ライフサイエンスコーパス: apoptosis induction

1 rface resulting in receptor crosslinking and apoptosis induction.

2 5 expression levels correlate with bystander apoptosis induction.

3 th the severity of colitis and the degree of apoptosis induction.

4 two organelles that critically contribute to apoptosis induction.

5 Fis1-Bap31 platform is an early event during apoptosis induction.

6 cessary for cleavage of caspase 3 and, thus, apoptosis induction.

7 link between ROS generation, autophagy, and apoptosis induction.

8 neuroprotectively to block S phase-dependent apoptosis induction.

9 AX have distinct mechanisms of action during apoptosis induction.

10 ells, in particular in response to extrinsic apoptosis induction.

11 ree culture model and was not accompanied by apoptosis induction.

12 proteins correlates with their potencies of apoptosis induction.

13 tained activation of JNK is critical for the apoptosis induction.

14 domain at lysine 120 as a critical event in apoptosis induction.

15 n (XIAP) plays a critical role in inhibiting apoptosis induction.

16 e in cells and isolated mitochondria and for apoptosis induction.

17 to growth inhibition in LNCaP cells through apoptosis induction.

18 sion and fusion also actively participate in apoptosis induction.

19 mpetitively inhibits FnE internalization and apoptosis induction.

20 c protein BAK and hinders BAK activation and apoptosis induction.

21 lar human telomerase inhibition activity and apoptosis induction.

22 a-7/IL-24 expression, growth inhibition, and apoptosis induction.

23 and in vivo by causing cell cycle arrest and apoptosis induction.

24 as associated with proteasome inhibition and apoptosis induction.

25 and in vivo by causing cell cycle arrest and apoptosis induction.

26 P-ribose) polymerase, which is indicative of apoptosis induction.

27 in repression, angiogenesis suppression, and apoptosis induction.

28 nvasive growth of 4T1 cells, and (f) lack of apoptosis induction.

29 -8, and caspase-9 were primarily involved in apoptosis induction.

30 gion as critical for the specificity in E2F1 apoptosis induction.

31 reovirus S1 and M2 genes as determinants of apoptosis induction.

32 sion (in androgen-dependent LNCaP cells) and apoptosis induction.

33 nking regions, with a potential role in E2F1 apoptosis induction.

34 spase-7 can be found in a cell-free model of apoptosis induction.

35 ancer cells is their increased resistance to apoptosis induction.

36 quence of targeting the MIZ-1 pathway during apoptosis induction.

37 mposition of oxidative stress and consequent apoptosis induction.

38 Rgamma), we studied the role of PPARgamma in apoptosis induction.

39 of caspase-8 activity significantly delayed apoptosis induction.

40 a heretofore unrecognized mediator of MDA-7 apoptosis induction.

41 a-7/IL-24 expression, growth inhibition, and apoptosis induction.

42 renders HCT116 cells completely resistant to apoptosis induction.

43 th virus replication, growth inhibition, and apoptosis induction.

44 xed complex formation as a means to regulate apoptosis induction.

45 on the expression of p53 target genes and on apoptosis induction.

46 gh inhibition of this pathway and consequent apoptosis induction.

47 te the molecular mechanism(s) accounting for apoptosis induction.

48 C1, leading to mitochondrial dysfunction and apoptosis induction.

49 compound-mediated cell growth inhibition and apoptosis induction.

50 d nonomers with an extremely high potency in apoptosis induction.

51 mplicated the transcription factor FoxO3a in apoptosis induction.

52 olysin contributes to both NO production and apoptosis induction.

53 spase-8 and caspase-10 to be responsible for apoptosis induction.

54 nctional gene groupings as being involved in apoptosis induction.

55 Fas and tumor necrosis factor (TNF)-alpha in apoptosis induction.

56 P < 0.025) providing biochemical evidence of apoptosis induction.

57 adation of survivin and cellular response to apoptosis induction.

58 ing dysregulation as a potential mediator of apoptosis induction.

59 se FA BM cells attenuates PKR activation and apoptosis induction.

60 Bcl-2 family members plays a crucial role in apoptosis induction.

61 ment, as did Bim mRNA, which correlated with apoptosis induction.

62 ults in full Bax toxicity even in absence of apoptosis induction.

