ライフサイエンスコーパス: apoptotic cell

1 ghbor cells form at their interface with the apoptotic cell.

2 or-mediated virus infection and clearance of apoptotic cells.

3 ss lipoproteins and cholesterol, and take up apoptotic cells.

4 situ from cell membranes, lipoproteins, and apoptotic cells.

5 nt colon epithelia showed a higher number of apoptotic cells.

6 promoting tolerance to antigens derived from apoptotic cells.

7 cently been linked to defective clearance of apoptotic cells.

8 mmatory responses via pathological levels of apoptotic cells.

9 by TIMD4, mediates the phagocytic uptake of apoptotic cells.

10 fer cells and were associated with uptake of apoptotic cells.

11 the mitochondrial fragmentation machinery in apoptotic cells.

12 rapid response to infection and clearing of apoptotic cells.

13 ccessfully tested by fluorescence imaging of apoptotic cells.

14 conversely that TRIM2 limits phagocytosis of apoptotic cells.

15 udy the mechanism of suppression elicited by apoptotic cells.

16 lood-stream and remove pathogens, toxins and apoptotic cells.

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

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

19 gocytes are highly specialized for engulfing apoptotic cells.

20 an "immunologically silent" clearance of the apoptotic cells.

21 ignals not to respond to the nucleic acid of apoptotic cells.

22 of macrophages following the phagocytosis of apoptotic cells.

23 ble for the silent uptake of vast numbers of apoptotic cells.

24 their dominant role in clearing the bulk of apoptotic cells.

25 city, high specificity, and high affinity to apoptotic cells.

26 idylserine (PtdSer) receptors that recognize apoptotic cells.

27 accine loaded with autologous HIV-1-infected apoptotic cells.

28 nding factors to promote the phagocytosis of apoptotic cells.

29 clearance of pathogens, immune complex, and apoptotic cells.

30 xtracellular particles, such as pathogens or apoptotic cells.

31 to promote resolution without administering apoptotic cells.

32 ell peritoneal macrophages after exposure to apoptotic cells.

33 ropagation also promotes apical extrusion of apoptotic cells.

34 encing after co-cultivating macrophages with apoptotic cells.

35 st maintaining their capacity to phagocytose apoptotic cells.

36 sue macrophages rapidly recognize and engulf apoptotic cells.

37 and human macrophages significantly impaired apoptotic cell (AC) engulfment.

38 Efficient clearance of apoptotic cells (AC) is likely an important component of

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

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

41 Clearance of apoptotic cells (ACs) by phagocytes (efferocytosis) prev

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

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

44 estrated morphological rearrangements of the apoptotic cell and its neighbors.

45 osphatidylserine (PS)-dependent clearance of apoptotic cells and also for their immune modulatory fun

46 of MZMs impairs the tolerogenic clearance of apoptotic cells and alters the serum cytokine profile, w

47 Apoptotic cells and cell fragments, especially those pro

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

49 tion of polyreactive B cells that bound both apoptotic cells and commensal bacteria from healthy adul

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

51 tion, and deficient efferocytotic removal of apoptotic cells and foam cells sustains lesion progressi

52 mediating transplantation tolerance by donor apoptotic cells and implicate MerTK agonism as a promisi

53 r by mutagenesis blocks vesicle formation in apoptotic cells and inhibits CPS, thus uncoupling apopto

54 earance of extracellular particles including apoptotic cells and pathogens.

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

56 more, 2-HOBA reduces inflammation and plaque apoptotic cells and promotes efferocytosis and features

57 We found that VDR deficiency induced more apoptotic cells and significantly increased cell death i

58 portant for the elimination of pathogens and apoptotic cells and stimulation of the adaptive immune s

59 l for the phagocytosis of infectious agents, apoptotic cells and synapses.

