ライフサイエンスコーパス: apoptosis by

1 Interestingly, apoptosis by 0.3 microg/mL ADI-PEG20 occurs 96 hours pos

2 rrest by 24 hours, and caspase induction and apoptosis by 40 hours postinfection.

3 f rosiglitazone reduced oxidized LDL-induced apoptosis by 40% and neutralizing antibody to IGF-1R (al

4 ed Bcl-2 expression, indicating induction of apoptosis by 48 hours after SP treatment.

5 nly avian viruses caused early and extensive apoptosis (by 6 h of infection) resulting in reduced vir

6 nine aminotransferase release, necrosis, and apoptosis by 70%, 100%, and 42%, respectively.

7 smic reticulum (ER) stress causes INS-1 cell apoptosis by a Ca(2+)-independent phospholipase A(2) (iP

8 er of regulation of cell differentiation and apoptosis by a lncRNA.

9 companied by a dramatic increase in myoblast apoptosis by a loss of p21 protein.

10 In contrast, Cdt holotoxin induced apoptosis by a mechanism independent of caspase- and apo

11 GDC-0623 plus ABT-263 induced a synergistic apoptosis by a mechanism that includes release of BIM fr

12 ly affect AcMNPV replication or induction of apoptosis by a mutant of AcMNPV lacking the antiapoptoti

13 Blockade of apoptosis by a pan-caspase inhibitor or by simvastatin s

14 emonstrates that AAT can regulate neutrophil apoptosis by a previously unidentified and novel mechani

15 eta) phagocytosis and have low resistance to apoptosis by Abeta.

16 f human neuroblastoma to doxorubicin-induced apoptosis by acting as a p53 phosphatase to downregulate

17 omising chemotherapeutic agent that promotes apoptosis by acting as a selective BH3 mimetic to neutra

18 et interconnected signaling pathways control apoptosis by activating a core intracellular machinery o

19 Bid is a Bcl-2 family protein that promotes apoptosis by activating Bax and eliciting mitochondrial

20 Furthermore, 8 induces apoptosis by activating caspase 3/7 and PARP cleavage, a

21 els of ALIX and ALG-2 are required to elicit apoptosis by activating ER stress-associated caspase 4/1

22 these cells protected them from PALA-induced apoptosis by activating p21, sustaining the expression o

23 ssed by renal epithelial cells, and triggers apoptosis by activating the apoptotic factor Bax.

24 -SDT mediates the switch from necroptosis to apoptosis by activating the caspase-3 and caspase-8 path

25 umor necrosis factor cytokine family-induces apoptosis by activating the extrinsic pathway through th

26 17beta-estradiol protects osteocytes against apoptosis by activating the NO/cGMP/PKG cascade; PKG II

27 ic NMDA-mediated neuritic bead formation and apoptosis by activating the phosphatidylinositol 3-kinas

28 Netrin-1 regulates cell survival and apoptosis by activation of its receptors, including UNC5

29 doplasmic reticulum (ER) stress and triggers apoptosis by activation of the unfolded-protein-response

30 AMPK, making them resistant to induction of apoptosis by adenosine 3',5'-cyclic monophosphate activa

31 hase, caffeine reduced oxygen-induced neural apoptosis by adenosine A2A receptor (A2AR)-dependent mec

32 and constitutively suppresses JNK1-mediated apoptosis by affecting expression of poly(ADP-ribose) po

33 ess response proteins, ATF-6, and subsequent apoptosis by alterations of CerS6/C(16)-ceramide.

34 The tumor suppressor p53 induces apoptosis by altering the transcription of pro-apoptotic

35 Depletion of zinc intracellularly leads to apoptosis by an unknown mechanism.

36 We interrogated E(2)-induced apoptosis by analysis of gene expression across time (2-

37 aluated cell survival by a clonogenic assay; apoptosis by Annexin V immunofluorescence; gammaH2AX, Ra

38 ected with miR-K10a showed less induction of apoptosis by annexin V staining and terminal deoxynucleo

39 been shown to induce myocyte detachment and apoptosis by anoikis through down-regulation of focal ad

40 The BCL-2 family member Noxa induces apoptosis by antagonizing the prosurvival protein MCL-1.

41 at 200muM at 48h confirmed the induction of apoptosis by apigenin and quercetagetin.