63 ell growth arrest, mitochondrial damage, and apoptosis induction.

64 e speckles into smaller foci with subsequent apoptosis induction.

65 l-tubulin levels and inhibited CSC growth by apoptosis induction.

66 . application was calculated relative to its apoptosis induction.

67 nuated the protumorigenic activity of WT1 by apoptosis induction.

68 (48 h) effects on cell cycle distribution or apoptosis induction.

69 ucture intactness of Cyt c was essential for apoptosis induction.

70 to VDAC1 and the release of cytochrome c for apoptosis induction.

71 eotidases is the main factor responsible for apoptosis induction.

72 es RNA replication and Bax/Bak for efficient apoptosis induction.

73 maging method for longitudinal monitoring of apoptosis induction.

74 ere associated with differences in bystander apoptosis induction.

75 PUMA, or Noxa with either Bax or Bak during apoptosis induction.

76 levels of p53 induced by MDM2 inhibition in apoptosis induction.

77 f Stattic upon cell viability inhibition and apoptosis induction.

78 76 treatment in 4 MCL cell lines resulted in apoptosis induction.

79 fibroblasts were resistant to AATF-mediated apoptosis induction.

80 ce signal compared to control cells 4h after apoptosis induction.

81 Bax, and increase cytochrome c release upon apoptosis induction.

82 liferative activity, cell cycle effects, and apoptosis induction.

83 as associated with proteasome inhibition and apoptosis induction.

84 HSP60 represents a common phenomenon during apoptosis induction; 2) cytosolic HSP60 accumulation dur

85 Second, on apoptosis induction, a greater amount of Bax was translo

86 ecisive for the proliferation inhibition and apoptosis induction ability.

87 several levels, including cell cycle arrest, apoptosis induction, accelerated cellular repopulation,

88 rs, we generated a dosage-response curve for apoptosis induction after i.c. delivery of fluorescence-

89 was produced by phototoxicity, H2O2 and the apoptosis induction agent staurosporine.

90 chondria and traffics into the nucleus after apoptosis induction, although AnkG lacks a predicted nuc

91 lly located in the center of control tumors, apoptosis induction and a single i.t. injection of virus

92 Both apoptosis induction and activation of the transcription

93 the multidrug resistance, cytotoxicity, and apoptosis induction and antiapoptotic defense; and the a

94 mpounds were more effective than curcumin in apoptosis induction and cell cycle arrest at G1 phase.

95 eral mesothelioma cell lines, accompanied by apoptosis induction and decreased mitogen-activated prot

96 ligomerization increasing substantially upon apoptosis induction and inhibited by apoptosis blockers.

97 in guarding the integrity of the OMM against apoptosis induction and open possibilities for more spec

98 among others, are intrinsically resistant to apoptosis induction and poorly responsive to current the

99 cells, and this interaction was enhanced by apoptosis induction and preceded the Bax conformational

100 diately after cytochrome c release 6 h after apoptosis induction and then decreased, but it was gradu

101 ads to impaired responses of cancer cells to apoptosis induction and to poor prognosis in patients wi

102 distinct pathways activated by c-MYC during apoptosis induction and transformation is crucial to the

103 tion and inactivated CRLs, which resulted in apoptosis induction and tumor suppression.

104 stabilization for Gal-1 ligand recognition, apoptosis induction, and cytokine modulation in a variet

105 ing pathway connecting microtubule damage to apoptosis induction, and help to clarify some of the con

106 p1, in modulating cell cycle progression and apoptosis induction, and provides a new cancer therapeut

107 of Opa1 are extremely sensitive to exogenous apoptosis induction, and some die spontaneously by a pro

108 lengthy period of phosphorylation preceding apoptosis induction, and with dephosphorylation closely

109 not sufficient for robust TNFalpha-dependent apoptosis induction, and X-linked inhibitor of apoptosis

110 ation did not have any appreciable effect on apoptosis induction, angiogenesis, or natural killer and

111 ons were confirmed by independent assays for apoptosis induction (annexin V binding, cleavage of poly

112 lines through multiple mechanisms including apoptosis induction, antibody-dependent cellular cytotox

113 Prior to apoptosis induction archazolid led to the activation of

114 e VD3 compound-induced growth inhibition and apoptosis induction are at least partially dependent on

115 mation of a proapoptotic p53/BAK complex and apoptosis induction are impaired, both in cultured cells

116 nts leading to IP3-gated Ca2+ release during apoptosis induction are not known.

