ライフサイエンスコーパス: growth suppression

1 ty, increased T cell infiltration, and tumor growth suppression.

2 ility and HuR is a mediator of RNPC1-induced growth suppression.

3 cannot bind phosphoinositide is defective in growth suppression.

4 ceptors, and is uncoupled from FLS2-mediated growth suppression.

5 tion of both prostate cell proliferation and growth suppression.

6 uence the transition between cell growth and growth suppression.

7 cells to chemotherapy-induced apoptosis and growth suppression.

8 3 inhibition resulted in tumor apoptosis and growth suppression.

9 irus infection and reversal of IFN-dependent growth suppression.

10 s cyclin D1-mediated repression of STAT3 and growth suppression.

11 triking increase in tumor cell apoptosis and growth suppression.

12 ive genes for transcriptional regulation and growth suppression.

13 which antagonizes full-length KLF6-mediated growth suppression.

14 tion, ablation of Rb impairs ARF function in growth suppression.

15 ession also interferes with RASSF1A-mediated growth suppression.

16 p53-dependent, RB-independent mechanism for growth suppression.

17 r in their sensitivity to TGF-beta1-mediated growth suppression.

18 olishes salinity tolerance without affecting growth suppression.

19 elevated levels of c-Myc are involved in HBC growth suppression.

20 B cell line responsive to TGF-beta1-mediated growth suppression.

21 ound that each kinase was active and induced growth suppression.

22 cell is unlikely to be the mechanism for the growth suppression.

23 down-regulation resulted in marked long-term growth suppression.

24 mediated effects on antigen presentation and growth suppression.

25 ARF-NPM association does not correlate with growth suppression.

26 esidues necessary for mediating Protein 4.1B growth suppression.

27 only partially rescues nuclear PTEN-mediated growth suppression.

28 C-terminal domain (RbC) is also required for growth suppression.

29 essor protein p53 in signaling apoptosis and growth suppression.

30 ms retain a potential in transactivation and growth suppression.

31 se substrate (HRS), both critical for merlin growth suppression.

32 nt role in chromatin remodeling and cellular growth suppression.

33 gnificance of 14-3-3 binding to Protein 4.1B growth suppression.

34 ng SFRP expression resulted in apoptosis and growth suppression.

35 at PIKE-L is an important mediator of merlin growth suppression.

36 s their response to 1,25(OH)(2)VD(3)-induced growth suppression.

37 the possible association of stimulants with growth suppression.

38 nhibit cyclin D1/cdk4 activity, resulting in growth suppression.

39 nse of OCa cells to 1,25(OH)(2)VD(3)-induced growth suppression.

40 gulating merlin subcellular localization and growth suppression.

41 he amino terminus of BRCA1 autoinhibited the growth suppression.

42 not required for transformation but mediates growth suppression.

43 ous level expressed in ARMS cells, result in growth suppression.

44 unique determinants for transactivation and growth suppression.

45 icient for alleviation of p107-mediated cell growth suppression.

46 olite, produced a synergistic effect on cell growth suppression.

47 ancer cells with exogenous SPARC resulted in growth suppression.

48 at it was, in part, responsible for the cell growth suppression.

49 of active STAT3, induction of apoptosis, and growth suppression.

50 in deficient C6 glioma cell lines results in growth suppression.

51 r DRA relevant to colon tumorigenesis, i.e., growth suppression.

52 ICS is beneficial despite possible risks of growth suppression.

53 hibiting a large cell phenotype that rescues growth suppression.

54 target rapamycin (mTOR) activity to enhance growth suppression.

55 human cancer cells and found that it caused growth suppression.

56 effects on both SEMA5B repression and tumor growth suppression.

57 Axl are required for TGF-beta2-mediated cell growth suppression.

58 bility, escalates with the degree of overall growth suppression.

59 sL expression and led to CD8-dependent tumor growth suppression.

60 by itself is sufficient, for Cx37 to mediate growth suppression.

61 roliferation and how cancer cells evade this growth suppression.

62 augments its induction of p21 and resultant growth suppression.

63 own of MIC-1 can decrease RNPC1-induced cell growth suppression.

64 olecules induced p53-dependent apoptosis and growth suppression.

