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1 strain germinated significantly faster than wild type cells.
2 ted to the airways by the chemokine CXCL2 as wild type cells.
3 ation of Rp mutant cells by competition with wild type cells.
4 els of the m.3243 A > G mutation compared to wild type cells.
5 oss of 1C enzymes increased the longevity of wild type cells.
6 in the GAT5 and GAT6 mutants compared to the wild type cells.
7 uced in GSDME-deficient cells comparing with wild type cells.
8 in near homoplasmic mutant cells compared to wild type cells.
9 lkylating agents, but they have no effect in wild-type cells.
10 n2 is constantly localized to the nucleus in wild-type cells.
11 Rgamma expression in knock-out cells than in wild-type cells.
12 SMARCA4/BRG1 mutant but not of SMARCA4/BRG1 wild-type cells.
13 in the tsetse flies at rates comparable with wild-type cells.
14 more sensitive to MET inhibitor SU11274 than wild-type cells.
15 s with the timing of DraRnl replenishment in wild-type cells.
16 rexpression of the Arg/N-end rule pathway in wild-type cells.
17 fungal load after fluconazole challenge than wild-type cells.
18 Wnt5a perturbed polarization of neighboring wild-type cells.
19 roduced less IFN-gamma, IL-5, and IL-13 than wild-type cells.
20 ow large deviations from what is observed in wild-type cells.
21 remethylate the Pdcd1 locus to the levels of wild-type cells.
22 n and caspase activation induced in adjacent wild-type cells.
23 levels of AngII in the mutant compared with wild-type cells.
24 tical to keeping incorporation levels low in wild-type cells.
25 osertib at concentrations that are lethal to wild-type cells.
26 arable to levels exhibited by ST-246-treated wild-type cells.
27 PY2R undergo signal-dependent ectocytosis in wild-type cells.
28 sion of Rec8 is sufficient to trigger UPD in wild-type cells.
29 increased median elastic modulus compared to wild-type cells.
30 n, similar to those induced by DNA damage in wild-type cells.
31 herichia coli and is essential for growth in wild-type cells.
32 4me2/3 levels observed at their promoters in wild-type cells.
33 Mek1 is excluded from synapsed homologues in wild-type cells.
34 R22beta(-/-) Sertoli cells moved faster than wild-type cells.
35 in expression to levels similar to analogous wild-type cells.
36 er apoptosis in Tsc2-deficient cells but not wild-type cells.
37 pported more efficient SVNI replication than wild-type cells.
38 of the N3 mutant was comparable with that of wild-type cells.
39 ivated protein kinase (MAPK) pathway in BRAF wild-type cells.
40 out, which depends upon PD-L1 expression by wild-type cells.
41 in under shear flow conditions compared with wild-type cells.
42 in the rate of exchange across the locus in wild-type cells.
43 ling was 50% lower in HD cells compared with wild-type cells.
44 ) BMDM long after they were downregulated in wild-type cells.
45 d WNT10A protein expression in comparison to wild-type cells.
46 bose) polymerase (PARP) 1(-/-) compared with wild-type cells.
47 inflammatory cytokine production compared to wild-type cells.
48 rway epithelia with varying ratios of CF and wild-type cells.
49 in the smc6 mutant is similar to that in the wild-type cells.
50 pensable for robust H3 eviction in otherwise wild-type cells.
51 have longer glycans in their PG relative to wild-type cells.
52 -catenin inhibition blocked this response in wild-type cells.
53 5 degrees C that is essentially identical to wild-type cells.
54 lipid mutant sta1 from a mixture of sta1 and wild-type cells.
55 n are coupled events during SPB formation in wild-type cells.
56 in nup116 mutants and increased longevity in wild-type cells.
57 telomere sequence was different from that of wild-type cells.
58 only 1% of the mutant cells in a mixture of wild-type cells.
59 sis and cell death not seen in KRAS and BRAF wild-type cells.
60 y in PTEN-deficient cells in comparison with wild-type cells.
