ライフサイエンスコーパス: induction of apoptosis

1 silencing a gene (caspase-3) responsible for induction of apoptosis.

2 bation of cell cycle progression rather than induction of apoptosis.

3 vity and annexin V-positive cell number upon induction of apoptosis.

4 ells causes G1 cell cycle arrest followed by induction of apoptosis.

5 37, and HL60 tumor and normal cell lines and induction of apoptosis.

6 on cell cycle regulation is followed by the induction of apoptosis.

7 due to cell-cycle regulation leading to the induction of apoptosis.

8 istic increase in caspase 3/7 activation and induction of apoptosis.

9 the onset of irreversible DNA damage and the induction of apoptosis.

10 g of gene expression, cell cycle arrest, and induction of apoptosis.

11 d SHP-1 activity, inhibition of p-STAT3, and induction of apoptosis.

12 by immune cells to kill cancer cells through induction of apoptosis.

13 erlying mechanism for this by using H2O2 for induction of apoptosis.

14 alpha, other interferon-stimulated genes and induction of apoptosis.

15 a mechanism of inhibiting metastasis via the induction of apoptosis.

16 ading to cessation of cell proliferation and induction of apoptosis.

17 3 activation and either cell cycle arrest or induction of apoptosis.

18 ned by a surprising, concentration-dependent induction of apoptosis.

19 cellular defense mechanisms is essential for induction of apoptosis.

20 ll death through activation of caspase-3 and induction of apoptosis.

21 uced in deguelin-treated mice along with the induction of apoptosis.

22 sed DCs could be partially attributed to the induction of apoptosis.

23 nd an increase in cell death consistent with induction of apoptosis.

24 -driven apoptosis) support a mechanism-based induction of apoptosis.

25 s (PIV5DeltaSH and PIV5VDeltaC) that enhance induction of apoptosis.

26 cells and evaluated the mechanism[s] in the induction of apoptosis.

27 ominant negative CDK5 results in synergistic induction of apoptosis.

28 ion of DNA DSBs, G2-M cell-cycle arrest, and induction of apoptosis.

29 ibitors, trigger cellular stress and lead to induction of apoptosis.

30 f the proapoptotic protein, BIM, followed by induction of apoptosis.

31 ndent elevation of cytosolic Ca(2+) prior to induction of apoptosis.

32 bility to secondary bacterial infection, and induction of apoptosis.

33 killing leukemic cells through the forcible induction of apoptosis.

34 enhanced host protein synthesis shutoff and induction of apoptosis.

35 n to be hypersensitive to CPT with prominent induction of apoptosis.

36 se activity, malondialdehyde production, and induction of apoptosis.

37 o dephosphorylation of Akt at serine-473 and induction of apoptosis.

38 ulting from a differentiation defect and the induction of apoptosis.

39 kinase (AMPK), activation of caspase-3, and induction of apoptosis.

40 elimination of Bcl-xL and Mcl-1 resulted in induction of apoptosis.

41 KT), because PI3K inhibitor results in early induction of apoptosis.

42 orrelate with protein kinase C inhibition or induction of apoptosis.

43 ICD target Hes1 gene in mouse brains without induction of apoptosis.

44 cells were then treated with doxorubicin for induction of apoptosis.

45 by RV metabolite treatments, as well as the induction of apoptosis.

46 cFLIP had been downregulated resulted in the induction of apoptosis.

47 lation of cytotoxic double-strand breaks and induction of apoptosis.

48 ulate Star-PAP control of BIK expression and induction of apoptosis.

49 promotes p53-dependent growth arrest and the induction of apoptosis.

50 nockdown or inactivation were accompanied by induction of apoptosis.

51 gulation, modulation of differentiation, and induction of apoptosis.

52 nts, may also contribute to piperlongumine's induction of apoptosis.

53 tivation of PI3-kinase (PI3K) signaling, and induction of apoptosis.

54 r of apoptosis, activation of caspase 9, and induction of apoptosis.

55 ctly links ErbB receptor inactivation to the induction of apoptosis.

56 proliferation of pancreatic cancer cells and induction of apoptosis.

57 ion of gamma-tubulin protein levels leads to induction of apoptosis.

58 ing electron transfer, enzyme catalysis, and induction of apoptosis.