65 c-Myc expression, facilitates RNPC1-mediated growth suppression.

66 oming free from growth factor dependence and growth suppression, altering their metabolism to cope wi

67 wth factor promoter but also Necdin-mediated growth suppression and antiangiogenic effects on cancer

68 doses markedly increased CFZ-mediated tumor growth suppression and apoptosis in a murine xenograft O

69 markedly enhances p53 expression, leading to growth suppression and apoptosis in a p53-dependent mann

70 iral-mediated delivery of mda-7/IL-24 causes growth suppression and apoptosis in a wide spectrum of c

71 Between 0.5 and 1.5muM CYT387 caused growth suppression and apoptosis in JAK2-dependent hemat

72 Lumefantrine promoted growth suppression and apoptosis in vitro in parental an

73 Growth suppression and apoptosis induction in tumor xeno

74 inhibitors of presenilin specifically induce growth suppression and apoptosis of a murine T-ALL cell

75 competent adenovirus (Ad), Ad.mda-7, induces growth suppression and apoptosis selectively in diverse

76 ells harboring deletions or mutations led to growth suppression and apoptosis that was alleviated by

77 ts dramatically impaired doxorubicin-induced growth suppression and apoptosis.

78 SEC61gamma expression in tumor cells led to growth suppression and apoptosis.

79 ormal p53 function in tumor cells and induce growth suppression and apoptosis.

80 7A conferred resistance to cisplatin-induced growth suppression and apoptotic cell death in EC cells.

81 Growth suppression and ATM activation required the ATPas

82 All treatments induced growth suppression and cell cycle arrest at the G(0)-G(1

83 Our data therefore suggest that both growth suppression and cell invasion may be differential

84 These data indicate a role for U19/Eaf2 in growth suppression and cell size control as well as argu

85 JNK activation abrogates protein 4.1B/DAL-1 growth suppression and cyclin A regulation.

86 Consistent with growth suppression and cytoprotection requiring differen

87 ed their expression as well as p21-dependent growth suppression and cytoprotection.

88 volved in many cellular processes, including growth suppression and differentiation.

89 of AR-responsive genes important to prostate growth suppression and differentiation.

90 the tumor suppressor protein's activities in growth suppression and E2F transcription factor inhibiti

91 ent of RbC for high-affinity E2F binding and growth suppression and establish a mechanism for the reg

92 l cellular response to high levels of PRL is growth suppression and furthermore, that PRL can counter

93 P5) can act as a suppresser of p53-dependent growth suppression and has been reported to associate wi

94 deaminase treatment provided stronger tumor growth suppression and increased mean survival time of t

95 Finally, cells deficient in IRF8 exhibited growth suppression and increased sensitivity to apoptosi

96 ated BCL2 inhibitor, ABT-263, restored tumor growth suppression and induced apoptosis.

97 stably overexpressing Id3 were resistant to growth suppression and induction of cell death induced b

98 ing of Myc to Miz1 is required to antagonize growth suppression and induction of senescence by TGFbet

99 modulates the efficacy of HDAC inhibitors in growth suppression and keratinocyte differentiation.

100 growth and migration can be shifted between growth suppression and migration promotion.

101 e targeted therapeutically to maximize tumor growth suppression and minimize collateral neurologic in

102 Depletion of Aly results in cell growth suppression and mRNA export reduction.

103 ngs shed light on how cancer cells can evade growth suppression and open a new avenue for future deve

104 events correlated with greater ARF-mediated growth suppression and p53 activation.

105 tor of androgen receptor (AR), with distinct growth suppression and promotion function in gender spec

106 adioresistant lung cancer H1299 cells caused growth suppression and radiosensitization, whereas overe

107 esults provide support for a role for tb1 in growth suppression and reveal the specific tissues where

108 cover a novel mode of IFN-induced anti-tumor growth suppression and suggest potential gene therapy ap

109 tal elements is essential for NORE1A-induced growth suppression and that the ERK pathway is a target

110 ild-type Rb were sensitive to BRCA1a-induced growth suppression and the status of p53 did not affect

111 Because androgen caused growth suppression and then reversion of androgen-indepe

112 which PAX3 functional domains are needed for growth suppression and transformation, inactivating muta

113 e conversion triggered by TMZ preceded tumor growth suppression and were not associated with changes

114 oxygen species (ROS), triggering DNA damage, growth suppression, and a senescent phenotype characteri

115 by enhanced levels of proteasome inhibition, growth suppression, and apoptosis induction, compared wi

116 resulting in mda-7/IL-24 protein production, growth suppression, and apoptosis.

