ライフサイエンスコーパス: control cell

1 ed placodal neurons make fewer synapses than control cells.

2 tases by TRCs are more efficient than by the control cells.

3 icantly upon chemically-induced hypoxia than control cells.

4 A375 melanoma cells in NSG mice, relative to control cells.

5 9 cells relative to Atg3- or Atg5-expressing control cells.

6 ted to TPC2 knockdown is less acidic than in control cells.

7 ability in Bth mutant OHCs than in wild-type control cells.

8 Cs produce less mature oligodendrocytes than control cells.

9 ncreased their release of EVs, compared with control cells.

10 thesized cartilage matrix more robustly than control cells.

11 ls developing blebs compared with 53% of the control cells.

12 lized Hb to the lysosomes in comparison with control cells.

13 nts, which rendered them similar to those in control cells.

14 lytic lesions, as compared with mice bearing control cells.

15 ivation, but had no effect in nontransformed control cells.

16 o the subendothelial matrix in contrast with control cells.

17 fferentially expressed between E7 and vector control cells.

18 fferentially expressed between E7 and vector control cells.

19 esulted in reduced NET formation relative to control cells.

20 d a lower rate of cholesterol synthesis than control cells.

21 ing IQGAP1 was significantly greater than in control cells.

22 eversal of migration direction compared with control cells.

23 to Coxsackie virus B3 (CVB3) infection than control cells.

24 F30-underexpressing cells when compared with control cells.

25 uent lung metastases than transplantation of control cells.

26 gher total LDLR protein levels compared with control cells.

27 ative to tumors generated by KLK5-expressing control cells.

28 A repair genes, BRCA2 or FANCD2, compared to control cells.

29 red HT-29 cells at 4 h compared to levels in control cells.

30 adding galectins impaired these processes in control cells.

31 significantly lower in KO alpha-cells versus control cells.

32 th of xenograft tumors in mice compared with control cells.

33 transcription of type I IFN genes in healthy control cells.

34 1 cells formed smaller xenograft tumors than control cells.

35 9 for transplantation than in mice receiving control cells.

36 mpared with corresponding NEDD4-1-proficient control cells.

37 dynein mutant cells was higher than that in control cells.

38 antly increased compared with differentiated control cells.

39 vels in TTP gene knockout (KO) cells than in control cells.

40 essing cells is unaltered in comparison with control cells.

41 maller and aberrantly positioned compared to control cells.

42 endocytic and exocytic domains compared with control cells.

43 SC cardiomyocytes when compared with healthy control cells.

44 als were decreased in comparison to those in control cells.

45 2b, IgG2c, and IgG3 were the same as C57BL/6 control cells.

46 mitochondrial matrix was lower than that in control cells.

47 alcium signaling and cell proliferation than control cells.

48 melanin expression levels, in comparison to control cells.

49 +) was higher in PC1-knock-out cells than in control cells.

50 y pre-edited mRNA was only one-fourth of the control cells.

51 ed in tumour-induced DCs compared to that in control cells.

52 nd angiogenesis compared to UMC-iPSC-ECs and control cells.

53 and resistance to apoptosis in vitro sparing control cells.

54 alignant hyperthermia-susceptible and normal controls cells.

55 munoglobulin (Ig) domain-containing proteins control cell adhesion and axonal navigation.

56 gh the depth of a scaffold, and to spatially control cell adhesion and morphology.

57 show that Unc5D interacts with FLRT2 in cis, controlling cell adhesion in response to externally pres

58 glycans of a small group of substrates, that controls cell adhesion and signaling.

59 ulation recapitulated cellular phenotypes in control cells and attenuated them in CFC cells.

60 nificantly higher in knockdown cells than in control cells and Gata2 knockdown rescued some of the ma

61 y siRNA led to an increase in ATP release in control cells and restoration of ATP release in cells tr

62 els of IL-6 and VEGF-A than that from vector control cells and significantly enhanced the proliferati

63 onfirmed that PAH P-EC proliferate more than control cells and stimulate more PA smooth muscle cell m

64 es purified from these treated cells or from control cells and treated with PKA degraded ubiquitinate

65 cence-activated cell sorting-isolated L- and control cells and was enriched in colonic L-cells.

