ライフサイエンスコーパス: growth suppression

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

2 tion of both prostate cell proliferation and growth suppression.

3 uence the transition between cell growth and growth suppression.

4 cells to chemotherapy-induced apoptosis and growth suppression.

5 3 inhibition resulted in tumor apoptosis and growth suppression.

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

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

8 triking increase in tumor cell apoptosis and growth suppression.

9 ive genes for transcriptional regulation and growth suppression.

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

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

12 ession also interferes with RASSF1A-mediated growth suppression.

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

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

15 olishes salinity tolerance without affecting growth suppression.

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

17 ICS is beneficial despite possible risks of growth suppression.

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

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

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

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

22 hibiting a large cell phenotype that rescues growth suppression.

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

24 esidues necessary for mediating Protein 4.1B growth suppression.

25 only partially rescues nuclear PTEN-mediated growth suppression.

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

27 essor protein p53 in signaling apoptosis and growth suppression.

28 ms retain a potential in transactivation and growth suppression.

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

30 human cancer cells and found that it caused 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 Axl are required for TGF-beta2-mediated cell growth suppression.

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

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

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

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

53 ndent protein synthesis, resulting in severe growth suppression.

54 he GADD45-induced cell cycle G2-M arrest and growth suppression.

55 proteins, GAP43, resulted in C6 glioma cell growth suppression.

56 of the tumour suppressor gene p16INK4a, and growth suppression.

57 s of HRS required for merlin binding and HRS growth suppression.

58 stantially abrogated the GADD45-induced cell growth suppression.

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

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

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

62 roliferation and how cancer cells evade this growth suppression.

63 mediated effects on antigen presentation and growth suppression.

64 augments its induction of p21 and resultant growth suppression.

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

66 olecules induced p53-dependent apoptosis and growth suppression.

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

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

69 cannot bind phosphoinositide is defective in growth suppression.

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

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

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

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

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

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

76 Growth suppression and apoptosis induction in tumor xeno

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

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

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

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

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

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

83 7A conferred resistance to cisplatin-induced growth suppression and apoptotic cell death in EC cells.

84 Growth suppression and ATM activation required the ATPas

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

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

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

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

89 Consistent with growth suppression and cytoprotection requiring differen

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

91 in vitro have associated these kinases with growth suppression and differentiation, their physiologi

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

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

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

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

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

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

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

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

100 CDK4 co-expression circumvents Ras growth suppression and induces invasive human neoplasia

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

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

103 dhesion, cytoskeletal and matrix remodeling, growth suppression and intracellular signaling cascades.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

127 24 include its ability to selectively induce growth suppression, apoptosis and radiosensitization in

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

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

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

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

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

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

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

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

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

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

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

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

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

141 Hypocotyl growth suppression by blue light was assessed by standar

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

143 that stably express 12S E1A are resistant to growth suppression by DRA, similar to HEK293 cells.

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

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

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

147 The growth suppression by miRNAs in PDFS cells is consistent

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

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

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

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

152 Growth suppression by p107 containing nonphosphorylatabl

153 Tumor growth suppression by PD0325901 relative to vehicle was

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

155 Importantly, growth suppression by SAG knockdown was partially rescue

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

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

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

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

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

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

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

163 Growth suppression depends on the CHES1 forkhead DNA-bin

164 This PTPRF-mediated growth suppression during cell proliferation functioned

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

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

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

168 E2F transactivation activity and inhibits Rb growth suppression function.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

189 7041 demonstrates robust p53-dependent tumor growth suppression in MDM2/MDMX-overexpressing xenograft

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

215 The growth suppression is associated with an increase in apo

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

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

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

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

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

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

222 This growth suppression is not correlated with impaired induc

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

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

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

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

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

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

229 cts transactivation function, apoptosis, and growth suppression mediated by wild-type p53 and TAp73,

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

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

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

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

234 mice was again required for T-cell-dependent growth suppression of CEA-expressing metastatic tumors.

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

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

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

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

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

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

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

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

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

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

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

246 Growth suppression of mutant IDH1 cells by BPTES was res

247 imatinib mesylate caused variable degrees of growth suppression of myeloid and erythroid progenitors

248 Growth suppression of nude mouse xenograft tumors carryi

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

272 activity, via the PI3K/AKT pathway, mediates growth suppression, there is accumulating evidence that

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

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

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

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

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

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

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

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

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

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

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

284 Tumor growth suppression was associated with increased accumul

285 Growth suppression was due primarily to E1 protein funct

286 This growth suppression was mediated by secreted soluble fact

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

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

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

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

291 This growth suppression was reversed by transduction of wild-

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

293 16 amino acids) and its fragments capable of growth suppression were localized to centrosomes and mic

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

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

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

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

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

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