1 MB cells upon re-transplantation of PTC-
028-
treated cells into secondary recipient mouse brains.
2 vopiridol, transcriptome analyses of FIT-
039-
treated cells revealed that FIT-039 specifically inhibit
3 ading to more ROS generation in hypoxic YC-
1-
treated cells.
4 depletion delays DNA repair in UV- and VP-
16-
treated cells and increases polyploid cells after VP-16
5 ion of c-Kit and IL-7 receptors on the IL-
18-
treated cells.
6 enation defects similar to those of ICRF-
193-
treated cells.
7 Interestingly, while IL-
1beta-
treated cells exhibited only minor changes in metabolism
8 enuated PGE2 and IL-6 release in HG+IL-
1beta-
treated cells than in NG+IL-1beta-treated cells.
9 G+IL-1beta-treated cells than in NG+IL-
1beta-
treated cells.
10 N-nitroso-guanidine-treated mice or H(2)O(
2)-
treated cells.
11 RNA reverses the reduction of TEER in IL-
22-
treated cells.
12 d to promote its self-aggregation in ABT-
263-
treated cells, shown using a bimolecular fluorescence co
13 o increased PDH activity in 1alpha,25(OH)
2D3-
treated cells (p = 0.09).
14 In 1alpha,25(OH)
2D3-
treated cells, mitochondrial volume and branching and ex
15 inase 4 (PDK4) decreased in 1alpha,25(OH)
2D3-
treated cells.
16 ion rate (OCR) increased in 1alpha,25(OH)
2D3-
treated cells.
17 mosan or bacteria was fully restored in IL-
4-
treated cells.
18 icient to induce enhanced cell death in IL-
5-
treated cells.
19 of cell viability were "rescued" in Ad.mda-
7-
treated cells incubated with Bcl-x(s) siRNA.
20 he mitochondria of rotenone- and antimycin
A-
treated cells was observed and may contribute to the enh
21 n were found to increase in the tubastatin
A-
treated cells compared with the control cells, suggestin
22 tor glioma-associated protein 1 (GLI1) in
AA-
treated cells is the underlying mechanism controlling BC
23 s, including BCL2, BFL1/A1, and 4-1BB, in
AA-
treated cells.
24 AB235-
treated cell pellets also integrated into the surroundin
25 Examination of
AB235-
treated cell pellets in both in vitro and in vivo experi
26 ABC-
treated cells and EMP had greater TF activity, while ten
27 Finally, EMP isolated from
ABC-
treated cells enhanced collagen-evoked platelet integrin
28 and transgenic mouse model, as well as
Abeta-
treated cells.
29 of IFI16 was absent in phosphonoacetic
acid-
treated cells, which blocks KSHV DNA replication and, co
30 olarized or ethylene glycol tetraacetic
acid-
treated cells, indicating that bacteria bind preferentia
31 arated with control cells, but not with
ADMA-
treated cells in PCA model.
32 rotein aggregation was more prominent in
ALA-
treated cells.
33 soproxil fumarate- and tenofovir
alafenamide-
treated cells and EMP displayed higher ectonucleotidase
34 Finally,
alcohol-
treated cells partially regained their ability to withst
35 , an inhibitor of p38 activity, to IFN-
alpha-
treated cells reversed, in part, the inhibition of telom
36 treated human cells, we challenged IFN-
alpha-
treated cells with HIV-G208R and found that MxB does not
37 tor that blocks HIV-1 infection in IFN-
alpha-
treated cells, this is a hard concept to grasp due to th
38 uced the expression of mTOR in peg-IFN-
alpha-
treated cells, whereas silencing of mTOR had no effect o
39 bute to the restriction imposed by IFN-
alpha-
treated cells.
40 -based library screening in interferon-
alpha-
treated cells, we sought to characterize further interfe
41 ivated in human inflamed colon and TNF-
alpha-
treated cells (false discovery rate < 0.05).
42 The absence of this pathway in TNF-
alpha-
treated cells suggests multiple regulatory pathways for
43 5 reduced TSLP mRNA in DEP but not TNF-
alpha-
treated cells.
44 s in some transformed or
aminobisphosphonate-
treated cells, rendering those cells a target for Vgamma
45 es upon stimulation with
aminobisphosphonate-
treated cells.