66 of ether lipids released more exosomes than control cells, and these exosomes were similar in size t

67 Through intracellular spatial control, cells are able to organize and regulate their m

68 spase 3 activity) in NZO cells compared with control cells at 3 and 6 hours after stimulation.

69 lecular and anatomical remodeling events are controlled cell autonomously by the phylogenetically con

70 Rusan investigates how centrosomes control cell behavior and differentiation during develop

71 Surface engineering to control cell behavior is of high interest across the che

72 biology is to build regulatory circuits that control cell behavior, for both basic research purposes

73 s of LGR5 could be used to pharmacologically control cell behavior.

74 tissues, maintaining organ architecture and controlling cell behavior, including cell differentiatio

75 g a fundamentally new molecular approach for controlling cell behavior.

76 um-starved cells were clearly separated with control cells, but not with ADMA-treated cells in PCA mo

77 NAD, and mitochondrial content compared with control cells, but show reduced mitochondrial membrane p

78 s have significantly larger melanosomes than control cells, but the number of organelles is unchanged

79 el transcriptional target of Hh signaling to control cell-cell adhesion by negative regulation of E-c

80 membrane receptors and extracellular ligands control cell-cell and cell-substrate adhesion, and envir

81 The formation of tightly controlled cell-cell adhesions and cell-matrix junctions

82 e, we show that p120-catenin (p120) not only controls cell-cell adhesion, but also acts as a critical

83 of an RCP-regulated endocytic pathway which controls cell:cell repulsion and metastasis in vivo.

84 nes (OVCAR3 and A2780), normal hamster ovary control cells (CHOK1) and alphavbeta3-deficient or trans

85 es in THP-1 gene expression as compared with control cell CM.

86 s higher in cells lacking PC1, compared with control cells containing PC1.

87 ound that NONO-silenced cells, compared with control cells, continued to synthesize DNA, failed to bl

88 haviour arise from intrinsic mechanisms that control cell cycle duration and involve a new doublesex-

89 final cell cycle prior to a developmentally controlled cell cycle exit leads to extra cell divisions

90 translation of CPE-containing mRNAs, thereby controlling cell cycle and differentiation or synaptic p

91 or suppressor is a transcription factor that controls cell cycle and genetic integrity.

92 of the cyclin-dependent kinase 2 (Cdk2) and controls cell cycle re-entry.

93 The retinoblastoma (Rb) tumor suppressor controls cell cycle, DNA damage, apoptotic, and metaboli

94 Mechanisms that control cell-cycle dynamics during tissue regeneration r

95 nvolved in translation, global transcription control, cell-cycle control, stress response, DNA topolo

96 omising anticancer drug targets because they control cell death and are structurally and functionally

97 ranscriptional signatures of developmentally controlled cell death are largely distinct from the ones

98 ing immune function and that it does this by controlling cell death and the activation of T cells.

99 The prominent role of IAPs in controlling cell death and their overexpression in a var

100 Although autophagy controls cell death and survival, underlying mechanisms

101 he embryo takes charge of gene expression to control cell differentiation and further development.

102 tokinin/WUS pathway and retrograde signaling control cell differentiation at the shoot apex.

103 ognized as vital components of gene programs controlling cell differentiation and function.

104 tor 6 ( IRF6) acts as a tumor suppressor and controls cell differentiation in ectodermal and craniofa

105 ling pathways regulating cofilin activity to control cell direction have been established, the molecu

106 colorectal CSCs (CR-CSC), where deiodinases control cell division and chemosensitivity.