117 rmation, migration/invasion, ERK activation, growth suppression, and changes in gene expression.

118 to transforming growth factor-beta-mediated growth suppression, and increased tumorigenesis are not

119 umor cell damage (double strand DNA breaks), growth suppression, and overall survival under clinical

120 oteins, resulting in enhanced G(2)-M arrest, growth suppression, and radiosensitization.

121 inhibition of PI3K and MEK signaling, marked growth suppression, and robust apoptosis of human KRAS m

122 underlying HIC1-mediated transcriptional and growth suppression, and the relevant targets of HIC1-med

123 24 include its ability to selectively induce growth suppression, apoptosis and radiosensitization in

124 well-tolerated and caused significant tumor growth suppression ( approximately 85.2% vs control, p =

125 owth factor-beta (TGF-beta) pathway-mediated growth suppression as a cause of BMF in FA.

126 mpacts on IRF-1-mediated gene repression and growth suppression as well as the rate of IRF-1 degradat

127 tributions that generate thallus shape given growth suppression at the apex.

128 with controls, consistent with inhibition of growth suppression attributed to SM alpha-actin.

129 We show that decorin causes marked growth suppression both in vitro and in vivo using a met

130 mportant for understanding the scar-mediated growth suppression, but also for developing novel and se

131 a novel mechanism to circumvent RB-mediated growth suppression by altered nucleocytoplasmic traffick

132 ogen-independent LNCaP 104-R1 cells adapt to growth suppression by androgen and then their growth is

133 KN1A (encoding p21) acted in part to mediate growth suppression by ARID1A.

134 Biochemical and functional studies linked growth suppression by BAF180 to its ability to form a ca

135 y protected cells from cell cycle arrest and growth suppression by BET inhibitors.

136 everses Cripto blockade of Activin B-induced growth suppression by blocking Cripto's association with

137 Hypocotyl growth suppression by blue light was assessed by standar

138 mutant for their survival and resistance to growth suppression by chemotherapeutic agents.

139 r a T100I point mutation (CSN5(3)), relieved growth suppression by DTrc8, whereas CSN5(1) (E160V) and

140 se viruses mutate to disrupt recognition and growth suppression by host miRNAs.

141 in vitro, suggesting that GPR56 may mediate growth suppression by interaction with a component in th

142 The growth suppression by miRNAs in PDFS cells is consistent

143 that p12 plays a role in TGF-beta1-mediated growth suppression by modulating CDK2 activities and pRB

144 n which the inhibition of TGF-beta1-mediated growth suppression by mutant p53 can be reversed by the

145 wever, the mechanism for cyclin D1-dependent growth suppression by nuclear PTEN has remained largely

146 Human breast cancer (HBC) cell growth suppression by okadaic acid (OA) was previously f

147 Tumor growth suppression by PD0325901 relative to vehicle was

148 m down-regulation of Survivin expression and growth suppression by pharmacological inhibitors of PI3K

149 Importantly, growth suppression by SAG knockdown was partially rescue

150 issive for regulation of gene expression and growth suppression by TGF-beta in LNCaP prostate adenoca

151 Resistance to growth suppression by TGF-beta1 is common in cancer; how

152 interaction is underscored by the fact that growth suppression by the dominant negative BAP1 mutant

153 down of mutant p53 sensitizes tumor cells to growth suppression by various chemotherapeutic drugs.

154 ption through TFIIIB may contribute to their growth-suppression capacities.

155 in the Caribbean (1495-1825 CE) with a tree-growth suppression chronology from the Florida Keys (170

156 dical problems, such as sleep disruption and growth suppression, continue to be better understood in

157 Growth suppression depends on the CHES1 forkhead DNA-bin

158 This PTPRF-mediated growth suppression during cell proliferation functioned

159 es that full transformation involves loss of growth suppression encoded by wild-type p53 together wit

160 of IL-1alpha abrogated vitamin D(3)-induced growth suppression, establishing a requirement for IL-1a

161 ated in the tumors, thereby inactivating its growth suppression function.

