ライフサイエンスコーパス: cell growth

1 r carbon and sulfur salvage, contributing to cell growth.

2 sterol and fatty acid synthesis, to restrict cell growth.

3 heme regulates mitochondrial biogenesis and cell growth.

4 duces prostatic oncogenic transformation and cell growth.

5 P1 expression and ablated FGF-mediated tumor cell growth.

6 ibrary of oncogenes and tumor suppressors on cell growth.

7 g other small molecules, also impairs cancer cell growth.

8 abolic regulation of protein trafficking and cell growth.

9 ume to match the increase of dry mass during cell growth.

10 tides and are indispensable for human cancer cell growth.

11 es required for acute myeloid leukemia (AML) cell growth.

12 hieved by coupling cell-cycle progression to cell growth.

13 reasing AR transcription and suppressing PCa cell growth.

14 FEN1 played a causal role in ERalpha-driven cell growth.

15 1 and a subsequent G(1) arrest and defect in cell growth.

16 and nutritional status, to direct eukaryotic cell growth.

17 others illustrated its inhibitory effects on cell growth.

18 variants impairs CHK2 negative regulation of cell growth.

19 essential enzyme lead to dramatically slower cell growth.

20 As(III) caused a 50% decrease in D. mccartyi cell growth.

21 in appropriate E2F protein levels for proper cell growth.

22 % of the integrations near genes involved in cell growth.

23 al of DNA damage response and restoration of cell growth.

24 nerated metabolic flux data to predict yeast cell growth.

25 ietic precursor differentiation and NPM-ALK+ cell growth.

26 whereas silencing of ZFP36L1 enhanced tumor cell growth.

27 creases FOXA1 expression and prostate cancer cell growth.

28 with an enhanced need for metabolites during cell growth.

29 replication and as a driver of dysregulated cell growth.

30 However, this amidase controls cell growth.

31 S-phase cell cycle arrest, and reduction in cell growth.

32 us to examine how LINE-1 expression affects cell growth.

33 d the Grh1-dependent effect of starvation on cell growth.

34 affect anti-tumor immune function and cancer cell growth.

35 rocess arrests at an early stage of daughter cell growth.

36 complex 1 (TORC1) is a central regulator of cell growth.

37 nisotropic cells and aligns with the axis of cell growth.

38 cancer cells, selectively suppresses cancer cell growth.

39 f OTUD5 is shown to significantly accelerate cell growth.

40 hylamine and cadaverine inhibited intestinal cell growth.

41 will divide independent of light and further cell growth.

42 duces target gene expression and reduces PEL cell growth.

43 oenergetic and biosynthetic demands of rapid cell growth.

44 ck cellular proteins and pathways to control cell growth.

45 ydrogel is cytocompatible and supports 2D/3D cell growth.

46 ramming, and thus the impact of mutations in cell growth.

47 modulating Hippo signaling to suppress tumor cell growth.

48 es in nutrient sensing, stress response, and cell growth.

49 eting four factors negatively regulating the cell growth.

50 he study of any kind of monolayer epithelial cells growth.

51 ipid peroxidation, NO production, and tumour cells growth.

52 nts on the global mechanisms that coordinate cell growth(1-3).

53 t is sufficient to establish the dynamics of cell growth and adherence to simple growth laws.

54 Mechanistically, PIERCE1 depletion inhibits cell growth and AKT phosphorylation (pAKT) at S473, whic

55 he HP protects genome fidelity by regulating cell growth and apoptosis in response to a myriad of del

56 We demonstrate its application to studies of cell growth and biofilm formation, automated in silico c

57 ull breadth of cellular processes, including cell growth and cell cycle control, signal transduction,

58 r-expression in MDA-MB-231 and MB-468 cells, cell growth and chemokine gene expression were evaluated

59 iguration greatly improves the efficiency of cell growth and chromosome segregation.

60 and GLUT1 inhibitors, respectively, inhibits cell growth and collective invasion.

61 ock-down of plectin inhibits prostate cancer cell growth and colony formation in vitro, and growth of

62 ious pathophysiological processes, including cell growth and development, metabolism, and cancer prog

63 ese proteins including their roles in normal cell growth and differentiation and in human disease.

