ライフサイエンスコーパス: control cell

1 to death induction by H(2)O(2) compared with control cells.

2 greater in FIT2 knockdown adipocytes than in control cells.

3 in semisolid medium (Matrigel) not seen with control cells.

4 nfirmed by immunocytochemistry compared with control cells.

5 ed BMSCs were increased compared to those of control cells.

6 unced in c-Myc knockdown Hep3B cells than in control cells.

7 fusion and autophagic flux to levels seen in control cells.

8 a more invasive phenotype, when compared to control cells.

9 d in FIT2 knockdown adipocytes compared with control cells.

10 vitro and as xenografted tumors compared to control cells.

11 tronger inhibition of TRPM8 activity than in control cells.

12 ion in OCT1-overexpressing cells compared to control cells.

13 and mouse mRNAs from LARP4 knockout (KO) and control cells.

14 k-in mouse model of human Batten disease and control cells.

15 tered accessibility between experimental and control cells.

16 imentin-deficient fibroblasts, compared with control cells.

17 differentially expressed between mutant and control cells.

18 cells compared with static, motion and flask control cells.

19 C1-deficient endothelial cells compared with control cells.

20 ed placodal neurons make fewer synapses than control cells.

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

22 9 cells relative to Atg3- or Atg5-expressing control cells.

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

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

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

26 SC cardiomyocytes when compared with healthy control cells.

27 2b, IgG2c, and IgG3 were the same as C57BL/6 control cells.

28 mitochondrial matrix was lower than that in control cells.

29 alcium signaling and cell proliferation than control cells.

30 eated compared with fewer than 2% of matched control cells.

31 melanin expression levels, in comparison to control cells.

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

33 ografts in mice, but had no effect on normal control cells.

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

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

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

37 and resistance to apoptosis in vitro sparing control cells.

38 wed reduced expression of GDF6 compared with control cells.

39 ed cells from children with SLE from healthy control cells.

40 3 and -7 and increased apoptosis compared to control cells.

41 tilise glucose to the same extent as healthy control cells.

42 lls, HCMV infection is reduced compared with control cells.

43 ids (including S1P and ceramides) in AML and control cells.

44 ease in ERK1/2 phosphorylation compared with control cells.

45 and mutant ultrastructure resembled healthy control cells.

46 s decreased in TRPC1/6(-/-) pmLF compared to control cells.

47 A549 cancer cell lines with VA13 and MCF10a control cells.

48 could be clearly distinguished from vehicle control cells (0 muM AMIO) and HepaRG cells from HepG2 c

49 Among PAH and control cells, 170 proteins and 240 phosphopeptides were

50 the ezrin, radixin, and moesin (ERM) family control cell and tissue morphogenesis.

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

52 imentin increases LBBM by ~50% compared with control cells and that vimentin overexpression and simva

53 ical roles as part of the RISC; rather, AGO1 controls cell and tissue growth by functioning as a dire

54 ty and intracellular S1P concentrations than control cells, and SKIP-transfected leukemia cell lines

55 ation, and spheroid formation, compared with control cells, and slowed growth of orthotopic tumors in

56 ed with IL-2 alone to serve as nonstimulated control cells, and then these expanded or nonstimulated

57 H approximately 0.2 units lower than that of control cells, and treatment with chloroquine normalized

58 We model the chromatin of the affected and control cells as networks and analyze the network topolo

59 like Nos2 and are significantly better than control cells at limiting M. tuberculosis replication.

60 We show that FPN controlled cell-autonomous iron efflux to stabilize and

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

62 Control cells became lodged in the first capillary bed e

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

64 c G proteins are key molecular switches that control cell behavior.

65 ligand, inducing intracellular signaling to control cell behavior.

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

67 s, access the intracellular environment, and control cell behavior.

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

69 egulation is essential for understanding and controlling cell behavior.

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

71 hese programs to reshape gene expression and control cell behavioral responses.

72 ide assemblies to mimic protein dynamics for control cell behaviors.

73 gives rise to mature-like cardiomyocytes in control cells but, mutant cells transition to a patholog

74 oforms of IL1RA were measured in patient and control cells by real-time polymerase chain reaction.