162 E2F transactivation activity and inhibits Rb growth suppression function.

163 f evidence indicates that ARF also possesses growth suppression functions independent of p53, the mec

164 nterest in therapeutic approaches to restore growth suppression functions to mutant p53.

165 target gene transactivations, apoptosis, and growth suppression functions.

166 gating the DNA binding, and subsequently the growth suppression, functions of wild-type p53.

167 umor tissues, resulting in significant tumor growth suppression (>77%).

168 EdU staining of RASSF8-depleted cells showed growth suppression in a manner dependent on contact inhi

169 s, breast cancer cells to DNA damage-induced growth suppression in a p53-dependent manner.

170 lly, we showed that Pirh2 knockdown leads to growth suppression in a TAp73-dependent manner.

171 regulation of gene expression and hypocotyl growth suppression in Arabidopsis.

172 ns-retinoic acid (RA) target genes linked to growth suppression in BEAS-2B human bronchial epithelial

173 ased expression of SPARC, which led to tumor growth suppression in bone in vivo These findings sugges

174 mage, and increased ECRG2 expression induced growth suppression in cancer cells but not in non-cancer

175 AP43 in deficient C6 glioma cells results in growth suppression in clonogenic assays, as well as in m

176 ur findings uncover a p53-ZMAT3-CD44 axis in growth suppression in CRC cells.

177 the key mediator of 1,25(OH)(2)D(3)-induced growth suppression in G(1) and show that the hormone ach

178 overexpression of hPNPaseold-35 resulted in growth suppression in HO-1 human melanoma cells.

179 IK3CA can lead to activation of p53-mediated growth suppression in human cells, indicating that p53 c

180 target sequence, causing strand cleavage and growth suppression in human colon cancer cells with G12D

181 inhibition of cap-dependent translation and growth suppression in intestinal epithelial cells.

182 Exogenous NmU "rescued" growth suppression in K562-MERT cells and stimulated the

183 Forced expression of ERbeta1 promoted growth suppression in MCF-7 cells, but the anti-prolifer

184 Smac-mimic significantly sensitized cells to growth suppression in MDA-MB-231 cells, but to a lesser

185 7041 demonstrates robust p53-dependent tumor growth suppression in MDM2/MDMX-overexpressing xenograft

186 our laboratory have shown that protein 4.1B growth suppression in meningioma is associated with the

187 paB activity leads to tumor rejection and/or growth suppression in mice.

188 ility of ARF to induce p53-independent tumor growth suppression in mouse xenograft models is signific

189 dependent, as T-cadherin could still mediate growth suppression in p53(-/-) mouse embryonic fibroblas

190 us targeting Pirh2 to restore TAp73-mediated growth suppression in p53-deficient tumors may be develo

191 orresponding signaling pathways that trigger growth suppression in tetraploid cells are not known.

192 ting USP2 is an effective approach to induce growth suppression in the cancer cells addicted to cycli

193 these and other endogenous target genes and growth suppression in the presence of mutant p53.

194 nsforming growth factor (TGF)-beta1-mediated growth suppression in tumor cells is often associated wi

195 Inhibition of signaling results in growth suppression in various cell types.

196 Ser110, effectively abolished KLF9's neurite growth suppression in vitro and promoted axon regenerati

197 F9-JNK3 interaction that contributes to axon growth suppression in vitro and regenerative failure in

198 more susceptible to NVP-BEZ235-mediated cell growth suppression in vitro and tumor shrinkage in vivo.

199 Relief from growth suppression in vitro but not in vivo by enzymatic

200 Combining erlotinib with bexarotene enhanced growth suppression in vitro compared with each single-ag

201 OR or AKT inhibitors resulted in synergistic growth suppression in vitro.

202 tosis and abrogates p53(3KR)-mediated tumour growth suppression in xenograft models.

203 tion of senescence, p53 contributes to tumor growth suppression, in a manner strictly dependent by it

204 as ectopic expression of DeltaNp63 inhibits, growth suppression induced by arsenic.