42 us background showed extensive renal tubular apoptosis by approximately 10 weeks of age in both male

43 Moreover, cells induced to undergo apoptosis by arsenite show increased R-CRT on their cell

44 ectably and became sensitive to Fas-mediated apoptosis by as early as day 1-2.

45 ction, might function redundantly to promote apoptosis by associating with Bcl-2 and exposing its pot

46 as been linked to such disorders and induces apoptosis by assuming an open-like conformation.

47 ysis protects keratinocytes from UVB-induced apoptosis by attenuating Cer levels.

48 om spontaneous and chemotherapy drug-induced apoptosis by attenuating the activation and cleavage of

49 ism in which nitric oxide prevents beta-cell apoptosis by attenuating the DNA damage response (DDR).

50 Synergistic induction of apoptosis by AZD8055 and ABT-737 is confirmed on the mol

51 a systems study of the intrinsic pathway of apoptosis by BCL2 family proteins and clinical translati

52 breakdown product that amplifies lymphocyte apoptosis by being phosphorylated to deoxyadenosine trip

53 /-) MEFs could be rescued from l-Hcy-induced apoptosis by beta-mercaptoethanol medium supplementation

54 n of Bcl-2 protects against Ca(2+)-dependent apoptosis by binding and inhibiting IP3Rs, although the

55 a pro-survival molecule, is known to inhibit apoptosis by binding and inhibiting p53, but its role in

56 er mitochondrial membrane, where it inhibits apoptosis by binding Bax and inhibiting Bax-induced oute

57 BCL2 suppresses apoptosis by binding the BH3 domain of proapoptotic fact

58 of ribonucleotide reductase (RR) to suppress apoptosis by binding to and blocking caspase-8.

59 pro-survival molecule, inhibits p53-induced apoptosis by binding to the sequence-specific DNA-bindin

60 Interestingly, extracellular Par-4 induced apoptosis by binding to the stress response protein, glu

61 In these cells, IL-6 prevented apoptosis by blocking caspase-3 and -7 activation throug

62 s validate that the nucleoside analog causes apoptosis by blocking cell cycle progression at G2/M.

63 RACK1 also induces apoptosis by blocking Src activation of the Akt cell sur

64 ather inhibits the capacity of Fas to induce apoptosis by blocking the association of FADD with Fas c

65 hat in the pluripotent epiblast they inhibit apoptosis by blocking the expression of the proapoptotic

66 e for the activation of JNK and induction of apoptosis by both agents.

67 target, is therefore required for efficient apoptosis by both caspase-independent and caspase-depend

68 nexin A5-CCPM allowed visualization of tumor apoptosis by both nuclear and optical techniques.

69 nism for the induction of DNA damage-induced apoptosis by c-Abl and illustrate network interactions b

70 otective autophagy in SPP1-depleted cells to apoptosis by calpain-mediated Atg5 cleavage.

71 ariants regulate death receptor (DR)-induced apoptosis by CASP8, the specific role of each isoform is

72 nal kinase activation, leading to hepatocyte apoptosis by caspase-8, caspase-3, and p21-activated kin

73 egulates TNFalpha-induced JNK activation and apoptosis by catalyzing the polyubiquitination of Miz1.

74 loss of PMCA2 expression at weaning triggers apoptosis by causing cellular calcium crisis.

75 anistically, regulation of ER-stress-induced apoptosis by CerS6/C(16)-ceramide was linked to the acti

76 ic apoptosis by death receptors or intrinsic apoptosis by chemotherapeutic agents.

77 y, SirT1 inhibition also sensitizes cells to apoptosis by chemotherapy drugs.

78 6-positive cervical cancer cell line SiHa to apoptosis by cisplatin, irradiation, recombinant human t

79 ponse to HGF but rendered cells resistant to apoptosis by cisplatin.

80 e the annexin V staining or the induction of apoptosis by Class II AMPs.

81 Additionally, MMP-7 promotes VSMC apoptosis by cleavage of N-cadherin.

82 Increased apoptosis by cleaved caspase-3 (P = 0.03) and decreased

83 ence, and Western blot were used to validate apoptosis by cleaved caspase-3, proliferation by Ki67, a

84 uman GzmB preferentially induces target cell apoptosis by cleaving the proapoptotic Bcl-2 family memb

85 n in the prevention of intestinal epithelial apoptosis by commensal bacteria.