60 g SFK signaling blocks both the expulsion of apoptotic cells and the rosette formation among their ne

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

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

63 lar Vesicles (EVs) were highly released from apoptotic cells, and contributed to macrophage productio

64 The viability of the cells, amount of apoptotic cells, and generation of reactive oxygen speci

65 cy resulted in failure of tolerance by donor apoptotic cells, and this failure could be effectively r

66 and IDO1 in tumor residual disease decreased apoptotic cell- and necrotic cell-induced immunosuppress

67 ge8(-/-) , leading to defective clearance of apoptotic cells; and either C1q(-/-) or C3(-/-) , leadin

68 that a therapeutic strategy combining donor apoptotic cells, anti-CD40L, and rapamycin effectively i

69 Efferocytosis is the process by which apoptotic cells are cleared from tissue by phagocytic ce

70 Although apoptotic cells are cleared quickly in almost all other

71 These data advance the concept that apoptotic cells are not inert cells waiting for removal,

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

73 How apoptotic cells are removed from this region during thes

74 rtant implications for the microenvironment; apoptotic cells are removed in an immune silent process,

75 Apoptotic cells are typically disposed of without activa

76 data implicate global protein aggregation in apoptotic cells as a mechanism that ensures the overlap

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

78 acellular signals from aminophospholipids on apoptotic cells, as well as unidentified ligands in the

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

80 cer effect than the RIATC prodrug that lacks apoptotic cell-binding property but having a similar deg

81 t the wound-site, impairment in clearance of apoptotic cell bioburden enables chronic inflammation.

82 ins, Yap/Taz also promoted the scavenging of apoptotic cell bodies and necrotic debris by PDA cells.

83 efferocytosis induced secondary necrosis of apoptotic cells, but failed to prevent increased tumor M

84 DNA release, has been extensively studied in apoptotic cells, but little is known about its role in l

85 Epithelia can eliminate apoptotic cells by apical extrusion.

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

87 bute to severe asthma, but whether uptake of apoptotic cells by lung phagocytes might dampen house du

88 Engulfment of apoptotic cells by macrophages (efferocytosis) resolves

89 Clearance of apoptotic cells by macrophages prevents excessive inflam

90 The engulfment of apoptotic cells by phagocytes, a process referred to as

91 The clearance of apoptotic cells by professional and non-professional pha

92 murine lung, myeloid phagocytes encountering apoptotic cells can deploy alphav integrin-mediated mech

93 Detection of apoptotic cells can therefore spatially compartmentalize

94 Apoptotic cell clearance (efferocytosis) elicits an anti

95 sted the role of inflammation, specifically, apoptotic cell clearance and complement activation in ki

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

97 ited the ease of manipulating cell death and apoptotic cell clearance in this model to identify that

98 Here, we examined the effect of blocking apoptotic cell clearance on anti-tumor immune response.

99 this model to identify that the loss of the apoptotic cell clearance receptor Six-microns-under (Sim

100 ctions such as blood pressure regulation(1), apoptotic cell clearance(2) and human oocyte development

101 gic signaling, including cancer progression, apoptotic cell clearance, inflammation, blood pressure r

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

103 Addition of 1% NaCl tended to increase apoptotic cells (cleaved caspase 3) in the renal papilla

104 vated viable LGCs numbers and decreased dead/apoptotic cell counts.

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

106 ine the mechanisms by which phagocytes sense apoptotic cell death and discuss how phagocytosis is int

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

108 ens, such as aflatoxin B(1) (AFB(1)), induce apoptotic cell death and the resulting cell debris stimu

109 he stress sensor, and protects cells against apoptotic cell death at both cellular and whole animal l

110 reduced proliferation with no difference in apoptotic cell death between control and Ddr1(-/-) anima

111 eath is not limited to this natural turnover-apoptotic cell death can be induced by infection, inflam

112 decreases during necrotic, necroptotic, and apoptotic cell death caused by demyelinating, ischemic,

113 events the NADPH oxidation, redox stress and apoptotic cell death caused by the activation of glycoly

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

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

116 Depleting ELP proteins promoted apoptotic cell death in an EGFR inhibition-dependent man

117 he unfolded protein response, and ultimately apoptotic cell death in breast and lung cancer cell line

118 5 was shown to be more effective in inducing apoptotic cell death in cancer cells as compared to norm

119 ewly synthesized mu1 protein does not affect apoptotic cell death in HeLa cells but enhances necropto

120 phorylation of p38MAPK and STAT1, as well as apoptotic cell death in HG-treated hRECs.

