ライフサイエンスコーパス: cell growth inhibition

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

2 HGF/Cpd 5 synergy in their actions on Hep3B cell growth inhibition.

3 ed HGF/Cpd 5-induced ERK phosphorylation and cell growth inhibition.

4 vation of NOTCH1 resulted in significant MTC cell growth inhibition.

5 sion may correlate to NPM-ALK-mediated tumor cell growth inhibition.

6 Cs) do not protect against VX-944-induced MM cell growth inhibition.

7 induced than with ionizing radiation-induced cell growth inhibition.

8 d by DNA-cleaving activity, as well as tumor cell growth inhibition.

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

10 racellular signal-regulated kinase (ERK) and cell growth inhibition.

11 rotein tyrosine phosphorylation that mediate cell growth inhibition.

12 ction of IL-10-mediated STAT3 activation and cell growth inhibition.

13 in lactate production in vitro, followed by cell growth inhibition.

14 s a repressor of MYC recently shown to cause cell growth inhibition.

15 NEMO-peptide had no effect on RANKL-induced cell growth inhibition.

16 n of Cdc25A correlated with their effects on cell growth inhibition.

17 sistance of tumor cells to TGF-beta-mediated cell growth inhibition.

18 cycle regulatory functions, correlated with cell growth inhibition.

19 U6027 has direct consequences for enzyme and cell growth inhibition.

20 n the absence of terminal differentiation or cell growth inhibition.

21 r DNA lesions than does cisplatin to achieve cell growth inhibition.

22 atment was sufficient to mediate FTI-induced cell growth inhibition.

23 drofolate reductase (DHFR) binding and tumor cell growth inhibition.

24 protein kinase --> downward arrow c-Myc --> cell growth inhibition.

25 involved in the mechanisms of Cpd 5-induced cell growth inhibition.

26 of this enzyme, which, in part, may lead to cell growth inhibition.

27 ransactivation, a p53 function essential for cell growth inhibition.

28 0.03 nM and D(max) > 95%, leading to potent cell growth inhibition.

29 odalities and reduced doses needed for tumor cell growth inhibition.

30 moter, led to restored expression of ST7 and cell growth inhibition.

31 k-down of EZH2 in NKTL cell lines results in cell growth inhibition.

32 micromolar IC(50) in PAD activity and cancer cell growth inhibition.

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

34 iation factor 2alpha (eIF2alpha), triggering cell growth inhibition.

35 und to be the most potent compound regarding cell growth inhibition.

36 inhibitor p21, and it reverses BMP-mediated cell growth inhibition.

37 p90 occupancy to be directly correlated with cell growth inhibition.

38 carboxylase phosphorylation at Ser(79), and cell growth inhibition.

39 ubulin binding by ITCs is an early event for cell growth inhibition.

40 l cycle progression, which may contribute to cell growth inhibition.

41 ctly linking tubulin-ITC adduct formation to cell growth inhibition.

42 ssion drastically attenuates CpdA-induced PC cell growth inhibition.

43 am cell signaling and contributing to cancer cell growth inhibition.

44 beta-dependent transcriptional responses and cell growth inhibition.

45 M-phase arrest and only partially prevented cell-growth inhibition.

46 ucts were derivatized and show potent cancer cell-growth inhibition.

47 (concentration that was able to cause 50% of cell growth inhibition; 24.8mug/ml) for 48h caused an in

48 The cell growth inhibition achieved by apigenin treatment re

49 -1, however, interferes with CFM-4-dependent cell growth inhibition, activation of caspases, and apop

50 Cell growth inhibition after MNP-mediated adiponectin pl

51 Furthermore, 9 demonstrated good cell growth inhibition against several human colorectal

52 ar relationships of cLogP with -log IC50 for cell growth inhibition and -log AE (AE = cell-free DNA a

53 s of interferon-alpha (IFN-alpha), including cell growth inhibition and antiviral protection, are ini

