ライフサイエンスコーパス: apoptotic

1 soluble receptor agonists are but weakly pro-apoptotic.

2 (p-FOXO3) has been shown to be specifically apoptotic.

3 brain, indicating a greater vulnerability to apoptotic activation.

4 een by reduced clonogenic survival, enhanced apoptotic activity and enhanced senescence post IR.

5 intracellular stress seem to directly induce apoptotic activity at the MOM.

6 In addition, differences in apoptotic activity between TRIM14-deficient and control

7 ding biochemical evidence that inhibition of apoptotic activity by the Diap1 gene product has been de

8 that ATF3 activated p53 and promoted its pro-apoptotic activity in mouse thymi and small intestines,

9 exhibited synergistic antiproliferative and apoptotic activity in multiple TNBC backgrounds.

10 egulation of Bcl-2 proteins, thus modulating apoptotic activity.

11 analogs of the hit with high cytotoxic, pro-apoptotic and anti-mitotic activities.

12 revealed that SETD8 ablation rescued the pro-apoptotic and cell-cycle arrest functions of p53 by decr

13 To explore the underlying mechanism, apoptotic and inflammatory factors were measured by qPCR

14 orative functions of M36 and M45 in blocking apoptotic and necroptotic cell death responses.

15 RK1/2 kinase and inhibited expression of pro-apoptotic and pro-fibrotic JNK and TGFbeta1 proteins in

16 (IAP) family and are key regulators of anti-apoptotic and pro-survival signaling pathways.

17 Furthermore, we show that the pro-apoptotic and pro-tumorigenic functions of PKCdelta also

18 AS of the anti-apoptotic and proliferation-associated survivin (BIRC5)

19 rrociphenolic entities generally operate via apoptotic and senescence pathways.

20 e-transcriptome RNA sequencing of untreated, apoptotic, and recovering HeLa cells.

21 and are characterized by a proinflammatory, apoptotic, and senescent endothelial phenotype.

22 These miRs regulate HIF-1alpha-regulated apoptotic, angiogenic, and immune pathways.

23 In vitro, adiponectin reduced apoptotic, anti-proliferative, and stress signals and re

24 1 expression in macrophages and confers anti-apoptotic attributes.NF-kappaB p65 silencing identified

25 The addition of apoptotic Bax protein to OxPls-containing vesicles drast

26 ngement requires the activity-dependent, non-apoptotic Bax/Bak-caspase signaling cascade.

27 Overexpression of anti-apoptotic Bcl-2 family proteins contributes to cancer pr

28 y radiotherapy increases the activity of pro-apoptotic BCL-2 pathway proteins, and lymphomas are exqu

29 Overexpression of anti-apoptotic BCL-2 proteins contributes to tumor developmen

30 need for mechanism-guided targeting of anti-apoptotic BCL-2 proteins to effectively activate the mit

31 a-cell mass, and more proliferative and less apoptotic beta-cells compared with the age-matched wild-

32 exhibited significantly decreased numbers of apoptotic beta-cells compared with those treated with ve

33 reases the expression of STAT-regulated anti-apoptotic BH3 family members MCL1 and BCL-XL sensitizing

34 Ngamma-induced tumour ischaemia resemble non-apoptotic blood vessel regression during development, wo

35 and internalization of sialic acid decorated apoptotic bodies and exosomes derived from tumors.

36 at encompasses microparticles, exosomes, and apoptotic bodies) are emerging as a novel mean of cell-t

37 lular vesicles (exosomes, microvesicles, and apoptotic bodies) are ubiquitous in human tissues, circu

38 ng microvesicles (distinct from exosomes and apoptotic bodies), which induce proliferation in neighbo

39 extracellular vesicles (EVs), which include apoptotic bodies, microvesicles, and exosomes, have emer

40 mechanisms could include antigens present in apoptotic bodies, necrotic debris, exosomes or even rele

41 rmation by constructing "blebbishields" from apoptotic bodies.

