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KSHV LANA and EBV LMP1 induce the expression of UCH-L1 following viral transformation.
[primary effusion lymphoma]
Ubiquitin
C-
terminal
Hydrolase
L
1
(
UCH-L
1
)
has
oncogenic
properties
and
is
highly
expressed
during
malignancies
.
We
recently
documented
that
Epstein-
Barr
virus
(
EBV
)
infection
induces
uch-l
1
expression
.
Here
we
show
that
Kaposi
's
Sarcoma
-associated
herpesvirus
(
KSHV
)
infection
induced
UCH-L
1
expression
,
via
cooperation
of
KSHV
Latency-
Associated
Nuclear
Antigen
(
LANA
)
and
RBP-J
κ
and
activation
of
the
uch-l
1
promoter
.
UCH-L
1
expression
was
also
increased
in
Primary
Effusion
Lymphoma
(
PEL
)
cells
co
-infected
with
KSHV
and
EBV
compared
with
PEL
cells
infected
only
with
KSHV
,
suggesting
EBV
augments
the
effect
of
LANA
on
uch-l
1
.
EBV
latent
membrane
protein
1
(
LMP
1
)
is
one
of
the
few
EBV
products
expressed
in
PEL
cells
.
Results
showed
that
LMP
1
was
sufficient
to
induce
uch-l
1
expression
,
and
co
-expression
of
LMP
1
and
LANA
had
an
additive
effect
on
uch-l
1
expression
.
These
results
indicate
that
viral
latency
products
of
both
human
γ-herpesviruses
contribute
to
uch-l
1
expression
,
which
may
contribute
to
the
progression
of
lymphoid
malignancies
.