46 ontrol, ataluren-treated, and
aminoglycoside-
treated cells.
47 inuclear regions of untreated and
amiodarone-
treated cells showed that the perinuclear region (i.e.,
48 clear region (i.e., cytoplasm) of
amiodarone-
treated cells had significantly elevated band intensitie
49 AFM topography maps revealed
amiodarone-
treated cells with enlarged cytoplasm and very thin regi
50 rescued impaired Abeta degradation in
ApoE4-
treated cells and reduced both ApoE and ABCA1 aggregatio
51 Experiments in
apyrase-
treated cells suggested involvement of a P2Y receptor un
52 induced translational repression in
arsenite-
treated cells expressing either wild-type or amyotrophic
53 The morphology of
avenaciolide-
treated cells was protoplast-like, which indicated that
54 sustained expression of the FMR1 gene in
AZA-
treated cells.
55 nase expression and activity in
azithromycin-
treated cells but not in cells treated with IL-4 and IL-
56 Interestingly, exosomes from AX-
B-
treated cells showed a positive biotin signal in electro
57 blast proliferation observed in NCaPP-PDGF-
B-
treated cells confirmed the functionality of these nanop
58 mulating factor, G-CSF) in the medium of
B20-
treated cells and in bronchoalveolar lavage fluid of mic
59 The supernatant from
BaPGN-
treated cells altered the growth of B. anthracis Sterne,
60 Moreover, treatment of
batimastat-
treated cells with recombinant sAPPalpha reversed the in
61 suggesting that suppression of mTOR in
BDNF-
treated cells resulted in excessive autophagy.
62 eath and accelerated autophagic flux in
BDNF-
treated cells.
63 reased binding to CPSF6 and CypA in IFN-
beta-
treated cells.
64 we adapted the RGDA/Q112D virus in IFN-
beta-
treated cells.
65 Interferon-
beta-
treated cells expressing wild-type STAT2 contain much le
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 dertook genome-wide analysis of
camptothecin-
treated cells at exon resolution.
72 ted off-target sites in a population of
Cas9-
treated cells further confirms high specificity of Cas9.
73 Cb-
treated cells formed midcell circumferential bulges, sug
74 ormal morphologies at the growth poles in
Cb-
treated cells, suggesting unipolar growth uses Cb-insens
75 ckdown of the autophagy protein Atg5 in
CCCP-
treated cells.
76 ully restored biotin production in
cerulenin-
treated cells.
77 expression was low in single agent
cisplatin-
treated cells, the opposite was true in cells treated wi
78 ing apoptosis in chemotherapy drug
cisplatin-
treated cells.
79 and up-regulated phospho-BRCA1 in
cisplatin-
treated cells, suggesting that T2AA increases DSBs.
80 een TR3 and mitochondrial Hsp60 in
cisplatin-
treated cells, which was associated with cytochrome c re
81 s found to be greatly disrupted in
cisplatin-
treated cells.
82 for TAB1 to regulate apoptosis in
cisplatin-
treated cells.
83 ced expression of RIP1 and IAPs in
cisplatin-
treated cells.
84 ines as mediators of miR486 expression in
CM-
treated cells.
85 e that SFN reverses the effects of PMI in
co-
treated cells by reducing the accumulation of p62 in mit
86 suspension cultures of GO-PEI/RNA
complexes-
treated cells dramatically increased the reprogramming e
87 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]
88 py in dynasore-treated cells than in
control-
treated cells.
89 N1A and FOXO3A in decitabine- versus
control-
treated cells.
90 markers by nearly 90% compared with
control-
treated cells (P<0.001).
91 abrogation of differences in
corticosteroid-
treated cell viability following siRNA knockdown of 2 TF
92 qPCR analysis showed that CPI and
CPH-
treated cells significantly inhibited PPARgamma expressi
93 Moreover, conditioned medium from
CR-
treated cells transmits the longevity benefit of CR to m
94 d calcium desensitization in control and
CRT-
treated cells, while HF(dys) cells were unaffected, impl
95 ame regions via the SSRP1 subunit in
curaxin-
treated cells.
96 id not observe this pattern in
cycloheximide-
treated cells or in cells lacking VID genes, required fo
97 on of inflammation-related genes in
cytokine-
treated cells.