86 c-FLIP can inhibit death receptor-mediated apoptosis by competing with caspase-8 for recruitment to

87 ng OSI-027-treatment and the potentiation of apoptosis by concomitant inhibition of such autophagy.

88 aimed at maximal activation of p53-mediated apoptosis by concomitant MDM2 and CRM1 inhibition.

89 blocks the hyperfusion response and leads to apoptosis by converting mTOR inhibitor action from cytos

90 re, we determined that syndecan-1 attenuated apoptosis by crosstalking with c-Met to potentiate its c

91 wth arrest, the induction of p53-independent apoptosis by D4476 suggested a critical role for the MDM

92 c CD8 T cells by day 7, followed by dramatic apoptosis by day 14.

93 rid screen, we cloned a factor that mediates apoptosis by DD1 and refer to this factor as DD1-interac

94 cells in response to induction of extrinsic apoptosis by death receptors or intrinsic apoptosis by c

95 that XIAP inhibition potentiates p53-induced apoptosis by decreasing p53-induced p21 and that p53 act

96 Overexpression of miR-29a/b/c also promoted apoptosis by decreasing the level of the antiapoptotic p

97 cl-2, selectively targets VDAC1 and inhibits apoptosis by decreasing VDAC1-mediated Ca(2+) uptake int

98 been reported to stimulate TNF-alpha-induced apoptosis by degradation of cellular IAP (cIAP)-1/2, we

99 dual role in breast cancer cell invasion and apoptosis by demethylating histone and the non-histone p

100 cose deprivation and Cdk5 inhibition promote apoptosis by dephosphorylating Noxa.

101 of drugs preferentially triggers tumor cell apoptosis by depleting mevalonate pathway metabolites fa

102 APs) were originally described as regulating apoptosis by direct binding to caspases.

103 Many viral polypeptides modulate apoptosis by direct interaction with highly conserved ap

104 duced p53 activation and resveratrol-induced apoptosis by direct targeting of G3BP1.

105 c signal that inhibits Xenopus laevis oocyte apoptosis by directly activating CaMKII.

106 ARC blocked hepatocyte apoptosis by directly interacting with members of the de

107 ouse gzmB is thought to predominantly induce apoptosis by directly processing pro-caspase-3.

108 these miRNAs down-regulate GRP78 and induce apoptosis by directly targeting its 3' untranslated regi

109 mir-200 abrogated KRAS-induced resistance to apoptosis by directly targeting the antiapoptotic gene B

110 ives leukemic cells into differentiation and apoptosis by dislodging from the osteogenic niche.

111 nhibition by shRNA sensitized tumor cells to apoptosis by DNA damage, resulting in caspase-3 and PARP

112 oapoptotic target genes and the induction of apoptosis by DNA-damaging agents.

113 idant enzyme genes, and enhancing epithelium apoptosis by down-regulating Bcl-2.

114 ) myoblasts display remarkable resistance to apoptosis by down-regulation of miR-1 (microRNA-1) and m

115 , revealing that it can block PAR-4-mediated apoptosis by downregulating trafficking of the PAR-4 rec

116 ficant caspase3/7 activity upon induction of apoptosis by doxorubicin.

117 ion markedly sensitized human fibroblasts to apoptosis by doxorubicin.

118 nd quantitatively evaluated the induction of apoptosis by drug combination therapies.

119 sequestration of Bim, a direct activator of apoptosis, by either Bcl-2 or Mcl-1, providing a surviva

120 in tumors, which not only induced tumor cell apoptosis by elevated oxidation stress but also served a

121 ant role in protecting invading T cells from apoptosis by elevating activity of the PI3K-Akt signalin

122 wound repair, synergize with FasL to induce apoptosis by elevating cellular levels of reactive oxyge

123 ged innate immune response signaling induces apoptosis by eliciting Noxa expression in reovirus-infec

124 ne attack (beta-cell homicide) and beta-cell apoptosis by endoplasmic reticulum stress (beta-cell sui

125 ever, the immature pro-neurotrophins promote apoptosis by engaging in a complex with sortilin and the

126 The induction of apoptosis by ErPC3 requires TSPO, a mitochondrial membra

127 gastric epithelial cells induced to undergo apoptosis by exposure to live H. pylori to study apoptot

128 animals are highly resistant to induction of apoptosis by expression of IAP-antagonists, DNA-damaging

