ライフサイエンスコーパス: cell growth

1 ts of Cryptolepis sanguinolenta, on melanoma cell growth.

2 cell lines to define oncogenes that promote cell growth.

3 inhibits cell differentiation and increases cell growth.

4 g AR transcriptional activity and inhibiting cell growth.

5 dination and control of plant cell shape and cell growth.

6 role for PS and membrane charge in polarized cell growth.

7 sight into fundamental mechanisms regulating cell growth.

8 FOXP1 in regulating normal HSPC and leukemic cell growth.

9 e inhibitory effects by fibroblasts on tumor-cell growth.

10 on of the NRF2 pathway, which promotes tumor cell growth.

11 mage/repair or signaling pathways related to cell growth.

12 o inhibit STAT5 phosphorylation and leukemic cell growth.

13 in the yeast complexes but are essential for cell growth.

14 ondrial UTP carrier (PNC1/SLC25A33) promotes cell growth.

15 ort purine and thymidine synthesis, and thus cell growth.

16 uous injection of oxygen bubbles to maintain cell growth.

17 of cell division, placing a finite limit on cell growth.

18 th would be significantly slower than normal cell growth.

19 ation) of histone H4 known to be involved in cell growth.

20 of the essential amino acids needed to drive cell growth.

21 activating CYLD mutations as drivers for NPC cell growth.

22 rcise-dependent suppression of breast cancer cell growth.

23 in TAF13, which is essential for supporting cell growth.

24 In contrast, inhibition of miR-503 reduces cell growth.

25 ase the frequency of apoptosis during normal cell growth.

26 that function in pathways critical to cancer cell growth.

27 d induced apoptosis, thus affecting leukemia cell growth.

28 A-binding activity, whose disruption reduces cell growth.

29 the Warburg effect, is important for cancer cell growth.

30 and found that they efficiently limit tumor cell growth.

31 e critical for mitochondrial homeostasis and cell growth.

32 control iron metabolism and promote optimal cell growth.

33 ion and systematically study their effect on cell growth.

34 (ABTS and DPPH assays) and inhibited Caco-2 cell growth.

35 acilitated FA-mediated anchorage-independent cell growth.

36 erase (HAT) MOF to be important for leukemia cell growth.

37 al toxin domains (CdiA-CT) to inhibit target-cell growth.

38 hypothesized to interfere with autophagy and cell growth.

39 he histone H4 and H2A and has been linked to cell growth.

40 nografted tumors significantly reduced tumor cell growth.

41 etabolic reprogramming that underlies cancer cell growth.

42 ells, lower pheromone doses elicit elongated cell growth.

43 de novo lipid synthesis, thereby suppressing cell growth.

44 gh a combination of radial intercalation and cell growth.

45 proved even to efficiently block cancer stem cell growth.

46 2 restored FBP1 expression and inhibited HCC cell growth.

47 e found that PUM1/2 sustain myeloid leukemic cell growth.

48 mediated glycolytic reaction, promoting PDAC cell growth.

49 s, inefficient energy generation and reduced cell growth.

50 down of KANK1 in neurofibroma cells promoted cell growth.

51 , colony formation and anchorage-independent cell growth.

52 the cell's immune response and restricting (cell) growth.

53 MAOA provides tumor cell growth advantages in the bone microenvironment by s

54 The tumor suppressor Trp53 (p53) inhibits cell growth after acute stress by regulating gene transc

55 2 inhibitor GSK343 in HepG2 cells suppressed cell growth and also revealed that local acquired DNA me

56 omal SOD3 had a stimulatory effect on cancer cell growth and an inhibitory effect on cancer cell migr

57 erlying the role of mcroRNAs in glioblastoma cell growth and apoptosis are not fully understood.

58 -colonizing capability through reduced tumor cell growth and bone remodeling in an intratibial mouse

59 aura cross-coupling reaction compatible with cell growth and carry out the cross-coupling chemistry i

60 and cell types, but the mechanisms coupling cell growth and cell cycle control with cell size regula

61 ctions in many cellular processes, including cell growth and cell cycle progression.