98 rinsic antiviral protection in actinomycin
D-
treated cells.
99 Comparative proteomic analysis of DNA
damage-
treated cells versus -untreated cells evidenced a diffus
100 Hence,
DD-
treated cells utilized transcriptional and mRNA stabilit
101 Expression of factors in
DDT-
treated cells was similar to that in estrogen-treated MS
102 mulated in the membrane fraction of
deguelin-
treated cells, as indicated by increased interaction of
103 n of JNK kinase function rendered
Delta24RGD-
treated cells resistant to autophagy.
104 with the G9/A16 EFC subcomplex in
detergent-
treated cell extracts.
105 s simplex virus type 1 (HSV-1) in
detergents-
treated cell culture medium containing various serum con
106 etween L-type Ca channels and RyR2 in T3+
Dex-
treated cells.
107 Overall,
DMP1-
treated cells showed increased expression of alkaline ph
108 ot alter cell viability in untreated or
DMSO-
treated cells; however it did increase CG effect.
109 Self dsRNA accumulation in
DNMTi-
treated cells leads to type I IFN production and IFN-sti
110 The anticancer drug (doxorubicin (
DOX))-
treated cells show slow increases of SPR signals in the
111 The
DOX-
treated cells further process plasma membrane disruption
112 hat RIP1 may promote survival in
doxorubicin-
treated cells and that ganetespib may synergize with dox
113 p53 activation, and apoptosis in
doxorubicin-
treated cells.
114 ygen species (ROS)- or chemotherapeutic
drug-
treated cell lines.
115 Results from
drug-
treated cells showed inhibited, but ongoing degradation
116 ate-velocity separation of lysates from
drug-
treated cells.
117 arizations and/or triggered activity in
drug-
treated cells (11/20 acutely and 8/15 chronically).
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 lied to MALDI-TOF mass spectral data of
drug-
treated cells to obtain classification models which assi
122 IL-13-stimulated eotaxin production in
dsRNA-
treated cells.
123 observed by electron microscopy in
dynasore-
treated cells than in control-treated cells.
124 K-mediated phosphorylation of AKT in 4-OH-
E2-
treated cells was inhibited by ROS modifiers as well as
125 Consequently, HB-
EGF-
treated cells exhibit higher double-strand break (DSB) r
126 nd were significantly higher in the
elastase-
treated cells compared with controls.
127 imately 50% compared with untreated and
EtOH-
treated cells.
128 EVR-
treated cells showed temporary slower growth, lower meta
129 ls of cytotoxicity were observed in
eyesalve-
treated cell lines representative of skin and immune cel
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 phosphoamino acid analysis revealed that
Fsk-
treated cells resulted in elevated serine phosphorylatio
139 hich we confirmed by showing that
fucosidase-
treated cells, largely, failed to activate complement.
140 by which ErbB3 is upregulated in
fulvestrant-
treated cells is unknown.
141 maintaining low ErbB3 levels in
fulvestrant-
treated cells.
142 coadministration of spermidine to IFN-
gamma-
treated cells.
143 s in the phosphoprotein profile of
genotoxin-
treated cells, largely mediated by the ATAXIA TELANGIECT
144 HLA class I peptide repertoire of
gentamicin-
treated cells and identified multiple peptides derived f
145 lfed cargo in palmitic acid (PA)- or
glucose-
treated cells, indicating suppressed autophagic turnover
146 reduced H3S28p levels in untreated and
GnRH-
treated cells and also affected H3K27ac levels.
147 es, were also increased in both N1KD and
GSI-
treated cells and responded to okadaic acid treatment.
148 acteristic of short-lived effector cells,
GW-
treated cells demonstrated enhanced persistence in vivo
149 In addition,
H2O2-
treated cells had elevated rates of point mutations (par
150 different PCD-inducing stimuli: low in
H2O2-
treated cells and high in the heat-shocked ones.
151 In
H2O2-
treated cells, the increase in NO was lower than in cell
152 source for S-nitrosylation, occurred in
H2O2-
treated cells, while a decrease in this metabolite was e
153 ibitor L-NAME or specific eNOS siRNA in
H2O2-
treated cells.
