ライフサイエンスコーパス: dying cell

1 ontrolling actin and microtubules within the dying cell.

2 an array of intracellular substrates in the dying cell.

3 on cooperation between the phagocyte and the dying cell.

4 eavage of anti-apoptotic Bcl-2 and Bcl-xL in dying cells.

5 spholipid that is produced and released from dying cells.

6 ation were examined by immunofluorescence in dying cells.

7 ll layer, proliferation, and phagocytosis of dying cells.

8 number of dividing cells with the number of dying cells.

9 ted dUTP nick end labeling)-staining labeled dying cells.

10 nition of extracellular self-DNA released by dying cells.

11 l death rather than simply being produced by dying cells.

12 response to intracellular Ags released from dying cells.

13 lable only on membrane disruption in dead or dying cells.

14 oparticles (MPs) are shed from activated and dying cells.

15 osis, but instead by more rapid clearance of dying cells.

16 ose signals drawing cells toward neighboring dying cells.

17 pathogens, but also to signals released from dying cells.

18 GTPase RAC1, promotes internalization of the dying cells.

19 they engulfed detectable amounts of labeled dying cells.

20 ells, leading to the prompt clearance of the dying cells.

21 of the anionic membrane surfaces of dead and dying cells.

22 and functions as a transcriptional sensor of dying cells.

23 eath program and facilitate packaging of the dying cells.

24 es or intrinsically associated with MPs from dying cells.

25 sis program is the swift phagocytosis of the dying cells.

26 ess the Mnl1-dependent weak acid response in dying cells.

27 tially harmful or immunogenic materials from dying cells.

28 enabled regional retinal analysis of labeled dying cells.

29 homeostatic role for C1q in the disposal of dying cells.

30 t shock protein 90 (hsp90) on the surface of dying cells.

31 gnal recently identified to be released from dying cells.

32 ding cell death, not merely a consequence of dying cells.

33 and contain a large number of quiescent and dying cells.

34 d have leaked from living cells and/or a few dying cells.

35 ologically showed a large number of dead and dying cells.

36 might attract mononuclear phagocytes to the dying cells.

37 uct, a putative holin, controls lysis of the dying cells.

38 h the release of intracellular antigens from dying cells.

39 various domains of the protein in living and dying cells.

40 that they derive, at least in part, from the dying cells.

41 t may contribute to the in vivo clearance of dying cells.

42 stent model for DIAP1 function in living and dying cells.

43 hered survival factors to their receptors on dying cells.

44 nction inhibitors decrease the clustering of dying cells.

45 death but does affect the morphology of the dying cells.

46 sentation of new cell surface ligands by the dying cells.

47 s a concomitant of a high burden of dead and dying cells.

48 e may due to intracellular self-digestion of dying cells.

49 hat mediate efficient uptake of proteins and dying cells.

50 or nucleolin in removing cleaved PARP-1 from dying cells.

51 their migration to, and thus engulfment of, dying cells.

52 motes the phagocytosis and immunogenicity of dying cells.

53 wild-type mice, produce IL-10 in response to dying cells.

54 irally infected cells and after release from dying cells.

55 w healthy cells interact with and respond to dying cells.

56 m, by degrading DNA that leaks from dead and dying cells.

57 molecular patterns expressed on stressed or dying cells.

58 paB (NF-kappaB)-induced transcription within dying cells.

59 ellular ATP as a danger signal released from dying cells.

60 y slow replacement of de-differentiating and dying cells.

61 -cell response to self-antigens displayed on dying cells.

62 indicating the presence of DNA from dead or dying cells.

63 e cells and passively released by injured or dying cells.

64 ic manner by infiltrating phagocytes purging dying cells.

65 indispensable for the efficient clearance of dying cells.

66 d autophagy, as well as reduced clearance of dying cells.

67 the cell surface of living cancer cells and dying cells.

68 he release of danger signals by stressed and dying cells, a process that leads to neuroinflammation.