62 shows that cell-autonomous co-ordination of cell growth and cell division previously observed in uni

63 d of Akt inhibition, including reductions in cell growth and cell viability and in the regulation of

64 nt mice or human patients with AML-inhibited cell growth and clonogenicity and induced apoptosis.

65 sts and AML stem/progenitor cells, inhibited cell growth and colony formation, and significantly prol

66 ptosis together with a dramatic reduction of cell growth and colony formation.

67 th of biomechanical changes leading first to cell growth and contraction and then cell deadhesion, sc

68 Unlike PagL, LpxL depletion caused reduced cell growth and defects in cell morphology, both of whic

69 naling has important functions in regulating cell growth and development, misregulation of which has

70 s a transcriptional repressor that regulates cell growth and differentiation in multiple tissues, inc

71 mportant mediator of hormonal stimulation of cell growth and differentiation through its activation o

72 a sequential cell order reflecting preceding cell growth and division variations.The quiescence-exit

73 when expressed in budding yeast, diminished cell growth and DNA replication, substantially decreased

74 amycin (mTOR) links nutrient availability to cell growth and function by regulating gene expression a

75 ential signaling routes of CD147 affecting T cell growth and function.

76 ucose homeostasis by insulin depends on beta-cell growth and function.

77 tion takes a significant part in lung cancer cell growth and in vivo tumorigenesis.

78 4a inhibited cancer cell growth and induced cell death by various mechanisms

79 /2 and ERK1/2 signaling, inhibiting melanoma cell growth and inducing apoptosis.

80 EBV expresses viral oncogenes that promote cell growth and inhibit the apoptotic response to uncont

81 Ectopic overexpression of miR-503 promotes cell growth and inhibits apoptosis by targeting PDCD4.

82 These alterations enhanced BC cell growth and invasive abilities.

83 ines favoring a permissive milieu for cancer cell growth and invasive behavior.

84 y optimized mechanical properties to sustain cell growth and limit scaffold contraction.

85 actors that may promote or support malignant cell growth and maintenance, and point out how we might

86 us physiological stimuli to regulate several cell growth and metabolic pathways.

87 mTOR complex 1 (mTORC1) regulates cell growth and metabolism in response to multiple envir

88 get of rapamycin complex 1 (mTORC1) controls cell growth and metabolism in response to nutrients, ene

89 t of rapamycin (mTOR) coordinates eukaryotic cell growth and metabolism with environmental inputs, in

90 with a large number of proteins critical for cell growth and metabolism, including the major oncogeni

91 has emerged as a major regulator of leukemia cell growth and metabolism.

92 The elevated mTORC2 promotes cancer cell growth and metastasis via Akt(S437) phosphorylation

93 YC degradation, and markedly inhibits cancer cell growth and metastasis.

94 ncreasing possibilities to control unchecked cell growth and metastasis.

95 r work showed that ribavirin inhibits glioma cell growth and migration, and increases cell cycle arre

96 The PI3K signaling pathway regulates cell growth and movement and is heavily mutated in cance

97 ORC1) integrates nutrient signals to control cell growth and organismal homeostasis across eukaryotes

98 tely linked to the regulation of metabolism, cell growth and physiology.

99 umor, as well as promoted cholangiocarcinoma cell growth and progression.

100 r (IGF) signaling plays an important role in cell growth and proliferation and is implicated in regul

101 Cell growth and proliferation are tightly coupled to met

102 Approved mTOR inhibitors effectively inhibit cell growth and proliferation but elicit AKT phosphoryla

103 , Pol III activity is tightly regulated with cell growth and proliferation by factors such as MYC, RB

104 Gene sets related to cell growth and proliferation generally associated posit

105 rotein kinase, which plays critical roles in cell growth and proliferation in several types of cancer

106 Aberrant cell growth and proliferation in T-ALL lymphoblasts are

107 In these tumors, p73 sustains cell growth and proliferation via regulation of glutamin

108 tivation that is exploited by EBV to promote cell growth and proliferation, offering new strategies t

109 and survival cues with pathways controlling cell growth and proliferation, yet how growth factors ta

110 timulates PI3Kalpha/Akt signaling, promoting cell growth and proliferation.

111 e biogenesis, a rate-limiting factor in both cell growth and proliferation.