64 eceptors with branched N-glycans coordinates cell growth and differentiation by controlling glycoprot

65 ncoded by the PTPN11 gene and is involved in cell growth and differentiation via the MAPK signaling p

66 luding synaptic transmission and plasticity, cell growth and differentiation, and infectivity of viru

67 -signalling in basophils promotes epithelial cell growth and differentiation, partly through histamin

68 nscription factors (TFs) that contributes to cell growth and differentiation.

69 ion by RNA polymerase (Pol) II and regulates cell growth and differentiation.

70 forms and participate in diverse aspects of cell growth and differentiation.

71 peed over several generations, provided that cell growth and division are coupled through a minimum-s

72 AF kinases activated by RAS GTPases regulate cell growth and division by signal transduction through

73 We show that the cell growth and division defects due to loss of this ami

74 indeed coupled to the cellular processes of cell growth and division to influence phenotypical trait

75 while those downregulated were critical for cell growth and division.

76 to maintain size homeostasis by coordinating cell growth and division.

77 es help in understanding the coordination of cell growth and division.

78 tion of DNA replication and segregation with cell growth and division.

79 and temporally regulated in order to support cell growth and division.

80 ironment, and are often used to study cancer cell growth and drug efficacy.

81 Nucleoid remodeling during cell growth and environmental adaptation correlate with

82 sence of DPP, resulting in attenuated cancer cell growth and eventually cell death.

83 ing siRNAs to silence genes vital for cancer cell growth and function could be an effective treatment

84 BXW7 inhibited diffuse large B-cell lymphoma cell growth and further sensitized cells to OxPhos inhib

85 atment with DNMTi decreased rhabdomyosarcoma cell growth and increased apoptosis and differentiation,

86 APIO-EE-07 inhibited cell growth and induced apoptosis and also increased exp

87 BD variants inhibits Ras signaling, reducing cell growth and inducing apoptosis.

88 dely recognised as a key integration hub for cell growth and intracellular stress signals upstream of

89 Furthermore, Rab7a inhibition promotes beta cell growth and islet survival, and protects against act

90 which resulted in a significant reduction of cell growth and loss of phenotype.

91 nt-sensing pathway is a central regulator of cell growth and metabolism and is dysregulated in diabet

92 The endocrine system controls cell growth and metabolism by providing extracellular cu

93 wo complexes (mTORC1 and mTORC2), regulating cell growth and metabolism.

94 lizing enzyme that also has a role in cancer cell growth and metabolism.

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

96 critical protein kinase that governs cancer cell growth and metabolism.

97 Cell size is believed to influence cell growth and metabolism.

98 OR Complex 1 (mTORC1), a master regulator of cell growth and metabolism.

99 have been implicated as critical drivers of cell growth and metastasis in numerous Ras-driven cancer

100 translation of proteins implicated in cancer cell growth and metastasis.

101 is an important regulator of prostate cancer cell growth and metastasis.

102 d SRC-3 oncoproteins, FBXL16 promoted cancer cell growth and migration and colony formation in soft a

103 and induction of ciliation, which restricts cell growth and migration in normal and breast cancer ce

104 in plays a central role in controlling plant cell growth and morphogenesis.

105 ey effectors of the Hippo pathway to control cell growth and organ size, of which dysregulation yield

106 capability of tunneling formation, vascular cell growth and osteogenic differentiation.

107 function, including regulation of epithelial cell growth and permeability, production of mucus and an

108 MET in beta-catenin-mediated prostate cancer cell growth and progression and implicate a molecular me

109 Hippo pathway signaling limits cell growth and proliferation and maintains the stem-cel

110 palladium complex, has been shown to inhibit cell growth and proliferation in pancreatic cancer, lymp

111 get of rapamycin complex 1 (mTORC1) promotes cell growth and proliferation in response to nutrients a

112 grates growth-promoting signals to stimulate cell growth and proliferation, at least in part, through

113 MYC drives cell growth and proliferation, but also, at high levels,

114 R signaling is known as a broad regulator of cell growth and proliferation, in neurons it regulates s

115 ling many normal cellular processes, such as cell growth and proliferation, metabolism, apoptosis, im

116 As one of the fundamental requirements for cell growth and proliferation, nitrogen acquisition and

117 nal through the PI3K/Akt pathway, regulating cell growth and proliferation.