59 leading from ligation of the Fas receptor to induction of apoptosis.

60 otes ADAM17 activity in neutrophils upon the induction of apoptosis.

61 osarcoma cells in the G2 cell cycle prior to induction of apoptosis.

62 the MDA-MB-231 cell line via complement and induction of apoptosis.

63 motes the DNA damage response leading to the induction of apoptosis.

64 accumulation of reactive oxygen species and induction of apoptosis.

65 esting that kinase activity is essential for induction of apoptosis.

66 active state of the MST kinases and favoring induction of apoptosis.

67 d-type colon cultures respond similarly upon induction of apoptosis.

68 lls in sub-G(1) phase of the cell cycle, and induction of apoptosis.

69 s of the molecular processes involved in the induction of apoptosis.

70 Z and DOX were mediated in part by selective induction of apoptosis.

71 otein, which is required for transcriptional induction of apoptosis.

72 in synergistic inhibition of cell growth and induction of apoptosis.

73 T laser power (2 W/cm(2)) to achieve maximal induction of apoptosis.

74 Chlamydia infection is known to block the induction of apoptosis.

75 a mechanism to promote BOK accumulation and induction of apoptosis.

76 lular trap formation, bacterial killing, and induction of apoptosis.

77 d redox ratio and ROS increased, followed by induction of apoptosis.

78 , accumulation of unrepaired DNA damage, and induction of apoptosis.

79 , reduced colony formation in soft agar, and induction of apoptosis.

80 horylated on Tyr142, high levels of p53, and induction of apoptosis.

81 ibition of JAK-STAT activity, leading to the induction of apoptosis.

82 oteins, reduction of cell proliferation, and induction of apoptosis.

83 limits both FasL and ceramide analogs in the induction of apoptosis.

84 udies showing the HEXIM1 is required for the induction of apoptosis.

85 rowth of the cell line A427, which is due to induction of apoptosis.

86 l squelching", while hid causes lethality by induction of apoptosis.

87 s results in irreversible DNA damage and the induction of apoptosis.

88 ions in the morphology of this organelle and induction of apoptosis.

89 mediated by both G0/G1 cell cycle block and induction of apoptosis.

90 chondria represents a critical signal in the induction of apoptosis.

91 believed to result directly or indirectly in induction of apoptosis, a better understanding of the bi

92 Induction of apoptosis activates Yorkie through the Jun

93 r-bearing mice with LV-tSMAC resulted in the induction of apoptosis, activation of antitumor immunity

94 PARP) cleavage were performed to measure the induction of apoptosis after nifurtimox treatment.

95 esolution by reducing neutrophil numbers via induction of apoptosis after tailfin injury.

96 least partially associated with an enhanced induction of apoptosis although triggered by distinct ap

97 mpairment of granule neuron differentiation, induction of apoptosis and abnormal localization of Purk

98 ogether with inhibited HDAC activity, led to induction of apoptosis and autophagy in WM cells.

99 6b leads to cell death by concomitant induction of apoptosis and autophagy, shows good pharmac

100 feration, motility, and invasion, as well as induction of apoptosis and autophagy.

101 o control OS tumor growth which involved the induction of apoptosis and cell cycle arrest, supporting

102 degradation by PS-341 occurred early before induction of apoptosis and could not be inhibited by a p

103 BP2 had reduced viability and proliferation, induction of apoptosis and cytotoxicity, and up-regulati

104 testing of their biological activity such as induction of apoptosis and evaluation of anti-cancer eff

105 grees than controls, which was attributed to induction of apoptosis and G2 cell cycle arrest.

106 cation transporter CNNM4 regulates growth by induction of apoptosis and identified a tumor suppressiv

107 downregulation of MYC expression, as well as induction of apoptosis and induces differentiation of pr

108 This was accompanied by induction of apoptosis and inhibition of cell growth and

109 y small-interfering (si) RNA caused a strong induction of apoptosis and inhibition of cell-cycle prog

110 Furthermore, significant induction of apoptosis and inhibition of epithelial-to-m

111 stress and p53 activation, resulting in the induction of apoptosis and inhibition of proliferation,

112 Further, the synergistic induction of apoptosis and inhibition of tumor growth we

113 n of pancreatic islet beta cell mass through induction of apoptosis and lack of regeneration.