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

122 rinsic antiviral control, it drove increased apoptotic cell death in infected fibroblasts.

123 e its deficiency results in TNFalpha-induced apoptotic cell death in luminal breast cancer subtype.

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

125 tion, inhibited proliferation, and triggered apoptotic cell death in primary neonatal pig GMCs.

126 of Wnt/beta-catenin activation and underwent apoptotic cell death in response to proliferative stimul

127 ite increased replication stress, leading to apoptotic cell death in S-phase and mitotic catastrophe.

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

129 an inhibitor of glutamate release, promoted apoptotic cell death in vitro and in vivo.

130 N3A caused reexpression of TSG, induced ALCL apoptotic cell death in vitro, and hindered ALCL tumorig

131 The proportion of cortical cells undergoing apoptotic cell death increased, suggesting that cell dea

132 The induction of apoptotic cell death involved loss of mitochondrial oute

133 Regulation of apoptotic cell death is an important component in the co

134 tion of VEGF is associated with induction of apoptotic cell death mainly through increasing activatio

135 ne potential loss, and lack of activation of apoptotic cell death markers.

136 Apoptotic cell death of the treated HeLa and BE(2)-C cel

137 at Galphaq/PKCzeta complexes link Galphaq to apoptotic cell death pathways.

138 ath (LCD) is a morphologically conserved non-apoptotic cell death process operating in Caenorhabditis

139 Ferroptosis-an iron-dependent, non-apoptotic cell death process-is involved in various dege

140 t, they become subject to elimination via an apoptotic cell death program known as anoikis.

141 block human B-cell proliferation and promote apoptotic cell death selectively in antibody-secreting B

142 ochondrial oxidative stress, DNA damage, and apoptotic cell death that were prevented by the antioxid

143 suppressed activation of STAT1 and decreased apoptotic cell death under HG conditions.

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

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

146 Simvastatin induced apoptotic cell death via the intrinsic apoptotic pathway

147 Apoptotic cell death was evaluated, and FITC conjugated

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

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

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

151 ers Bax and Bak are known to be resistant to apoptotic cell death, and previous we have shown that th

152 ion of G4C2 repeats of varying length caused apoptotic cell death, but failed to generate DPRs.

153 As a cell undergoes apoptotic cell death, it experiences changes in morpholo

154 erate light illumination induces substantial apoptotic cell death, transient mild light illumination

155 esult of downregulation of M1BP also induces apoptotic cell death, which can be significantly restore

156 In the BubR1 mutant, massive apoptotic cell death, which is likely due to the comprom

157 heir stress response, followed by a surge in apoptotic cell death.

158 ow a wider community of researchers to study apoptotic cell death.

159 cancer cell proliferation and induces their apoptotic cell death.

160 also recognized as an important mediator of apoptotic cell death.

161 owed by nucleolar stress, p53 activation and apoptotic cell death.

162 that act directly on mitochondria to trigger apoptotic cell death.

163 tion in that leads to MESN-subtype-dependent apoptotic cell death.

164 s in impaired mitochondrial function and non-apoptotic cell death.

165 hondrial dysfunction and sensitized cells to apoptotic cell death.

166 gets cell proliferation, mitosis and induces apoptotic cell death.

167 on, rescued TSG expression, and induced ALCL apoptotic cell death.

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

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

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

171 ects mitochondria dynamics and protects from apoptotic cell death.

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

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

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

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

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

177 tubular epithelial cells to progress towards apoptotic cell death.

178 deficiency increases cIAP1 stability during apoptotic cell death.

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

180 rtant ramifications in diseases that involve apoptotic cell death.

