1 vopiridol, transcriptome analyses of FIT-
039-
treated cells revealed that FIT-039 specifically inhibit
2 CHT in both vehicle- and SIN-
1-
treated cells colocalizes with Rab7, Rab9, and Lamp-1 in
3 Thus, CHT inhibition in SIN-
1-
treated cells is mediated by proteasomal degradation, wh
4 ecreased levels of cell surface CHT in SIN-
1-
treated cells is related to alterations in its trafficki
5 ading to more ROS generation in hypoxic YC-
1-
treated cells.
6 eatment but absent in [A(11)]hRFRP-1((8-
12))-
treated cells was consistent with this result.
7 depletion delays DNA repair in UV- and VP-
16-
treated cells and increases polyploid cells after VP-16
8 ion of c-Kit and IL-7 receptors on the IL-
18-
treated cells.
9 enation defects similar to those of ICRF-
193-
treated cells.
10 Interestingly, while IL-
1beta-
treated cells exhibited only minor changes in metabolism
11 enuated PGE2 and IL-6 release in HG+IL-
1beta-
treated cells than in NG+IL-1beta-treated cells.
12 G+IL-1beta-treated cells than in NG+IL-
1beta-
treated cells.
13 N-nitroso-guanidine-treated mice or H(2)O(
2)-
treated cells.
14 RNA reverses the reduction of TEER in IL-
22-
treated cells.
15 d to promote its self-aggregation in ABT-
263-
treated cells, shown using a bimolecular fluorescence co
16 o increased PDH activity in 1alpha,25(OH)
2D3-
treated cells (p = 0.09).
17 In 1alpha,25(OH)
2D3-
treated cells, mitochondrial volume and branching and ex
18 inase 4 (PDK4) decreased in 1alpha,25(OH)
2D3-
treated cells.
19 ion rate (OCR) increased in 1alpha,25(OH)
2D3-
treated cells.
20 Bax 'activation' and caspase cleavage in
2DG-
treated cells.
21 -2 dramatically enhanced the survival of
2DG-
treated cells that was negated by a Bcl-2 antagonist.
22 bserved decrease in glutathione in As(2)O(
3)-
treated cells, as this could increase intracellular reac
23 mosan or bacteria was fully restored in IL-
4-
treated cells.
24 Chk2 at nanomolar concentrations in LMP-
400-
treated cells.
25 icient to induce enhanced cell death in IL-
5-
treated cells.
26 of cell viability were "rescued" in Ad.mda-
7-
treated cells incubated with Bcl-x(s) siRNA.
27 he mitochondria of rotenone- and antimycin
A-
treated cells was observed and may contribute to the enh
28 n were found to increase in the tubastatin
A-
treated cells compared with the control cells, suggestin
29 tor glioma-associated protein 1 (GLI1) in
AA-
treated cells is the underlying mechanism controlling BC
30 s, including BCL2, BFL1/A1, and 4-1BB, in
AA-
treated cells.
31 AAT-
treated cells displayed enhanced chemokine-dependent mig
32 AB235-
treated cell pellets also integrated into the surroundin
33 Examination of
AB235-
treated cell pellets in both in vitro and in vivo experi
34 and transgenic mouse model, as well as
Abeta-
treated cells.
35 of IFI16 was absent in phosphonoacetic
acid-
treated cells, which blocks KSHV DNA replication and, co
36 olarized or ethylene glycol tetraacetic
acid-
treated cells, indicating that bacteria bind preferentia
37 arated with control cells, but not with
ADMA-
treated cells in PCA model.
38 rotein aggregation was more prominent in
ALA-
treated cells.
39 Finally,
alcohol-
treated cells partially regained their ability to withst
40 , an inhibitor of p38 activity, to IFN-
alpha-
treated cells reversed, in part, the inhibition of telom
41 treated human cells, we challenged IFN-
alpha-
treated cells with HIV-G208R and found that MxB does not
42 tor that blocks HIV-1 infection in IFN-
alpha-
treated cells, this is a hard concept to grasp due to th
43 uced the expression of mTOR in peg-IFN-
alpha-
treated cells, whereas silencing of mTOR had no effect o
44 bute to the restriction imposed by IFN-
alpha-
treated cells.