69 Consequently, in SCARF1-deficient mice, dying cells accumulated in tissues, which led to a lupus

70 nal IL-33, which is released from damaged or dying cells, achieves its effects via the IL-1R family m

71 In one of them--apoptosis--the dying cell affects others minimally.

72 nervous tissue formed during phagocytosis of dying cells after injury, and the failure of many adult

73 In summary, the release of histones from dying cells aggravates AKI via both its direct toxicity

74 essional phagocytes recognize and respond to dying cells, albeit in a manner partially distinct from

75 bule targeting to the cortex and whether the dying cell also controls the extrusion direction were un

76 se to promote elimination of mitochondria in dying cells, an event that could facilitate cell-death e

77 d a bridge between phosphatidylserine on the dying cell and formyl peptide receptor 2 on the phagocyt

78 UTP nick end labeling (TUNEL) to detect the dying cells and 5-bromodeoxyuridine (BrdU) to label newl

79 portant in vivo role for MBL in clearance of dying cells and adds the MBL null animals to the few ani

80 1 (HMGB1) and nucleic acids are released by dying cells and bind Toll-like receptors (TLRs).

81 , and aging and is required for clearance of dying cells and coagulation.

82 in Drosophila has identified a link between dying cells and compensatory proliferation of neighbouri

83 Histones are released from dying cells and contribute to antimicrobial defense duri

84 such, annexin A1 promotes the engulfment of dying cells and dampens the postphagocytic production of

85 Abs form ICs with nucleosomes released from dying cells and elicit spontaneous formation of anti-Id

86 ectin receptor that binds F-actin exposed by dying cells and facilitates cross-presentation of dead c

87 ns, ced-12 is required for the engulfment of dying cells and for cell migration.

88 e physiological waste-disposal mechanisms of dying cells and immune complexes.

89 er the release of nucleotides by damaged and dying cells and in the development of neuropathic and in

90 observation of newly exposed ligands on the dying cells and new evidence for direct inhibition of up

91 pro-inflammatory signals upon engulfment of dying cells and prevention of autoantigen presentation t

92 aalpha in mice and is specialized to capture dying cells and process antigens for MHC class I "cross-

93 lls, which are critical for the clearance of dying cells and rapid resolution of inflammation.

94 Since DNA is a major component of dying cells and recent studies indicate that mammalian n

95 ble in hepatic inflammation predominantly on dying cells and stimulate cytokine secretion as well as

96 mechanisms: protein aggregates released from dying cells and taken up by macropinocytosis, and exosom

97 ciency include a decreased capacity to clear dying cells and the establishment of a lupus-like autoim

98 ave direct implications for the clearance of dying cells and the roles played by different phagocytes

99 ng them to release tumor associated Ags from dying cells and then prime antitumor immunity against th

100 ty group box-1 protein (HMGB1) released from dying cells and thereby neutralized its stimulatory acti

101 s necessary to prevent secondary necrosis of dying cells and to avoid immune responses to autoantigen

102 Tissues have a natural capacity to replace dying cells and to heal wounds.

103 Injury, phagocytosis of dying cells, and CD36 inflammatory signaling were determ

104 ch engulf and digest pathogens, infected and dying cells, and debris, and can recruit and regulate ot

105 signal gradient, and in turn the presence of dying cells, and migrate to their vicinity.

106 h a death domain) complexes were detected in dying cells, and neither of these initiator caspases nor

107 ecular signaling events between macrophages, dying cells, and other tissue-resident cells.

108 Cell death density, total number of dying cells, and regional volume were determined in 16 r

109 Ligands from dying cells are a source of Toll-like receptor (TLR) act

110 Dying cells are capable of activating the innate immune

111 t has been shown, however, that senescent or dying cells are capable of eliciting inflammatory respon

112 Dying cells are distinguished by their biochemical and m

113 These dying cells are distributed in an anterior to posterior

114 efferocytosis - the process by which dead or dying cells are engulfed and digested by phagocytes.

115 When we trigger apoptosis in epithelia, dying cells are extruded to preserve a functional barrie

116 odels of necroptosis and apoptosis, in which dying cells are generated by receptor-interacting protei

117 When dying cells are injected into LAP-deficient mice, they a

118 site is changed, cell death is reduced, and dying cells are instead engulfed by stand-in phagocytic

119 Dying cells are localized to regions of TPIT expression

120 Strikingly, >95% of these dying cells are not productively infected but instead co

121 nstrated that danger signals associated with dying cells are not sufficient to initiate alloimmunity,

122 To preserve epithelial barrier function, dying cells are squeezed out of an epithelium by "apopto

123 Surprisingly, the vast majority of dying cells arrested the apoptotic process and recovered

124 genous heat shock proteins on the surface of dying cells as a mechanism of immunogenic death of human

125 Dendritic cells can acquire infected dead or dying cells as exogenous sources of antigens for present

126 e S1P(2) receptor in the cells neighboring a dying cell, as S1P(2) knockdown in these cells or its lo

127 s likely derive from the remains of dead and dying cells, as well as from disturbances in clearance.