118 n of ERK1/2 or Src, the kinases that lead to cell growth and proliferation.

119 nding processes in human cells, critical for cell growth and proliferation.

120 , and inhibition of either pathway disrupted cell growth and proliferation.

121 ell into two daughter cells-is a key step in cell growth and proliferation.

122 RNA and DNA synthesis, which is required for cell growth and proliferation.

123 nucleic acid synthesis required for anabolic cell growth and proliferation.

124 dicating hypoxic like damage and endothelial cell growth and proliferation.

125 eal how Myc controls antigen receptor driven cell growth and proteome restructuring in murine T cells

126 tandardized wound healing assay by observing cell growth and quantifying cell detachment processes.

127 hondria generate ATP and building blocks for cell growth and regeneration, using pyruvate as the main

128 genic REGgamma-proteasome, attenuates cancer cell growth and sensitizes p53-compromised cells to chem

129 mass spectrometry, which were decoupled from cell growth and showed high specific turnover rates (~1

130 ession of Rig-G led to significantly reduced cell growth and suppressed migration in A549 and NCI-H19

131 t role in tumorigenesis by supporting cancer cell growth and suppressing oncogene-induced senescence.

132 strategy to target oncogene-dependent tumor cell growth and survival by enhancing Cu chelator effica

133 sults further demonstrate that GNL1 promotes cell growth and survival by inducing cytoplasmic retenti

134 rative medicine approaches to enhancing beta cell growth and survival represent potential treatments

135 cellular and genetic responses that improve cell growth and survival under culture conditions.

136 such as insulin, IGF-1 and HGF support beta cell growth and survival, but in people with type 2 diab

137 s of enhancers/promoters interactions to PEL cell growth and survival, here we produce H3K27ac HiChIP

138 l cellular signalling pathways implicated in cell growth and survival.

139 ment of libraries of transgenes that perturb cell growth and survival.

140 rce PRMT5's relevance for promoting lymphoma cell growth and survival.

141 A 2'-O-methylation is essential for leukemia cell growth and survival.

142 g proliferative response, but also for tumor cell growth and survival.

143 ption factor CUC3 is a negative regulator of cell growth and that its expression dynamics in a small

144 nd that loss of either ZFX or ZNF711 reduced cell growth and that the double knockout cells have majo

145 y role in mediating the action of insulin on cell growth and the development of diabetes.

146 ression of ~2,400 genes essential for robust cell growth and to construct an in silico sgRNA library

147 ed by methionine, despite conditions of high cell growth and translation (in which the roles of Gcn4

148 GE overexpression is shown to inhibit cancer cell growth and tumorigenicity.

149 nzymatic assay, while also inhibiting cancer cell growth and viability and activating p53-dependent t

150 n of RUNX1 in ccRCC cell lines reduced tumor cell growth and viability in vitro and in vivo.

151 scaffolds were cytocompatible and supported cell growth and viability.

152 wever, a complete deletion of BCCIP arrested cell growth and was lethal in mice.

153 Cell growth and/or proliferation may require the reprogr

154 negatively impact osteoblast and fibroblast cells growth and were capable of reducing bacterial load

155 oncogenic transformation, accelerated tumor cell growth, and aggressive tumor phenotypes in the comp

156 nscriptional activity, prostate cancer (PCa) cell growth, and androgen sensitivity.

157 viable cells, with an EC(50) of 0.9-1.9 muM, cell growth, and colony survival, and induced apoptosis

158 d proteins shown to regulate gene silencing, cell growth, and differentiation.

159 amental processes, such as organogenesis and cell growth, and elevated TEAD activity is associated wi

160 naling, cell division, membrane trafficking, cell growth, and gene expression.

161 , including alterations in ECM organization, cell growth, and interferon signaling.

