ライフサイエンスコーパス: cellular proliferation

1 in both positively and negatively regulating cellular proliferation.

2 reased patient survival, and is required for cellular proliferation.

3 d, they were all found capable of inhibiting cellular proliferation.

4 to reduced metabolic rate and inhibition of cellular proliferation.

5 s, as well as growth retardation and reduced cellular proliferation.

6 egulation are therefore necessary for proper cellular proliferation.

7 cytoplasmic PI3K-AKT pathway and suppresses cellular proliferation.

8 forces outstanding anabolic requirements for cellular proliferation.

9 he proper temporal and spatial regulation of cellular proliferation.

10 Telomerase is essential for continuous cellular proliferation.

11 e cells in lymph nodes, indicating extensive cellular proliferation.

12 tant cell lines and plays essential roles in cellular proliferation.

13 recruitment and contribute independently to cellular proliferation.

14 T) is a functional radiotracer used to study cellular proliferation.

15 transcription factors are key regulators of cellular proliferation.

16 ts regarding the role of Mfn2 in controlling cellular proliferation.

17 ndependently associated with tumor growth or cellular proliferation.

18 iary lymphoneogenesis with active centers of cellular proliferation.

19 tating RUNX1 regulation of transcription and cellular proliferation.

20 ads to an increase of nearly 100% in overall cellular proliferation.

21 TBI penumbra and hippocampus had higher cellular proliferation.

22 Skp2 regulates its protein levels to control cellular proliferation.

23 d BMP5 results in a significant reduction of cellular proliferation.

24 lar dosage levels required for inhibition of cellular proliferation.

25 elomerase enables chromosome survival during cellular proliferation.

26 xia, which elicited both exaggerated HVR and cellular proliferation.

27 gand and did not occur solely as a result of cellular proliferation.

28 in tumors is solely an artifact of increased cellular proliferation.

29 (-8) M) induced an Erk-dependent increase in cellular proliferation.

30 ube defect prevention through stimulation of cellular proliferation.

31 imal thickening, leukocyte infiltration, and cellular proliferation.

32 es p53 pathway, leading to the inhibition of cellular proliferation.

33 ns, intimately involved in the regulation of cellular proliferation.

34 d cell cycle progression, leading to reduced cellular proliferation.

35 one of its splice variants in up-regulating cellular proliferation.

36 and extracellular signal-related kinase and cellular proliferation.

37 ht junction assembly, fluid accumulation and cellular proliferation.

38 tive tyrosine kinase activity and influences cellular proliferation.

39 cycle regulators, with concomitant increased cellular proliferation.

40 s to microRNA biogenesis and is required for cellular proliferation.

41 oting cellular differentiation to aggressive cellular proliferation.

42 ay be a response to, rather than a cause of, cellular proliferation.

43 hondrial volume, and a severe suppression of cellular proliferation.

44 elin with inflammation and myo-inositol with cellular proliferation.

45 in pro-neural gene expression and increased cellular proliferation.

46 phenotypes, including insulin secretion and cellular proliferation.

47 hat RIF is primarily associated with reduced cellular proliferation.

48 ng sites of transcription factors that drive cellular proliferation.

49 l enhancers that control gene expression and cellular proliferation.

50 utative oncogene with roles in secretion and cellular proliferation.

51 nhibiting critical cell functions, including cellular proliferation.

52 endent effect on immunoblotting), stimulated cellular proliferation (about 1.8-fold increase in cell

53 ults in unopposed ERalpha mediated increased cellular proliferation, activation of the ERE and increa

54 Our model simulates the effect of cellular proliferation, actomyosin contractility, cell-c

55 l as the effects of PD-1 pathway blockade on cellular proliferation after T-cell receptor stimulation

56 genic allele of K-ras resulting in increased cellular proliferation and accelerated tumor growth.

57 ivation, trigger induction of p53 that halts cellular proliferation and allows cells to be repaired.

58 d from A-T [M] mutant mice exhibited reduced cellular proliferation and an altered DNA damage respons

59 of Cx43, but not Cx26, significantly reduced cellular proliferation and anchorage-independent growth

60 vPK also augments cellular proliferation and anchorage-independent growth.

61 e cells' proliferation rate, suggesting that cellular proliferation and apoptosis are concurrent.