45 hereas for tumor necrosis factor (TNF)-
alpha-
treated cells, PARP-1 protein alone was sufficient.
46 ivated in human inflamed colon and TNF-
alpha-
treated cells (false discovery rate < 0.05).
47 The absence of this pathway in TNF-
alpha-
treated cells suggests multiple regulatory pathways for
48 5 reduced TSLP mRNA in DEP but not TNF-
alpha-
treated cells.
49 es upon stimulation with
aminobisphosphonate-
treated cells.
50 ontrol, ataluren-treated, and
aminoglycoside-
treated cells.
51 nuclear structures called PML bodies in
ATO-
treated cells.
52 The morphology of
avenaciolide-
treated cells was protoplast-like, which indicated that
53 sustained expression of the FMR1 gene in
AZA-
treated cells.
54 Interestingly, exosomes from AX-
B-
treated cells showed a positive biotin signal in electro
55 blast proliferation observed in NCaPP-PDGF-
B-
treated cells confirmed the functionality of these nanop
56 mulating factor, G-CSF) in the medium of
B20-
treated cells and in bronchoalveolar lavage fluid of mic
57 The supernatant from
BaPGN-
treated cells altered the growth of B. anthracis Sterne,
58 Moreover, treatment of
batimastat-
treated cells with recombinant sAPPalpha reversed the in
59 suggesting that suppression of mTOR in
BDNF-
treated cells resulted in excessive autophagy.
60 eath and accelerated autophagic flux in
BDNF-
treated cells.
61 Interferon-
beta-
treated cells expressing wild-type STAT2 contain much le
62 significantly different in iron or TGF-
beta-
treated cells compared with untreated control cells.
63 resence of SMAD proteins in iron or TGF-
beta-
treated cells, including of SMAD4, did confirm convergen
64 ion of hepatitis B virus in iron or TGF-
beta-
treated cells.
65 In both resting and TGF-
beta1-
treated cells, ectopic expression of miR-29 repressed th
66 In
BM-
treated cells, apoptosis tended to be suppressed via inc
67 BMP2-
treated cells displayed marked increase in calcification
68 tantly, the ability of NELL-1 to direct
BMP2-
treated cells toward osteogenesis and away from adipogen
69 from heat-mediated induction, in
bortezomib-
treated cells, HSF1 and HSF2 interact directly, forming
70 s been shown to be sufficient to separate
BP-
treated cells from coexposed or control cells.
71 n cold (4 degrees C) and heat (49 degrees
C)-
treated cells.
72 ellular release of IL-36gamma from poly(I:
C)-
treated cells.
73 dertook genome-wide analysis of
camptothecin-
treated cells at exon resolution.
74 ted off-target sites in a population of
Cas9-
treated cells further confirms high specificity of Cas9.
75 Cb-
treated cells formed midcell circumferential bulges, sug
76 ormal morphologies at the growth poles in
Cb-
treated cells, suggesting unipolar growth uses Cb-insens
77 ckdown of the autophagy protein Atg5 in
CCCP-
treated cells.
78 d not induce DNA double-strand breaks in
CEM-
treated cells but prevented the formation of Top2alpha-
79 ully restored biotin production in
cerulenin-
treated cells.
80 ing apoptosis in chemotherapy drug
cisplatin-
treated cells.
81 strate that extracts prepared from
cisplatin-
treated cells are fully capable of NHEJ catalyzed repair
82 and up-regulated phospho-BRCA1 in
cisplatin-
treated cells, suggesting that T2AA increases DSBs.
83 een TR3 and mitochondrial Hsp60 in
cisplatin-
treated cells, which was associated with cytochrome c re
84 ced expression of RIP1 and IAPs in
cisplatin-
treated cells.