129 surface, thereby sensitizing cancer cells to apoptosis by extracellular PAR-4 or GRP78 agonistic anti

130 Induced-apoptosis by F-I on MDA-MB-435 was confirmed by Tunnel n

131 on of TGF-beta, (ii) the promotion of T-cell apoptosis by Fas-Fas ligand or granzyme-B pathways, and

132 investigated cancer cell lines, induction of apoptosis by FasL or DR5 agonist antibody can be inhibit

133 mblies were shown to contribute to beta-cell apoptosis by forming discrete pores that destabilize the

134 ts RIPK3-dependent necrosis without inducing apoptosis by functioning in a proteolytically active com

135 ion of the previously reported regulation of apoptosis by Gene 33 via the c-Abl/p73 pathway.

136 Interestingly, inhibiting apoptosis by genetic ablation of TNFr1 significantly inc

137 null genotype increased their sensitivity to apoptosis by genotoxic agents.

138 e present study indicates that ROS-dependent apoptosis by GL is regulated by JNK signaling axis.

139 After induction of apoptosis by H. pylori or camptothecin, there was a 5-fo

140 l-2-ERK complex, as well as the induction of apoptosis by H2O2.

141 astrocytes against oxidative stress-induced apoptosis by improving metabolism functioning, particula

142 nds to CED-9, suggesting that DRE-1 promotes apoptosis by inactivating CED-9.

143 nherent genetic damage, but avoid arrest and apoptosis by inactivating p53.

144 endent proliferation and become resistant to apoptosis by inactivating the Hippo signaling pathway, r

145 1 (CAV1) on Tyr-14 facilitates mitochondrial apoptosis by increasing BCL2 phosphorylation in response

146 a suggest that cocaine induces CD4(+) T-cell apoptosis by increasing intracellular reactive oxygen sp

147 Moreover, oxamate induced GH3 cell apoptosis by increasing mitochondrial reactive oxygen sp

148 Bit-1 expression protected cells from apoptosis by increasing phospho-IkappaB levels and subse

149 te cancer cells, we found that ERbeta causes apoptosis by increasing the expression of pro-apoptotic

150 e activation of the mitochondrial pathway of apoptosis by indomethacin.

151 f c-mip in differentiated podocytes promotes apoptosis by inducing caspase-3 activity and up-regulati

152 cancer tumorigenesis and protects cells from apoptosis by inducing prosurvival targets, it was hypoth

153 nduced phosphorylation of eIF2alpha promotes apoptosis by inducing the cytoplasmic accumulation of hn

154 AFF (rBAFF) rescues B cells from CSE-induced apoptosis by inhibiting activation of nuclear factor-kap

155 ncreased superoxide products and endothelial apoptosis by inhibiting AngII-induced Kynurenines genera

156 g that E. faecalis protects macrophages from apoptosis by inhibiting caspase 3 activation.

157 rprisingly, rBAFF blocked CSE-induced B-cell apoptosis by inhibiting CSE-induced NF-kappaB activation

158 eting rat pitutitary adenoma cell lines from apoptosis by inhibiting cytochrome c release from mitoch

159 data indicated HGF abrogated Ang II-induced apoptosis by inhibiting cytochrome c release, caspase-3

160 demonstrates that each gold-indole enhances apoptosis by inhibiting DNA repair.

161 , we found that CQ induced blood cancer cell apoptosis by inhibiting histone deacetylases (HDACs).

162 usceptibility or resistance to TRAIL-induced apoptosis by inhibiting key functional proteins.

163 roup that sensitized hypoxic cancer cells to apoptosis by inhibiting the kinases GSK-3beta and cyclin

164 moted reactive oxygen species production and apoptosis by inhibiting thioredoxin.

165 oid deposition and thereby reduces beta-cell apoptosis, by inhibiting fibril formation.

166 lpha expression and prevention of hepatocyte apoptosis by inhibition of both death receptor and mitoc

167 howed that blunting autophagy and augmenting apoptosis by inhibition of eEF-2 kinase could modulate t

168 and were sensitized to plasminogen-mediated apoptosis by inhibition of SPARC or beta-catenin.