112 dates metabolic programs that sustain cancer cell growth and proliferation.

113 e of external glutamine supply for mammalian cell growth and proliferation.

114 maintenance and proteostasis, and away from cell growth and proliferation.

115 s real-time and simultaneous measurements of cell growth and protein expression.

116 LCs, and found that AL LC expression alters cell growth and proteostasis and confers PI sensitivity.

117 for the real-time, non-invasive analysis of cell growth and response to treatment in tissue-engineer

118 pha, and is critical for alveolar epithelial cell growth and self-renewal.

119 of bacterial growth using multigenerational cell growth and shape data for single Caulobacter cresce

120 otein coupled receptors (S1P1-5) to regulate cell growth and survival and has been implicated in a va

121 Autophagy supports cell growth and survival autonomously by recycling intra

122 dulator (KPT-9274) significantly impacted MM cell growth and survival in a large panel of MM cell lin

123 Metastatic tumor cell growth and survival in distant organs is facilitate

124 ose unique to the respective organs, various cell growth and survival pathways and functions are diff

125 PAK4 promoted MM cell growth and survival via activation of MM survival s

126 ng cancer (NSCLC) and is required for cancer cell growth and survival.

127 oding for a variety of proteins essential to cell growth and survival.

128 tor of cellular anabolic processes linked to cell growth and survival.

129 e cancer cell lines without affecting normal cell growth and survival.

130 11) signaling was essential for osteosarcoma cell growth and survival.

131 treated cells, confirming that tsRNAs affect cell growth and survival.

132 as to how growth--dependent signals control cell growth and the cell cycle.

133 Atg9 and TOR signaling in the regulation of cell growth and tissue homeostasis.

134 for the accumulation of biomass required for cell growth and tolerance of nutrient-poor, anaerobic en

135 rostate epithelial cell line, exhibited fast cell growth and transformation, while knock down of MCM8

136 onse factors, which can promote an arrest in cell growth and trigger cell death.

137 is and response in Phaeodactylum NO inhibits cell growth and triggers triacylglycerol (TAG) accumulat

138 reover, MYCN was essential to retinoblastoma cell growth and tumor formation, and ectopic MYCN partia

139 NO2-OA reduced TNBC cell growth and viability in vitro, attenuated TNFalpha-

140 ession knockdown via siRNA greatly inhibited cell growth and viability.

141 ns that are essential for various aspects of cell growth and virulence, including nutrient uptake, si

142 not only eliminates Pin1, but also inhibits cells growth and metastasis.

143 decreased glycolysis, anchorage-independent cell growth, and cell migration and invasion in HPV-tran

144 -2 expression leading to suppression of sAML cell growth, and enhancement of DNR cytotoxicity.

145 tinct resistance mechanisms, inhibited tumor cell growth, and increased cell death.

146 and cellulose synthesis is pivotal to plant cell growth, and its regulation is poorly understood.

147 mice, and genes associated with cell cycle, cell growth, and proliferation were differentially expre

148 time for APEX2 fusion construct validation, cell growth, and solidification of embedding resins.

149 ferent classes of PGs may support or inhibit cell growth, and their functions are determined in part

150 of stress-responsive kinases that modulates cell growth, apoptosis, proliferation and development.

151 embrane growth, which ensures that events of cell growth are coordinated with each other and with the

152 f MCM8 in PC3, DU145 and LNCaP cells induced cell growth arrest, and decreased tumour volumes and mor

153 factor alpha (TNF-alpha) that induced tumor cell growth arrest.

154 displayed additive or synergistic effects in cell growth assays in 10 of 11 cell lines evaluated as w

155 Preliminary cell growth behavior was carried out by culturing epider

156 ation of KANK1 in human MPNST cells inhibits cell growth both in human cell culture and xenograft mic

157 The siRNA delivered by the DNPs inhibited cell growth both in vitro and in vivo, which suppressed

158 rug NPs show significant inhibition of tumor cell growth both in vitro and in vivo.

159 r, miR-26a overexpression inhibits the tumor cell growth both in vitro and in vivo.