54 on of survivin and vitamin D3 (VD3)-mediated cell growth inhibition and apoptosis have been extensive

55 n by cDNA transfection abrogated DIM-induced cell growth inhibition and apoptosis in both prostate ca

56 S100A4 downregulation results in significant cell growth inhibition and apoptosis in response to TGF-

57 Whereas TM-2-51 selectively induced cell growth inhibition and apoptosis in SH-SY5Y cells, i

58 , STAT3 decoy, and gossypol further enhanced cell growth inhibition and apoptosis in vitro, and it do

59 he current study significantly increased the cell growth inhibition and apoptosis inducing activities

60 These results suggest that B-DIM-induced cell growth inhibition and apoptosis induction are partl

61 rvivin plays a role in VD3 compound-mediated cell growth inhibition and apoptosis induction.

62 ed the MT-hTers, also caused p53-independent cell growth inhibition and apoptosis, and when coexpress

63 ndolylmethane treatment resulted in enhanced cell growth inhibition and apoptosis, whereas overexpres

64 ering RNA transfection increased DIM-induced cell growth inhibition and apoptosis, whereas overexpres

65 A before ERRP treatment resulted in enhanced cell growth inhibition and apoptosis.

66 tion abrogated 3,3'-diindolylmethane-induced cell growth inhibition and apoptosis.

67 before TW-37 treatment resulted in enhanced cell growth inhibition and apoptosis.

68 arget hub genes and subsequently resulted in cell growth inhibition and apoptosis.

69 DNA damage response, ultimately resulting in cell growth inhibition and apoptosis.

70 increases genomic instability, resulting in cell growth inhibition and apoptosis.

71 hat reduction of cellular Na/K-ATPase causes cell growth inhibition and cell death in renal proximal

72 stigated the in vitro effect of As(2)O(3) on cell growth inhibition and cell death mechanisms in huma

73 urvivin-2B sensitizes cells to taxol-induced cell growth inhibition and cell death, while silencing o

74 tion, respectively, which resulted in cancer cell growth inhibition and cell death.

75 aS26X cells at concentrations sufficient for cell growth inhibition and complete suppression of EGFR

76 ar macromolecular synthesis concomitant with cell growth inhibition and compromised the integrity of

77 eclin 1 using siRNA significantly suppresses cell growth inhibition and death induced by phycocyanin,

78 ntial, aiming at a higher efficacy regarding cell growth inhibition and decreased angiogenesis and in

79 lasmid (C62S) partially abolished PL-induced cell growth inhibition and decreased the enhanced expres

80 suggest that the mechanism of breast cancer cell growth inhibition and differentiation via erbB rece

81 and TGF-beta1 significantly impaired myeloid cell growth inhibition and differentiation.

82 d breast and colon cancer cells also induces cell growth inhibition and differentiation.

83 ere was a generally good correlation between cell growth inhibition and E. coli farnesyl diphosphate

84 or p27 individually did not alter IP6-caused cell growth inhibition and G(1) arrest; however, their s

85 generally more active in human breast cancer cell growth inhibition and human leukemia cell different

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

87 ture studies, apigenin treatment resulted in cell growth inhibition and induction of apoptosis, which

88 rophage-like cells was associated with yeast cell growth inhibition and killing.

89 r current study, we found that TW-37 induces cell growth inhibition and S-phase cell cycle arrest, wi

90 tyrosine phosphorylated Jak3 correlated with cell growth inhibition and terminal granulocytic differe

91 as sufficient to antagonize TGF-beta-induced cell growth inhibition and that dysregulation of TGF-bet

92 hibition of NRG1 signaling leads to melanoma cell growth inhibition and tumor growth delay.

93 as shown to exhibit cellular activity (i.e., cell-growth inhibition and cell-cycle arrest) in mammali

94 ly inactive CD148 mutants attenuates the Ab1-cell growth inhibition, and (3) bivalent Ab1 suppresses

95 luding gene expression, the triple response, cell growth inhibition, and accelerated senescence.