169 these results indicate that TnBVANK1 induces apoptosis by interacting with Alix, suggesting a role of

170 acellular Par-4 induces cancer cell-specific apoptosis by interaction with the cell-surface receptor

171 r necrosis factor alpha (TNFalpha)-initiated apoptosis by interfacing with the NF-kappaB signaling pa

172 nfected cells against death receptor-induced apoptosis by interfering with caspase 8/FLICE activation

173 note on the assay in studying mechanisms of apoptosis by ITCs and other electrophilic and thiol-reac

174 additive effect with AG1478 but also induced apoptosis by itself.

175 Inhibition of anti-IgM-induced apoptosis by K13 may contribute to the development of KS

176 also attenuated the oxidative stress-induced apoptosis by knockdown of PP2A/Calpha and increased the

177 ium-dependent vasorelaxation, and attenuated apoptosis by limiting cytochrome c release, caspase 3 ac

178 esting that STAT3 might protect T-cells from apoptosis by limiting their production of IL-2 through u

179 a caspase substrate whose cleavage promotes apoptosis by limiting, in a target-specific fashion, its

180 lar granule neurons (CGNs) primed to undergo apoptosis by low potassium treatment, expression of HDAC

181 Exosomal TAR RNA down-regulated apoptosis by lowering Bim and Cdk9 proteins in recipient

182 Suppression of SMC apoptosis by maintenance of nuclear GAPDH/Ape1 interacti

183 hanism of ER stress-induced cancer-selective apoptosis by mda-7/IL-24.

184 ation and induction of cell cycle arrest and apoptosis by mechanisms independent of p53.

185 Notably, ILC3 could be induced to undergo apoptosis by microbial products through the TLR2 (lipote

186 destruction motif inhibits the induction of apoptosis by microtubule poisons.

187 We propose that modulation of apoptosis by miRNAs may determine congenital nephron end

188 1 depletion lead to increases in spontaneous apoptosis by mitochondria-mediated intrinsic mechanism a

189 pression of genes involved in senescence and apoptosis by modulating chromatin structure.

190 e phosphorylation (OXPHOS) in cancer inhibit apoptosis by modulating ROS production and cellular sign

191 f this study was to explore the induction of apoptosis by MTX.

192 Here, we show that induction of apoptosis by Myc in breast epithelial cells requires ass

193 which can be converted to active full-blown apoptosis by navitoclax or ABT-199 for therapeutic benef

194 Protection from TLR4-induced enterocyte apoptosis by NOD2 required a novel pathway linking NOD2

195 with these nanoparticles in vitro triggered apoptosis by NuBCP-9-mediated mechanism, with a potency

196 Induction of apoptosis by OSI-027 appears to negatively correlate wit

197 ytic activity, Skp2 also blocks p53-mediated apoptosis by outcompeting p53 for binding p300.

198 Genetically blocking apoptosis by over-expressing BCL2 ameliorates muscle wea

199 Inhibiting apoptosis by overexpression of antiapoptotic proteins Bc

200 Here, we describe an induction of apoptosis by p21 in sarcoma cell lines that is p53-indep

201 the downregulation of EGFR and induction of apoptosis by p73 in HNSCC cells.

202 gulation of p53 subcellular localization and apoptosis by PARC as a contributing factor in CDDP resis

203 tion of normal cells, such as suppression of apoptosis by pharmacological inhibition of p53 or activa

204 at Mst1 coordinately regulates autophagy and apoptosis by phosphorylating Beclin1 and consequently mo

205 On the other hand, the induction of apoptosis by PIK-75 did not require the expression of th

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

207 + cells, and protected oligodendrocytes from apoptosis by preventing decreases in Gli2 and Bcl-2 expr

208 ates that in melanoma cell lines, CQ induces apoptosis by preventing degradation of the pro-apoptotic

209 ecifically interacts with Bcl-2 and promotes apoptosis by preventing the formation of protective Bcl-

210 augmented BMP signaling induces p53-mediated apoptosis by prevention of p53 degradation in developing

211 molar quantities) during the early stages of apoptosis by primary thymocytes and cell lines.

212 These results suggest that TWEAK triggers apoptosis by promoting assembly of a RIP1-FADD-caspse-8

213 metabolic stress, and that TAT-p27 inhibits apoptosis by promoting autophagy in glucose-deprived car

214 the pro-apoptotic proteins, tBid, can induce apoptosis by promoting Bax activation, Bax homo-oligomer

215 ondrial translocation of p53 and spontaneous apoptosis by promoting K63-linked ubiquitination of p53

216 ted with DLE-HuM195 induce rapid target cell apoptosis by promoting simultaneous conjugates to multip

217 ents retinal capillary cells from undergoing apoptosis by protecting mitochondrial ultrastructure and

218 demonstrated that cytosolic HMGB1 regulates apoptosis by protecting the autophagy proteins beclin 1

219 ytokine with anti-tumor potential, initiates apoptosis by re-organizing TRAIL receptors into large cl

220 nsitized chemoresistant PaC cells to undergo apoptosis by recombinant TRAIL.