114 Strikingly, induction of apoptosis and necroptosis effectors was sha

115 00E mutant melanoma xenograft tumors through induction of apoptosis and necrosis.

116 n mouse model of prostate cancer through the induction of apoptosis and proliferation block.

117 eckpoint both contributed to the synergistic induction of apoptosis and proliferation inhibition in A

118 esulting in inhibition of FAK/Src signaling, induction of apoptosis and re-sensitization to chemother

119 lted in secretion of inflammatory cytokines, induction of apoptosis and reduction in trophoblast cell

120 gh PERK-eIF2alpha-dependent pathways, of the induction of apoptosis and reduction of autophagy by Sub

121 The induction of apoptosis and repression of the cell adhesi

122 lective DNA damage at telomeric level and to induction of apoptosis and senescence on tumor cells is

123 A] and its downstream substrate FOXO1 in the induction of apoptosis and the synthesis of catalase.

124 nteracts with E2F1, and is required for E2F1 induction of apoptosis and transcription of a number of

125 cytotoxic effect appeared to be mediated by induction of apoptosis and was inhibited in a concentrat

126 GI-1776 results in a concentration-dependent induction of apoptosis and we investigated its effect on

127 DCP inhibitory effects were attributed to induction of apoptosis and/or increased production of in

128 Cell-intrinsic effects such as induction of apoptosis and/or inhibition of cell prolife

129 ell-based assays to evaluate cell viability, induction of apoptosis, and accumulation of ROS followin

130 ession of the pro-survival protein MCL-1, an induction of apoptosis, and an enhanced reduction of tum

131 on of Sp-regulated genes, growth inhibition, induction of apoptosis, and antiangiogenic responses.

132 alization along with osteonectin expression, induction of apoptosis, and cytotoxicity assays were per

133 cells by RNAi resulted in aberrant mitoses, induction of apoptosis, and decreased ability of human b

134 he most potent effects on growth inhibition, induction of apoptosis, and delay of acquired resistance

135 The mechanism of action of IAD is largely induction of apoptosis, and each mechanism of resistance

136 luding loss of epithelial barrier functions, induction of apoptosis, and inflammation.

137 4 results in efficient degradation of Mcl-1, induction of apoptosis, and inhibition of tumor growth i

138 ulting in a shut-off of general translation, induction of apoptosis, and inhibition of virus replicat

139 al dysfunction, generation of peroxynitrite, induction of apoptosis, and oxidative stress due to disr

140 APDH are associated with anti-proliferation, induction of apoptosis, and oxidative-stress protection.

141 ociated with the inhibition of angiogenesis, induction of apoptosis, and reduction in keloid phenotyp

142 rosurvival Bcl-2 proteins leads to effective induction of apoptosis, and strongly support the concept

143 ibition-induced down-regulation of c-Myc and induction of apoptosis are mitigated when the cells are

144 correction of mitochondrial dysfunction and induction of apoptosis are promising strategies in cance

145 e main function ascribed so far has been the induction of apoptosis as a crucial mediator of KRAS-dri

146 the cytotoxic effect may be associated with induction of apoptosis as evidenced by increased percent

147 an intrinsic innate immune response and the induction of apoptosis as mechanisms to restrict viral r

148 This effect is related to a synergistic induction of apoptosis as seen in the combination of 4j

149 miR-205 overexpression resulted in induction of apoptosis, as evidenced by increased cleave

150 An opposite pattern was observed regarding induction of apoptosis, as studied by Western blotting f

151 osphocholine, inhibition of cell growth, and induction of apoptosis at low micromolar concentrations.

152 e mediated by the block of autophagy and the induction of apoptosis; (b) decreased metastatic potenti

153 r fate by regulating both cytoprotection and induction of apoptosis based on the metabolic state.

154 Induction of apoptosis because of aggresomal compartment

155 v toxin is linked to V. vulnificus dependent induction of apoptosis, but the region of the large mult

156 e inhibition of tumor cell proliferation and induction of apoptosis, but their effect on tumor cell i

157 x and decreased Bcl-2 expression, indicating induction of apoptosis by 48 hours after SP treatment.