61 and had reduced proliferation compared with wild-type cells.
62 l mouse kidney cells with minimal effects on wild-type cells.
63 amma-glutamylcysteine synthetase relative to wild-type cells.
64 ses H3K9 methylation from tethering sites in wild-type cells.
65 ion start sites becomes broader than that in wild-type cells.
66 ecreased levels of p65 protein compared with wild-type cells.
67 d accumulation of SERCA levels compared with wild-type cells.
68 ATPase proton transport in inositol-deprived wild-type cells.
69 ndogenous Ags were more readily deleted than wild-type cells.
70 kines in response to TLR stimulation than do wild-type cells.
71 R)-induced, mutations than similarly treated wild-type cells.
72 more acidic phagolysosomal compartments than wild-type cells.
73 crete more proinflammatory cytokines than do wild-type cells.
74 in of Num1, an event that is not observed in wild-type cells.
75 nd breaks, and cell death compared with IDH1 wild-type cells.
76 nse granules in Ctr2(-/-) mast cells than in wild-type cells.
77 creased intracellular Ca(+) flux relative to wild-type cells.
78 tivate the Th2 pathway in vitro than similar wild-type cells.
79 mediators in response to infection than did wild-type cells.
80 ore ROS in the presence of DOX compared with wild-type cells.
81 levels of Rho1-GTP at the division site than wild-type cells.
82 tely repressed in 2-KO cells, in contrast to wild-type cells.
83 for accurate comparisons between mutant and wild-type cells.
84 terminate BIR at a significant frequency in wild-type cells.
85 il to upregulate Foxp3 to the same extent as wild-type cells.
86 LT1 protease-deficient (MALT(PD/PD)) mice to wild-type cells.
87 e rounded cell body and fewer dendrites than wild-type cells.
88 bstrate levels and P-body counts to those of wild-type cells.
89 lcytosine (5hmC) decreased to 30% of that in wild-type cells.
90 acellular growth of P. falciparum similar to wild-type cells.
91 78A confers a dominant negative phenotype in wild-type cells.
92 all respiratory rate that is comparable with wild-type cells.
93 l gene expression profiles compared with the wild-type cells.
94 control of the pathogen after infection with wild-type cells.
95 es were significantly less elongated than in wild-type cells.
96 resistance to oxidative injury compared with wild-type cells.
97 ) gene htpG turn over FtsZ more rapidly than wild-type cells.
98 levels of active and total beta-catenin than wild-type cells.
99 ted chromosome segregation fidelity in Sli15 wild-type cells.
100 th of DeltahtpG cells is reduced compared to wild-type cells.
101 vels corresponding to H3K27me3 deposition in wild-type cells.
102 ion, conferring a competitive advantage over wild-type cells.
103 of ATP7B-knockout HepG2 cells compared with wild-type cells.
104 luding MAP1LC3A, known as LC3) compared with wild-type cells.
105 he surface before departing was the same for wild-type cells (12 s) and pilus-minus mutant cells (13
107 cts more rapidly in the pkd2 mutant than the wild-type cells (50% higher), the cell separation in the
108 Moreover, reversible adhesion events in wild-type cells (6.8 events/min) occur twice as frequent
109 in TbRFT1 null parasites when compared with wild-type cells, a defect that is corrected by expressin
111 esses promote phenotypic plasticity, letting wild-type cells adapt to unfavourable environments witho
112 ate with sites of SmcHD1 enrichment on Xi in wild-type cells, additionally adopt features of active X
113 orthogonal methods we validated that PIK3CA wild-type cells adopt MAPK-dependent circuitries in brea
115 e activator aphB, and ompR overexpression in wild-type cells also repressed virulence through aphB We
116 ller in deletion mutants for Tol-Pal than in wild-type cells, although it is still larger than would
117 equency, in competition with matrix mutants, wild-type cells always increase in relative abundance in
118 3D genome folding using Hi-C experiments on wild type cells and ataxia telangiectasia mutated (ATM)
119 erexpressing, GFP-positive cells outcompeted wild type cells and dominated the peripheral blood compa
120 ecifically, we assume that fitness values of wild type cells and mutants at different locations come
121 herwise lethal disease more efficiently than wild-type cells and bypassed the requirement for interle
122 by comparing genome-wide DNA repair rates in wild-type cells and cells defective in the global genome
123 phenomenon was initially recognized between wild-type cells and cells with mutations in ribosomal pr
124 acterize the magnetosome arrangement in both wild-type cells and DeltamamJ mutants, which exhibit dif
125 re rings, including treadmilling velocity in wild-type cells and ftsZ(GTPase) mutants, lifetimes of F
126 tely accounts for the variable phenotypes of wild-type cells and more than 20 mutant yeast strains si
127 ells, thiol levels were similar to untreated wild-type cells and not significantly depleted by AS-HK0
128 false alarm and miss error probabilities in wild-type cells and provide a formulation which shows ho
129 nothione were identified in AS-HK014-exposed wild-type cells and reproduced by chemical reaction.