221 ctase (hBVR), a Ser/Thr/Tyr kinase, inhibits apoptosis by reducing biliverdin-IX to antioxidant bilir

222 t inhibition of Met kinase activity, induced apoptosis by reducing integrin alpha3beta1 levels, activ

223 rtain Cl(-) channels are proposed to promote apoptosis by reducing intracellular pH, we tested whethe

224 vastatin (1) prevented CM-induced renal cell apoptosis by reducing stress kinases activation and (2)

225 R-34a indicates that miR-34a may be inducing apoptosis by reducing the levels of anti-apoptotic prote

226 and suggest that NPM may protect cells from apoptosis by reducing the mitochondrial level of p53.

227 and reducing Bcl-2, but otherwise inhibiting apoptosis by reduction of caspase-3 and cytochrome c.

228 e relevant in vivo, for example, in blocking apoptosis by reduction of ferric cytochrome c, and gentl

229 ant cells to DNA damage and the induction of apoptosis by regulating activity of the TP53 signaling p

230 out to assess whether isoflurane can induce apoptosis by regulating Bcl-2 family proteins, enhancing

231 tion by d-flow induces endothelial cell (EC) apoptosis by regulating p53.

232 Our results show that bortezomib induces apoptosis by regulating pathways that are mechanisticall

233 estigated the possibility that Rheb controls apoptosis by regulating the interaction of FKBP38 with B

234 ast, selective inhibition of Rac induces CGN apoptosis by repressing unique MEK5/ERK5, p90Rsk, and Ak

235 The induction of apoptosis by RNAi-mediated depletion or pharmacologic in

236 atal day 7 rat pups prevents ethanol-induced apoptosis by scavenging reactive oxygen species in the e

237 1 potently suppresses lung tumour growth via apoptosis by selectively activating Bax in vivo without

238 horylation during hypertonic stress promotes apoptosis by sequestration of specific mRNAs in SGs in a

239 YAP-dependent necrosis and p73/YAP-dependent apoptosis by shifting the interaction partner of YAP fro

240 nized link between metabolism and Drosophila apoptosis by showing that cellular NADPH levels modulate

241 Induction of apoptosis by SHP activation inhibits peritoneal pancreat

242 oxvirus genera, encode inhibitors that block apoptosis by simultaneously binding the proapoptotic Bcl

243 cellular p53 and attenuation of p53-mediated apoptosis by siRNA were dose- and time-dependent.

244 regulation of tumor metabolism and possibly apoptosis by SIRT1 mechanistically contribute to the obs

245 We suggest that the regulation of apoptosis by Six and Eya family members is conserved in

246 RA synovial fibroblasts to TNFalpha-induced apoptosis by specifically blocking Mcl-1 expression and,

247 a molecular mechanism in suppression of cell apoptosis by stabilizing Sirt1 in response to DNA damage

248 leukin 6 protects pancreatic beta cells from apoptosis by stimulation of autophagy.

249 ism by which Bcl-xL lowers the threshold for apoptosis by suppressing acetyl-CoA production, which, i

250 Simvastatin reduces mouse hepatocyte apoptosis by suppressing expression of the TNF-alpha/cas

251 Rituximab induces B-lymphocyte apoptosis by targeting CD20 antigen and has shown effica

252 FBW7 as the F-box protein) governs cellular apoptosis by targeting MCL1, a pro-survival BCL2 family

253 ARL), can suppress mitochondrial fission and apoptosis by targeting miR-539 and PHB2.

254 t Nur77, an orphan nuclear receptor, induces apoptosis by targeting mitochondria.

255 of miR-503 promotes cell growth and inhibits apoptosis by targeting PDCD4.

256 PHB2 and regulates mitochondrial fission and apoptosis by targeting PHB2.

257 se inhibitor that induces mitotic arrest and apoptosis by targeting Polo-like kinase.