154 pression decreased ERK1/2 activation in
H2O2-
treated cells.
155 as compared with wild-type-FLAG-MLK3 in
H2O2-
treated cells.
156 Cell proliferation of
HAN-
treated cells was suppressed for as long as 43 to 52 h.
157 tment induced mitosis override, and that
HAN-
treated cells proceeded into S phase and directly into t
158 e and restores metformin resistance in
hemin-
treated cells and tumours(7).
159 l formation and H2A.X phosphorylation in
HNE-
treated cells in vitro.
160 K1A cells but to a lesser extent in
HPK1ARas-
treated cells.
161 , RNA pol II-mediated RNA synthesis in 24
hr-
treated cells was upregulated, indicating that, in contr
162 Ase1 isoforms localize at the spindle in
HU-
treated cells and overexpression of the short Ase1 isofo
163 UV (ultraviolet light)- or HU (
hydroxyurea)-
treated cells, PIAS3 is required for efficient ATR autop
164 n prevents spindle elongation in
hydroxyurea-
treated cells.
165 stalled DNA replication forks in
hydroxyurea-
treated cells.
166 Cytosol from type I
IFN-
treated cells abolished IAV hemagglutinin (HA) transport
167 A (siRNA) knockdown of MxA expression in
IFN-
treated cells.
168 Tsg101 is itself ISGylated in
IFN-
treated cells.
169 Paradoxically, even in infected,
IFN-
treated cells in which NAE inhibition substantially resc
170 Untreated or
IFN-
treated cells infected by this mutant virus (AdEasyE1Sub
171 ate whether particles released from
IFNalpha-
treated cells have a reduced capacity to establish infec
172 When the systolic functions of the NE/Ang
II-
treated cells were measured, a maintained or failed cont
173 y, immunofluorescence microscopy of
imatinib-
treated cells revealed a marked colocalization of intern
174 crophages, as well as in FABP4/aP2
inhibitor-
treated cells, but partially rescued in FABP4/aP2-null m
175 RNA sequencing of BET
inhibitor-
treated cells followed by Gene Ontology analysis showed
176 In both alpha2M* and
insulin-
treated cells, the mRNA levels of SREBP1-c, SREBP2, fatt
177 ted Nox1 expression and suppressed EMT in
IR-
treated cells.
178 PCBP1 bound to DOHH in
iron-
treated cells but not in control or iron-deficient cells
179 ly reduced compared with untreated and
KBrO3-
treated cells; and significant up-regulation of DNA repa
180 6 ns compared to 2.57 +/- 0.14 ns in
KU60019-
treated cells).
181 (diffusion coefficient and velocity) in
LatA-
treated cells was dependent on the level and activity of
182 In
Li(+)-
treated cells, cytoplasmic Ca(2+) signals evoked by an a
183 In
Li(+)-
treated cells, recovery of the cytoplasmic Ca(2+) oscill
184 untreated cells to 4.06 +/- 0.9 mum in
LiCl-
treated cells.
185 utophagy precedes apoptosis in Sigma1
ligand-
treated cells.
186 nt amount of succinate is accumulated in
LND-
treated cells.
187 e in lipid composition on the surface of
LPA-
treated cells.
188 and improved viability in palmitate- and
LPS-
treated cells.
189 Conditioned media from
LPS-
treated cells also induced angiogenic tube and network f
190 Transcriptional profiling of
LPS-
treated cells revealed that 22 genes were up-regulated m
191 d the levels of ROS and TNF-alpha in the
LPS-
treated cells isolated from UC patients.
192 o observed in the culture supernatants of
LT-
treated cells.
193 mahanine and N-methylated dehydroxy-
mahanine-
treated cells exhibited apoptosis only at higher concent
194 ced apoptosis compared to dehydroxy-
mahanine-
treated cells, indicating significant contribution of th
195 ere identified between control and
metformin-
treated cells at three time points.
196 the immature CA-SP1 lattice; virions from
MI-
treated cells retain an immature-like CA-SP1 lattice, wh
197 senger RNA and protein levels in
milatuzumab-
treated cells.
198 ail and vimentin, and a subpopulation of
MMS-
treated cells displayed an elongated fibroblast-like mor
199 imeter)(2)] from 0.47 +/- 0.06 units in
mock-
treated cells to 0.09 +/- 0.03 units in S6K-overexpressi
200 ximately fourfold less abundant than in
mock-
treated cells.