130 icked by the fusion inhibitor chloroquine in wild-type cells and rescued by expression of Munc13-4 bu
131 largest 102-kbp genomic island was lethal to wild-type cells and resulted in a reduction of up to 2.5
132 m hole and ring are circular and centered in wild-type cells and that in the absence of a functional
133 ustained higher levels of WNV infection than wild-type cells and that this difference was greater und
134 eshold to predetermine methylation levels in wild-type cells and the magnitude of methylation reducti
135 can be significantly affected, compared to a wild-type cell, and the method is able to model and meas
136 cerevisiae and found that 1-3% of all ECs in wild-type cells, and 5-7% of all ECs in cells lacking pr
137 ed p53-dependent G1 cell-cycle arrest in p53 wild-type cells, and a p53-independent pathway impaired
138 Fe(II) efflux is physiologically relevant in wild-type cells, and null mutants accumulate elevated le
139 ial drug susceptibilities of KRAS mutant and wild-type cells, and predict relapse based on increased
141 nt to UVB-triggered cell death compared with wild-type cells, and tumor necrosis factor-alpha release
142 h was found at both enhancer and promoter in wild-type cells, appeared to have been replaced by H3K27
144 evidence that most spontaneous SCE events in wild-type cells are not due to the repair of DNA double-
146 ransporters (i.e. xCT, LAT1, and y(+)LAT2 in wild-type cells) are crucial to control reactive oxygen
147 exhibit a strongly impaired SOCE compared to wild-type cells as a result of reduced calcium release a
148 st and demonstrate its ability to 3D segment wild-type cells as well as classical size and shape muta
149 hemotaxing Dictyostelium cells, and examined wild-type cells as well as mutants with defects in contr
151 in rings at approximately 90% of the rate of wild-type cells at 30 degrees C and 36 degrees C, sugges
152 icroglia lacking CR3 are more efficient than wild-type cells at degrading extracellular Abeta by secr
154 re normally weakly coupled to one another in wild-type cells become strongly synchronized following a
156 both Tcon and Treg cell function compared to wild-type cells but disproportionally affected Treg cell
157 d phosphorylated eEF-2 cycle in abundance in wild-type cells but not in cells deleted for OS-2 or the
160 ed as that caused by extensive DNA damage in wild-type cells but showed genetic dependencies distinct
161 of Hsp90, was degraded relatively slowly in wild-type cells but was rapidly destroyed in naa10Delta