128 ages ensures the nonimmunogenic clearance of dying cells, as well as the maintenance of self-toleranc

129 horylation events, produced in living versus dying cells at ERK-inducible versus ERK-independent site

130 TUNEL staining identified dying cells at P14 through P60, mainly in the CA3 subfie

131 ic effects of death - by making resources in dying cells beneficial to others.

132 ndogenous molecules released from damaged or dying cells both through direct binding of ligands and i

133 tigens not only by delaying the clearance of dying cells but also by altering intracellular processin

134 ively inhibited the inflammatory response to dying cells but not to microbial molecules or sterile ir

135 rectly to histones exposed on the surface of dying cells but we did not detect significant interactio

136 and the specific recognition and removal of dying cells by a clearance 'crew' composed of profession

137 othelial cell sprouts that extend toward the dying cells by a mechanism that involves endothelial cel

138 In infarcted heart, improper clearance of dying cells by activated neighboring phagocytes may prec

139 f Treml4 expression did not impair uptake of dying cells by CD8alpha(+) dendritic cells or cross-pres

140 However, uptake of dying cells by dendritic cells (DCs) is generally a noni

141 s can be achieved through the replacement of dying cells by differentiating precursors or self-renewa

142 ntain an intact barrier, epithelia eliminate dying cells by extrusion.

143 nate immunity is designed/poised to identify dying cells by their unique surface-associated molecular

144 cid-containing debris released from dead and dying cells can be recognized as damage-associated molec

145 The inefficient clearance of dying cells can lead to abnormal immune responses, such

146 ls in the other compartment, indicating that dying cells can release long-range death factors.

147 ixture of lipids called oxPAPC, derived from dying cells, can hyperactivate dendritic cells (DCs) but

148 nimals are morphologically distinct from the dying cells characteristic of C. elegans programmed cell

149 Mice lacking molecules associated with dying cell clearance develop SLE-like disease, and phago

150 tophagy but not LAP do not display defective dying cell clearance, inflammatory cytokine production,

151 Dying cells contained DNA strand breaks with overhanging

152 the release of histones, specifically, from dying cells contributes to the inflammation of AKI is un

153 agocyte must discriminate between living and dying cells; current concepts for this discrimination de

154 zed is that endogenous molecules released by dying cells (damage-associated molecular patterns; DAMPs

155 onsidered only a passive process of dead and dying cells, data from multiple laboratories worldwide h

156 Remarkably, dying cells did not stain positively for terminal deoxyn

157 Flow cytometry showed that MPs derived from dying cells displayed light scatter and DNA staining sim

158 evated apoptotic microparticles derived from dying cells during acute HIV-1 infection.

159 We now know that the phagocytic clearance of dying cells (efferocytosis), particularly by macrophages

160 any different cellular stresses in which the dying cell essentially 'packages' itself for removal.

161 Dying cells exhibited classical hallmarks of apoptosis,

162 ore morphologically intact neurons and fewer dying cells existed in the ipsilateral frontal cortex ar

163 rface, a hallmark of apoptosis, prepares the dying cell for engulfment and elimination by phagocytes.

164 may impact the clearance and consequences of dying cells for host physiology.

165 y conserved process that efficiently removes dying cells from animal bodies during development.

166 re activated not just to kill but to prevent dying cells from triggering a host immune response.

167 Later, the chloroplasts of dying cells generate NO, which only slightly affects cel

168 rammed cell death (PCD), but its function in dying cells has been unclear.

169 The visualization of autophagosomes in dying cells has led to the belief that autophagy is a no

170 Defects in clearance of dying cells have been proposed to underlie the pathogene

171 Finally, the mitochondria in dying cells have dramatically altered movements and cell

172 rs that are responsible for the clearance of dying cells have recently been found to mediate envelope

173 erform critical functions in both living and dying cells; however, how caspases perform physiological

174 The phagocytic clearance of dying cells in a tissue is a highly orchestrated series

175 Dronc may play roles in dying cells in addition to activating downstream effecto

176 Dying cells in aging DBA/2J mice exhibited nuclear local

177 Dying cells in autophagy gene null EBs fail to express t

178 The analysis of the percentage of dying cells in FVB-GFP <--> B6-ROSA chimeras yielded an

179 ion correlated positively with the number of dying cells in HVC.