201 Compared with
mock-
treated cells, rapamycin-pretreated human ECs (rapa-ECs)
202 had higher levels of Myt1 compared with
mock-
treated cells.
203 enyl had no effect on DAcyt levels in
MPP(+)-
treated cells and produced only a moderate effect on the
204 Nanostraw-
treated cells were fully functional and viable, with no
205 ing function, were greatly attenuated in
NCR-
treated cells.
206 Nicotine-
treated cells formed spheres at a higher efficiency than
207 onsistent with previous literature,
nicotine-
treated cells demonstrated a greater capacity for surviv
208 that SAF-A interacts with PLK1 in
nocodazole-
treated cells, and that serine 59 is dephosphorylated by
209 ed mitotic cell viability and, in
nocodazole-
treated cells, increased expression of the promitotic pr
210 ents inactivation of the APC/C in
nocodazole-
treated cells.
211 of uracil occurrence both in treated and
non-
treated cells.
212 etabolic activities of treated cells and
non-
treated cells.
213 rmed spheres at a higher efficiency than
non-
treated cells, formed larger tumors when injected into m
214 rs and other genomic features shows that
non-
treated cells possess uracil in the late replicating con
215 , but caused more than 75% lethality in
nsEP-
treated cells (300 ns, 1.8-7 kV/cm, 50-700 pulses).
216 stimulated by eIF4E availability in
nuclease-
treated cell-free extracts.
217 der conditions of hyperlipidemia/obesity,
OA-
treated cells gain or reduce GSK3 substrate expression i
218 istration with AZD6738 releases the
olaparib-
treated cells from G2 arrest.
219 62 translocated to the NE and nLDs of
oleate-
treated cells.
220 with wild-type or scrambled
oligonucleotide-
treated cells, respectively.
221 Transcriptome analysis of FPPa-
OmoMYC-
treated cells indicated that the fusion protein inhibite
222 ing of AIF release by cyclosporine A in
OmpU-
treated cells further suggests that OmpU may be inducing
223 sed release of lactate dehydrogenase in
OmpU-
treated cells indicates that the OmpU-mediated cell deat
224 hough the same markers are elevated in mu-
OR-
treated cells from methadone users.
225 culum distention, and vacuolar changes in
PA-
treated cells.
226 2A (PP2A) became more eNOS-associated in
PA-
treated cells; the PP2A inhibitor okadaic acid reversed
227 e tissue of overweight humans, and
palmitate-
treated cells.
228 ivated protein kinase signaling in
palmitate-
treated cells.
229 f IL-17A and compared with TGF-beta- and
PBS-
treated cells as positive and negative controls, respect
230 ates Pkc1, which prevents lysis of
pheromone-
treated cells by inhibiting polarized growth.
231 In the
phosphonates-
treated cells with the high and low DHTKD1 expression, a
232 itment at CyclinD1 and c-Myc promoters in
pM-
treated cells.
233 gulation of Janus kinase/Stat3 pathway in
pM-
treated cells.
234 reased in the supernatant from spike
protein-
treated cells.
235 despite increased prion titers in
quinacrine-
treated cells, transmission of the resulting prions prod
236 ation of protein kinase B compared with
RAPA-
treated cells.
237 Rapamycin-
treated cells maintained a higher capacity to proliferat
238 clear Cap Binding Complex (CBC) in
rapamycin-
treated cells.
239 Transcriptome analysis of
rapamycin-
treated cells reveals genome-wide changes in alternative
240 the decrease in glycolytic state,
rapamycin-
treated cells displayed reduced sensitivity to low-gluco
241 ws similar vacuole size scaling to
rapamycin-
treated cells and is itself insensitive to rapamycin tre
242 control and with 0.1 mug/mul MNPs@SiO2(
RITC)-
treated cells.
243 ls compared with nontarget short hairpin
RNA-
treated cells.
244 decreased antiviral genes in IL-13- and
RV16-
treated cells.
245 ion of glycoconjugates in alkynyl-
saccharide-
treated cells at extremely low concentration (0.1 muM).
246 d with increased autophagic activity in
SAHA-
treated cells.