158 t significantly affect AcMNPV replication or induction of apoptosis by a mutant of AcMNPV lacking the

159 signaling to AMPK, making them resistant to induction of apoptosis by adenosine 3',5'-cyclic monopho

160 The induction of apoptosis by an unresolvable unfolded prote

161 n of Caspase3 at 200muM at 48h confirmed the induction of apoptosis by apigenin and quercetagetin.

162 Synergistic induction of apoptosis by AZD8055 and ABT-737 is confirm

163 as responsible for the activation of JNK and induction of apoptosis by both agents.

164 erent primary cells and cell lines after the induction of apoptosis by different stimuli.

165 ance of significant caspase3/7 activity upon induction of apoptosis by doxorubicin.

166 we examined and quantitatively evaluated the induction of apoptosis by drug combination therapies.

167 The induction of apoptosis by ErPC3 requires TSPO, a mitocho

168 Early L3 animals are highly resistant to induction of apoptosis by expression of IAP-antagonists,

169 After induction of apoptosis by H. pylori or camptothecin, the

170 ruption of Bcl-2-ERK complex, as well as the induction of apoptosis by H2O2.

171 92 or a D-box destruction motif inhibits the induction of apoptosis by microtubule poisons.

172 The aim of this study was to explore the induction of apoptosis by MTX.

173 Here, we show that induction of apoptosis by Myc in breast epithelial cells

174 he NF-kappaB pathway by nucleolar stress and induction of apoptosis by nucleolar sequestration of NF-

175 Here, we describe an induction of apoptosis by p21 in sarcoma cell lines that

176 On the other hand, the induction of apoptosis by PIK-75 did not require the exp

177 wnregulation that contributes to synergistic induction of apoptosis by PP242 plus TRAIL.

178 vity of elephant cells to DNA damage and the induction of apoptosis by regulating activity of the TP5

179 The induction of apoptosis by RNAi-mediated depletion or pha

180 small cell lung cancer cell lines toward the induction of apoptosis by the DNA-damaging agent etoposi

181 us, mutation of cleavage sites inhibited the induction of apoptosis by treatment with tumor necrosis

182 It is thought that induction of apoptosis can lead to enhanced antigen pres

183 AKT2-amplified PDAC, was able to bypass the induction of apoptosis caused by KRAS* ablation, highlig

184 is demonstrates that BIM is critical for the induction of apoptosis caused by potentially oncogenic D

185 time-dependent inhibition of proliferation, induction of apoptosis, cell-cycle arrest, and terminal

186 showed the largest inhibition of growth and induction of apoptosis compared with the double combinat

187 Induction of apoptosis correlated with increased express

188 ed to significant inhibition of cell growth, induction of apoptosis, decreased invasiveness and decre

189 on (that resulted in loss of nuclear CK2 and induction of apoptosis) demonstrated dynamic modulation

190 The induction of apoptosis depend on the BAPO and the irradi

191 However, induction of apoptosis does not explain how scrib(-) cel

192 as a scaffold for pro-caspase-8 binding and induction of apoptosis downstream of induced-proximity a

193 Here we show the efficient induction of apoptosis even by a non-toxic nsEP exposure

194 Usp9x in myeloma cells resulted in transient induction of apoptosis, followed by a sustained reductio

195 Thus, despite the preferential induction of apoptosis following exogenously induced gen

196 TRAIL receptors facilitate induction of apoptosis for selective elimination of mali

197 The induction of apoptosis has long been proposed as a targe

198 ape as well as retardation of cell cycle and induction of apoptosis have been analyzed and found to v

199 MV-4-11 human leukemia cells, showed potent induction of apoptosis (IC(50)'s approximately 20 muM) w

200 The best binders showed induction of apoptosis in a human cancer cell line with

201 lence functions for P. aeruginosa, including induction of apoptosis in a variety of target host cells

202 immunoregulatory activity via B7-H1-mediated induction of apoptosis in activated T cells.

203 genes, decreased dendritic spine density and induction of apoptosis in astrocytes may contribute to t

204 function of WT p53 is directly linked to the induction of apoptosis in both cancer cells and tumor xe

205 domain protein Miz-1 restricts p53-dependent induction of apoptosis in both pro-B and DN3a pre-T cell

206 imary myoblasts and C2C12 cultures, chemical induction of apoptosis in C2C12 cells results in indiscr

207 The induction of apoptosis in CACs by microparticles derived

208 Inhibition of phagocytosis prevents the induction of apoptosis in CACs by microparticles.

209 Induction of apoptosis in cells infected by Sendai virus

210 tion protects stalled forks from collapse or induction of apoptosis in CHK1 inhibited cells during re

211 , irreversible DNA damage, and ATM-dependent induction of apoptosis in cytokine-treated beta cells.