85 s found to be greatly disrupted in
cisplatin-
treated cells.
86 for TAB1 to regulate apoptosis in
cisplatin-
treated cells.
87 ines as mediators of miR486 expression in
CM-
treated cells.
88 e that SFN reverses the effects of PMI in
co-
treated cells by reducing the accumulation of p62 in mit
89 ohistochemical analysis, in drug
combination-
treated cells, microtubule-associated protein light chai
90 ucose-regulated protein, in drug
combination-
treated cells.
91 suspension cultures of GO-PEI/RNA
complexes-
treated cells dramatically increased the reprogramming e
92 s was 2.3 times greater than that by
control-
treated cells (mean 5.66 mug/mL [SD 0.77] vs 2.45 [0.36]
93 py in dynasore-treated cells than in
control-
treated cells.
94 N1A and FOXO3A in decitabine- versus
control-
treated cells.
95 markers by nearly 90% compared with
control-
treated cells (P<0.001).
96 abrogation of differences in
corticosteroid-
treated cell viability following siRNA knockdown of 2 TF
97 qPCR analysis showed that CPI and
CPH-
treated cells significantly inhibited PPARgamma expressi
98 Moreover, conditioned medium from
CR-
treated cells transmits the longevity benefit of CR to m
99 d calcium desensitization in control and
CRT-
treated cells, while HF(dys) cells were unaffected, impl
100 ame regions via the SSRP1 subunit in
curaxin-
treated cells.
101 Finally, phagocytosis of actinomycin
D-
treated cells caused apoptosis in macrophages, and suppr
102 immune repression mediated by actinomycin
D-
treated cells did not require phagocytosis or cell-cell
103 Comparative proteomic analysis of DNA
damage-
treated cells versus -untreated cells evidenced a diffus
104 Expression of factors in
DDT-
treated cells was similar to that in estrogen-treated MS
105 mulated in the membrane fraction of
deguelin-
treated cells, as indicated by increased interaction of
106 tially mimicked the effects observed in
DEHP-
treated cells.
107 n of JNK kinase function rendered
Delta24RGD-
treated cells resistant to autophagy.
108 s simplex virus type 1 (HSV-1) in
detergents-
treated cell culture medium containing various serum con
109 l amounts in extracts from untreated and
Dex-
treated cells.
110 etween L-type Ca channels and RyR2 in T3+
Dex-
treated cells.
111 -1 mRNA by cytoplasmic extracts from the
Dex-
treated cells.
112 Overall,
DMP1-
treated cells showed increased expression of alkaline ph
113 respond to DNA-bearing ACs, but not to
DNase-
treated cells, by secreting IL-10.
114 hat RIP1 may promote survival in
doxorubicin-
treated cells and that ganetespib may synergize with dox
115 p53 activation, and apoptosis in
doxorubicin-
treated cells.
116 Results from
drug-
treated cells showed inhibited, but ongoing degradation
117 ate-velocity separation of lysates from
drug-
treated cells.
118 icant source of increased ROS levels in
drug-
treated cells.
119 In data from 498 individual
drug-
treated cells, we found a linear dependence of degradati
120 accumulation of PolH in the nucleus of
drug-
treated cells along with direct binding to damaged DNA.
121 IL-13-stimulated eotaxin production in
dsRNA-
treated cells.
122 observed by electron microscopy in
dynasore-
treated cells than in control-treated cells.
123 K-mediated phosphorylation of AKT in 4-OH-
E2-
treated cells was inhibited by ROS modifiers as well as
124 Consequently, HB-
EGF-
treated cells exhibit higher double-strand break (DSB) r
125 nd AP-1 promoter activation are noted in
EGF-
treated cells with VPS4B knockdown.
126 In
EGF-
treated cells, Tks4 is tyrosine-phosphorylated and assoc
127 nd were significantly higher in the
elastase-
treated cells compared with controls.