258 9), that exhibits higher potency in inducing apoptosis by targeting the Akt-NF-kappaB signaling netwo

259 ession of miR-497 effectively induced HUVECs apoptosis by targeting VEGFR2 and downstream PI3K/AKT si

260 nd to sensitize cisplatin-resistant cells to apoptosis by targeting WEE1 and CHK1.

261 r, cytochrome c release by Western blot, and apoptosis by terminal deoxynucleotidyl transferase-media

262 Remarkably, quantification of apoptosis by terminal deoxynucleotidyltransferase-mediat

263 nclusion, Elmo1 and Dock180 protect ECs from apoptosis by the activation of the Rac1/PAK/AKT signalin

264 Spi6(-/-) Tregs were rescued from apoptosis by the addition of a GrB inhibitor (Z-AAD-CMK)

265 ation systems, cellular transformation after apoptosis by the blebbishield emergency program and the

266 ng cancer cell lines toward the induction of apoptosis by the DNA-damaging agent etoposide.

267 o prove that the inhibition of TRAIL-induced apoptosis by the ECD predominantly comes from the disrup

268 ed apoptosis-inducing ligand (TRAIL)-induced apoptosis by the ECD, although TRAIL is still able to bi

269 f these lipids rapidly enter cells to induce apoptosis by the intrinsic pathway, but how such lipids

270 sruption is independent of the initiation of apoptosis by the ion transporter.

271 Inhibition of FDH-induced apoptosis by the Jun N-terminal kinase inhibitor SP60012

272 eatment of 4-HNE to HepG2 cells also induces apoptosis by the p53 pathway through activation of Bax,

273 at least some conditions, the modulation of apoptosis by the R72P polymorphism does not affect the p

274 le of counteracting genotoxic stress-induced apoptosis by the suppression of caspase-3 activation.

275 ells are protected from chemotherapy-induced apoptosis by their interactions with bone marrow mesench

276 hts a common mechanism unveiling RHIM-driven apoptosis by therapeutic or genetic perturbation of RIP3

277 GR antagonist RU486 sensitized the cells to apoptosis by these agents.

278 ve regulation of the cell-division cycle and apoptosis by these oncogenes.

279 While observing monocytes undergoing apoptosis by time-lapse microscopy, we discovered a new

280 ished both DR5 induction and potentiation of apoptosis by TRAIL.

281 da-7/IL-24-induced ER stress response causes apoptosis by translational inhibition of the antiapoptot

282 of cleavage sites inhibited the induction of apoptosis by treatment with tumor necrosis factor alpha

283 d hepatocyte proliferation toward hepatocyte apoptosis by triggering a JNK signal, which allows activ

284 rmore, RA/IFN-alpha combination also induces apoptosis by triggering both caspases-8 and -9 resulting

285 cell cycle arrest and induction of cellular apoptosis by triggering intrinsic apoptotic pathway thro

286 at various days postinoculation for in situ apoptosis by TUNEL analysis and Fas/FasL expression.

287 lular acidification with a flux analyzer and apoptosis by TUNEL assay.

288 Caspase 3 enzymatic activity and apoptosis by TUNEL staining were also increased after 12

289 Also, potentiation of TRAIL-induced apoptosis by UA was significantly reduced by both ROS qu

290 plays an important role in the induction of apoptosis by unrepaired O(6)MeGs.

291 on in the placenta, (ii) increased germ cell apoptosis by up-regulating p53/p27-Bax-caspase-3 protein

292 loss sensitized keratinocytes to UVB-induced apoptosis by up-regulating the expression of the proapop

293 ancer cell lines evades Smac mimetic-induced apoptosis by up-regulation of cIAP2, which although init

294 We show that SR20 triggers tumor apoptosis by up-regulation of gene expression of tumor n

295 oids sensitize cancer cells to TRAIL-induced apoptosis by upregulating expression of TRAIL-R1.

296 e radiomimetic compound doxorubicin promoted apoptosis by upregulating the tumor suppressor p73.

297 ith AD and healthy donors were used to study apoptosis by using annexin V/7-aminoactinomycin D staini

298 The infected macrophages were scored for apoptosis by using DAPI (4',6-diamindino-2-phenylindole

299 role of p53 in proteasome inhibitor-induced apoptosis by using isogenic human cancer cell lines with

300 2 has been shown to sensitize tumor cells to apoptosis by various chemotherapeutic drugs and tumor ne