181 al number of donor cells are lost because of apoptotic cell death.

182 ly, mitochondria also have a central role in apoptotic cell death.

183 y tissue abnormalities, such as necrosis and apoptotic cell death.

184 one of the most fundamental processes during apoptotic cell death.

185 ilization (MOMP) is a crucial event enabling apoptotic cell death.

186 cribe its biological activity and effects on apoptotic cell death.

187 l or, in the event of chronic damage, induce apoptotic cell death.

188 n of ER homeostasis; that failing, it drives apoptotic cell death.

189 totic cell death into immunologically silent apoptotic cell death.

190 new insights into how mitochondria regulate apoptotic cell death.

191 haperone protein BiP, inducing ER stress and apoptotic cell death.

192 iating immune and inflammatory responses and apoptotic cell death.

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

194 ase of self antigens and danger signals from apoptotic cell-derived constituents that can result in i

195 uniquely programmed to process internalized apoptotic cell-derived fatty acids, cholesterol and nucl

196 formed after validating the disappearance of apoptotic cell-derived RNA sequences.

197 trated that Tregs were necessary for maximal apoptotic cell-directed enhancement of resolution, and a

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

199 Here, we utilize apoptotic-cell disintegration to develop a novel label-f

200 ificities that may facilitate the removal of apoptotic cells during development and shape gut microbi

201 Macrophages encounter and clear apoptotic cells during normal development and homeostasi

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

203 ylserine (PS) receptors mediate clearance of apoptotic cells-efferocytosis-by recognizing the PS expo

204 Expression of Rho in apoptotic cells enables them to secrete EGFs, which stim

205 This study investigated whether apoptotic cell engulfment in the murine lung impacts the

206 ingle-nucleotide polymorphisms (SNPs) in the apoptotic cell-engulfment genes ELMO1, DOCK2, and RAC1 l

207 Intratracheal instillation of apoptotic cells enhances resolution of experimental lung

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

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

210 riguingly, the sessile epithelia is prone to apoptotic cell extrusion upon crowding, whereas the pend

211 of these results, we propose a mechanism for apoptotic cell extrusion: spontaneously formed topologic

212 cells by CD103(+) dendritic cells, exogenous apoptotic cells failed to induce transforming growth fac

213 Extrusion of apoptotic cells from epithelial tissues requires orchest

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

215 Clearance of apoptotic cells has been intensively studied, but the ef

216 Poor clearance of apoptotic cells has been suggested to contribute to seve

217 t target macrophages, endothelial cells, and apoptotic cells have also been tested in small groups of

218 hways modulated in phagocytes in response to apoptotic cells have been linked to chronic inflammatory

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

220 red to stimulate the phagocytic clearance of apoptotic cells; however, these therapies can cause off-

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

222 hibited by peritransplant infusions of donor apoptotic cells in combination with anti-CD40L and rapam

223 ls, fewer dividing cells, and an increase in apoptotic cells in KO mice.

224 Apoptotic cells in PBMCs and tissues increased during pe

225 sion of BCL2 in B cells could largely rescue apoptotic cells in the absence of Fbw7.

226 ated with increase in both proliferative and apoptotic cells in the affected tissue and were largely

227 is associated with phagocytes that eliminate apoptotic cells in the chick.

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

229 therosclerotic plaque is the accumulation of apoptotic cells in the necrotic core.

230 tide (termed Apo-15) that selectively stains apoptotic cells in vitro and in vivo in a calcium-indepe

231 The detection and quantification of apoptotic cells in vivo is hampered by the need for fixa

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

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

234 on of surface molecules required for NKT and apoptotic cell interactions and developed suppressive im

235 ively studied, but the effects of macrophage-apoptotic cell interactions on macrophage behaviour are

236 x morphogenetic event where expulsion of the apoptotic cell is accompanied by rearrangement of its im

237 Recipient infusion of donor apoptotic cells is an emerging strategy for inducing rob

238 The clearance of apoptotic cells is an essential process to maintain home

239 In ced-11 mutants, the degradation of apoptotic cells is delayed.

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

241 ese defects and reveals that phagocytosis of apoptotic cells is not necessary for their anti-inflamma

242 Phagocytosis of apoptotic cells is thus coupled to specific functions, f

243 iabetic retinopathy (DR) is characterized by apoptotic cell loss in the retinal vasculature.