160 d signaling pathway is not essential to beta-cell growth but is involved in regulating beta-cell func

161 t Rrp2's ATPase activity is not required for cell growth, but experimental evidence supporting this n

162 stromal cells have been shown to favor FL B-cell growth, but the mechanisms of their protumoral effe

163 Ribosomes drive cell growth, but translation of ribosomal proteins compe

164 rapamycin complex 1 (mTORC1) kinase promotes cell growth by activating biosynthetic pathways and supp

165 te across cell membranes, halts liver cancer cell growth by altering both energy production and mamma

166 MSI2 influenced breast cancer cell growth by altering ESR1 function.

167 OCDO stimulates BC cell growth by binding to the glucocorticoid receptor (G

168 ecific IgEs were reported to restrict cancer cell growth by engaging high-affinity Fc receptors on mo

169 evidence that PRMT5 promotes prostate cancer cell growth by epigenetically activating transcription o

170 In conclusion, simvastatin may suppress TamR cell growth by inhibiting MCM7 and Rb and subsequently i

171 of nutrients that dictate the regulation of cell growth by mechanistic target of rapamycin complex 1

172 We postulate that the suppression of Th cell growth by SF through tryptophan catabolism may play

173 gs indicate that HIF-2alpha increases cancer cell growth by up-regulating YAP1 activity, suggesting t

174 Aberrant regulation of uterine cell growth can lead to endometrial cancer and infertili

175 on line can form when both cell movement and cell growth cease at low nutrient levels.

176 in vitro cellular activities for inhibiting cell growth, clonogenicity, and cellular glutamate produ

177 mice displayed striking impairment of tumor cell growth compared with wild-type mice, along with dec

178 and IL-22 production in PBMCs cultured in T-cell growth conditions was observed.

179 vely, produced additive effects on p-Akt and cell growth, consistent with direct Akt phosphorylation

180 e from an ancient program for unidirectional cell growth coopted for root hair development during vas

181 endogenous FAM46C enhanced multiple myeloma cell growth, decreased Ig light chain and HSPA5/BIP expr

182 some interaction in vitro and for pronounced cell growth defects upon translation inhibition in vivo,

183 of Rph1 during DNA damage stress results in cell growth defects.

184 e ability to divide asymmetrically, nor show cell-growth defects or undergo apoptosis.

185 tosis, and caspase-2-dependent inhibition of cell growth, demonstrating that the NPM1-dependent nucle

186 actor complex, which plays a pivotal role in cell growth, differentiation, and survival as well as th

187 ough Start increases with cell size, because cell growth dilutes the cell-cycle inhibitor Whi5 in G1.

188 ulation in EZH2 suppressed cells and rescued cell growth disadvantage.

189 However, a cell-growth disadvantage was observed, suggesting a poss

190 gnment, cell-specific mechanical properties, cell growth, division and apoptosis.

191 leton network has an important role in plant cell growth, division, and stress response.

192 asteful oxygen consumption and inappropriate cell growth during hypoxia.

193 odel predicts the size-independent amount of cell growth during the full cell cycle.

194 49 and 50 showed a remarkable anticlonogenic cell growth effect on MLL-AF9 human leukemia cells.

195 A long-term cell growth experiment revealed an extensive remodeling

196 The tyrosine kinase mast/stem cell growth factor receptor KIT is an example of a clini

197 strongly with autoantibodies to endothelial cell growth factor, matrix metalloproteinase 10, and apo

198 stages, fast growing clones exhibit greater cell growth heterogeneity.

199 tabolic homeostasis, inflammation and cancer cell growth highlighting its potential as a therapeutic

200 essential for intracellular protein sorting, cell growth, hormone secretion, and neurotransmission.

201 hanced the inhibitory potency of ATRA on HCC cell growth, improving IC50 by over 3-fold.

202 and low nanomolar potencies in inhibition of cell growth in acute leukemia cell lines.

203 esis and has been implicated in uncontrolled cell growth in cancer.

204 indeed suppresses beta-catenin signaling and cell growth in colon cancer via binding RXRalpha, which

205 Pex36 is required for cell growth in conditions that require peroxisomes for t

206 GLUT5 transport activity is associated with cell growth in fructose-based media or assayed by fructo

207 and highlight the importance of postmitotic cell growth in gut epithelial repair.