107 Cyclin-dependent kinases (CDKs) control cell division in eukaryotes by phosphorylating p

108 ulatory subunits of AMPK are not required to control cell division in response to nitrogen stress, pr

109 Controlled cell division is central to the growth and de

110 s on Z-ring stability during developmentally controlled cell division via a network of protein-protei

111 nase of the spindle assembly checkpoint that controls cell division and cell fate.

112 The RhoGEF Ect2 controls cell division and exerts oncogenic functions in

113 ase-promoting complex/cyclosome (APC), which controls cell division by ubiquitinating cell cycle regu

114 Since Notch signalling controls cell division timing downstream of Cdc25, ECs i

115 quently Miro1(-/-) MEFs migrated slower than control cells during both collective and single-cell mig

116 perimental data revealed how mechanisms that control cell dynamics are altered at the earliest stages

117 Apoptosis is a metazoan process of controlled cell elimination that plays critical roles in

118 kinin regulates shootward auxin transport to control cell elongation and root growth.

119 or, LiaR (a member of the LiaFSR system that controls cell envelope homeostasis), from daptomycin-res

120 V-1 and had a survival advantage compared to control cells ex vivo In a hu-PBL mouse study, GPI-scFv

121 , a superfamily of approximately 80 members, control cell excitability, ion homeostasis, and many for

122 ftly navigate the multitude of pathways that control cell fate [4].

123 of implanted stem cells must be optimized to control cell fate and enhance therapeutic efficacy.

124 etworks, regulated by extracellular signals, control cell fate decisions and determine the size and c

125 trate that cell cycle regulators Cyclin D1-3 control cell fate decisions in human pluripotent stem ce

126 ropic viral integration site (MEIS) proteins control cell fate decisions in many physiological and pa

127 y suppressing endogenous DNA damage, and may control cell fate through the regulation of CHK1.

128 ssion of transcription factors (TFs) aims to control cell fate with the degree of precision needed fo

129 cells to mediate cell-cell communication and control cell fate, proliferation, and survival.

130 nd duration of ER stress stimuli in order to control cell fate.

131 y defines how c-FLIP isoforms differentially control cell fate.

132 n integrate inputs from multiple pathways to control cell fate.

133 clear how they integrate with one another to control cell fate.

134 may exert bimodal transcriptional effects to control cell fate.

135 th factor beta (TGF-beta) signaling pathways controlling cell fate and proliferation.

136 ammed mechanism that plays a pivotal role in controlling cell fate and, consequently, many physiologi

137 Notch has a well-defined role in controlling cell fate decisions in the embryo and the ad

138 s and the sub-temporal program, spatial cues controlling cell fate in the latter part of the 5-6 line

139 h scales can improve traditional methods for controlling cell fate.

140 ing an unexpected role for these proteins in controlling cell fate.

141 he importance of a Ddx5-miR125b-Rybp axis in controlling cell fate.

142 slational modification with ubiquitin chains controls cell fate in all eukaryotes.

143 The transcription factor TLX1 controls cell fate specification and organ expansion dur

144 and highly conserved signaling pathway that controls cell fate specification and tissue patterning i

145 We show that ACD of developing T cells controls cell fate through differential inheritance of c

146 ispensable for cell-identity maintenance, it controls cell fate transition by orchestrating p300-medi

147 ns in all embryos, from flies to humans, and controls cell fate, proliferation and metabolic homeosta

148 crosstalk between the two TOR complexes that controls cell-fate decisions in response to nutrient ava

149 natorial libraries to select antibodies that control cell fates.

150 unfolding proteins to activating enzymes to controlling cell fates, aggregates of small molecules ar

151 e precision, and combined synergistically to control cell function.

152 Controlling cell functions for research and therapeutic

153 ing of how arrestin-dependent GPCR signaling controls cell functions.

154 lex 1 (TORC1) integrates nutrient signals to control cell growth and organismal homeostasis across eu

155 ases of the Rab family and has been shown to control cell growth and proliferation, actin-cytoskeleto

156 nscriptional coactivators YAP and TAZ, which control cell growth and proliferation.