162 F-L (NFEL) and NF-M (NFEM) were expressed in wild-type cells but were virtually absent in 2-KO cells.
163 an4c is also able to induce 2C-like cells in wild-type cells but, in contrast to Dux, can no longer d
164 of NF-kappaB dynamics that is unaltered from wild-type cells, but activation of the TNFalpha promoter
165 that TLR4 activation inhibits growth of TP53 wild-type cells, but promotes growth of TP53 mutant brea
166 activity was higher apically than basally in wild-type cells, but upon transformation this gradient w
167 hat peroxisomes form de novo continuously in wild-type cells by heterotypic fusion of endoplasmic ret
168 , both of which are dynamically modulated in wild-type cells by TOR kinase activity and the presence
171 nsitive to compaction, that interaction with wild-type cells causes their compaction and that crowdin
172 wnregulated in CMD1 mutant cells compared to wild-type cells, causing a reduced capacity for photopro
173 cells elicited a dominant-negative effect in wild-type cells, causing paralyzed short flagella with h
176 s, suggesting that other methods that target wild-type cells could be valuable in arresting tumor pro
179 we also find that tRNA thiolation levels in wild-type cells decrease when cells are grown at elevate
181 Displacement of MukBEF from ter by MatP in wild-type cells directs MukBEF colocalization with the r
182 ng IgV R-loops by RNase HI overexpression in wild-type cells does not affect IgV diversification, sho
184 se of Ssb from ribosomes is also observed in wild-type cells during growth in poor synthetic medium.
185 that H2O2 exposure caused bacteriostasis in wild-type cells during which time SCVs appeared spontane
187 etabolically resistant 5-InsP(7) analog into wild-type cells elevated levels of NUDT3 mRNA substrates
188 d it is Gaussian-like for immotile bacteria, wild-type cells exhibit anomalous non-Gaussian deviation
189 o osteoclasts was similar in TRAF6[L74H] and wild-type cells, explaining why the bone structure and t
190 mutations in epithelial polarity genes, and wild-type cells exposed to 'super-competitor' cells with
193 e but migrate significantly more slowly than wild-type cells; expressing Flag-AbpG in mutant cells el
200 omparing their impact before malignancy with wild-type cells have limited the understanding of their
201 terozygous iPSCs remained largely similar to wild-type cells, homozygosity for PIK3CA (H1047R) caused
202 viable but produce more robust biofilms than wild-type cells in both in vitro and in vivo conditions.
203 st-translational modification, we first grew wild-type cells in buffered tryptone broth with glucose
206 r vesicles that did not differ from those of wild-type cells in quantity, surface molecule expression
207 ll cells transform phenotypes of neighboring wild-type cells in vivo in such manner that they become
208 had enhanced effector function compared with wild-type cells, including increased production of IL-2
209 in CypA knockdown chondrogenic cells than in wild-type cells, indicating that CypA plays a functional
210 d lipid accumulation similar to those of the wild-type cells, indicating that DEX-bound GR accelerate
211 colocalize with HNF-1beta-occupied sites in wild-type cells, indicating widespread reciprocal bindin
212 er cisternae per Golgi apparatus relative to wild-type cells, indicative of protein trafficking defec
213 amics of fluorescently-labeled mutant and/or wild-type cells individually or in co-culture using a su
216 5alpha is present within the mitochondria in wild-type cells, it is instead located mostly outside in
217 ed a perinuclear pattern in undifferentiated wild-type cells, it predominantly localized to the nucle
219 e Pfn2 open reading frame alone in otherwise wild-type cells largely recapitulates these phenotypes.
220 romatid cohesion in STAG2 mutated but not in wild-type cells leading to mitotic catastrophe, defectiv
221 complex presenilin 1 from Tsc1-null cells to wild-type cells leading to the activation of Notch and R
222 athways in the stem cell compartment and how wild-type cells limit the proliferation of mutant cells
223 subsequent reanalysis of the remaining TP53 wild type cell lines clearly demonstrated that unfortuna
225 cell lines would be more sensitive than BRAF wild-type cell lines to three MEK1/2 inhibitors tested.
231 bstrates with a spread morphology similar to wild-type cells on stiff substrates and to cells undergo
232 th STAT1 and STAT3 were activated by mOSM in wild type cells or by mLIF/hOSM in wild type and Osmr(-/
233 n active hippo pathway signaling compared to wild-type cells or cells lacking both Mst1 and Mst2.