42 duced by lymphoid radiation, suggesting that apoptotic body ingestion by CD8(+) DCs initiates toleran

43 SMCs were not apoptotic but displayed senescence associated-ss-galacto

44 The IO-LAHP NPs are able to induce efficient apoptotic cancer cell death both in vitro and in vivo th

45 , immune system phagocytes continually clear apoptotic cancer cells in a process known as efferocytos

46 Mer tyrosine kinase-dependent recognition of apoptotic cancer cells.

47 Apoptotic cancer stem cells can evade cell death by unde

48 instability and phagocytosis checkpoints by apoptotic cancer stem cells.

49 However, the connections between the apoptotic cascade and events leading to extrusion are no

50 Using this probe, we discover that the apoptotic caspases are O-GlcNAcylated, which we confirme

51 ected from the potentially harmful action of apoptotic caspases is largely unknown.

52 Apoptotic CD4(+) T cells from patients with rheumatoid a

53 tin ring (EAAR) that is assembled within the apoptotic cell and drives epithelial extrusion.

54 We examined the cause of impaired apoptotic cell clearance in human and murine lupus.

55 idized low-density lipoprotein and promoting apoptotic cell clearance.

56 -inspired nanovesicle can efficiently induce apoptotic cell death and significantly inhibit tumor gro

57 Transient activation of apoptotic cell death during early age correlated well wi

58 ed tumor cells to CQ, resulting in increased apoptotic cell death following treatment.

59 5 was shown to be more effective in inducing apoptotic cell death in cancer cells as compared to norm

60 nstitutively activates caspase-8 and induces apoptotic cell death in human lung epithelial cells.

61 ith the anti-HSF1 compounds strongly induced apoptotic cell death in MM cells.

62 ic potential, anoikis resistance and induced apoptotic cell death in therapy-resistant EOC cells.

63 eld duodenum, there was a trend for elevated apoptotic cell death under most irradiation conditions;

64 cumulation of ZnPc in MCF-7 cells, improving apoptotic cell death upon irradiation.

65 Simvastatin induced apoptotic cell death via the intrinsic apoptotic pathway

66 se activation or ultrastructural features of apoptotic cell death were observed.

67 cells exhibited increased susceptibility and apoptotic cell death with oxidative stress.

68 CX-5461 (ie, the induction of p53-dependent apoptotic cell death), the inhibition of Pol I transcrip

69 ells exposed to KA or NMDA appear to undergo apoptotic cell death.

70 ough induction of G2/M cell cycle arrest and apoptotic cell death.

71 spase and plays a central role in activating apoptotic cell death.

72 to induce severe aneuploidy and, ultimately, apoptotic cell death.

73 tubular epithelial cells to progress towards apoptotic cell death.

74 deficiency increases cIAP1 stability during apoptotic cell death.

75 tion, and loss of TAX1BP1 is associated with apoptotic cell death.

76 age, culminating in activity-dependent, non-apoptotic cell death.

77 roptosis, parthanatos, or other forms of non-apoptotic cell death.

78 reast cancer cells to doxorubicin leading to apoptotic cell death.

79 ects mitochondria dynamics and protects from apoptotic cell death.

80 is an iron-dependent, oxidative form of non-apoptotic cell death.

81 rescue, we observe a significant increase in apoptotic cell density in Foxg1(-/-);Wnt8b(-/-) double m

82 y DFNA5 as a central molecule that regulates apoptotic cell disassembly and progression to secondary

83 Here we show that apoptotic cell extrusion is provoked by singularities in

84 ing of old and new phagocyte functions after apoptotic cell phagocytosis demonstrates the enormity of

85 Some studies have linked apoptotic cell receptors on cardiac macrophages to tissu

86 in the dying cell to promote the increase in apoptotic cell refractility.