62 ions in the expression of well characterized cellular proliferation and apoptosis guards (NF-kappaB,

63 Cellular proliferation and apoptosis were similar in MPh

64 on and degradation of multiple regulators of cellular proliferation and apoptosis, including the tumo

65 strating downregulation of genes involved in cellular proliferation and B cell activation.

66 is regulated by estrogen and contributes to cellular proliferation and cancer progression.

67 In vitro studies demonstrated defects in cellular proliferation and cell cycle entry, which were

68 fractions (NHFs) have a remarkable effect on cellular proliferation and collective migration, and exh

69 n in the cells led to profound reductions in cellular proliferation and colony-formation capacities.

70 The induction of cellular proliferation and cyclin D1 abundance, but not

71 enic HSCT and allowed visualisation of early cellular proliferation and detection of patterns of cell

72 gnalling secondary messengers that influence cellular proliferation and differentiation in a variety

73 Spatiotemporal balancing of cellular proliferation and differentiation is crucial fo

74 G5) functions in cell polarity and regulates cellular proliferation and differentiation via undefined

75 reasing host resistance, reducing control of cellular proliferation and differentiation, and diminish

76 tential of 2-hydroxyglutarate, the impact on cellular proliferation and differentiation, and the infl

77 tissue homeostasis, notably via controlling cellular proliferation and differentiation.

78 ly regulated biological system that controls cellular proliferation and differentiation.

79 In response to cellular proliferation and DNA damage, proteasome and HS

80 Inhibition of BCL-2 expression can decrease cellular proliferation and enhance the efficacy of chemo

81 d by viral etiology must exhibit deregulated cellular proliferation and evade immune recognition.

82 providing a rationale for their function in cellular proliferation and for the apoptotic effect of t

83 es to DNA damage in pancreatic beta-cells on cellular proliferation and glucose homeostasis.

84 which is secreted by the ovaries and induces cellular proliferation and growth of the uterus and mamm

85 vel mechanism how matrix stiffness regulates cellular proliferation and highlights the importance of

86 or abolished the IL-21-mediated increases in cellular proliferation and IgM secretion.

87 tion of H3 by other kinases, which regulates cellular proliferation and immediate early gene activati

88 hibitory site on the kinase Mst1, to inhibit cellular proliferation and induce apoptosis.

89 ized HMECs (TRIM24 iHMECs) greatly increased cellular proliferation and induced malignant transformat

90 a co-activator and a co-repressor to enhance cellular proliferation and inhibit myogenic differentiat

91 to monitor acute effects of chemotherapy on cellular proliferation and its recovery in bone marrow,

92 These integrants appear to be maintained by cellular proliferation and longevity of infected cells,

93 GLTSCR2 controls cellular proliferation and metabolism via the transcript

94 ylindrical structures called crypts in which cellular proliferation and migration are tightly regulat

95 Cells expressing the S114A/S446A mutant have cellular proliferation and migration defects.

96 vacaine reduced cell viability and inhibited cellular proliferation and migration in both cell lines.

97 methyltransferase activity of G9a inhibited cellular proliferation and migration in vitro and tumor

98 Cyclin D1-mediated cellular proliferation and migration is Dicer-dependent.

99 elligent model to investigate its effects on cellular proliferation and migration.

100 ous Ca(2+)-selective conductance involved in cellular proliferation and migration.

101 structural alterations as well as increased cellular proliferation and motility.

102 MTS-p53 decreased cellular proliferation and mtDNA abundance in HepG2 cell

103 n factor complex, has important functions in cellular proliferation and oncogenic transformation.

104 gnaling pathway is an important regulator of cellular proliferation and organ size.

105 ant to the pathogenesis of asthma, including cellular proliferation and pathways associated with gluc

106 oreover, overexpression of HDAC5 accelerated cellular proliferation and promoted acridine mutagen ICR

107 PHOS complex activity and increased in vitro cellular proliferation and promoted tumor development in

108 se to infection, while 223R showed increased cellular proliferation and recruitment.

109 SRC-3 deletion impaired cellular proliferation and reduced tumor size.

110 C1/2 have essential and pleiotropic roles in cellular proliferation and regulate stem cell self-renew

111 for Delta133p53 and p53beta in regulation of cellular proliferation and senescence in vivo.