157 ew clues as to how growth--dependent signals control cell growth and the cell cycle.

158 X3 and RUNX1 transcription is manipulated to control cell growth.

159 in and ecdysone, that act synergistically by controlling cell growth and cell division.

160 lular growth and survival cues with pathways controlling cell growth and proliferation, yet how growt

161 nal transducers and transcription factors in controlling cell growth and tumorigenesis.

162 in complex 1 (mTORC1), which is important in controlling cell growth in response to nutrient availabi

163 -Jun transactivation, an important factor in controlling cell growth, apoptosis, and stress response.

164 mTORC1 is a central signaling node in controlling cell growth, proliferation, and metabolism t

165 ion with the RNA template molecule TERC, and controlling cell growth.

166 alian target of rapamycin complex 1 (mTORC1) controls cell growth and anabolic metabolism and is a cr

167 investigates how the microbial cytoskeleton controls cell growth and division.

168 istic target of rapamycin complex 1 (mTORC1) controls cell growth and metabolism in response to nutri

169 These data indicate that RSL4 controls cell growth by controlling the expression of ge

170 A targets in vivo and whether Msi2 primarily controls cell growth in all cell types.

171 novel glucocorticoid-mediated mechanism that controls cell growth in Leydig cell tumors.

172 al. from 1996, the first suggesting that TOR controls cell growth in response to nutrients.

173 The cytoplasmic tyrosine kinase SRC controls cell growth, proliferation, adhesion, and motil

174 ssed nonradially oriented processes, whereas control cells had long, radially oriented monopolar or b

175 lf5 had reduced proliferation, compared with control cells, had reduced expression of ductal markers,

176 wever, a synaptic priming protocol, which in control cells has no effect on synaptic plasticity, lead

177 Control cells have high fractal dimension and low lacuna

178 MM and control cells have similar sensitivities to cisplatin, a

179 Compared to control cells, HEK293T cells transfected with an express

180 s, peroxides, and oxidized proteins than the control cells (i.e. not treated with NaCl) exposed to H2

181 ns (PcG) are transcriptional repressors that control cell identity and development.

182 Transcription factors control cell identity by regulating diverse developmenta

183 or signaling pathways to regulate genes that control cell identity during development and tumorigenes

184 e an emerging subclass of regulatory regions controlling cell identity and disease genes.

185 and derived cells, we demonstrate that Brd4 controls cell identity gene induction and is essential f

186 n Srf mutant SCs rescued their fusion with a control cell in vitro and in vivo and reestablished over

187 the TCDD-exposed fetal cells to compete with control cells in a mixed competitive irradiation/reconst

188 uency and produced smaller neurospheres than control cells in vitro, indicating reduction of self-ren

189 - 30.79 mm(3) vs 121.44 +/- 34.90 mm(3) from control cells) in flanks of mice.

190 significantly slower than those formed from control cells, indicating a reduced proliferation of tum

191 nt cancer progression and metastasis through controlling cell invasion.

192 A common motif in dynamically controlled cells is a dual-timescale regulatory network:

193 hnology represents an efficient strategy for controlling cell labeling and directing cell fate or beh

194 l lines (PsPC-1 and BXPC-3) and a non-cancer control cell line (HEK293) were infected with reovirus s

195 IMR90-iPSC cells were used as the control cell line.

196 due to lower cell-substrate adhesion in the control cell line.

197 feration of HNSCC cells with 3q gain but not control cell lines.

198 and exposed to light irradiation compared to control cells maintained in the dark.

199 s, which shows the possibility to access and control cell membrane structures with conductive polyele

200 reveal an instrumental function of Cdc25A in controlling cell metabolism, which is essential for EGFR

201 Chemokines and their receptors control cell migration during development, immune system

202 Controlling cell migration is important in tissue engine

203 However, the role these forces play in controlling cell migration speed remains largely unknown

204 wide array of functions for this complex in controlling cell migration, shape, and adhesion.