128 he clathrin machinery in control and
ethanol-
treated cells.
129 imately 50% compared with untreated and
EtOH-
treated cells.
130 FA-
treated cells also had higher amounts of small activator
131 cell death and the long-term survival of
FA-
treated cells.
132 on was lower in plasma rich in growth
factor-
treated cells compared to non-stimulated cells, although
133 usative because supplementation of
fendiline-
treated cells with exogenous PtdSer rapidly restores K-R
134 inant ASM or exogenous ceramide to
fendiline-
treated cells rapidly relocalizes K-Ras4B and PtdSer to
135 cumulated fructose 1,6-bisphosphate in
FK866-
treated cells mainly derived from dihydroxyacetone phosp
136 Moreover, cell viability in
FK866-
treated cells supplemented with extracellular NMN was st
137 phate and sedoheptulose 1-phosphate in
FK866-
treated cells.
138 of protein extracts obtained from
flavonoid-
treated cells.
139 phosphoamino acid analysis revealed that
Fsk-
treated cells resulted in elevated serine phosphorylatio
140 hich we confirmed by showing that
fucosidase-
treated cells, largely, failed to activate complement.
141 by which ErbB3 is upregulated in
fulvestrant-
treated cells is unknown.
142 maintaining low ErbB3 levels in
fulvestrant-
treated cells.
143 ppaBalpha were found to be accumulated in
FZ-
treated cells.
144 Chromatin immunoprecipitation of IFN-
gamma-
treated cells indicates that Nlrc5 reduced the silencing
145 coadministration of spermidine to IFN-
gamma-
treated cells.
146 point kinase 1-dependent manner in
genotoxin-
treated cells.
147 HLA class I peptide repertoire of
gentamicin-
treated cells and identified multiple peptides derived f
148 lfed cargo in palmitic acid (PA)- or
glucose-
treated cells, indicating suppressed autophagic turnover
149 reduced H3S28p levels in untreated and
GnRH-
treated cells and also affected H3K27ac levels.
150 es, were also increased in both N1KD and
GSI-
treated cells and responded to okadaic acid treatment.
151 different PCD-inducing stimuli: low in
H2O2-
treated cells and high in the heat-shocked ones.
152 In
H2O2-
treated cells, the increase in NO was lower than in cell
153 source for S-nitrosylation, occurred in
H2O2-
treated cells, while a decrease in this metabolite was e
154 ibitor L-NAME or specific eNOS siRNA in
H2O2-
treated cells.
155 pression decreased ERK1/2 activation in
H2O2-
treated cells.
156 as compared with wild-type-FLAG-MLK3 in
H2O2-
treated cells.
157 Cell proliferation of
HAN-
treated cells was suppressed for as long as 43 to 52 h.
158 tment induced mitosis override, and that
HAN-
treated cells proceeded into S phase and directly into t
159 uptake as well as glucose utilization in
HG-
treated cells.
160 rritin promotes adhesion and survival of
HKa-
treated cells and restores key survival and adhesion sig
161 l formation and H2A.X phosphorylation in
HNE-
treated cells in vitro.
162 K1A cells but to a lesser extent in
HPK1ARas-
treated cells.
163 Ase1 isoforms localize at the spindle in
HU-
treated cells and overexpression of the short Ase1 isofo
164 at a replication fork "collapse point" in
HU-
treated cells describes the point at which accumulated D
165 UV (ultraviolet light)- or HU (
hydroxyurea)-
treated cells, PIAS3 is required for efficient ATR autop
166 stalled DNA replication forks in
hydroxyurea-
treated cells.
167 Cytosol from type I
IFN-
treated cells abolished IAV hemagglutinin (HA) transport
168 A (siRNA) knockdown of MxA expression in
IFN-
treated cells.
169 Tsg101 is itself ISGylated in
IFN-
treated cells.