117 IM-induced cell proliferation inhibition and apoptosis induction are partly mediated through the down

118 hat B-DIM-induced cell growth inhibition and apoptosis induction are partly mediated through the regu

119 the functions of PKCalpha and PKCepsilon in apoptosis induction are redundant, such that either one

120 GL-induced growth inhibition correlated with apoptosis induction as evidenced by an increase in cytop

121 aB p65 activation is essential for 3-Cl-AHPC apoptosis induction as evidenced by the fact that inhibi

122 tural proteasome substrates p27 and Bax) and apoptosis induction (as shown by caspase activation and

123 nd Bax was followed by cell-cycle arrest and apoptosis induction, as shown by 5-bromo-2'-dUTP incorpo

124 The cytotoxic effects correlated with apoptosis induction, as was evidenced by increase of apo

125 nducer with EC(50) of 2 nM in our cell-based apoptosis induction assay.

126 imal compounds, 33 and 44, were effective in apoptosis induction at low micromolar concentrations irr

127 um (ER) and translocated to the nucleus upon apoptosis induction but prior to INDF manifestation, mak

128 rmined that these genes are not required for apoptosis induction but rather that their products play

129 R172P background; these mice have defects in apoptosis induction, but not cell cycle arrest.

130 ncer cells in culture and in vivo by causing apoptosis induction, but the sequence of events leading

131 enuated the protein level of Bcl-XL and that apoptosis induction by 2,3-DCPE could be blocked by enfo

132 , this decrease correlated with reduction in apoptosis induction by 4HPR.

133 tion has also been shown to be essential for apoptosis induction by a number of agents.

134 ed alone or on bone marrow stromal cells--to apoptosis induction by ABT-737, a molecule that releases

135 Moreover, we found that apoptosis induction by AITC depended entirely on mitotic

136 ling, including calcium signals that mediate apoptosis induction by anticancer drugs.

137 vitro, Taxol enhanced caspase activation and apoptosis induction by Apo2L/TRAIL.

138 Apoptosis induction by BH3 mimetics is a therapeutic str

139 Thus, apoptosis induction by CARP-1 involves sequestration of

140 PPARgamma inhibitor significantly diminished apoptosis induction by CDDO.

141 ocyte cultures also protected CLL cells from apoptosis induction by chlorambucil.

142 inal tissues were collected and analyzed for apoptosis induction by cleaved caspase 3 immunohistochem

143 Apoptosis induction by CSA and PSC-833 was measured by d

144 kinase Akt (PKB), and active Akt can nullify apoptosis induction by DAP3.

145 3 cells were significantly more resistant to apoptosis induction by DATS compared with vector-transfe

146 transcriptional network and contributing to apoptosis induction by DNA damage.

147 rcinoma A549 cells are markedly resistant to apoptosis induction by EGCG (even at 100 microm for 72 h

148 nterference rendered cells more sensitive to apoptosis induction by EGCG and classical prooxidants.

149 ed HO-1 overexpression confers resistance to apoptosis induction by EGCG; therefore, its inactivation

150 mine whether AMG655 possibly interferes with apoptosis induction by endogenous TRAIL, which could be

151 OS are required for FLIP down-regulation and apoptosis induction by Fas ligand (FasL) in primary lung

152 fectively inhibited FLIP down-regulation and apoptosis induction by FasL.

153 cl-x(L) overexpression, effectively inhibits apoptosis induction by hPNPase(old-35).

154 rase-mediated nick-end labeling positive) to apoptosis induction by IFN-alpha2 and IFN-beta (ACHN, SK

155 verexpression of XAF1 overcame resistance to apoptosis induction by IFN-beta.

156 Postulating that genes important for apoptosis induction by IFNs might be silenced by methyla

157 transferase 1 (DNMT1) overcame resistance to apoptosis induction by IFNs with up to 85% apoptotic cel

158 Resistance to antiproliferative effects and apoptosis induction by interferons (IFNs) was postulated

159 reactive oxygen species (ROS) generation in apoptosis induction by isothiocyanates (ITCs).

