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1
Basal and high-glucose-induced nuclear factor-kappaB activation were suppressed in the PARP-
deficient
cells
.
2
Moreover, enforced repression of cryptic exons prevented cell death in TDP-43-
deficient
cells
.
3
Although both encode stable products, neither reverses the NHEJ defects in DNA-PKcs-
deficient
cells
.
4
Functional relevance was confirmed by in vitro expression studies in cytosolic HMGS-
deficient
cells
.
5
In contrast, cyclin E expression in Rb-
deficient
cells
is deregulated in two ways.
6
However, end joining in XRCC4-
deficient
cells
has not been examined.
7
Expression profiling revealed several miRs and many mRNAs are differently expressed in folate-
deficient
cells
.
8
Furthermore, we show that autophagy-
deficient
cells
contained significantly elevated levels of reactive oxidized phospholipids.
9
Consistently, caspase-9-
deficient
cells
were defective in the release of Smac after induction of apoptosis.
10
However, the TAR defect may be associated with a general transcription defect in CSB-
deficient
cells
.
11
Both antifunctional antibodies and genetically
deficient
cells
were used.
12
We also observed intracellular lipid droplet accumulation in both acutely Fe-S-
deficient
cells
and iron-starved cells.
13
Therapeutic screening revealed that RB-
deficient
cells
were particularly resistant to agents targeting PI3K and MEK pathway.
14
Spindle assembly in NuSAP-
deficient
cells
is highly inefficient and chromosomes remain dispersed in the mitotic cytoplasm.
15
Interestingly, we also detect reduced IR-induced toxicity in HR
deficient
cells
when inhibiting post-DNA damage replication.
16
In ERp57-
deficient
cells
,
we found short-lived interaction of MHC class I molecules with the loading complex.
deficient
cells
deficient
cell