170 Paradoxically, even in infected,
IFN-
treated cells in which NAE inhibition substantially resc
171 Untreated or
IFN-
treated cells infected by this mutant virus (AdEasyE1Sub
172 ate whether particles released from
IFNalpha-
treated cells have a reduced capacity to establish infec
173 When the systolic functions of the NE/Ang
II-
treated cells were measured, a maintained or failed cont
174 y, immunofluorescence microscopy of
imatinib-
treated cells revealed a marked colocalization of intern
175 crophages, as well as in FABP4/aP2
inhibitor-
treated cells, but partially rescued in FABP4/aP2-null m
176 RNA sequencing of BET
inhibitor-
treated cells followed by Gene Ontology analysis showed
177 Overexpression of ubiquitin in
inhibitor-
treated cells partially reverses the inhibitor effect on
178 p38 kinase
inhibitor-
treated cells had 50% more U6 RNA than the control cells
179 easome subunit level in proteasome
inhibitor-
treated cells and confirm that PcG protein levels are re
180 In both alpha2M* and
insulin-
treated cells, the mRNA levels of SREBP1-c, SREBP2, fatt
181 and increased BrdU incorporation in
insulin-
treated cells as well as in HT22 cells overexpressing PK
182 ted Nox1 expression and suppressed EMT in
IR-
treated cells.
183 n the membrane, cytoplasm, and nucleus of
IR-
treated cells and CSC.
184 PCBP1 bound to DOHH in
iron-
treated cells but not in control or iron-deficient cells
185 This change was not observed in
iron-
treated cells.
186 We found that
IS-
treated cells exhibited a phenotype of mixed apoptosis/a
187 ly reduced compared with untreated and
KBrO3-
treated cells; and significant up-regulation of DNA repa
188 s and reactive oxygen species in beta-
lactam-
treated cells.
189 (diffusion coefficient and velocity) in
LatA-
treated cells was dependent on the level and activity of
190 In
Li(+)-
treated cells, cytoplasmic Ca(2+) signals evoked by an a
191 In
Li(+)-
treated cells, recovery of the cytoplasmic Ca(2+) oscill
192 untreated cells to 4.06 +/- 0.9 mum in
LiCl-
treated cells.
193 utophagy precedes apoptosis in Sigma1
ligand-
treated cells.
194 nt amount of succinate is accumulated in
LND-
treated cells.
195 a general increase in N-glycans on
lobeline-
treated cells rather than specific alterations in cell s
196 e in lipid composition on the surface of
LPA-
treated cells.
197 and improved viability in palmitate- and
LPS-
treated cells.
198 Conditioned media from
LPS-
treated cells also induced angiogenic tube and network f
199 Transcriptional profiling of
LPS-
treated cells revealed that 22 genes were up-regulated m
200 d the levels of ROS and TNF-alpha in the
LPS-
treated cells isolated from UC patients.
201 o observed in the culture supernatants of
LT-
treated cells.
202 mahanine and N-methylated dehydroxy-
mahanine-
treated cells exhibited apoptosis only at higher concent
203 ced apoptosis compared to dehydroxy-
mahanine-
treated cells, indicating significant contribution of th
204 ts suggest that the rapid lysis of
meropenem-
treated cells is the result of synergistically inhibitin
205 ere identified between control and
metformin-
treated cells at three time points.
206 the immature CA-SP1 lattice; virions from
MI-
treated cells retain an immature-like CA-SP1 lattice, wh
207 senger RNA and protein levels in
milatuzumab-
treated cells.
208 ail and vimentin, and a subpopulation of
MMS-
treated cells displayed an elongated fibroblast-like mor
209 brin cytotoxicity compared with control
mock-
treated cells.
210 imeter)(2)] from 0.47 +/- 0.06 units in
mock-
treated cells to 0.09 +/- 0.03 units in S6K-overexpressi
211 ximately fourfold less abundant than in
mock-
treated cells.