205 0c was associated with upregulation of genes controlling cell migration.

206 TMIGD1 controls cell migration, cell morphology, and protects r

207 The Abl tyrosine kinase signaling network controls cell migration, epithelial organization, axon p

208 ignaling pathway downstream of Sema4A, which controls cell migration.

209 observed throughout the layer of surrounding control cells, mimicked by Bdnf (brain-derived neurotrop

210 O-MDSCs, which has recently been reported to control cell motility in monocytes, alongside reduced VL

211 ed RhoGAP that specifically targets RhoA for controlling cell motility.

212 rmation and open the possibility that CRMP-1 controls cell motility by modulating Arp2/3 activation.

213 iate the signal transduction that ultimately controls cell motility.

214 There are several ways to control cell number, including readouts of organ functio

215 o regulate normal brain growth trajectory by controlling cell number, and disruption of this pathway

216 regulates normal brain growth trajectory by controlling cell number, and imbalance in this relations

217 formed tumors more slowly in nude mice than control cells or cells that expressed a mutant form of D

218 but also offers the capability of spatially controlling cell organization for fundamental studies, a

219 the Dchs1-Fat4 planar cell polarity pathway controls cell orientation in the early skeletal condensa

220 T2 relaxation times compared with unlabeled control cells (P = .0012).

221 ed cell survival to 34% compared with 51% in control cells (*, p < 0.01).

222 Compared with donor control cells, PAH pericytes had significant enrichment

223 REC domains control cell physiology through diverse mechanisms, many

224 d Msps, a known microtubule-binding protein, control cell polarity and spindle orientation of NBs.

225 NC migration in amphibians and zebrafish by controlling cell polarity in a cell contact-dependent ma

226 oupling between individual actin oscillators controls cell polarization and directional movement.

227 ostate cancer, and provide a new strategy on controlling cell populations by manipulating noise stren

228 They assess how a DNA-binding factor Satb2 controls cell position, molecular identity, pre-and post

229 When compared with controls, cell pretreatment with ST247 diminished the ef

230 sights for canonical signaling pathways that control cell proliferation (ERK), DNA-damage responses (

231 ulation of compartmentalized cAMP pools that control cell proliferation and CFTR-driven fluid secreti

232 ns impacts the redox signaling cascades that control cell proliferation and death.

233 e all developmental phase transitions and to control cell proliferation during organ growth and devel

234 sms of Fat4-Dchs1 signalling have evolved to control cell proliferation within the developing vertebr

235 or (EGFR) or the Hippo signaling pathway can control cell proliferation, apoptosis, and differentiati

236 propriate cellular signaling is essential to control cell proliferation, differentiation, and cell de

237 l and physical properties of the environment control cell proliferation, differentiation, or apoptosi

238 ide concentration within neurons and seem to control cell proliferation, migration, differentiation,

239 grates stimulatory and inhibitory signals to control cell proliferation.

240 e between positive and negative signals that control cell proliferation.

241 s at the hub of signal transduction pathways controlling cell proliferation and survival.

242 The tumor suppressor PTEN controls cell proliferation by regulating phosphatidylin

243 To understand how PLCgamma1 controls cell proliferation, we turned to its downstream

244 an essential transcriptional regulator that controls cell proliferation.

245 ucleoside diphosphate kinase A (NDPK-A) that controls cell proliferation.

246 The Frz pathway of Myxococcus xanthus controls cell reversal frequency to support directional

247 tion of the endothelial cell cytoskeleton to control cell shape and polarity.

248 Steering stem cell fate - through controlling cell shape - may substantially accelerate pr

249 l filaments to conduct many different tasks, controlling cell shape, division, and DNA segregation.

250 portant regulators of the cell cytoskeleton, controlling cell shape, migration and proliferation.