75 as restored in the recircularized plasmid in control cells by using the endogenous homologous transcr

76 ction incidence was elevated 6.665-fold over control cells carrying the CC genotype.

77 ndividuals showed higher CBS expression than control cells; CBS localization was both cytosolic and m

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

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

80 tenin-dependent membrane function that helps control cell-cell interactions.

81 e equally, implicating additional mechanisms controlling cell-cell cooperation and individualization.

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

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

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

85 Here we report that the NMDA receptor controls cell competition of epithelial cells and Myc su

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

87 ose this codon bias as a regulatory layer to control cell context-specific expression and explain the

88 link between the molecular machineries that control cell cycle progression and EHT.

89 ctasia-mutated (ATM) and Rad3-related (ATR), control cell cycle progression, DNA repair, and apoptosi

90 horylates the regulatory T-loop of CDKs that control cell cycle progression.

91 esults reveal an important role for RECQ1 in controlling cell cycle checkpoint activation in response

92 egulate the differentiation of adult HSCs by controlling cell cycle gene regulatory module.

93 Among the different cyclins controlling cell cycle progression, cyclin F does not pa

94 display specific functions by differentially controlling cell cycle progression.

95 a great variety of pathways, including those controlling cell cycle, metabolism, and ribosomal and mi

96 olutionarily conserved ubiquitin ligase that controls cell cycle progression through spatiotemporally

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

98 The ATR kinase controls cell cycle transitions and the DNA damage respo

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

100 mplex phosphorylates the T-loop of CDKs that control cell-cycle progression.

101 a well-known posttranslational modification controlling cell-cycle transitions and levels or/and act

102 cysts form significantly fewer tubules than control cell cysts, and Exoc5-KD cysts did not undergo t

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

104 revealed it did not depend on pathways that control cell death and engulfment or muscle arm extensio

105 dual independent functions because they also control cell death checkpoints.

106 against cisplatin must target molecules that control cell death pathways in the oocytes of primordial

107 ated into these polymers to enable spatially controlled cell death by the localized generation of (1)

108 As an alternative pathway of controlled cell death, necroptosis can be triggered by t

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

110 The PTEN tumor suppressor controls cell death and survival by regulating functions

111 d in significantly lower amounts compared to control cells, demonstrating the efficiency of the lipid

112 yzing Notch activation in single cells while controlling cell density and ligand expression level, we

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

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

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

116 ation, raising the question of what actually controls cell directionality.

117 roduce the pathogenic variant into unrelated control cells (disease modeled) to determine the necessi

118 e cell cycle inhibitor p57 has been shown to control cell division in human beta cells.

119 orchestration of programs and processes that control cell division, cell-type specification, cell mig

120 upregulation of genes involved in cell cycle control, cell division, mitosis, DNA replication, and DN

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

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

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

124 e-promoting complex/cyclosome (APC/C), which controls cell division and many aspects of neurobiology,

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

126 Intrinsically disordered proteins control cell elongation and carbon reserves via an order

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

128 of genetically engineered proteins that can control cell excitability with light have revolutionized

129 tion have largely been elucidated, how auxin controls cell expansion is only now attaining molecular-

130 ngle, comprehensive explanation of how auxin controls cell expansion, and where more research is warr

131 In comparison with the control cells, exposure to 10 muM MeHg for 0.5 h signifi

132 pulmonary metastasis within 5 weeks, whereas controls cells failed to do so.

133 of two key regulatory histidine kinases that control cell fate and differentiation.

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

135 used by prokaryotes and eukaryotes alike to control cell fate and generate cell diversity.

136 nal mechanisms enabling these metabolites to control cell fate and review evidence that nutrient avai

137 insight into the biochemical reactions that control cell fate and state.

138 into the complex regulatory mechanisms that control cell fate choice.

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

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

141 that engage alternate signaling networks to control cell fate decisions.

142 ant regulator of tissue growth, but can also control cell fate or tissue morphogenesis.

143 the communication between adjacent cells to control cell fate specification.