112 ough all variants induced cytokine-dependent cellular proliferation and STAT3 phosphorylation via CNT

113 of the mTOR signalling pathways and inhibits cellular proliferation and stem-cell-derived organoid fo

114 The resulting altered metabolism supports cellular proliferation and survival but leaves cancer ce

115 The Hippo signaling pathway regulates cellular proliferation and survival, thus exerting profo

116 The Hippo signaling pathway regulates cellular proliferation and survival, thus exerting profo

117 genesis, in particular to aspects other than cellular proliferation and survival, we generated three

118 (PTEN) is a lipid phosphatase implicated in cellular proliferation and survival.

119 y immune regulation and DNA repair, but also cellular proliferation and survival.

120 ly active kinase that plays crucial roles in cellular proliferation and survival.

121 pathways in the naive T cell that result in cellular proliferation and the acquisition of particular

122 to maintain morphology through regulation of cellular proliferation and tissue integrity.

123 velopment in Drosophila requires coordinated cellular proliferation and tissue patterning.

124 s a critical factor in determining long-term cellular proliferation and tissue renewal.

125 emodeling that is characterised by increased cellular proliferation and tissue stiffness.

126 pathway, an essential event for uncontrolled cellular proliferation and transformation.

127 sociated protein 1 (KEAP1) signaling promote cellular proliferation and tumorigenesis are poorly unde

128 ine signaling, which can aberrantly modulate cellular proliferation and tumorigenesis.

129 ssion in primary human fibroblasts decreases cellular proliferation and ultimately triggers oncogene-

130 multi-faceted complex pathophysiology, with cellular proliferation and vascular remodeling being the

131 s a cardiopulmonary disease characterized by cellular proliferation and vascular remodeling.

132 ed for HIV infection yet are dispensable for cellular proliferation and viability.

133 They had reduced cellular proliferation and were less dependent on oxidat

134 e that activates epithelial beta-catenin and cellular proliferation, and (2) the simultaneous inhibit

135 ellular molecules (p < 0.01) and accelerated cellular proliferation, and (3) significantly increased

136 o changes in gene expression, a reduction in cellular proliferation, and an inability to differentiat

137 ement of cell death, mitochondrial function, cellular proliferation, and anchorage-independent growth

138 sal feature of cancer, promoting glycolysis, cellular proliferation, and angiogenesis.

139 t and chromosome segregation during mitosis, cellular proliferation, and apoptosis.

140 suppressor and regulates genomic integrity, cellular proliferation, and apoptosis; however, its role

141 inted gene that has roles in growth control, cellular proliferation, and insulin signaling.

142 e profiles with antiapoptosis, inhibition of cellular proliferation, and proinflammatory processes.

143 ant AKT(ser473) and p70S6 signalling, slowed cellular proliferation, and reversed mitochondrial abnor

144 e being uncovered in autophagy, hypoxia, and cellular proliferation, and the lipids are now implicate

145 oxidative endurance, tumorigenic potential, cellular proliferation, and tumor growth.

146 omelanocortin transcription, ACTH secretion, cellular proliferation, and tumor invasion rates in vitr

147 processes essential for anabolic metabolism, cellular proliferation, and tumorigenesis.

148 in human cancer and has significant roles in cellular proliferation, apoptosis, differentiation and d

149 While low-dose paclitaxel did not affect cellular proliferation, apoptosis, or cytoskeletal integ

150 rent tubular injuries but was independent of cellular proliferation as determined in physiological gr

151 Furthermore, infection did not induce cellular proliferation, as it does in B cells, but inste

152 These findings suggest that cellular proliferation, as occurs in cancer cells but al

153 es such as the balance between apoptosis and cellular proliferation, as well as the influence of othe

154 icient PAR1 was more effective at increasing cellular proliferation, associated with Gq signaling, th

155 dasatinib led to apoptosis and inhibition of cellular proliferation, associated with reduced phosphor

156 d that lack of CDK2 protein does not prevent cellular proliferation, both during somatic development

157 zation of p53, leading not only to continued cellular proliferation but also to further accumulation

158 les in cell cycle progression and control of cellular proliferation, but the precise functional roles

159 ially regulate histone H3K14 acetylation and cellular proliferation by altering HBO1 levels.