162 ssion in proliferating cells is dependent on cell growth, and the extent of growth required for cell

163 nd activates rDNA transcription, transformed cell growth, and tumor formation.

164 xtracellular enzymes, lignin degradation and cell growth are crucial phenotypes of lignin-utilizing b

165 xogenous ASM or ceramide enhanced epithelial cell growth arrest and death.

166 , leading to inhibition of mTORC1 and cancer cell growth arrest.

167 be ideal for the support of mesenchymal stem cell growth, as shrinkage of fibers normally found with

168 enging by nonstatic environments during host cell growth, as well as variability introduced by manual

169 smotic stress, and oxidative treatment using cell growth assays and found increased resistance to eac

170 Cell growth assays in two NKTCL cell lines (YT and SNK-6

171 M-808 effectively inhibits leukemia cell growth at low nanomolar concentrations and is capab

172 g release profile of FGF from PXDDA film and cell growth behavior were measured.

173 a function of macropinocytosis in mammalian cell growth beyond Ras-transformed tumor cells via susta

174 otein expression in ATC cell lines decreased cell growth both in culture and in mouse xenografts.

175 nbalancing protein abundances and inhibiting cell growth but also accelerating genetic diversificatio

176 ring not only how the environment influences cell growth, but also how microbes shape their chemical

177 encing of an ERV-derived enhancer suppresses cell growth by inducing apoptosis in leukemia cell lines

178 n external uridine and enables us to control cell growth by modulating the uridine supply, both in vi

179 tative basis for predictive understanding of cell growth-cell cycle relationships.

180 Under our cell growth conditions and the concentrated conditions o

181 phosphoprotein that plays a critical role in cell growth control as the central regulator of RNA poly

182 d eIF4A1 and provides novel insight into the cell growth controlled by WDR77.

183 nal target Axl was found to be essential for cell growth dependent on the uptake of dead cells and ce

184 To identify additional effectors that enable cell growth dependent on the uptake of extracellular pro

185 Chromatin organization is critical for cell growth, differentiation, and disease development, h

186 c BET proteins for their ability to modulate cell growth, differentiation, and gene expression.

187 ngers regulating biologic processes, such as cell growth, differentiation, migration, and apoptosis.

188 The Hippo pathway plays critical roles in cell growth, differentiation, organ development and tiss

189 for providing a niche and for directing stem cell growth, differentiations and function pertinent to

190 fied, the molecular mechanisms through which cell growth drives cell division have remained elusive.

191 ial for stromal cells to modulate epithelial cell growth during intestinal regeneration and tumorigen

192 We show that cell growth during the G(1) phase of the cell division c

193 It suggested cell growth, dye-decolorizing peroxidase (DyP) and react

194 y host transcription factors that regulate B cell growth (e.g., IKZF1 and RUNX3), factors that enhanc

195 We find that cell growth efficiency increases, plateaus, and then dec

196 Second, size-dependent cell growth ensures that larger and smaller cells grow s

197 agnitude upon T cell activation to support T cell growth even under amino acid (AA) replete condition

198 "multiple fission": a long G1 with >10-fold cell growth followed by multiple rapid divisions.

199 h they are frequently postulated to regulate cell growth following stress, few null phenotypes for TA

200 s, mutant Pop1/6 have little or no effect on cell growth, global protein levels, the abundance of Est

201 ations important to tumorigenesis and cancer cell growth, here we report a chemoproteomic analysis of

202 which AHR cooperates with MYC in supporting cell growth, here we used LC-MS-based metabolomics to ex

203 e shift signal provide information about the cell growth in a confluent cell layer.

204 ribosome biogenesis, nucleolar expansion and cell growth in a manner dependent on Myc abundance.

205 factors resulted in synergistic decreases in cell growth in cell lines and patient-derived organoid m

206 3-Bromotyrosine formed both during cell growth in culture and in the isolated decellularize

207 Thus, Rb dilution through cell growth in G(1) provides one of the long-sought mole

208 e show that tumor ADORA1 deletion suppresses cell growth in human melanoma cell lines in vitro and tu

209 eraction screen identifies genes that impact cell growth in response to mTOR pathway inhibition.