96 cells RhoB-GG induced phenotypic reversion, cell growth inhibition, and activation of the cell cycle

97 aP sublines (C4, C4-2, and C4-2B), conferred cell growth inhibition, and at least one of the PY motif

98 me potent FPPS inhibitors had no activity in cell growth inhibition, and based on the result of Catal

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

100 intracellular 20S activity correlating with cell growth inhibition, and bortezomib IC(50) values (co

101 cells were resistant to bicalutamide-induced cell growth inhibition, and CSE overexpression could reb

102 p16 expression, cell growth inhibition, and G1 cell cycle arrest by 5-Az

103 RXR retinoid receptor transactivation, tumor cell growth inhibition, and transglutaminase (TGase) ind

104 e mycobacterial phosphatase, correlated with cell growth inhibition, and we found that M. smegmatis c

105 eir diverse pharmacologic activities such as cell growth inhibition, anti-inflammatory effects and tu

106 d with a reduction of IFN-induced apoptosis, cell growth inhibition, antiviral defense, and chemotaxi

107 ed LNCaP cells showed striking resistance to cell growth inhibition/apoptosis mediated by the wt p53.

108 tion, specific examples of integrin-mediated cell growth inhibition are few.

109 s elevated IL-10 and TGF-beta 1, and cause T cell growth inhibition as effector CD8+ T cells.

110 2 was identified as the key mediator of skin cell growth inhibition as evidenced by complete protecti

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

112 nthesized and evaluated in a colon carcinoma cell growth inhibition assay using HCT116 and SW480 cell

113 A cell growth inhibition assay was used to measure variati

114 TGF-beta was measured by the CCL-64 cell growth inhibition assay.

115 However, potency in cell growth inhibition assays ranged over 2 orders of ma

116 liminary biological studies using short-term cell growth inhibition assays show that some of the liga

117 ed or exceeded the potency of vinblastine in cell growth inhibition assays.

118 PT-11 toxicity by both drug accumulation and cell growth-inhibition assays.

119 and in vivo that silencing of GCK induces MM cell growth inhibition, associated with blocked MKK4/7-J

120 cell culture study, analogue 8 exhibited 88% cell growth inhibition at a concentration of 10 muM and

121 acted to achieve significant prostate cancer cell growth inhibition at approximately 2 to 10 times lo

122 Cell growth inhibition at increasing concentrations of e

123 Cytotoxicity was determined as cell-growth inhibition at increasing concentrations of c

124 th factor-beta1 (TGF-beta1) induces not only cell growth inhibition but also apoptosis in hepatocytes

125 vely active Akt construct partially relieved cell growth inhibition but was less effective than inhib

126 erin binding to beta-catenin is required for cell growth inhibition, but beta-catenin/T-cell factor t

127 g the genetic contribution to sensitivity to cell growth inhibition by anticancer agents.

128 The synthesis and tumor cell growth inhibition by doxazolidine carbamate prodrug

129 Cell growth inhibition by ENZ in breast cancer with low

130 and the role of p27(KIP1) in G1/S arrest and cell growth inhibition by erlotinib, we determined its e

131 n of p27(KIP1) is required for G1 arrest and cell growth inhibition by erlotinib.

132 Our results suggest that cell growth inhibition by IFN-gamma is due to apoptosis

133 These findings show a unique mechanism of cell growth inhibition by integrins and point to beta1C

134 The biochemical mechanisms of cell growth inhibition by ITCs are not fully understood.

135 Mechanistically, we show that MTC cell growth inhibition by NOTCH1 is mediated by cell cyc

136 MSA was used to elucidate the mechanisms of cell growth inhibition by selenium.

137 ing the possibility that p202 contributes to cell growth inhibition by the interferons, at least in p

138 These results suggest that Hep3B cell growth inhibition by these K vitamin analogues may

139 These results suggest that cell growth inhibition by thioether analogs is closely a

140 E. coli) between experimental and predicted cell growth inhibition by using DNA DeltaTm and UPPS IC5

141 than error induction, is the major cause of cell growth inhibition by viomycin.

