uxt
interacted
specifically
inside
nucleus
p65
signal-dependent
manner
went
address
whether
interaction
important
regulating
nf-κb
activity
genes
responsive
transfected
293t
cells
uxt
other
control
plasmids
prepared
nuclear
extracts
performed
electrophoretic
mobility
shift
assay
emsa
indicated
consistently
nf-κb
binding
cognate
probe
without
tnf-α
treatment
notably
overexpression
uxt
alone
induce
detectable
basal
nf-κb
binding
activity
overexpression
uxt
markedly
affect
nf-κb
activation
induced
tnf-α
293t
cells
transfected
equal
amount
uxt
a20
control
vector
transfection
cells
stimulated
ng/ml
tnf-α
indicated
times
equal
amounts
nuclear
extracts
subjected
emsa
competition
analysis
100-fold
excess
unlabeled
wild-type
mutant
probes
added
reaction
mixtures
supershift
assays
nuclear
extracts
incubated
antibody
indicated
emsa
performed
test
endogenous
nf-κb
sp1
binding
cognate
probes
via
emsa
analyzed
endogenous
nf-κb
dna
binding
activity
cells
reduced
uxt
expression
expectedly
tnf-α
alone
induced
endogenous
nf-κb
bind
cognate
probe
strongly
specifically
considerably
interaction
markedly
diminished
nuclear
extracts
from
uxt-specific
knockdown
cells
addition
reduction
correlated
effectiveness
sirna
administered
fig.
emsa
performed
test
endogenous
nf-κb
sp1
binding
cognate
probes
furthermore
emsa
confirmed
loss
uxt
also
suppressed
constitutive
dna
binding
activity
nf-κb
control
sp1
fig.
results
indicate
elevated
expression
uxt
strongly
correlates
constitutive
nf-κb
activity
prostate
cancer
cell
lines
again
substantiates
notion
uxt
essential
nf-κb
function
nucleus