160 dometrial cancer show that metformin reduces cellular proliferation by inhibition of the PI3K-AKT-mTO

161 the high-risk HPV16 E7 oncogene can promote cellular proliferation by interacting with the DREAM (DP

162 ose that CHERP acts in the nucleus to impact cellular proliferation by regulating the function of the

163 We demonstrate that G9a enhances cellular proliferation by two distinct mechanisms.

164 otein kinase known to play multiple roles in cellular proliferation, cell cycle regulation, and carci

165 melanoma cells resulted in (i) a decrease in cellular proliferation, colony formation, and cellular m

166 o show that overexpression of EphB4 promotes cellular proliferation, colony formation, and motility,

167 man melanocytes, which resulted in increased cellular proliferation, colony formation, invasion, and

168 number of known ER target genes involved in cellular proliferation (cyclin D1, CDKs) and morphogenes

169 use large B-cell lymphomas (DLBCLs) inhibits cellular proliferation, decreases cholesterol biosynthes

170 Cellular proliferation depends on the integration of mit

171 an aggressive phenotype including increased cellular proliferation, deregulated G2-M checkpoint foll

172 sses in most eukaryotic organisms, including cellular proliferation, development, and protein turnove

173 lation of BMP-2 production mediates rates of cellular proliferation, differentiation and tissue produ

174 oad array of biological processes, including cellular proliferation, differentiation, and apoptosis.

175 development of guiding tissue scaffolds for cellular proliferation, differentiation, and apoptosis.

176 mutations in signaling pathways that control cellular proliferation, differentiation, and survival.

177 eraction network analysis suggested enriched cellular proliferation/differentiation pathways in truck

178 insight into the role of APA in controlling cellular proliferation during biological processes such

179 Dnmt3a delayed tumorigenesis by suppressing cellular proliferation during disease progression.

180 or, a downstream target of K-Ras, stimulates cellular proliferation during embryogenesis, organ repai

181 Our results suggest that p44/wdr77 controls cellular proliferation during lung development, and this

182 s involved in the induction of pluripotency, cellular proliferation, early ocular genes and genes imp

183 ived growth factor (PDGF)-DD, which promotes cellular proliferation, epithelial-mesenchymal transitio

184 CV LT shows a decreased potential to support cellular proliferation, focus formation, and anchorage-i

185 ex and targets several proteins required for cellular proliferation for ubiquitin-mediated destructio

186 gulate diverse biological processes, such as cellular proliferation, gene transcription, and tumorige

187 rmal growth factor receptor (EGFR)-dependent cellular proliferation, has been achieved.

188 Non-invasive imaging biomarkers of cellular proliferation hold great promise for quantifyin

189 f NEAT1 in hypoxia also leads to accelerated cellular proliferation, improved clonogenic survival and

190 have investigated the dynamics of growth and cellular proliferation in a murine vestibular organ, the

191 UTS leads to increased apoptosis and reduced cellular proliferation in a PTEN-dependent manner.

192 ning BH3 mimetics and gamitrinib-TPP blunted cellular proliferation in a synergistic manner by massiv

193 creased SFRP1 mRNA expression, and decreased cellular proliferation in a trophoblast cell line.

194 iated genetic mutation resulted in increased cellular proliferation in all cell lines tested, the gen

195 orothymidine ((18)F-FLT) was used to measure cellular proliferation in bone marrow (BM), whereas MRI

196 Rapid cellular proliferation in early development and cancer d

197 proto-oncogene whose overexpression promotes cellular proliferation in hematopoietic cells.

198 039 did not affect cell cycle progression or cellular proliferation in host cells.

199 ox1)-dependent ROS generation and consequent cellular proliferation in intestinal stem cells upon ini

200 CD25 expression, STAT5 phosphorylation, and cellular proliferation in Jurkat cells following activat

201 se cell cycle arrest and suppressed in vitro cellular proliferation in NSCLC cancer cells.