244 How apoptotic cells mediate such diverse effects is not full

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

246 on, there is a positive relationship between apoptotic cell numbers and fluorescence intensities.

247 Expression of CD44 and apoptotic cell numbers in tendon tissue from patients wi

248 Phagocytosis of various targets, such as apoptotic cells or opsonized pathogens, by macrophages i

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

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

251 The removal of apoptotic cells prevents them from undergoing secondary

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

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

254 much has been learnt about the mechanisms of apoptotic cell recognition and uptake, several key areas

255 cytes coexpressed many receptors involved in apoptotic cell recognition.

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

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

258 that is activated in neighbor cells when the apoptotic cell relaxes shortly after injury.

259 Daily clearance of billions of self-apoptotic cells relies on homeostatic engagement of phag

260 This 'switch' to pro-inflammatory sensing of apoptotic cells resulted from the disruption of the chlo

261 ors trigger widespread Rho expression in non-apoptotic cells, resulting in chronic EGF signaling.

262 rovide new insights into the consequences of apoptotic cell sampling, advance our understanding of ho

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

264 l cycle analysis and flow cytometry detected apoptotic cell shrinkage in cetuximab-treated DiFi cells

265 y, treatment of infected wild-type mice with apoptotic cells significantly increased GM-CSF productio

266 e observed a large number of binucleated and apoptotic cells-signs of failed cytokinesis that we also

267 und parameter changes from those of in vitro apoptotic cells, suggesting that these different methods

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

269 e display of so-called eat-me signals on the apoptotic cell surface, the most fundamental of which is

270 regulates phagocytosis of myelin debris and apoptotic cells that can accumulate and inhibit tissue r

271 After exposure to apoptotic cells, the F4/80(+) MHCII(LO) subset significa

272 nds with high affinity to PS externalized by apoptotic cells, thereby hindering their interaction wit

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

274 stablished in the neighboring epithelium for apoptotic cells to be extruded.

275 Dendritic cells carry apoptotic cells to lymph nodes where they signal the eme

276 process and present antigens associated with apoptotic cells to MHC class I-restricted T cells.

277 er, an outstanding question is if allogeneic apoptotic cells trigger the same receptor system for ind

278 Here we show that phagocytosis of apoptotic cells triggers a coordinated transcriptional p

279 Apoptotic cells undergo a series of morphological change

280 Apoptotic cell uptake by lung alveolar macrophages suppr

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

282 and show that CD300f-dependent regulation of apoptotic cell uptake is essential for suppressing overa

283 cess the metabolic cargo they receive during apoptotic cell uptake; the links between efferocytosis a

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

285 Phagocytosis of apoptotic cells via the receptor MerTK is important for

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

287 However, the percentage of apoptotic cells was similar to conventional embryos.

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

289 Furthermore, CD44 expression and apoptotic cells were co-stained in tendinopathic tendon.

290 In comparison with saline rats, many apoptotic cells were found in rats injected with 100 mug

291 ange in astrocytes, microglia, and number of apoptotic cells were found.

292 Apoptotic cells were infused into the lungs of mice chal

293 The most important number of apoptotic cells were observed in animals injected with 3

294 After intratracheal instillation, labeled apoptotic cells were observed in most CD11c(+)CD103(+) m

295 ammatory mediators, NF-kappaB expression and apoptotic cells when compared with the Con group, and th

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

297 Loss of Oga resulted in a doubling of apoptotic cells within the bone marrow and transcription

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

299 lockade of MerTK resulted in accumulation of apoptotic cells within tumors and triggered a type I int

300 , activating mAbs increased the frequency of apoptotic cells without affecting proliferation.