210 wth in the early stage of NSCLC, but promote cell growth in the advanced stage of NSCLC.

211 that the plasma-like B cells inhibit cancer cell growth in the early stage of NSCLC, but promote cel

212 GBM) cells, identifying 467 hits that modify cell growth in the presence of clinically relevant doses

213 showed that FECH is required for endothelial cell growth in vitro and choroidal neovascularization in

214 d UNC0631) significantly inhibited human CCA cell growth in vitro and in severe combined immunodefici

215 PARK2 overexpression reduces melanoma cell growth in vitro and in vivo and induces apoptosis.

216 itor approved for clinical trials, blocks MB cell growth in vitro and in vivo, and prolongs survival

217 IM25 leads to ER stress and attenuates tumor cell growth in vitro and in vivo.

218 , inhibited FGFR signaling and reduced tumor cell growth in vitro and in vivo.

219 s to Enz treatment and further suppress EnzR cell growth in vitro and in vivo.

220 egulation of YAP1, ablating rhabdomyosarcoma cell growth in vitro and trending toward decreased tumor

221 tantly, CYR61 overexpression rescued MITF.KO cell growth in vitro and tumor growth in vivo.

222 trongly associated with airway smooth muscle cell growth in vitro.

223 of MEK and p110beta/PI3K reduced mouse tumor cell growth in vitro.

224 to perform its essential role in supporting cell growth in vivo.

225 HeLa cells growth in the very close vicinity of the working e

226 EPA and DHA promoted cell growth indicated by higher cell viability and cell

227 GF2, PDGF, and hGF and readily prevented MBC cell growth induced by these factors.

228 c acid exhibited the highest potency both in cell growth inhibition and in suppressing beta-cell deat

229 Interestingly, a real-time cell growth inhibition assay demonstrated that a single

230 In contrast to the broad range of cell growth inhibition induced by DbBi, the antiprolifer

231 ces antimicrobial activity, rescues bacteria cell growth inhibition, and blocks induced cell permeabi

232 SCs), where loss of PRDM10 results in severe cell growth inhibition.

233 onine sulfoximine (BSO) leads to synergistic cell growth inhibition.

234 Plant cell growth involves a complex interplay among cell-wall

235 Plant cell growth is constrained by the rate of water uptake a

236 eukaryotes, conserved mechanisms ensure that cell growth is coordinated with nutrient availability.

237 dividing epidermal stem cells, we found that cell growth is coupled to division through a sizer opera

238 The rate of cell growth is crucial for bacterial fitness and drives

239 Coordination of cell growth is essential for the development of the brai

240 In mouse models of LM, cancer cell growth is supported by the LCN2/SLC22A17 system and

241 inated regulation between the cell cycle and cell growth machineries.

242 essential role in prostate tumorigenesis and cell growth mediated by growth regulatory factors.

243 lex 1 (mTORC1) senses amino acids to control cell growth, metabolism, and autophagy.

244 pression of YBX1-R205A significantly reduced cell growth, migration and anchorage-independent growth

245 ate that DZIP3 is a crucial driver of cancer cell growth, migration, and invasion.

246 on multiple signaling pathways to coordinate cell growth, migration, and the formation of the extrace

247 r pharmacological PGM3 inhibition reduces PC cell growth, migration, invasion, in vivo tumor growth a

248 ts revealed roles for SEMA7A in breast tumor cell growth, motility, invasion, and tumor-associated ly

249 Now, we identified that PAX2 inhibits cell growth of ER+/HER2- tumor cells in a dose-dependent

250 When expressed in yeast, OsLHT1 supported cell growth on a broad spectrum of amino acids, and effe

251 correctly predicts the effects of inhibiting cell growth or cycle progression.

252 Directed cell growth or migration are critical for the developmen

253 cteriocytes of low- versus high-titer hosts: Cell-growth pathways are up-regulated in low-titer genot

254 We conclude that mTORC1 appears to regulate cell growth, perhaps in part through AKAP8L.

255 association with eIF4A or eIF4E, and reduces cell growth, polysome assembly, and translation of repor

256 selective USP7 inhibition suppresses cancer cell growth predominantly through a p53-dependent mechan

257 lso sufficient to reveal unknown features of cell growth, previously unmeasurable.