212 These in vitro studies show that induction of apoptosis in DC by MVA vectors is detriment

213 synergistic effect in growth inhibition and induction of apoptosis in DLBCL cells.

214 es during cisplatin treatment with strongest induction of apoptosis in each of the MPM cell lines, bu

215 e importance of hnRNP A1 was demonstrated by induction of apoptosis in eIF2alpha phosphorylation-defi

216 ailable for clinical studies potentiates the induction of apoptosis in glioma CSCs.

217 and evaluate their inhibition of growth and induction of apoptosis in human cancer cells.

218 ection gonorrhea, protects against exogenous induction of apoptosis in human cervical epithelial cell

219 lpain, CAPN1, which were requisite steps for induction of apoptosis in MDS cells and in acute myeloid

220 Although induction of apoptosis in melanoma cells by melphalan in

221 tion, MVA-B13R showed a significant delay in induction of apoptosis in muscle cells derived from mice

222 +) DCs from rhesus macaques, compared to the induction of apoptosis in MVA-infected cells.

223 ensory epithelium (OSE) in hamsters and that induction of apoptosis in olfactory receptor neurons (OR

224 Strong induction of apoptosis in one compartment of the Drosoph

225 ment of multiple oncogenic processes and the induction of apoptosis in pancreatic and breast cancer c

226 on causes reduction in adipogenesis, through induction of apoptosis in pre-adipocytes, by inhibition

227 cept in cancer therapy, coiled-coil mediated induction of apoptosis in Raji B cells, for treatment of

228 the expression of IFN-beta and the efficient induction of apoptosis in reovirus-infected cells.

229 ied the molecular mechanisms involved in the induction of apoptosis in response to cisplatin, and fou

230 tical role in cell-cycle progression and the induction of apoptosis in response to DNA damage.

231 activation plays a major regulatory role in induction of apoptosis in response to ER stress and indi

232 of E2F regulation is critical for the normal induction of apoptosis in response to irradiation.

233 these two microRNAs in mediating p16-related induction of apoptosis in response to this genotoxic str

234 sclerosis (RRMS) is not well understood, but induction of apoptosis in specific leukocyte subsets is

235 ation between GFI1 and p53 that controls the induction of apoptosis in T cells.

236 s revealed that Dicer1 deficiency led to the induction of apoptosis in T-ALL cells, whereas cell cycl

237 depletion causes impaired proliferation and induction of apoptosis in the OP9 cell line and in prima

238 catenin S45F mutants, resulting in decreased induction of apoptosis in these cells.

239 ly demonstrated that Heme is involved in the induction of apoptosis in vascular endothelial cells.

240 nducing ligand (TRAIL) for markedly enhanced induction of apoptosis in VHL-null 786-O cells but not i

241 ulting in viral RNA replication and a potent induction of apoptosis in vitro and antitumor effects in

242 inical Akt and CDK inhibitors, demonstrating induction of apoptosis in vitro and providing a preclini

243 PE induced a rapid and dose-dependent induction of apoptosis in wild-type (WT) and Bax knockou

244 siParp1 inhibits cell growth, primarily by induction of apoptosis, in Brca1-deficient cells both in

245 play a role in G(2)/M cell cycle arrest and induction of apoptosis, in contrast to the function of t

246 c protein that forms a complex with Bax upon induction of apoptosis, in the presence of gamma-secreta

247 ents that require BID activation for maximal induction of apoptosis, including topoisomerase inhibito

248 The induction of apoptosis increased osteocytic Rankl expres

249 To investigate if EBOV blocks the induction of apoptosis, infected cells were treated with

250 tinoblastoma and current models propose that induction of apoptosis is a key p53 tumor suppressive fu

251 We further demonstrated that the induction of apoptosis is associated with the GNMT nucle

252 The regulation of neutrophil lifespan by induction of apoptosis is critical for maintaining an ef

253 in the activation of Bid, and the consequent induction of apoptosis is inhibited by Noxa silencing.