160 dose when compared with what is required for apoptosis induction by itself.

161 se to replication stress, a major pathway of apoptosis induction by many chemotherapeutic agents.

162 Additionally, radiation augments apoptosis induction by mda-7/IL-24 in parental and neomy

163 ection, association with sigma3 may regulate apoptosis induction by micro1.

164 ight be an important transcription factor in apoptosis induction by MSA.

165 f DeltapsiM and increased [Ca(2+)](i) during apoptosis induction by neferine with increased expressio

166 ken together, we report a novel mechanism of apoptosis induction by PAR-4/ceramide-enriched exosomes,

167 Apoptosis induction by PPARgamma ligands may be importan

168 To do so, we tested how AMG655 affected apoptosis induction by recombinant TRAIL.

169 ors of reovirus replication demonstrate that apoptosis induction by reovirus requires viral disassemb

170 igated its contribution in growth arrest and apoptosis induction by SFN using HL60 and K562 human leu

171 inoid receptor antagonists failed to prevent apoptosis induction by SHetA2.

172 xicity, oxidative stress induced by H2O2 and apoptosis induction by staurosporine was characterised i

173 members Bax and Bak play a critical role in apoptosis induction by sulforaphane.

174 cer cells by small interfering RNA abrogates apoptosis induction by the inhibitor of NF-kappaB and bl

175 Determinants of differentiation and apoptosis induction by the novel histone deacetylase inh

176 We examined the mechanisms of apoptosis induction by the novel synthetic triterpenoid

177 Apoptosis induction by this combinatorial treatment was

178 ibution of individual p53-regulated genes to apoptosis induction by this protein, whereas in this rev

179 d perform biological functions, evidenced by apoptosis induction by transported cytochrome c.

180 -xL overexpression protects LNCaP cells from apoptosis induction by troglitazone and Delta2-TG in an

181 (PPARgamma-deficient) cells are sensitive to apoptosis induction by troglitazone and its PPARgamma-in

182 okine signaling pathway might be involved in apoptosis induction by VES and MSA, respectively.

183 This hypoxia-specific apoptosis induction by YC-1 involved excessive reactive

184 bition on RNA levels and protein expression, apoptosis induction, caspase activation and lymphocyte p

185 a novel role for this GTP-binding protein in apoptosis induction caused by cell detachment.

186 breast cancer cell viability correlated with apoptosis induction characterized by DNA condensation, c

187 proliferation (Ki-67 staining; p < 0.03) and apoptosis induction (cleaved Caspase-3 staining; p < 0.0

188 oteasome inhibition, growth suppression, and apoptosis induction, compared with cells treated with na

189 Apoptosis induction contributed to the observed antiprol

190 Apoptosis induction correlated with increased cellular r

191 vered i.v. reached the brain tumor, but that apoptosis induction declined quickly within 24 hours.

192 mation and melanoma growth via senescence or apoptosis induction depending on the RB and p53 pathway

193 The apoptosis induction due to As2O3 treatment of LNCaP cell

194 vity has primarily been linked to defects in apoptosis induction during central tolerance.

195 Moreover, the apoptosis induction elicited by specific inhibitors (PP2

196 ty, and G(1) arrest, ultimately resulting in apoptosis induction, events consistent with potent NF-ka

197 However, as we show here, Tat apoptosis induction fails in PBMCs cultured at physiolog

198 N1A, also known as p21(WAF1/CIP1)) increases apoptosis induction following telomerase inhibition in a

199 onal phosphatases, especially their powerful apoptosis induction function.

200 This inhibition resulted in apoptosis induction, G(2)-M arrest, polyploidy cells, an

201 ytochrome c, released from mitochondria upon apoptosis induction, gradually accumulates in the nucleu

202 ct on the normal cell cycle distribution and apoptosis induction in a human breast tumor cell line.

203 poietic cells deprived of IL-3, resulting in apoptosis induction in a variety of hematopoietic cells

204 mall interfering RNA (Akt3 siRNA) to analyze apoptosis induction in Akt1 and Akt2 double knock-out mo

205 her levels of proteasome target proteins and apoptosis induction in breast cancer cells.