202 ated knockdown of RBMS3 expression increased cellular proliferation in PBMCs, consistent with the rol

203 evealed abundant lung neovascularization and cellular proliferation in PE that was distinctly absent

204 miR-130/301 family is a master regulator of cellular proliferation in PH via regulation of subordina

205 the first evidence that InsP(6) can inhibit cellular proliferation in plants under growth conditions

206 ority of repopulation occurred by stochastic cellular proliferation in situ in a macrophage colony-st

207 ncogene expression only marginally increased cellular proliferation in the epidermis of Tg animals, c

208 Flox/Flox mice was a consequence of reduced cellular proliferation in the midface, aberrant vasculog

209 Herein, cyclin D1 inactivation reduced cellular proliferation in the murine prostate in vivo an

210 Metformin inhibited cellular proliferation in the presence of glucose, but i

211 d the hypothesis that metformin would reduce cellular proliferation in vivo in atypical endometrial h

212 e upregulated genes, known to be involved in cellular proliferation, included c-Myc along with its ta

213 ically bind to key transcription factors for cellular proliferation, including NF-Y, p53, and sp1, in

214 deficient embryonic stem cells have impaired cellular proliferation, increased apoptosis, defective c

215 Additionally, there was an increase in cellular proliferation, increased proteoglycan distribut

216 c signaling is an effective strategy to halt cellular proliferation, induce apoptosis and eliminate c

217 Depletion of HDAC5 by shRNA hindered cellular proliferation, induced G1 cell cycle arrest, an

218 Mostly because of its effects on metabolism, cellular proliferation, inflammation, and immunity, the

219 EYA1 enhanced cellular proliferation, inhibited apoptosis, and induced

220 nsduction for multiple receptors, regulating cellular proliferation, invasion, and metastasis in huma

221 ls showed that SPZ1 was able to regulate the cellular proliferation, invasion, and tumorigenic activi

222 Cellular proliferation is antagonistically regulated by

223 Defining the genes that are essential for cellular proliferation is critical for understanding org

224 enzymatic activity, and consequently promote cellular proliferation, is compromised by mutations with

225 he STAT5A and STAT5B isoforms did not affect cellular proliferation, loss of STAT5 significantly decr

226 Using the cellular proliferation marker 3'-deoxy-3'-(18)F-fluoroth

227 unostaining with antibodies against Ki-67, a cellular proliferation marker.

228 The cellular proliferation markers Cyclin D1, Bcl-Xl, and c-

229 dependent second messengers, with effects on cellular proliferation, migration, and invasiveness.

230 -signal-regulated kinases, and regulation of cellular proliferation (miR20b, miR10b, and miR141 throu

231 lipid sphingosine-1-phosphate (S1P) mediates cellular proliferation, mitogenesis, inflammation, and a

232 lpha stimulation demonstrated an increase in cellular proliferation, monocyte cells, osteoclast diffe

233 to maintain the increased rRNA synthesis and cellular proliferation observed in the absence of Arf.

234 cation factor 1 may explain the reduction in cellular proliferation observed on MINCR knockdown.

235 In addition, the knockout of HuR decreased cellular proliferation of CD4(+) T cells.

236 Furthermore, castration did not suppress cellular proliferation of either basal-derived or lumina

237 ulenin, a small molecule antibiotic, blocked cellular proliferation of KRAS-associated lung cancer ce

238 1 inhibitor was shown to effectively inhibit cellular proliferation of NSCLC cells in a dose-dependen

239 erived exosomes exerted a positive effect on cellular proliferation of recipient RMS cells and fibrob

240 n demonstrated a synergistic decrease in the cellular proliferation of several ATC cells.

241 gnificantly increases both IgM secretion and cellular proliferation of these cells with no effect on

242 central memory T cell pool occurs in lieu of cellular proliferation or activation, but with the expec

243 Abnormalities in cellular proliferation or differentiation in any of thes

244 n species (ROS), immunoinflammatory effects, cellular proliferation, or apoptosis with concomitant up

245 matin, which is necessary for DNA repair and cellular proliferation, our results suggest that MAGE-C2

246 n burn patients expressed Ki67, a marker for cellular proliferation (P < 0.05).

247 locked aspartate production and reprogrammed cellular proliferation pathways, while application of as

248 ease in mucin was comparable to increases in cellular proliferation (Pearson R = 0.978).

249 emin (NS) has been associated with increased cellular proliferation potential and tumor malignancy du

250 suggests that I-PTH plays a critical role in cellular proliferation, proteoglycan distribution, and m

251 ssion and mutations in TRAIP therefore limit cellular proliferation, providing a potential mechanism

252 el of ROS production was proportional to the cellular proliferation rate.