236 ed media alone (no LIF or inhibitors) and in wild-type cells passaged in media containing only calcit
238 se regulations within the heterogeneity of a wild-type cell population growing in optimal conditions.
239 down cells being more sensitive than matched wild type cells potentially providing cancer-specific ta
241 Finally, overexpressing the RQ-mutant in wild type cells produced no effect on either docking or
242 ent and LDIR reverses this effect, promoting wild-type cell proliferation and p53 mutant differentiat
243 K induction, the isogenic KRAS mutant versus wild-type cells remained resistant to GDC-0623-induced a
247 tion rates in TSC1/2-deficient cells, unlike wild-type cells, sensitizes these cells to endoplasmic r
248 on in lamin-A/C-deficient cells, whereas the wild-type cells show much less plastic deformation.
249 rved in smtA and smtB mutants, DeltasmtA and wild-type cells showed a similar 9,Me-GlcCer content, re
250 ensitivity to polyphosphate and, compared to wild-type cells, showed increased killing of phagocytose
251 as effective in cisplatin-resistant cells as wild-type cells, signifying that they circumvent cisplat
253 TP7A enhanced cell proliferation compared to wild type cells, suggesting that these proteins compete
254 longest cell-cell communication distance in wild-type cells, suggesting that criticality provides an
255 a level equivalent to or even higher than in wild-type cells, suggesting that the four hypersensitive
256 -3 exerts its cytotoxic effects on A549 (p53 wild-type) cell survival through a mechanism that depend
258 cells was indistinguishable from that of the wild-type cells, the mutant did exhibit reduced chemotax
260 at equalizes the mean cell size with that of wild-type cells, the size distributions of cells with ga
261 reintroduced by CRISPR-Cas9 gene editing of wild-type cells, these mutations reversed both ISRIB-med
263 enhances cell death of FLT3 mutant, but not wild-type, cells through GC-receptor-dependent upregulat
265 an AML cells were more sensitive than IDH1/2 wild-type cells to ABT-199, a highly specific BCL-2 inhi
269 in-mutated cells required higher forces than wild-type cells to reach high indentation depths, where
272 AS1 to 3 are highly resistant to AZA, as are wild-type cells treated with a small-molecule inhibitor
273 The lipid-based probe could also rescue wild-type cells treated with an inhibitor of cell wall b
278 Heterochromatin heritability might allow wild-type cells under certain conditions to acquire epim
280 but only the PKBR1 activity was increased in wild-type cells under the equivalent conditions, indicat
282 N survival, but the proportion of mutant and wild-type cells undergoing cell death was not affected b
283 bolomics revealed a broad metabolic shift in wild type cells upon biotin withdrawal which was blunted
284 more intense unfolded protein response than wild-type cells upon treatment with inducers of this pat
285 eated Ewing sarcoma cells were compared with wild-type cells using an isobaric mass-tag quantitative
286 nt APC(-/-) tumors induce rho in neighboring wild-type cells via acute, non-autonomous activation of
288 tation to indole caused a bipartite response-wild-type cells were attracted to regions of high indole
289 more abundant in dcl3 mutant strains than in wild-type cells were not due to sRNA-targeted RNA degrad
290 ls showed a dependency on PDHK4 whereas KRAS wild-type cells were significantly resistant to PDHK4 kn
291 expression was reduced by half, relative to wild-type cells, whereas focal adhesion kinase (FAK) act
293 diurnal rhythms of cellular fluorescence in wild-type cells, which persist in continuous light condi
294 fibroblasts was reduced by 80% compared with wild-type cells, which was in line with a reduced expres
295 mpaired caffeine-induced Ca(2+) release from wild type cells while promoting intracellular Ca(2+) rel
296 i.e., diffusion pathlength) and by comparing wild-type cells with hemoglobin H (HbH) thalassemia (sho
298 in vivo cassette-inversion method that marks wild-type cells with the endogenous EGFP-tagged protein,
300 t of genes that were essential for growth in wild-type cells yet dispensable when pbp1a was deleted.