206 n of ectopic Par-4 or its SAC (selective for apoptosis induction in cancer cells) domain, which induc

207 inflammasome activation in myeloid cells and apoptosis induction in cancer cells.

208 creased p53 levels was supported by enhanced apoptosis induction in cells cotreated with Nutlin-3a an

209 ed activation of JNK1/2, but not ERK1/2, and apoptosis induction in DU145 cells suggesting involvemen

210 n also decreases both cell proliferation and apoptosis induction in functional assays.

211 The results of apoptosis induction in human Burkitt's B-cell non-Hodgki

212 tion and cytokinesis, growth inhibition, and apoptosis induction in human cancer cell lines.

213 suggest a hierarchical model of 2ME-related apoptosis induction in human leukemia cells in which 2ME

214 This represents the first description of apoptosis induction in infected cells triggered as a res

215 hosphorylation of histones H2B and H2AX, and apoptosis induction in K-ras-transformed cells.

216 In contrast, the rapid kinetics of apoptosis induction in monocytic THP-1 cells correlated

217 chemotherapeutics revealed high potency for apoptosis induction in neuroblastoma cells, etoposide wa

218 in vitro evidence linking ZIKV infection and apoptosis induction in neurons and progenitors to microc

219 this study, we investigated p53 protein and apoptosis induction in PLHC-1 (desert topminnow hepatoce

220 We recently demonstrated that apoptosis induction in primary human cells strictly requ

221 onsistently, this effect was associated with apoptosis induction in prostate cancer cells.

222 ) and bcl-2 prevents these changes including apoptosis induction in prostate tumor cells by Ad.mda-7.

223 detailed structure of the nanoconjugates and apoptosis induction in Raji cells to allow system optimi

224 expression cassette altered the kinetics of apoptosis induction in recombinant MVA-infected cells to

225 two mechanistically distinct pathways of DC apoptosis induction in response to an extracellular bact

226 the ubiquitin-proteasome system, facilitates apoptosis induction in response to cellular stress.

227 itor of caspase-12 activation, did not delay apoptosis induction in rM51R-M virus-infected L929 cells

228 ncluding the role of caspase-2 activation in apoptosis induction in the BxPC-3 human pancreatic carci

229 , with IC(50) values in PDK-1 inhibition and apoptosis induction in the low microM range.

230 s of IVIG and RAPA on cell proliferation and apoptosis induction in the MLR.

231 from LMP2A transgenic mice were sensitive to apoptosis induction in the presence of specific inhibito

232 pulates the CD4(+)-lymphocyte cell cycle and apoptosis induction in the progressive CD4(+)-lymphocyte

233 e efficacy of chemotherapy, led to amplified apoptosis induction in the tumor, and minimized the side

234 modification of Top2alpha may contribute to apoptosis induction in transformed cells by ITCs.

235 of the disease was associated with increased apoptosis induction in transgenic T cells and decreased

236 e inhibition, proliferation suppression, and apoptosis induction in tumor tissues.

237 ted with increased proteasome inhibition and apoptosis induction in tumor tissues.

238 Growth suppression and apoptosis induction in tumor xenografts in vivo by oral

239 ide-engineered CAFs were highly sensitive to apoptosis induction in vitro and in vivo by the addition

240 point mutants of p53, resulting in efficient apoptosis induction in vitro and in vivo in mice.

241 from Hmgb2(-/-) mice are more susceptible to apoptosis induction in vitro.

242 TM disrupt trimerization in vitro and reduce apoptosis induction in vivo, indicating the essential ro

243 iated with proteasome inhibition and massive apoptosis induction in vivo.

244 r data support a model whereby the degree of apoptosis induction is regulated by the conformation of

245 However, apoptosis induction is significant only when more than 8

246 er, we found that the key commitment step in apoptosis induction is the ability of E2F1, and not E2F2

247 pically expressed, however, the mechanism of apoptosis induction is unclear.

248 The mechanism of apoptosis induction is unknown.

249 hocytes, but the dependency of PPARgamma for apoptosis induction is unknown.

250 of OT-1 CTL with target cells and increased apoptosis induction lasting up to six days postadoptive

251 However, apoptosis induction may not depend on the receptor, beca

252 Strikingly, apoptosis induction occurred predominantly in uninfected

253 This apoptosis induction occurs through the recruitment by th

254 cascade, thereby lowering thresholds for the apoptosis induction of glioma cells.