208 nuclear mobility, as well as lower rates of cell growth in HeLa cells, further supporting a role for

209 2 half-life, and enhanced JAK2 signaling and cell growth in human cell lines as well as primary murin

210 ompound 18 potently and selectively inhibits cell growth in human leukemia cell lines harboring MLL t

211 d we found increased Erk phosphorylation and cell growth in malignant B cells cocultured with CD40L-e

212 ished MART-10-induced inhibition of NGAL and cell growth in SNU308 cells.

213 kinase activity and excellent inhibition of cell growth in the drug-resistant cell line H1975, witho

214 d development of therapies against malignant cell growth in the future.

215 Consistently, 6ha inhibited tumor cell growth in the NCI 60 cell line panel and induced ap

216 Quantitative analysis of hypocotyl cell growth in the nek6-1 mutant demonstrated that NEK6

217 AS at the plasma membrane and induced tumour cell growth in vitro and in vivo.

218 served that GSK126 significantly reduced CCA cell growth in vitro and intrahepatic metastasis in vivo

219 tion and lactate secretion and inhibited HCC cell growth in vitro and tumor growth in mice.

220 pertussis-like toxin that inhibits mammalian cell growth in vitro We found that this protein, EcPlt,

221 Trametinib effectively inhibited tumor cell growth in vitro, but the combination of trametinib

222 and that miR-32 can improve prostate cancer cell growth in vitro.

223 ibitor of EphA2 effectively suppressed tumor cell growth in vivo, including TNBC patient-derived xeno

224 beta signaling is required to sustain cancer cell growth in which the tumor suppressor phosphatase an

225 extracellular lumican decreases PDAC tumour cell growth in xenograft and syngeneic orthotopic animal

226 rk phosphorylation and increased malignant B cell growth, indicating that CD40L in the tumor microenv

227 dyl transfer at a rate sufficient to support cell growth, indicating that it is accommodated by trans

228 in HL-60 and Jurkat leukemia cells, inhibit cell growth, induce apoptosis and differentiation, and d

229 ate dehydrogenase complex, caused a profound cell growth inhibition in tumour cells harbouring KRAS m

230 to downregulation of EGFR protein and tumor cell growth inhibition.

231 les which were screened for effects on tumor cell growth, inhibition of tubulin polymerization, and i

232 at displays anti-inflammatory properties and cell growth inhibitory activity against tumor cells.

233 sm underlying the effect of ILT3.Fc on tumor cell growth involves inhibition of the p70S6K signaling

234 lative timer phase before constriction where cell growth is correlated to its initial size, followed

235 Theory shows that cell growth is maximized when all expressed ribosomes ar

236 However, cell growth kinetics in the presence of anidulafungin re

237 pression of miR-6883-5p and miR-149* blocked cell growth leading to G0-G1 phase cell-cycle arrest and

238 inhibition may directly inhibit malignant T-cell growth, making duvelisib a promising candidate for

239 r model organism, we show that during active cell growth, matrix production enables biofilm-dwelling

240 l suited to spinal cord repair by supporting cell growth mechano-biology.

241 Studies of cell growth media conditioned after autophagy blockade r

242 hased miRNA-like RNAs function in process of cell growth metabolism and play roles in protein kinase.

243 The TUG1/miR-455-3p/AMPKbeta2 axis regulates cell growth, metastasis, and glycolysis through regulati

244 The up-regulation of these aggressive tumor cell growth, migration, and invasion phenotypes is media

245 Cell growth necessitates extensive membrane remodeling e

246 d a higher potency than gefitinib to inhibit cell growth of EGFR-overexpressing tumor cell lines in v

247 other GOF p53 mutants enhances the invasive cell growth of p53-deficient head and neck squamous cell

248 oliferation and its overexpression inhibited cell growth of prostate cancer.

249 ons show our model applies to scans based on cell growth or binding and handles common experimental e

250 tions such as drug and energy metabolism and cell growth or death, which are often involved in the de

251 anscription are observed without a change in cell growth or survival; analysis of such pairs identifi

252 hich plays an essential role in development, cell growth, organ size and homeostasis.