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

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

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

147 mbers in response to extracellular cues that control cell fate.

148 gen directly affects chromatin regulators to control cell fate.

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

150 may exert bimodal transcriptional effects to control cell fate.

151 SOX) genes that encode transcription factors controlling cell fate and differentiation in many develo

152 s affects the instructive signaling pathways controlling cell fate is poorly understood.

153 we identified novel transcriptional programs controlling cell fate specification of populations arisi

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

155 The transcriptional repressor Blimp1 controls cell fate decisions in the developing embryo an

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

157 -type diversity and transcriptional networks controlling cell-fate specification.

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

159 will ultimately contribute to our ability to control cell fates at will.

160 dynamically changing protein concentrations control cell fates.

161 ring content mixing between compartments and controlling cell fluorescence.

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

163 wth plate and whether chondrocyte metabolism controls cell function.

164 of biological membranes play a vital role in controlling cell functions that require local reorganiza

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

166 s growth, nutrient and energy status cues to control cell growth and metabolism.

167 Z) are key effectors of the Hippo pathway to control cell growth and organ size, of which dysregulati

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

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

170 endent on external uridine and enables us to control cell growth by modulating the uridine supply, bo

171 rewiring complicated signaling networks that control cell growth, cell death, and homeostasis.

172 TOR complex 1 (mTORC1) senses amino acids to control cell growth, metabolism, and autophagy.

173 As, hijack cellular proteins and pathways to control cell growth.

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

175 ogen-activated protein kinase (MAPK) pathway controlling cell growth, differentiation, and oncogenic

176 In summary, we demonstrate that miR-193b controls cell growth and differentiation in liposarcoma

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

178 The endocrine system controls cell growth and metabolism by providing extrace

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

180 istic target of rapamycin complex 1 (mTORC1) controls cell growth and proliferation by sensing fluctu

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

182 lian) target of rapamycin complex 1 (mTORC1) controls cell growth, proliferation, and metabolism in r

183 However, this amidase controls cell growth.

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

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

186 led that a clique of self-regulated core TFs control cell identity and cell state.

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

188 DNA, RNA, and protein synthesis collectively control cell identity and function.

189 Transcription factors control cell identity by regulating diverse developmenta

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

191 gand that regulates the expression of a gene controlling cell identity.

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

193 n example of a "terminal selector" gene that controls cell identity.

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

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

196 - 30.79 mm(3) vs 121.44 +/- 34.90 mm(3) from control cells) in flanks of mice.

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

198 Eph receptors (Eph) and their ephrin ligands control cell interactions during normal development, and

199 nt cancer progression and metastasis through controlling cell invasion.

200 C) maturation, whereas NPCs from age-matched control cell lines did so efficiently.

201 As control cell lines HEK 293 from embryonic kidney and RC

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

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

204 e show that Sdf1 and Sema3A antagonistically control cell-matrix adhesion via opposite effects on Rac

205 0 nanoparticles) as well as their respective controls (cell media and both blank nanoparticles) were

206 ucible factor (HIF) transcription factors to control cell metabolism, erythrogenesis, and angiogenesi

207 tissue-restricted cytoskeleton modulation to control cell migration and angiogenesis in development a

208 f the cellular and molecular mechanisms that control cell migration and axon guidance at the vertebra

209 involved in mammalian signaling pathways and control cell migration toward endogenous CC chemokine li

210 0c was associated with upregulation of genes controlling cell migration.

211 hat integrates the timing of wound repair by controlling cell migration.

212 trate that this autoregulatory feedback loop controls cell migration in cSCC by blocking epithelial-m

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

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

215 ing activities of the Rac and Rho GTPases to control cell morphology.

216 involves Rap1, a noncanonical activator, and controls cell morphology and EGF-induced membrane protru

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

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

219 sed Atrogin-1 expression compared to healthy control cells (P < 0.05).

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 REC domains control cell physiology through diverse mechanisms, many

223 the kinase PAR1 are essential proteins that control cell polarity.