255 Third, the apoptosis induction of maspin-transfected cells was asso

256 ions related to tumorigenesis, one involving apoptosis induction of normal hematopoietic cells and th

257 this study, we investigated the mechanism of apoptosis induction of obatoclax (GX15-070), a novel Bcl

258 t Cks proteins are important determinants of apoptosis induction of replication stress-inducing chemo

259 including inhibition of IAPs (inhibitors of apoptosis); induction of IAP degradation; inhibition of

260 ing arrest of proliferation without inducing apoptosis, induction of a neuronal morphology, upregulat

261 n species (ROS), induction of DNA damage and apoptosis, induction of DNA damage repair pathways and R

262 l differences were noted in MDM2 expression, apoptosis, induction of or recovery from mitotic blockag

263 tiple antitumor effects including oncolysis, apoptosis, induction of T-cell responses, and upregulati

264 Which property of RASSF1A, apoptosis induction or microtubule regulation, is respon

265 ysis of the growth inhibitory properties and apoptosis induction potentials of tyrosine kinase inhibi

266 g by cells overexpressing BCL-xL even before apoptosis induction raise interesting questions as to th

267 ut the link between pneumococcal killing and apoptosis induction remains undefined.

268 However, apoptosis induction requires high doses of ligands, sugg

269 revention and therapy, is thought to act via apoptosis induction resulting from increased reactive ox

270 The mechanism of apoptosis induction results from the capacity of human T

271 benzodithiophenes (i.e., differentiation and apoptosis induction) support further development of thes

272 SCs are more sensitive to all three types of apoptosis induction than are lineage-non-specific, retin

273 vy metal ions play a role in determining the apoptosis induction threshold of the inflammatory respon

274 77, leading to the accumulation of Nur77 for apoptosis induction triggered by cisplatin.

275 ded protein response and dramatically lowers apoptosis induction typically associated with ERAD inhib

276 by generation of reactive oxygen species and apoptosis induction under conditions of oxidative stress

277 that VDAC1 also exists as a dimer that upon apoptosis induction undergoes conformational changes and

278 Apoptosis induction (up to 14- to 17-fold in both cell l

279 come by BCL2 overexpression, suggesting that apoptosis induction upon lymphocyte activation limits ce

280 CD28(null) T cells in ACS were resistant to apoptosis induction via Fas-ligation or ceramide.

281 Here, we report a nonnuclear role for pRB in apoptosis induction via pRB's direct participation in mi

282 First, apoptosis induction was accompanied by changes in expres

283 uman cancer cells through apoptosis; nuclear apoptosis induction was accompanied by G0/G1 phase arres

284 First, apoptosis induction was accompanied by the upregulation

285 Apoptosis induction was also independent of B-cell lymph

286 Sensitivity of T cells to apoptosis induction was analyzed in vitro following stim

287 induced apoptosis in FLT3 mutant AML cells, apoptosis induction was diminished under stromal cocultu

288 Apoptosis induction was found to be more profound with t

289 Apoptosis induction was preceded by an initial phase of

290 d cytoplasmic TR3 translocation required for apoptosis induction was regulated by JNK activation and

291 ompound 2-mediated proteasome inhibition and apoptosis induction were completely blocked by addition

292 wth, proliferation, mitogenic signaling, and apoptosis induction were observed in vivo.

293 n association with Mcl-1 down-regulation and apoptosis induction, whereas agents administered individ

294 midine incorporation resulted primarily from apoptosis induction, whereas at lower concentrations, th

295 internalization is known to be essential for apoptosis induction, whereas survival signaling is initi

296 ss-cleavage of precursor dimers, formed upon apoptosis induction, which are not only enzymatically co

297 -(2-phenylpropyl)thioanalogue 4c showed huge apoptosis induction, while some sulfinyl and sulfonyl de

298 e has provided new tools to target cells for apoptosis induction with temporal and spatial control.

299 assembly of VDAC1 was shown to be coupled to apoptosis induction, with oligomerization increasing sub

300 ontoxic compound DSF, resulting in selective apoptosis induction within tumor cells.