205 cle arrest in G(2)/M and sensitizes cells to growth suppression induced by DNA damage or MDM2 inhibit

206 Interestingly, we found that growth suppression induced by HDAC inhibitors is attenua

207 ies indicate that TSP-1 contributes to tumor growth suppression induced by LDC and suggest that tumor

208 L tumor suppressor controls key pathways for growth suppression, induction of apoptosis, and cellular

209 AS gene, but not either gene alone, promotes growth suppression, induction of apoptosis, and suppress

210 However, much greater growth suppression is achieved by combinatorial inhibiti

211 The growth suppression is associated with an increase in apo

212 Moreover, response to TGF-beta1-mediated growth suppression is compromised in MOK(p12-/-) cells.

213 r genetic results confirm that DTrc8-induced growth suppression is CSN5 (and CSN6) dependent.

214 Nuclear compartment-specific PTEN-induced growth suppression is dependent on possessing a function

215 While TGF-beta growth suppression is independent of activin, TGF-beta t

216 Surprisingly, BAP1-mediated growth suppression is independent of wild-type BRCA1.

217 Petiole growth suppression is likely attributed to a cell cycle

218 evity-related transcription factors-mediated growth suppression is necessary to promote cancer develo

219 This growth suppression is not correlated with impaired induc

220 tical step connecting apyrase suppression to growth suppression is the inhibition of polar auxin tran

221 One candidate for mediating retinoid-induced growth suppression is the novel class II tumor suppresso

222 A key mechanism of KLF6-mediated growth suppression is through p53-independent transactiv

223 from many natural populations indicate that growth suppression is widespread but not universal and,

224 -negative p53, resulted in the rescue of the growth suppression mediated by Cyr61 in the H520-Cyr61 c

225 Moreover, we also found that the melanoma growth suppression mediated by mitogen-activated protein

226 n of translation initiation factor eIF4E and growth suppression mediated upon PRMT5 knockdown is inde

227 ated cells was observed, indicating that the growth suppression observed upon NOTCH1 activation is in

228 thoxygeldanamycin yielded virtually complete growth suppression of aggressive breast tumors.

229 ancers, MLN4924 was found to be effective in growth suppression of cancer cells.

230 ) signaling in cancer has been implicated in growth suppression of early lesions and enhancing tumor

231 n of CRAD and ad-IGF-1R/482 induced stronger growth suppression of established lung cancer xenografts

232 Conversely, growth suppression of fast-growing cells by cellular for

233 ng of TRAF2 using siRNA caused a significant growth suppression of glioblastoma U251 cells and modera

234 and p21, as well as partially reversing the growth suppression of H520-Cyr61 cells.

235 effective as ~30 daily oral doses of TLZ in growth suppression of homologous recombination-defective

236 ion by PLZF was inhibited, and PLZF-mediated growth suppression of leukemia cells was partially block

237 Inhibition of NR4A2 was associated with growth suppression of LKB1 null tumors, but showed littl

238 mma agonist rosiglitazone provides effective growth suppression of mammary epithelial cells, potentia

239 ABT-263 treatment led to rapid and sustained growth suppression of MCC xenografts from a representati

240 ising agents for both specific detection and growth suppression of metastatic ovarian cancer.

241 Sindbis vector infection and growth suppression of murine MOSEC tumor cells indicate

242 Growth suppression of mutant IDH1 cells by BPTES was res

243 Growth suppression of nude mouse xenograft tumors carryi

244 ther, these ultimately result in significant growth suppression of pancreatic cancer cells in vitro.

245 Overexpression of MnSOD may be effective in growth suppression of pancreatic cancer.

246 Thus, growth suppression of PPARgamma-expressing tumor cells b

247 calize to defined nuclear foci and result in growth suppression of the host cells.

248 s, and TP53 knockout rescues XL177A-mediated growth suppression of TP53 wild-type (WT) cells.