87 on Env-CD4-coreceptor complexes triggers non-apoptotic cell surface exposure of the membrane lipid ph

88 Impaired apoptotic cell uptake by MPhi also was seen in mice trea

89 ve found that dendritic cells expressing the apoptotic cell-recognizing receptor CD300f play a crucia

90 Efficient clearance of apoptotic cells (AC) is pivotal in preventing autoimmuni

91 aling maintains immune tolerance by clearing apoptotic cells (ACs) and inducing immunoregulatory sign

92 Although apoptotic cells (ACs) contain nucleic acids that can be

93 red ability of arterial phagocytes to uptake apoptotic cells (efferocytosis) promotes lesion growth a

94 ssue repair, wound healing, and clearance of apoptotic cells and cellular debris.

95 urther contained less proliferating and more apoptotic cells and exhibited lower numbers of infiltrat

96 earance of extracellular particles including apoptotic cells and pathogens.

97 flow cytometry; annexin-V status identified apoptotic cells and phosphorylation of intracellular kin

98 The nature of signaling between apoptotic cells and their neighboring cells remains larg

99 If apoptotic cells are not scavenged, they progress to a ly

100 Apoptotic cells are typically disposed of without activa

101 over, the CD31(+)F4/80(+) cells phagocytosed apoptotic cells as functionally matured macrophages, adh

102 etains its ability to preferentially bind to apoptotic cells at a level comparable to the native prot

103 polyinosinic acid inhibited phagocytosis of apoptotic cells by CD138(+) MPhi.

104 Detection of apoptotic cells can therefore spatially compartmentalize

105 To this end, apoptotic cells express specific eat-me signals, such as

106 tricted to the peritoneum and may help clear apoptotic cells from tissues such as the lung, helping t

107 Genetic ablation of sensors of apoptotic cells impaired the proliferation of tissue-res

108 ere associated with abnormal accumulation of apoptotic cells in the gut.

109 sufficient, but IL-4 or IL-13 together with apoptotic cells induced the tissue repair program in mac

110 tissue physiology, and the prompt removal of apoptotic cells is equally essential to avoid the undesi

111 Here we show that a fraction of apoptotic cells produce and release CrkI-containing micr

112 Apoptotic cells undergo a series of morphological change

113 fferent doses, and the immunolabeling of the apoptotic cells using quantum dot reporters.

114 By contrast, the recognition of apoptotic cells was dispensable for cytokine-dependent i

115 elated with the fraction of slow cycling and apoptotic cells within the four TPA subsets.

116 h increased survival and a reduced number of apoptotic cells, and adult male offspring exhibited high

117 th their defect in the cross-presentation of apoptotic cells, DC-specific Vps34-deficient animals dev

118 ll death, coupled with impaired clearance of apoptotic cells, have been implicated as causes of failu

119 murine and human macrophage efferocytosis of apoptotic cells, independent of macrophage polarization

120 Following MFG-E8-mediated engulfment of apoptotic cells, myofibroblasts acquired antiinflammator

121 of plaque necrosis is defective clearance of apoptotic cells, or efferocytosis, by lesional macrophag

122 higher levels of MerTK and, when exposed to apoptotic cells, secreted proreparative cytokines, inclu

123 for the maturation of phagosomes containing apoptotic cells, through recruitment of the Rab GTPase U

124 isoform BAX-beta, exclusively transcribed in apoptotic cells, was negatively correlated.

125 cells displayed hyperactive phagocytosis of apoptotic cells, which stimulated excessive TNF-alpha se

126 robe was fabricated to have high affinity to apoptotic cells.

127 ote the shrinkage, death, and degradation of apoptotic cells.

128 kage is consistent with the hypothesis of an apoptotic ceramide channel, we have used here assays of

129 MZ) treatment induced greater DNA damage and apoptotic changes in mutant glioma cells.

130 Defective apoptotic death of activated macrophages has been implic

131 cted by inflammatory response, fibrosis, and apoptotic death of hepatocytes.