258 ector stimulation of a c-Myc controlled host cell growth program can contribute to pathogenesis.

259 the signalling pathways that are involved in cell growth, proliferation and death.

260 eonine kinases which play important roles in cell growth, proliferation, survival, and differentiatio

261 identify connections between the cell-growth-promoting transcription factor YAP/Yorkie an

262 rve a pronounced, significant maximum of the cell-growth rate at a specific SAW amplitude, resulting

263 he nucleoid is not significantly affected by cell growth rates and by prior treatment with rifampicin

264 Consistent with theory, Jurkat T cell growth rates increase with size for small cells, bu

265 s us to determine the distribution of single-cell growth rates, cell division sizes and replication i

266 Unlike SN38, SN22 inhibited NB cell growth regardless of ABCG2 expression levels.

267 c target of rapamycin complex 1 (mTORC1) and cell growth-regulating processes.

268 Exactly how mTORC1 promotes cell growth remains unclear.

269 2 knockout leads to increased R-loop levels, cell growth retardation and accumulation of gammaH2AX, a

270 ve mitochondrial biosynthesis and clearance, cell growth retardation, and cellular senescence of DC f

271 might indicate that anchorage-dependence of cell growth signaling is disturbed.

272 ile adriamycin inhibited SM-164-resistant BC cell growth, similar to parental cells.

273 o understand the factors that greatly impact cell growth, specific productivity and product qualities

274 We report on in vitro wound-healing and cell-growth studies under the influence of radio-frequen

275 ncer and serves to disconnect the control of cell growth, survival and metabolism from exogenous grow

276 Platelets also promote cancer cell growth, survival in circulation, and angiogenesis a

277 ns that control vital cell processes such as cell growth, survival, and differentiation.

278 signaling network plays fundamental roles in cell growth, survival, and migration and is frequently a

279 n of critical hallmarks of cancer, including cell growth, survival, metastasis, migration, and angiog

280 utoff mechanism in the design of a bacterial cell-growth system.

281 ellular signal-regulated kinase (ERK) and of cell growth than SHP099, a potent SHP2 inhibitor, in KYS

282 t in sphingolipid abnormalities and impaired cell growth that are corrected by treatment with myrioci

283 enic CD44 isoforms (CD44v) and increased CRC cell growth that was rescued by concurrent knockdown of

284 and transcripts reveal barley COM1 regulates cell growth, thereby affecting cell wall properties and

285 variable response from complete blockade of cell growth to absolute resistance.

286 Such variation highlights the sensitivity of cell growth to environmental variations and the limitati

287 on of organosulfur auxotrophy to better tune cell growth to the metabolic environment.

288 nine nucleotide exchange factor, rescues the cell growth, translation, and neuronal differentiation d

289 s important as deleting CNC1 allows enhanced cell growth under mild starvation.

290 parib sensitivity to better suppress the HCC cell growth via a synergistic mechanism that may involve

291 Norrin inhibited cell growth via beta-catenin signaling in GSCs that had

292 There was a significant decrease in cell growth via inhibition of AKT, NF-kB, CREB and AP-1

293 tor of PTP4A3 and human A2780 ovarian cancer cell growth was reduced.

294 cell proliferation and anchorage-independent cell growth were markedly inhibited.

295 ive (Ph+) acute lymphoblastic leukemia (ALL) cell growth, whereas expression of the closely related C

296 that PABPN1 deficiency inhibits keratinocyte cell growth, which can be rescued by ectopic DeltaNp63al

297 can restore Enz sensitivity to suppress EnzR cell growth, which may indicate that these antidepressio

298 tute for the native polyamines in supporting cell growth while stimulating polyamine homeostatic cont

299 s as a serine/threonine kinase that inhibits cell growth, while the HipB antitoxin neutralizes the to

300 ation have been widely applied to relate the cell growth with substrate availability.