251 ntifies a primary role for alpha-Spectrin in controlling cell shape, perhaps by modulating actomyosin

252 -dependent spindle-positioning mechanism and controls cell shape and alignment through a transcriptio

253 d tissue homeostasis, how adhesion molecules control cell shapes and cell patterns in tissues remains

254 This effect was specific for RA because control cells showed opposite effects (e.g., osteoarthri

255 The ability to spatially control cell signaling can help resolve fundamental biol

256 al states can serve as lipid recognition and controlled cell signaling mechanisms.

257 phytochromes and describe their use in light-controlled cell signaling, gene expression, and protein

258 ites of posttranslational modifications that control cell-signaling pathways.

259 on of this mutant showed that ClpXP activity controls cell size and is required for growth at low tem

260 In contrast to control cells, SMAD4-deficient cells did not migrate aga

261 es utilize the transcription factor STAT5 to control cell-specific genes at a larger scale than unive

262 typic hybrids, suggesting that multiple loci control cell specification at the onset of female meiosi

263 to the same level of activity as channels in control cells stimulated by significantly higher IP3 con

264 one (VZ) and cortical plate (CP) compared to control cells, suggesting that IE2 concurrently dysregul

265 activity to extracellular dsRNA relative to control cells, suggesting that SR-As do not possess sign

266 s phosphorylation signals may differentially control cell surface density of GPR15 through endocytosi

267 se temporarily limits cell growth, and might control cell survival on plants by limiting their growth

268 General anesthetics may control cell survival via their effects on autophagy by

269 ng with abnormalities in immune-inflammatory control, cell survival, intracellular signaling, protein

270 uding cleaving and activating chemokines and controlling cell survival and proliferation.

271 pid kinases that activate signaling cascades controlling cell survival, proliferation, protein synthe

272 paB activation, and plays a critical role in controlling cell survival.

273 In contrast to control cells, the probands' cells showed mitochondrial

274 Compared with control cells, they failed to decidualize in vitro as de

275 Compared with control cells, thin sections of STIM1-transfected cells

276 Furthermore, compared with control cells, TNFalpha-treated cells exhibited reduced

277 antagonism between the GTPases Rac1 and RhoA controls cell-to-cell heterogeneity in isogenic populati

278 iption pre-initiation complex is proposed to control cell type-specific gene expression.

279 vel epigenetic mechanisms of transcriptional control, cell type-specific analysis of nuclear mRNA and

280 nt, a single orthologous locus (MAT/MTL) has controlled cell type throughout ascomycete evolution.

281 Transcriptional enhancers control cell-type-specific gene expression.

282 nd CReP-containing eIF2alpha phosphatases to control cell viability.

283 family of stress responsive proteins, which controls cell viability via antioxidant activity and reg

284 We control cell volume by modulating media osmotic pressure

285 n channels (VRACs) play an important role in controlling cell volume by opening upon cell swelling.

286 a widespread family of morphogenic proteins controlling cell wall biogenesis by the PBPs.

287 R as a regulator of cell wall synthesis that controls cell wall homeostasis in response to antibiotic

288 We describe a system that controls cell wall metabolism in response to starvation,

289 NA 5' ends in infected DBR1 knockdown versus control cells was eliminated by in vitro incubation of i

290 Intracellular Cu in control cells was similar for all three species (2.5-3.2

291 nerated a similar amount of MVs as uninduced control cells, we found that MVs isolated from onco-Dbl-

292 H2.35 cells with knockdown of ANLN or control cells were injected into FRG mice, which develop

293 s of ETV1-overexpressing PDAC and respective control cells were performed.

294 ased cancerous cell death while noncancerous control cells were unaffected.

295 As control, cells were plated on the insert membrane withou

296 ced replication fork progression compared to control cells; whereas no additive effect was observed b

297 press less ATGL and accumulate more fat than control cells, while knock down of Egr1 in 4E-BP1/2-null

298 s cause mitochondrial DNA disorganization in control cells, while mitochondrial DNA aggregation in th

299 Incubating control cells with disease bronchoalveolar lavage recapi

300 sh operational principles for quantitatively controlling cells with BMP ligands.