132 ysfunction of proteostasis and the resultant apoptotic death of neurons represent common pathways for

133 f visible light and the extent of CO-induced apoptotic death of the cancer cells has been determined

134 cling in quiescent HSPCs, resulting in their apoptotic death.

135 mplex balance between cell proliferation and apoptotic death.

136 tial proliferative burst that is followed by apoptotic death.

137 ficient macrophages were more susceptible to apoptotic death.

138 or genetic inactivation of cIAP1 reverts the apoptotic deficit of LAR-RPTP-deficient embryos.

139 Greater apoptotic depletion of class-switched and IgM memory cel

140 is of thalassemia pathology is the premature apoptotic destruction of erythroblasts causing ineffecti

141 The apoptotic effect of 10 microM YC-1 was enhanced by addit

142 Consistent with an anti-apoptotic effect of autophagy, rapamycin-induced apoptos

143 nd (v) complete abrogation of the normal pro-apoptotic effect of dexamethasone and fluticasone furoat

144 nstitutively active TEL-SYK counteracted the apoptotic effect of HSP90 inhibition.

145 ly of proteins, preventing activation of the apoptotic effectors, BAX and BAK, and promoting cell sur

146 of Akt1, suggesting CD40 involvement in anti-apoptotic effects observed.

147 e renoprotective, anti-inflammatory and anti-apoptotic effects of octreotide after HIR.

148 Thus, anti-nucleolar and pro-apoptotic effects of protein C are flavivirus-species sp

149 nslocate to mitochondria, mediate downstream apoptotic effects of tumor suppressor P53, and inhibit t

150 depletion of endogenous SF3B1 abrogated the apoptotic effects, but not the G2/M cell cycle arrest in

151 Associated with these cell cycle and pro-apoptotic effects, we observed increased CCNA2 and BAX g

152 nd shows survival properties due to its anti-apoptotic effects.

153 in primary and metastatic tumors, leading to apoptotic elimination of advanced invasive and metastati

154 onspecific nuclease family that includes the apoptotic endonuclease EndoG.

155 gnized roles of myofibroblasts in regulating apoptotic engulfment and a fundamental importance of the

156 mal growth factor 8 (MFG-E8), which promotes apoptotic engulfment, and determined that serum response

157 Cases presented with severe apoptotic enterocolitis resembling acute intestinal graf

158 Individual apoptotic enterocytes promote divisions by loss of E-cad

159 regulation of neuroinflammation and neuronal apoptotic events.

160 d mitochondria, as well as the activation of apoptotic events.

161 Apoptotic executioner caspase-3, -6, and -7, but not the

162 Here, we characterize an apoptotic extrusion apical actin ring (EAAR) that is ass

163 ely and downregulated the expression of anti-apoptotic factors and multidrug resistance proteins.

164 In addition, the pro-apoptotic factors FoxO1/3 are overly degraded by acetyla

165 creased Egr-2 expression, which induces anti-apoptotic factors like MCL-1.

166 tion, leading to the release of pro- or anti-apoptotic factors which mediate cell survival or death.

167 peroxiredoxins-1, heme oxygenase-1, and anti-apoptotic factors, including BCL2, BCL-XL, and MCL1.

168 tors in mediating these proliferative versus apoptotic fates.

169 ne biosynthesis, triggers ferroptosis, a non-apoptotic form of cell death.

170 tylation is permissive for generation of the apoptotic form of FOXO3 and the activity of SIRT1 and pa

171 ity of GIMAP6 was not essential for its anti-apoptotic function in Huh-7 cells.

172 tumor suppressor while antagonizing the anti-apoptotic function of Bcl-2 is highly active in preclini

173 This platform requires a non-apoptotic function of caspase-8, but no caspase-3 or cas

174 independently or in concert to regulate the apoptotic function of FOXO3.