254 Induction of apoptosis is often necessary for successful

255 Killing cancer cells through the induction of apoptosis is one of the main mechanisms of

256 impaired growth and proliferation in vitro, induction of apoptosis, loss of colony formation in meth

257 Furthermore, we demonstrate that, upon induction of apoptosis, lymphoma cells not only activate

258 ificant inhibition of cell proliferation and induction of apoptosis, making it an attractive target f

259 R (PKR) was blocked in EBOV-infected cells, induction of apoptosis mediated by dsRNA was not suppres

260 in orchestrating various pathologies via the induction of apoptosis, necroptosis, and nuclear factor-

261 blood-brain barrier integrity during ECM by induction of apoptosis of brain vascular endothelial cel

262 e capacity to help GC-B cells because of the induction of apoptosis of GC-B cells through the FAS/FAS

263 B-ALL development, which was accompanied by induction of apoptosis of leukemic B-lymphoid progenitor

264 : (i) inhibition of cell proliferation, (ii) induction of apoptosis of tumor xenograft cells, (iii) d

265 receptor, death receptor 5 (DR5), leading to induction of apoptosis, offers a promising anticancer st

266 lthough p53 limits tumorigenesis through the induction of apoptosis or cell cycle arrest, its molecul

267 on state of the Bnip3 LIR signals either the induction of apoptosis or pro-survival mitophagy.

268 f c-Jun N terminal kinases (JNK)1/2, but not induction of apoptosis or the JAK/STAT pathway that is n

269 is ameliorates these phenotypes, while acute induction of apoptosis phenocopies these defects and rev

270 lts in suppression of cell proliferation and induction of apoptosis process.

271 Furthermore, induction of apoptosis proved to be dependent on the sub

272 70alpha is AR-dependent and mediated through induction of apoptosis rather than cell cycle arrest.

273 f breast cancer cells, which correlated with induction of apoptosis, reduced expression of SOX2 but e

274 ation of oxidant and antioxidant levels, and induction of apoptosis-related proteins in the lung tiss

275 , including cell activation, protection from/induction of apoptosis, release of inflammatory cytokine

276 Degradation of FAT10 is accelerated after induction of apoptosis, suggesting that it plays a role

277 lts in loss of MCL-1 expression prior to the induction of apoptosis, suggesting that MCL-1 may be an

278 Combination treatment resulted in rapid induction of apoptosis that coincided with increased DNA

279 pevonedistat treatment of cells resulted in induction of apoptosis that could be partially rescued b

280 M-phase arrest and the consequent induction of apoptosis that follows could possibly be at

281 spase-3, Bax and Bcl-2 factors specified the induction of apoptosis that helped in significant inhibi

282 These findings indicate that induction of apoptosis through Fas is dependent on recep

283 strong anticancer activity exhibited as the induction of apoptosis through p53 activation.

284 um by down-regulation of XIAP expression and induction of apoptosis through specific targeting of a S

285 We unexpectedly found that induction of apoptosis triggered high-level viral replic

286 Independent cell cycle arrest and increased induction of apoptosis underlies the synergistic effect

287 is inducing factor (AIFM1) have roles in the induction of apoptosis upon association with PA.

288 ation, can trigger transcription-independent induction of apoptosis upon mitotic aberrations.

289 of Lmo4 in nitroxidative conditions and the induction of apoptosis upon repression of Lmo4.

290 BID and BIM have nonoverlapping roles in the induction of apoptosis via BAK and BAX, affecting chemot

291 t that cellular levels of PPARgamma regulate induction of apoptosis via caspase-8 activation, whereas

292 Induction of apoptosis was caspase dependent, as it was

293 rimary epidermal keratinocytes, photodynamic induction of apoptosis was elicited by the combined acti

294 Induction of apoptosis was increased using a combination

295 Induction of apoptosis was observed in Cucurbitacin D tr

296 lation, profound cell growth inhibition with induction of apoptosis was observed in response to singl

297 served that, in clade B infected astrocytes, induction of apoptosis was significantly higher than in

298 ynthesis inhibition, cell cycle effects, and induction of apoptosis were determined for two character

299 or, significant reduction in cell viability, induction of apoptosis were observed when treated with a

300 These effects were due to striking induction of apoptosis, which was mediated by Bim upregu