212 Compared with
mock-
treated cells, rapamycin-pretreated human ECs (rapa-ECs)
213 enyl had no effect on DAcyt levels in
MPP(+)-
treated cells and produced only a moderate effect on the
214 ing function, were greatly attenuated in
NCR-
treated cells.
215 Nicotine-
treated cells formed spheres at a higher efficiency than
216 onsistent with previous literature,
nicotine-
treated cells demonstrated a greater capacity for surviv
217 that SAF-A interacts with PLK1 in
nocodazole-
treated cells, and that serine 59 is dephosphorylated by
218 ed mitotic cell viability and, in
nocodazole-
treated cells, increased expression of the promitotic pr
219 In
non-
treated cells the amount of IL-8 was unchanged following
220 rmed spheres at a higher efficiency than
non-
treated cells, formed larger tumors when injected into m
221 , but caused more than 75% lethality in
nsEP-
treated cells (300 ns, 1.8-7 kV/cm, 50-700 pulses).
222 stimulated by eIF4E availability in
nuclease-
treated cell-free extracts.
223 der conditions of hyperlipidemia/obesity,
OA-
treated cells gain or reduce GSK3 substrate expression i
224 with wild-type or scrambled
oligonucleotide-
treated cells, respectively.
225 ing of AIF release by cyclosporine A in
OmpU-
treated cells further suggests that OmpU may be inducing
226 sed release of lactate dehydrogenase in
OmpU-
treated cells indicates that the OmpU-mediated cell deat
227 culum distention, and vacuolar changes in
PA-
treated cells.
228 and protein kinase C (PKC) activation in
PA-
treated cells.
229 2A (PP2A) became more eNOS-associated in
PA-
treated cells; the PP2A inhibitor okadaic acid reversed
230 e tissue of overweight humans, and
palmitate-
treated cells.
231 ivated protein kinase signaling in
palmitate-
treated cells.
232 f IL-17A and compared with TGF-beta- and
PBS-
treated cells as positive and negative controls, respect
233 pletion of lipid II precursors in
penicillin-
treated cells.
234 mitochondria isolated from hydrogen
peroxide-
treated cells led to degradation of the S-glutathionylat
235 lation, similar to PKCdelta in
peroxynitrite-
treated cells.
236 poptosis only in 1-methyl-4-
phenylpyridinium-
treated cells.
237 mal tau aggregation, increased 3-fold in
PHF-
treated cells.
238 itment at CyclinD1 and c-Myc promoters in
pM-
treated cells.
239 gulation of Janus kinase/Stat3 pathway in
pM-
treated cells.
240 despite increased prion titers in
quinacrine-
treated cells, transmission of the resulting prions prod
241 Rapamycin-
treated cells maintained a higher capacity to proliferat
242 clear Cap Binding Complex (CBC) in
rapamycin-
treated cells.
243 Transcriptome analysis of
rapamycin-
treated cells reveals genome-wide changes in alternative
244 the decrease in glycolytic state,
rapamycin-
treated cells displayed reduced sensitivity to low-gluco
245 ws similar vacuole size scaling to
rapamycin-
treated cells and is itself insensitive to rapamycin tre
246 control and with 0.1 mug/mul MNPs@SiO2(
RITC)-
treated cells.
247 ls compared with nontarget short hairpin
RNA-
treated cells.
248 RNAi-
treated cells had suppressed Akt signaling and exogenous
249 RNAi-
treated cells were smaller, had higher proliferation rat
250 N-acetyl cysteine (NAC) rescued Blp-
RNAi-
treated cells from cell cycle arrest, indicating that in
251 decreased antiviral genes in IL-13- and
RV16-
treated cells.
252 s proteasome-mediated, was slower in HDL-
S1P-
treated cells as compared with cells treated with albumi
253 ion of glycoconjugates in alkynyl-
saccharide-
treated cells at extremely low concentration (0.1 muM).
254 d with increased autophagic activity in
SAHA-
treated cells.