142 In MCF-7 mammary carcinoma cells, growth inhibition by RA entails an early cell cyc

143 In MCF-7 and MCF-7/IGF-IR cells, growth inhibition by Tam was associated with the

144 Moreover, we have identified that cell growth inhibition can be achieved by expressing mod

145 X overexpression not only reversed the tumor cell growth inhibition caused by MnSOD overexpression bu

146 M, 10S-3 Ki = 180 nM) that exhibit effective cell growth inhibition (CCRF-CEM IC50 = 80 and 50 nM, re

147 PPARgamma, induced dose- and time-dependent cell growth inhibition, cell cycle arrest in G(1)-S and

148 nuating TGFbeta-mediated Smad2/3 activation, cell growth inhibition, cell migration and apoptosis.

149 t role in cellular homeostasis by regulating cell growth inhibition, cellular senescence, differentia

150 d DOX-TEG-TAM, was found to possess superior cell growth inhibition characteristics relative to clini

151 igand leads to significantly increased tumor cell growth inhibition compared with one method alone, s

152 h inhibition, and we found that M. smegmatis cell growth inhibition could be well predicted by using

153 s and overproduction of the protein leads to cell growth inhibition, decreased protein synthesis and

154 The most pronounced cell growth inhibition effect was obtained in the breast

155 Ironomycin also induced significant cell growth inhibition, ferroptosis, and autophagy.

156 cts on client protein degradation and cancer cell growth inhibition has not been thoroughly investiga

157 he synthetic samples were screened for tumor cell growth inhibition, HDAC inhibition, and Mycobacteri

158 se model of ovarian cancer resulted in tumor cell growth inhibition, impaired cell invasion, and seve

159 Cell growth inhibition in 324 Centre d' Etude du Polymor

160 DC-antizyme has been shown to correlate with cell growth inhibition in a variety of different cell ty

161 ls with wortmannin, a PI3K inhibitor, caused cell growth inhibition in a way similar to the effects o

162 1 nM and has low nanomolar IC(50) values in cell growth inhibition in cancer cell lines.

163 hown to be responsible for TGF-beta-mediated cell growth inhibition in Chinese hamster ovary (CHO) ce

164 uggest that IL-4 activates Stat1, leading to cell growth inhibition in colon cancer cells.

165 ses butHinfp levels remain constitutive upon cell growth inhibition in culture.

166 Here, we demonstrate that erlotinib-induced cell growth inhibition in EGFR high-expressing human H32

167 re tested at 25-500 mug/mL, showed up to 50% cell growth inhibition in four selected tumoral cell lin

168 ctor E2F-1 is consistent with ZD1694-induced cell growth inhibition in HCT-8 cells.

169 iously found that K vitamin analogues caused cell growth inhibition in Hep3B hepatoma cells in vitro,

170 ortant mediator of RA- and TGF-beta2-induced cell growth inhibition in human breast cancer cells.

171 Dox to induce p21 expression and subsequent cell growth inhibition in MCF-7 cells.

172 STAT activation was correlated with cell growth inhibition in response to EGF and IFN-gamma.

173 tion of the cell cycle inhibitor p27Kip1 and cell growth inhibition in response to TGF-beta occur in

174 tency than INZ in both of p53 activation and cell growth inhibition in several human cancer cell line

175 o C-1027, as it did not cause hypersensitive cell growth inhibition in the absence of ATM nor require

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

177 3-oxo analogues (11 and 16) exhibited potent cell growth inhibition in vitro (GI(50): 9 nM and 20 nM)

178 ration of KLF4 expression resulted in marked cell growth inhibition in vitro and significantly attenu

179 hermore, we found that CED-4 is required for cell-growth inhibition in animals lacking TFG-1.