175 podocyte survival by inhibiting dendrin pro-apoptotic function.

176 KDM3A suppressed pro-apoptotic functions of p53 by erasing p53-K372me1, as th

177 unique carboxyl terminus with specific anti-apoptotic functions.

178 nery also have important non-cell-death (non-apoptotic) functions in flies, nematodes, and mammals.

179 rogenesis by conditional deletion of the pro-apoptotic gene Bax in stem cells reduced excitatory post

180 slocated to the nucleus, and induced the pro-apoptotic gene BCL2-like 11 (Bim).

181 conjugated to an adenovirus carrying the pro-apoptotic gene PUMA, has therapeutic efficacy in a rat a

182 mutated p53 to induce the expression of pro-apoptotic genes in breast cancer with mutant p53.

183 e, PEITC treatment induced expression of pro-apoptotic genes in tumor cells, which was partially reve

184 was confirmed (annexin-PI, SubG1/cell-cycle, apoptotic genes, caspase-3 and poly ADP ribose polymeras

185 cell types, including MAPK pathway genes and apoptotic genes.

186 fment and impaired LAP-mediated clearance of apoptotic germ cells as miR-471-5p transgenic mice show

187 Phagocytic clearance of apoptotic germ cells by Sertoli cells is vital for germ

188 ile Bai1 overexpression rescues clearance of apoptotic germ cells in the testes of Mertk (-/-) mice i

189 -1, but not in cells dependent on other anti-apoptotic homologs.

190 ficantly (p < 0.05) decreased acute necrotic/apoptotic injury and significantly (p < 0.05) improved f

191 ncentrations of anisomycin induced selective apoptotic killing of Mtb-infected human macrophages, whi

192 ependent migratory DCs potentially acquiring apoptotic LECs.

193 A miniPEG8 spacer was effective in enhancing apoptotic levels in contrast to a miniPEG2 spacer.

194 re, we provide context for the argument that apoptotic-like cell death occurs in plants.

195 While the removal of apoptotic M. tuberculosis (Mtb)-infected cells, or effer

196 stochemical analysis revealed a reduction in apoptotic M1, but not apoptotic M2 macrophages.

197 evealed a reduction in apoptotic M1, but not apoptotic M2 macrophages.

198 ncreases in alanine aminotransferase levels, apoptotic markers, and human inflammatory cytokines retu

199 ugh VDR-dependent anti-proliferative and pro-apoptotic mechanisms.

200 of the unfolded protein response and the pro-apoptotic mediators CamkII and Stat1 was impaired in Trp

201 ewborns, which underscores the importance of apoptotic modulation during urinary tract morphogenesis.

202 , display striking differences in density of apoptotic neurons during the early postnatal period.

203 deprivation leads to exacerbated amounts of apoptotic neurons in the corresponding functional area o

204 ve microglia phenotype after phagocytosis of apoptotic neurons.

205 Furthermore, we show that endonuclease G, an apoptotic nuclease downstream of Caspase-3, is directly

206 selectivity and antitumor efficacy of IP pro-apoptotic NWs.

207 The physical interaction between Malat1 and apoptotic or inflammatory factors was measured by RNA im

208 RIPK1 limit virus spread by executing either apoptotic or necroptotic cell death in response to infec

209 iruses, HBoV1 infection did not activate the apoptotic or necroptotic cell death pathway.

210 howed trabecular thinning, higher numbers of apoptotic osteocytes, and imbalanced metabolism, leading

211 d requires the nuclear and mitochondrial pro-apoptotic p53 program to induce and execute apoptosis, w

212 a critical role in the cellular response to apoptotic pathway activation in the embryo.

213 While the p53 apoptotic pathway has clearly been associated with Abeta

214 on, and induced both intrinsic and extrinsic apoptotic pathway in vitro with a dose-dependent manner.

215 s exposed to Ru(II) compounds die through an apoptotic pathway triggered by ROS production.