255 SB202190-
treated cell nuclear extract had about 50% increase in O
256 (1)O2 level and H2O2, but not OH in the
SDT-
treated cells.
257 f experiment, progressed normally in
Sephin1-
treated cells.
258 optosis to levels seen in normotensive
serum-
treated cells, and preventing the premature trophoblast
259 6, and ErbB3] to those in normotensive
serum-
treated cells.
260 Gene expression profiling of
SFB-
treated cells was consistent with a shift toward aerobic
261 pletion and Gravin short hairpin RNA (
shRNA)-
treated cells, an increase in cells containing micronucl
262 y two to three times compared with
siControl-
treated cells.
263 8 and hnRNP A1 small interfering RNA (
siRNA)-
treated cells.
264 e analysis reveals that neurites of C2-
siRNA-
treated cells have a net negative change in neurite leng
265 K and AKT can be partially restored in
siRNA-
treated cells by introduction of wild type (WT) GFP-NM I
266 Analysis of
siRNA-
treated cells by electron microscopy and Western blottin
267 In
siScrib-
treated cells, reinduction of the wild-type protein but
268 tments, were reduced in the siX3- and
siUL54-
treated cells.
269 eir ability to increase TNF production of
SM-
treated cells.
270 rface proteins were down-regulated in
statin-
treated cells compared to untreated cells because statin
271 with stabilized microtubules, such as
taxane-
treated cells.
272 of the striking physical features of
taxane-
treated cells is the localization of their microtubules,
273 ieved to arrest mitotic progression in
taxol-
treated cells.
274 be greater if the more numerous
teduglutide-
treated cells could be stimulated toward a more fully di
275 capable of binding Samd3 and E2F4 in
TGFbeta-
treated cells.
276 ll viability in lactacystin and
thapsigargin-
treated cells.
277 apping and pausing were also reduced in
THZ1-
treated cells.
278 Tivantinib-
treated cells showed typical microtubule disruption simi
279 rmore, compared with control cells,
TNFalpha-
treated cells exhibited reduced focal adhesion kinase an
280 a from Galpha(s) knockdown and cholera
toxin-
treated cells on FSHbeta expression.
281 cued production of TLR-inducible NO in
toxin-
treated cells.
282 tective effect of NRG1 and HGF in
trametinib-
treated cells.
283 immunoprecipitated VEGFR2 complexes from
TSR-
treated cells.
284 s-related genes were detected in
tunicamycin-
treated cells.
285 Relative to controls,
U0126-
treated cells showed constitutive decreases in phosphory
286 is article, we show that EPCR-positive
UM171-
treated cells, as opposed to EPCR-negative cells, exhibi
287 In
UV-
treated cells, Rad18 S409 phosphorylation was inhibited
288 ion of BPLF1 1-246 decreased viability of
UV-
treated cells and led to cell death, presumably through
289 impaired in extracts prepared from FICZ/
UVA-
treated cells.
290 efficient targeted gene disruption in
vector-
treated cell lines and primary cells.
291 aling compared with their respective
vehicle-
treated cell lines.
292 NA copy number between rapamycin and
vehicle-
treated cells.
293 ged from <30 to >120% of the mean of
vehicle-
treated cells for molecules known to lower and increase
294 lasmic reticulum, in contrast to the
vehicle-
treated cells, the cells treated with NLF or RuR also de
295 hasone-treated podocytes compared to
vehicle-
treated cells.
296 uptake up to 2.5-fold compared with
vehicle-
treated cells and up to 1.1-fold compared to PT-1.
297 phase cell cycle entry compared with
vehicle-
treated cells as determined by 5'-bromo-2'-deoxyuridine
298 did it induce vacuolar fragmentation in
VPA-
treated cells, suggesting that perturbation of the V-ATP
299 fibers at distal sites that fused with
Wnt7a-
treated cells were hypertrophic, suggesting that the tra
300 tain early changes in gene expression of
Zol-
treated cells, a 3 times higher dose of Zol IC(50 72 h)