249 ed and nontransformed cells was required for growth suppression of transformed cells in this system;

250 ry activity, SC66 manifests a more effective growth suppression of transformed cells that contain a h

251 Re-expression of Smyd4 resulted in growth suppression of tumor cells and inhibition of tumo

252 G5-FI-FA-MTX or G5-FA-MTX for targeting and growth suppression of tumor cells that overexpress FA-re

253 ral injection of the adenovirus also induces growth suppression of tumor xenografts in mice in a p53-

254 ion of OTUB1 destabilized SLC7A11 and led to growth suppression of tumor xenografts in mice, which wa

255 as a skin probiotic for in vitro and in vivo growth suppression of USA300, the most prevalent communi

256 that let-7 miRNAs inhibit proliferation and growth, suppression of let-7 miRNAs via Lin28a overexpre

257 atment of mice resulted in significant tumor growth suppression only in tumors with functional Rb, an

258 n days 0 and 3 resulted in significant tumor growth suppression (P < 0.0001).

259 anti-PDL1 and RT and observed similar tumor growth suppression, particularly at early time-points.

260 A novel PTPRF-mediated growth suppression pathway was identified by way of a fu

261 mponents, finding that laminin mitigates the growth suppression properties of the matrix metalloprote

262 dence that BRCA1 is involved in p53-mediated growth suppression rather than apoptosis.

263 tion to the DNA-binding domain, p73-mediated growth suppression requires the N-terminal activation do

264 sustaining proliferative signaling, evading growth suppression, resisting cell death, reprogramming

265 ive benchmarks for the design of Li dendrite growth suppression strategies in all-solid-state batteri

266 GK1 and AKT resulted in significantly higher growth suppression than inhibiting either PI3K or AKT al

267 have greater sensitivity to aspirin-mediated growth suppression than their wild-type counterparts.

268 PTEN/low levels of pAkt exhibited T3-induced growth suppression that could be bypassed by small inter

269 of KLF7, although resulting in multilineage growth suppression that extended to hematopoietic stem c

270 After initial growth suppression, there is a rapid increase in growth

271 LF6 mutants lead to the loss of p21-mediated growth suppression through an unknown mechanism.

272 lates p53 mRNA translation and p53-dependent growth suppression through dephosphorylation of RBM38.

273 re required for estrogen antagonist-mediated growth suppression through the estrogen receptor, and th

274 s), we narrowed the domain required for 4.1B growth suppression to a fragment containing a portion of

275 harboring mutations in BMPR-II and restored growth suppression to BMP4 in mutant PASMCs.

276 , further mechanistic evidence linking DTrc8 growth suppression to CSN5 was lacking.

277 deletion eliminates normal integrin-mediated growth suppression, ultimately leading to cellular trans

278 ects, bone regeneration potential, and tumor growth suppression under NIR laser radiation are the mai

279 ensitized cancer cells to DNA damage-induced growth suppression via enhanced p53 stabilization and ac

280 uster is known to overcome TGF-beta-mediated growth suppression via targeting p21 and BIM, we demonst

281 reviously we reported that TGF-beta1-induced growth suppression was associated with a decrease in mut

282 ECRG2-mediated growth suppression was associated with activation of cas

283 Tumor growth suppression was associated with increased accumul

284 Growth suppression was due primarily to E1 protein funct

285 This growth suppression was mediated by secreted soluble fact

286 ATP-dependent ER Ca(2+) release and loss of growth suppression was observed in cycling cells.

287 A steroid-hormone-dependent growth suppression was observed in Escherichia coli effl

288 The early growth suppression was preceded by up-regulation of IFNb

289 Shh-induced growth suppression was reversed by exogenous Fgf10, but

290 This growth suppression was reversed by transduction of wild-

291 To establish a molecular mechanism for this growth suppression, we investigated the effects of celec

292 16 amino acids) and its fragments capable of growth suppression were localized to centrosomes and mic

293 targeting oAd elicited greater in vivo tumor growth suppression when compared with naked oAd and 9.5

294 ain is necessary for transformation, but not growth suppression; whereas the paired box is not requir

295 Thus, a loss of Lrp5 leads to profound growth suppression, whether growth is induced by serum o

296 via RNA interference results in marked cell growth suppression, which is associated with morphologic

297 unctionally, GSK3beta enhanced KLF6-mediated growth suppression, which was abrogated by the KLF6-4A p

298 dinaciclib would be most effective in tumor growth suppression, which we demonstrated in neuroblasto

299 ssion of PLZF leads to cell cycle arrest and growth suppression, while disruption of normal PLZF func

300 ls, KR12 infusions induce significant tumour growth suppression, with low host toxicity in KRAS-mutat