216 ti-tumor effects by activating the extrinsic apoptotic pathway which could overcome the cytoprotectiv

217 Cytotoxicity was mediated by the intrinsic apoptotic pathway, as shown by an increase in Bcl2-like

218 tosis of CLL cells through the mitochondrial apoptotic pathway.

219 duced apoptotic cell death via the intrinsic apoptotic pathway.

220 kemia cell death through a caspase-dependent apoptotic pathway.

221 ts which involves the PI3K/Akt signaling and apoptotic pathway.

222 is without affecting the caspase-independent apoptotic pathway.

223 considered the guardian of the mitochondrial apoptotic pathway.

224 mbine MEK inhibitors with agents that target apoptotic pathways may be a promising therapeutic approa

225 mozygous deletion of Sirt1 triggers cellular apoptotic pathways, increases cell death, diminishes aut

226 cing inflammasome activation and suppressing apoptotic pathways.

227 initiate cell death through induction of pro-apoptotic pathways.

228 triggers of apoptosis, including apoptosome apoptotic peptidase activating factor 1 (APAF-1).

229 lature-homing peptide (CGKRK) fused to a pro-apoptotic peptide [D(KLAKLAK)2] coated on iron oxide nan

230 t a "cancer-like" pro-proliferative and anti-apoptotic phenotype.

231 chemokine receptor D6/ACKR2 is expressed on apoptotic PMN and plays an important role in regulating

232 e on macrophages when acting in concert with apoptotic PMN-expressed D6.

233 -treated mice had increased efferocytosis of apoptotic polymorphonuclear leukocytes instilled into th

234 Apoptotic population elevation, mitochondrial membrane p

235 homodimers multimerize to form the putative apoptotic pore is unknown.

236 nalling and explained the differences in pro-apoptotic potential between soluble and membrane-bound C

237 A-21 as a STAT3 target gene with strong anti-apoptotic potential, suggesting that noncoding RNAs have

238 Here, we examined the mechanisms of apoptotic priming in ASFs and explored a combined target

239 Cs from primary human-monocytes display anti-apoptotic profile, exhibited by elevated phosphorylated-

240 e this pathway is normally halted by the pro-apoptotic protease caspase-8 and the IAP ubiquitin ligas

241 se 3 levels with a parallel decrease in anti-apoptotic protein B-cell leukemia/lymphoma 2 levels.

242 konin also attenuated DM/hypoxia-induced pre-apoptotic protein BAX expression as well as the producti

243 n circumstances where expression of the anti-apoptotic protein BCL2 is high, Casp8p41 instead binds B

244 Increasing Grx1 reduces the pro-apoptotic protein Bim expression through regulating Akt-

245 Survivin, an overexpressed anti-apoptotic protein in cancer, represents a pharmacologica

246 th computational modeling and selective anti-apoptotic protein inhibitors, uncovers new mechanistic d

247 apoptosis, suggesting that GIMAP6 is an anti-apoptotic protein.

248 and Bcl-xL), while reduced expression of pro-apoptotic proteins (AIF and Bax).

249 0.05) increased expression of p-Akt and anti-apoptotic proteins (Bcl-2 and Bcl-xL), while reduced exp

250 Extracts decreased expression of anti-apoptotic proteins (survivin, cIAP-2, XIAP), induced apo

251 ays or of altered expression of pro- or anti-apoptotic proteins can thus be compared.

252 ed the regulatory mechanism by which the pre-apoptotic proteins translocate from mitochondria to the

253 itochondrial envelope and the release of pro-apoptotic proteins, leading to cell death.

254 s show selectivity for Mcl-1 over other anti-apoptotic proteins, possess cytotoxicity to cancer cell

255 plementary set of anti-proliferative and pro-apoptotic proteins.

256 the expression of inflammatory cytokines and apoptotic proteins.

257 impact the expression of oncogenes and anti-apoptotic proteins.