247 (1)O2 level and H2O2, but not OH in the
SDT-
treated cells.
248 f experiment, progressed normally in
Sephin1-
treated cells.
249 optosis to levels seen in normotensive
serum-
treated cells, and preventing the premature trophoblast
250 6, and ErbB3] to those in normotensive
serum-
treated cells.
251 Gene expression profiling of
SFB-
treated cells was consistent with a shift toward aerobic
252 pletion and Gravin short hairpin RNA (
shRNA)-
treated cells, an increase in cells containing micronucl
253 y two to three times compared with
siControl-
treated cells.
254 8 and hnRNP A1 small interfering RNA (
siRNA)-
treated cells.
255 e analysis reveals that neurites of C2-
siRNA-
treated cells have a net negative change in neurite leng
256 mbrane fractions compared with control
siRNA-
treated cells.
257 te to a greater extent than in control
siRNA-
treated cells.
258 S1619, rescued BK(G354S) cells but not
siRNA-
treated cells, by selectively blocking the mutant channe
259 Analysis of
siRNA-
treated cells by electron microscopy and Western blottin
260 In
siScrib-
treated cells, reinduction of the wild-type protein but
261 eir ability to increase TNF production of
SM-
treated cells.
262 rface proteins were down-regulated in
statin-
treated cells compared to untreated cells because statin
263 viability in untreated or dimethyl
sulfoxide-
treated cells; however, it did increase the CG effect.
264 aggregation inhibitors that protected p-
tau-
treated cells.
265 with stabilized microtubules, such as
taxane-
treated cells.
266 of the striking physical features of
taxane-
treated cells is the localization of their microtubules,
267 ieved to arrest mitotic progression in
taxol-
treated cells.
268 be greater if the more numerous
teduglutide-
treated cells could be stimulated toward a more fully di
269 te were significantly higher in
temozolomide-
treated cells compared with controls.
270 everal metabolic alterations in
temozolomide-
treated cells, including a significant increase in stead
271 capable of binding Samd3 and E2F4 in
TGFbeta-
treated cells.
272 ll viability in lactacystin and
thapsigargin-
treated cells.
273 apping and pausing were also reduced in
THZ1-
treated cells.
274 Tivantinib-
treated cells showed typical microtubule disruption simi
275 proteomic profile between untreated- and
TIZ-
treated cells.
276 Significantly,
TM-
treated cells secreted increased insulin under condition
277 rmore, compared with control cells,
TNFalpha-
treated cells exhibited reduced focal adhesion kinase an
278 differentiated macrophages, but not
TNFalpha-
treated cells.
279 Torin1-
treated cells had an increased relative maximum force of
280 cued production of TLR-inducible NO in
toxin-
treated cells.
281 tective effect of NRG1 and HGF in
trametinib-
treated cells.
282 immunoprecipitated VEGFR2 complexes from
TSR-
treated cells.
283 rences between thapsigargin- and
tunicamycin-
treated cells upon inflammation suggest that different c
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 impaired in extracts prepared from FICZ/
UVA-
treated cells.
288 efficient targeted gene disruption in
vector-
treated cell lines and primary cells.
289 aling compared with their respective
vehicle-
treated cell lines.
290 NA copy number between rapamycin and
vehicle-
treated cells.
291 lasmic reticulum, in contrast to the
vehicle-
treated cells, the cells treated with NLF or RuR also de
292 hasone-treated podocytes compared to
vehicle-
treated cells.
293 uptake up to 2.5-fold compared with
vehicle-
treated cells and up to 1.1-fold compared to PT-1.
294 phase cell cycle entry compared with
vehicle-
treated cells as determined by 5'-bromo-2'-deoxyuridine
295 spiratory burst of PMN compared with
vehicle-
treated cells.
296 resolving receptor ALX compared with
vehicle-
treated cells.
297 ptor human resolvin E1 compared with
vehicle-
treated cells.
298 did it induce vacuolar fragmentation in
VPA-
treated cells, suggesting that perturbation of the V-ATP
299 arch and lipid accumulation, whereas
WD30030-
treated cells accumulate only lipids.
300 fibers at distal sites that fused with
Wnt7a-
treated cells were hypertrophic, suggesting that the tra