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YGLF motif in the Kaposi sarcoma herpes virus G-protein-coupled receptor adjusts NF-κB activation and paracrine actions.
[primary effusion lymphoma]
Kaposi
sarcoma
(
KS
)
and
primary
effusion
lymphoma
(
PEL
)
are
two
pathologies
associated
with
KS
herpes
virus
(
KSHV
/
HHV-
8
)
infection
.
KSHV
genome
contains
several
oncogenes
,
among
which
,
the
viral
G-
protein-coupled
receptor
(
vGPCR
open
reading
frame
74
)
has
emerged
as
a
major
factor
in
KS
pathogenicity
.
Indeed
,
vGPCR
is
a
constitutively
active
receptor
,
whose
expression
is
sufficient
to
drive
cell
transformation
in
vitro
and
tumour
development
in
mice
.
However
,
neither
the
role
of
vGPCR
in
KSHV-infected
B-
lymphocytes
nor
the
molecular
basis
for
its
constitutive
activation
is
well
understood
.
Here
,
we
show
that
vGPCR
expression
contributes
to
nuclear
factor
-κ
B
(
NF-κB
)
-
dependent
cellular
survival
in
both
PEL
cells
and
primary
B
cells
from
HIV-negative
KS
patients
.
We
further
identified
within
vGPCR
an
AP
2
consensus
binding
motif
,
Y
326
GLF
,
that
directs
its
localization
between
the
plasma
membrane
and
clathrin-coated
vesicles
.
The
introduction
of
a
mutation
in
this
site
(
Y
326
A
)
increased
NF-κB
activity
and
proinflammatory
cytokines
production
.
This
correlated
with
exacerbated
morphological
rearrangement
,
migration
and
proliferation
of
non-infected
monocytes
.
Collectively
,
our
work
raises
the
possibility
that
KSHV-infected
B-
lymphocytes
use
vGPCR
to
impact
ultimately
the
immune
response
and
communication
within
the
tumour
microenvironment
in
KSHV-associated
pathologies
.
Oncogene
advance
online
publication
,
2
December
2013
;
doi
:
10
.
1038
/
onc
.
2013
.
503
.
Diseases
Validation
Diseases presenting
"exacerbated morphological rearrangement, migration and proliferation"
symptom
primary effusion lymphoma
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