253 Inhibiting cellular proliferation reduced Ki67 expression and HIV-1

254 sis and regeneration require coordination of cellular proliferation, regulated in part by secreted gr

255 denylation (APA) that occurs during enhanced cellular proliferation represents an important, yet poor

256 Cellular proliferation requires increased production of

257 Analysis of cellular proliferation revealed many Ki67(+) cells durin

258 ulated ERK/MAPK pathway is a key conduit for cellular proliferation signals and a therapeutic target

259 ulators, mTORC1 and tp53 and correlated with cellular proliferation status.

260 itude of genes involved in the regulation of cellular proliferation, stemness, and epithelial-mesench

261 ne expression is critical for the control of cellular proliferation, survival, and development.

262 activation of signaling pathways involved in cellular proliferation, survival, and differentiation.

263 spects of AML disease development, including cellular proliferation, survival, and differentiation.

264 se and human prostate cancer cells decreased cellular proliferation, survival, Erk signaling and tumo

265 mage, epigenetic deregulation, and increased cellular proliferation that eventually culminate in the

266 Recent evidence shows that it is not only cellular proliferation that is heavily compromised in DS

267 etastasis, and MYC is a central regulator of cellular proliferation that is upregulated in many cance

268 cluding proinflammatory cytokine release and cellular proliferation that were induced after potent T

269 n by restoring hepatic homeostasis, limiting cellular proliferation through reduced cyclinD1 expressi

270 ene expression allows the virus to stimulate cellular proliferation to support viral genome replicati

271 1 (HIV-1) reservoir and the contribution of cellular proliferation to the maintenance of the reservo

272 sory epithelium during development, confines cellular proliferation to the organ's periphery, and eve

273 pecific consequences ranging from effects on cellular proliferation, to surfactant production and/or

274 ivo tumor-initiating capacity, while leaving cellular proliferation unaltered.

275 study how chronic inflammation and abnormal cellular proliferation underlie tumorigenesis and tumor

276 thin stratified epithelia included increased cellular proliferation, unscheduled DNA synthesis, incre

277 for RNA splicing, cell migration, controlled cellular proliferation, vasculogenesis, extracellular ma

278 Finally, we found that Tcfap2c promotes cellular proliferation via direct repression of p21 tran

279 of these drugs are mediated by inhibition of cellular proliferation via the retinoblastoma (Rb) pathw

280 Cellular proliferation was assessed by Ki-67 proliferati

281 Decreased cellular proliferation was associated with G0/G1 cell cy

282 the Ras signaling pathway was prolonged and cellular proliferation was enhanced after ligand binding

283 Cellular proliferation was evaluated with 5-bromo-2'-deo

284 The rate of cellular proliferation was higher in mutant cells under

285 Importantly, IL-2-dependent cellular proliferation was inhibited upon blocking both

286 Cellular proliferation was significantly greater in the

287 Cellular proliferation was significantly increased in ba

288 ta, matrix metalloproteinase expression, and cellular proliferation were markedly increased.

289 ermore, reduced tumor necrosis and increased cellular proliferation were seen after radiation treatme

290 mune response, inflammation, cell cycle, and cellular proliferation were stimulated.

291 demonstrated to be effective in stimulating cellular proliferation when the sera from mice are injec

292 3) phosphorylation in Mvt-1 cells as well as cellular proliferation, whereas cholesterol depletion in

293 ted genes are mainly components that control cellular proliferation, whereas the down-regulated genes

294 has a secondary function, as a regulator of cellular proliferation, which is independent of its cata

295 ls accelerated lymphomagenesis by increasing cellular proliferation, which suggests that Dnmt3b funct

296 only the nuclear fraction of p53 controlled cellular proliferation, which was supported by the MTS-p

297 not required for viability or even efficient cellular proliferation, while in humans, RNase H2 hypomo

298 t histological analysis revealed evidence of cellular proliferation with an absence of histological e

299 ce is needed, it appears that the imaging of cellular proliferation with PET and 3'-deoxy-3'-(18)F-fl

300 hysiologic upregulation of c-Myc can lead to cellular proliferation without DNA replication stress.