulating
the
function
of
these
cytoskeletal
proteins
.
Diseases
Validation
Diseases presenting
"dynamic molecular interactions"
symptom
wiskott-aldrich syndrome
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