253 We conclude that HDAC6 inhibition reduces cell growth primarily by reducing intracellular cAMP and

254 ulator YAP controls organ size by regulating cell growth, proliferation and apoptosis.

255 rs are signaling molecules which orchestrate cell growth, proliferation and differentiation.

256 ynamics which are shown to impact epithelial cell growth, proliferation and intestinal cell function.

257 PK-related protein kinases (ARKs) coordinate cell growth, proliferation, and migration with environme

258 ons, including endothelial and smooth muscle cell growth, proliferation, and migration; angiogenesis;

259 STAT3 is known to play critical roles in cell growth, proliferation, differentiation, immunity an

260 ics and that the embryonal theory for cancer cell growth/proliferation is overly simplistic, as meiot

261 he molecular mechanisms accounting for the B-cell growth-promoting activity of vp17s.

262 al epitope(s), masked in refp17, to elicit B-cell growth-promoting signals after its interaction with

263 High salinity inhibited the cell growth rate but increased the viability and bacteri

264 ultures where we could precisely control the cell growth-rate.

265 ion kinetics, diffusion could support normal cell growth rates.

266 Nutrient starvation usually halts cell growth rather than causing death.

267 Cell growth regulation by CM and TRAIL was associated wi

268 reserving the coupling of cell division with cell growth, remain uninvestigated.

269 Significant cell growth retardation could be observed for pathogenic

270 sion by activating the ARK Cdr2 according to cell growth signals.

271 tumor marker and regulator of cytoskeleton, cell growth, stress response, or immune cell function; h

272 inflammation plays a critical role in cancer cell growth, studies remain uncharacterized on the role

273 ators of key biological processes, including cell growth, survival, and differentiation, and were est

274 S1P promotes cell growth, survival, and migration and is a key regula

275 racellular RNA processing that contribute to cell growth, survival, and regenerative capabilities of

276 lved in many biological processes, including cell growth, survival, inflammation, and development.

277 ource of signalling cues that affects cancer cell growth, survival, movement and metastasis.

278 Pooled screens based on cell growth/survival, as well as fluorescence-activated

279 complex 1 (mTORC1) is a central regulator of cell growth that responds to diverse environmental signa

280 Thus, KANK1 inhibits MPNST cell growth though CXXC5 mediated apoptosis.

281 EZH2 and DNA methylation, which promotes CCA cell growth through activation of the Notch pathway.

282 onstrate that stromal lumican restrains PDAC cell growth through mediating cell entry into a quiescen

283 sults suggest that NEK6 promotes directional cell growth through phosphorylation of beta-tubulin and

284 e diploid-polyploid conversion and polyploid cell growth through the Akt-Skp2 axis.

285 t FOXP1 by itself supports HSPC and leukemic cell growth, thus mimicking PUM activities.

286 250 h of acclimation, which was followed by cell growth to an even higher density than the control (

287 nd investigated changes in colorectal cancer cell growth, transcriptome, metabolome, and kinome in re

288 demethylate genes important for EBV-driven B-cell growth transformation.

289 r a critical mass of either Gea1 or Gea2 for cell growth under stress conditions.

290 IGF-I signaling, two critical regulators of cell growth via CSNK-2.

291 the expression of multiple genes involved in cell growth, viability and tissue-specific differentiati

292 cytometry revealed that inhibition of tumor cell growth was related to an induction of G2/M phase ce

293 cular mechanisms of estrogen-induced uterine cell growth, we removed the estrogen receptor alpha (Esr

294 ecreased amino acid metabolism and depressed cell growth were related to RS consumption.

295 nce mechanism contributes to xenograft tumor cell growth, which is prevented with mTOR plus IGFR inhi

296 g effect and the inhibition of breast cancer cell growth, which may serve as a useful approach to inh

297 uppressor-oncogene cascade to control cancer cell growth with FBXW2 acting as a tumour suppressor by

298 reaction in 2D cultures results in transient cell growth, with poor yield and short-term survival.

299 EMCN knockdown reduced migration, inhibited cell growth without compromising cell survival, and supp

300 e metabolic resources that are important for cell growth yet leak into the environment.