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

225 increases activity of PKCzeta, a PKC isoform controlling cell polarity, and that addition of a PKCzet

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

227 as greater in Notch2(tm1.1Ecan) BMMs than in control cells, possibly contributing to the actions of T

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

229 uripotent archaeocytes upregulate genes that control cell proliferation and gene expression, as in ot

230 y, tissue mechanics, and nutritional cues to control cell proliferation and tissue growth in both Dro

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

232 to cells via mechanotransduction pathways to control cell proliferation, differentiation and death.

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

234 CK2alpha-dependent molecular mechanisms that control cell proliferation, we established a myoblast-de

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

236 novo and taxonomically restricted genes that control cell proliferation:cell death ratio.

237 ily, and inhibiting the transcription factor controlling cell proliferation and differentiation.

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

239 velopmental biology, mediating organ size by controlling cell proliferation through the activity of a

240 phogenesis, homeostasis, and regeneration by controlling cell proliferation, apoptosis, and different

241 all GTPases that regulate signaling pathways controlling cell proliferation, differentiation, and sur

242 ssion via modulating the expression of genes controlling cell proliferation.

243 pathways, including the Hippo pathway which controls cell proliferation and differentiation in eukar

244 e transmembrane protein angiomotin (AMOT130) controls cell proliferation and migration of many cell t

245 The tumor suppressor PTEN controls cell proliferation by regulating phosphatidylin

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

247 ly powerful opportunities to investigate and control cell regulatory mechanisms.

248 of telomeres and, in turn, could be used to control cell replication and growth.

249 mtDNA levels of 0.9% and 17.9% compared with control cells, respectively.

250 Aberrant signaling through pathways controlling cell response to extracellular stimuli const

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

252 embrane-cortex attachment plays key roles in controlling cell shape and integrity.

253 a regulated process, the regulatory pathways controlling cell shape transitions in V. cholerae and th

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

255 omyosin networks driven by myosin activation controls cell shape changes and tissue morphogenesis dur

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

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

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

259 nd coordinating two cycles, a division cycle controlling cell size and a DNA replication cycle contro

260 thway mediates a key signaling mechanism for controlling cell size and number in organ growth.

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

262 , while another unidentified secreted factor controls cell size.

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

264 l number of master splicing regulators might control cell-specific splicing networks and that these R

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

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

267 Thus, BMP-9 levels can control cell surface levels of ALK-1, via CAV-1, to regu

268 associated trafficking regulator 1 (ENTR1), controls cell surface levels of Fas and Fas-mediated apo

269 this pathogen's physiology and mechanisms to control cell survival is critical in the identification

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

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

272 IM regulation by miRNAs serves as a rheostat controlling cell survival in specific physiological cont

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

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

275 In contrast to control cells, T cell subsets from methadone users show

276 three to four-fold higher uptake compared to control cells that do not overexpress EGFR.

277 Bs from PAS cases to gestational age-matched control cells that invaded to the normal depth from pret

278 In control cells, the addition of extracellular sodium (+40

279 In proliferating wild-type control cells, the addition of the growth factors promot

280 Compared with control cells, the B-to-A permeability of mIBG increased

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

282 physiological properties similar to those of control cells, their morphology is significantly more co

283 nhancing angiogenesis compared with diabetic control cell therapy.

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

285 thy adult organs, robust feedback mechanisms control cell turnover to enforce homeostatic equilibrium

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

287 other transcription factors under normoxia, control cell-type-specific hypoxia responses is observed

288 s demonstrated, optojasps can be employed to control cell viability, cell motility, and cytoskeletal

289 f mitochondrial reactive oxygen species that control cell viability.

290 hannels coordinate electrical signalling and control cell volume by gating in response to membrane de

291 We control cell volume by modulating media osmotic pressure

292 identifying candidate regulatory genes that control cell wall formation.

293 k1 in FgBck1-MKK1-Mgv1 cascade to negatively control cell wall integrity.

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

295 nd beta-chains of sorted nickel-specific and control cells were studied by high-throughput sequencing

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

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

298 mmon, inherited variants in a few genes that control cell-wide changes but also respond to the enviro

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

300 ncreased SEAP secretion by ~ 82% relative to control cells, with lesser effects at other field streng