180 nt of PKR relieved c-Myc down-regulation and cell growth inhibition, indicating that PKR is directly

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

182 Consistent with the hypothesis that cell growth inhibition is due to competitive inhibition

183 ed in vivo bystander effect leading to tumor cell growth inhibition is mediated, at least in part, by

184 The compounds were studied for cell growth inhibition mediated by partial depletion of

185 by increased expression of genes involved in cell growth, inhibition of apoptosis, and embryogenesis

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

187 with several orders of magnitude more potent cell growth inhibition on a variety of cultured cancer c

188 DFMO and SAM486A caused rapid cell growth inhibition, polyamine depletion, and G1 cell

189 ites showed lowered antioxidant activity and cell growth inhibition potential.

190 S287A-STAT2 increased cell growth inhibition, prolonged protection against ves

191 AP70, SYK, or LCK showed additive effects on cell growth inhibition, providing a rationale for combin

192 inding a poor correlation between enzyme and cell growth inhibition (R(2) = 0.06).

193 ree QSAR models showed that the experimental cell growth inhibition results could be well predicted.

194 n in Escherichia coli is consistent with the cell growth inhibition results.

195 lyses relating the polar termini with cancer cell growth inhibition revealed that length and van der

196 ight on the biochemical mechanism of aglycon cell growth inhibition, showing as it remarkably influen

197 In Ambit kinome screens, cell growth inhibition studies, and surrogate kinase ass

198 ed greater or comparable potency to VP-16 in cell growth-inhibition studies and were less affected by

199 ogated erlotinib-induced G1 phase arrest and cell growth inhibition, suggesting that induction of p27

200 uch more potent effects on pancreatic cancer cell growth inhibition than free curcumin.

201 -O-glucuronide, and studied their effects on cell growth inhibition, the cell cycle and apoptosis usi

202 Nevertheless, with respect to cell growth inhibition, the methanolic extract was the m

203 Moreover, 10 displays superior cell growth inhibition to the parent G9a/GLP inhibitor U

204 Selectivity for tumor cell growth inhibition versus normal human fibroblast gr

205 yclin E versus cyclin A, we demonstrate that cell growth inhibition was absolutely dependent on the a

206 Colon cancer cell growth inhibition was accompanied by downregulation

207 The cell growth inhibition was accompanied by increased apop

208 Cancer cell growth inhibition was also demonstrated either as a

209 Furthermore, this anti-miR-21-mediated cell growth inhibition was associated with increased apo

210 The direct involvement of IGFBP-3 in cell growth inhibition was further confirmed by its acti

211 FLT3's likely contribution to pacritinib's cell growth inhibition was further demonstrated by siRNA

212 rations of eight chemotherapeutic drugs, and cell growth inhibition was measured at each dose with ha

213 Cell growth inhibition was measured with the sulforhodam

214 mediating this effect, as the enhancement of cell growth inhibition was not observed in cells lacking

215 phospho(Ser(139))histone H2AX induction and cell growth inhibition was observed.

216 Cell growth inhibition was partially or completely rescu

217 The cell growth inhibition was reversed by the removal of th

218 persistent ERK phosphorylation might induce cell growth inhibition, we used Cpd 5 as a tool to exami

219 DU145 cell culture medium and a strong DU145 cell growth inhibition were observed that were irreversi

220 nt type II PRMT, produces synergistic cancer cell growth inhibition when combined with GSK3368715.

221 ses, cell cycle delays and DNA synthesis and cell growth inhibition, which can be rescued by restorin

222 ons of 15, 30, and 45 micromol/L resulted in cell growth inhibition, which was accompanied by the exp

223 ells with PTX-loaded MNPs caused significant cell growth inhibition, which was not observed under non

224 ne with mainly MET phosphorylation, profound cell growth inhibition with induction of apoptosis was o

225 ntify an active region responsible for tumor cell growth inhibition within exon 4, which harbors two