258 TAT1 in cell-based assays, and increases the apoptotic rate of cultured NSCLC cells in a STAT3-depend

259 masks compartment-specific proliferative and apoptotic regulation that is not present under homeostat

260 tors, uncovers new mechanistic details about apoptotic regulators that are predictive of drug sensiti

261 Animal apoptotic regulators, including Bcl-2 family members, ha

262 analysis of BCL-2 family proteins and other apoptotic regulators, together with computational modeli

263 f RAS-induced self-renewal, and during which apoptotic resistance is not necessarily the directly sel

264 ges enhances chronic arthritis by conferring apoptotic resistance to activated macrophages.

265 We demonstrate that this apoptotic response provides a cell-extrinsic signal that

266 nes that promote cell growth and inhibit the apoptotic response to uncontrolled proliferation.

267 ation fork speed, and increased R-loops), an apoptotic response, and a dependence upon cyclin E expre

268 nd a rapid p53-independent ATR-Chk1-mediated apoptotic response.

269 absent in RIP1-deficient Jurkat cells during apoptotic responses to chemotherapeutic agents.

270 as a rheostat that fine-tunes autophagic and apoptotic responses.

271 induced microglia/macrophages associate with apoptotic retinal neurons.

272 ing that this difference may result from the apoptotic role of Trp53.

273 ion of A3A expression in AML cells, enabling apoptotic sensitivity to inhibitors of the DNA replicati

274 differentially regulate the endocytosis and apoptotic signaling downstream of TNF-related apoptosis-

275 Compromised apoptotic signaling is a prerequisite for tumorigenesis.

276 K, and ATF6) and allows them to activate the apoptotic signaling pathway.

277 The NS3 TCR induced a rapid expression of apoptotic signaling pathways and formation of embryonic

278 rapamycin (mTOR), proinflammatory, and anti-apoptotic signaling pathways, as well as downregulation

279 ed hepatotoxicity and the rapid induction of apoptotic signaling pathways, the noncytotoxic T cell ac

280 The resulting release of pro-apoptotic signaling proteins leads to cell destruction t

281 nd kidneys, are profoundly refractory to pro-apoptotic signaling, leading to cellular resistance to c

282 regulates integrin-mediated pro-survival and apoptotic signaling.

283 The extrusion process can be triggered by apoptotic signalling, oncogenic transformation and overc

284 nt transformation, our study reveals how pro-apoptotic signals can elevate ROS past a previously hypo

285 Injection of naive mice with apoptotic spleen cells generated by irradiation led to D

286 avage division, epigenetic reprogramming and apoptotic status of bovine preimplantation cloned embryo

287 rvive caspase activation following transient apoptotic stimuli, a process called anastasis.

288 otably the modulation of cell sensitivity to apoptotic stimuli.

289 oteins inside the membrane in the absence of apoptotic stimuli.

290 iculum and sensitization to Ca(2+)-dependent apoptotic stimuli.

291 characterized by an increased sensitivity to apoptotic stimuli.

292 with treatment resistance and upregulated by apoptotic stressors such as chemotherapy.

293 eport a technique termed two-photon chemical apoptotic targeted ablation (2Phatal) that uses focal il

294 duces only minimal cell death, it lowers the apoptotic threshold in a subset of patient-derived gliob

295 S past a previously hypothesised 'lethal pro-apoptotic threshold' to induce death; an observation tha

296 efect in efferocytosis, the process by which apoptotic tissue is recognized for engulfment by phagocy

297 t and ovarian cancer cells and released from apoptotic tumor cells, whereupon it interacts with the c

298 99m)Tc-duramycin specifically accumulates in apoptotic tumors in which (18)F-FDG was not able to diff

299 sed levels of surface activation markers and apoptotic vesicle formation, and also formed aggregates

300 tumor cell killing and the identification of apoptotic vulnerabilities to overcome drug resistance in