180 TUNEL labeling of dying cells in mutants revealed a transient period of ap

181 sms possess mechanisms to dismantle and mark dying cells in response to diverse noxious stimuli and s

182 detection of activated caspase-3 to identify dying cells in the brains of male and female mice from p

183 urological deficit, edema, and the number of dying cells in the core and periinfarct area.

184 Here we show that dying cells in the developing ganglion and inner nuclear

185 A widely accepted hypothesis is that dying cells in the graft release "danger" molecules that

186 Thus, they are unable to effectively replace dying cells in the injured heart.

187 -associated molecular patterns released from dying cells in the injured spinal cord likely activate d

188 mice and caused the accumulation of damaged, dying cells in the mammary gland.

189 bly caused by cell fragments and debris from dying cells in the meshwork, ciliary body, and other ant

190 The dying cells in the MTZs send 'danger' signals that attra

191 We hypothesize that dying cells in the retina generate a gap junction-permea

192 showed profound in vivo defects in clearing dying cells in the thymus and testes.

193 lls are responsible for replacing damaged or dying cells in various adult tissues throughout a lifeti

194 onocyte-derived cells that directly engulfed dying cells in vitro were not the major APCs stimulating

195 ammatory cytokine production when exposed to dying cells in vitro.

196 of Treml4 in the uptake and presentation of dying cells in vivo.

197 atory proliferation signaling (CPS), whereby dying cells induce proliferation in neighboring cells as

198 Dying cells initiate adaptive immunity by providing both

199 Repeated injection of dying cells into LAP-deficient, but not LAP-sufficient,

200 y convert 5'-AMP generated by neutrophils or dying cells into the anti-inflammatory mediator adenosin

201 Moreover, Rac1 restricts the extrusion of dying cells into the lumen, thus promoting their eradica

202 egans an increase in the refractility of the dying cell is a hallmark morphological change that is ca

203 onucleosomal fragmentation of chromosomes in dying cells is a hallmark of apoptosis.

204 The release of histones from dying cells is associated with microvascular thrombosis

205 Disassembly and phagocytic removal of dying cells is critical to maintain immune homeostasis.

206 nd humans suggest that the prompt removal of dying cells is crucial for immune tolerance and tissue h

207 l-free circulating DNA (cfDNA) released from dying cells is emerging as a diagnostic tool for monitor

208 able p75 mutant, mitochondrial morphology of dying cells is maintained, and loss of plasma membrane i

209 ysiological conditions, self-DNA released by dying cells is not detected by intracellular DNA sensors

210 lar adenosine triphosphate (ATP) released by dying cells is sensed as a danger associated molecular p

211 the outer surface of the plasma membrane of dying cells is unknown, as are the molecular mechanisms

212 to the actin cortex in cells surrounding the dying cell, it does so by controlling actin and microtub

213 mpensatory cell division can be triggered by dying cells, it is unknown how cell death might relieve

214 ants could account for persistent dsDNA from dying cells leading to an aberrant immune response in th

215 disproportionate to the accumulation of old dying cells, leading to cardiac decompensation.

216 disruption of MyD88 may consequently render dying cells less sensitive to proinflammatory stimuli in

217 cells with the TLR7/8 ligand ssRNA, whereas dying cells loaded with TLR3 ligand were less efficient.

218 Dying cells localise to the fusing foregut epithelial ri

219 How does the number of dying cells match those dividing to maintain constant nu

220 e of endogenous danger signals released from dying cells may aid in a better understanding of mechani

221 genous TLR ligands such as the products from dying cells may also engage with TLRs as damage-associat

222 During viral infection, dying cells may also release nucleic acids into the tiss

223 We speculate that dying cells may communicate cell fate or behavior instru

224 ding protein and factor H also interact with dying cells, most likely to decrease complement activati

225 Apoptosis and the subsequent clearance of dying cells occurs throughout development and adult life

226 e recognition of these two classes of native dying cells occurs via distinct and noncompeting mechani

227 the growth-stimulating effect of irradiated, dying cells on living melanoma cell growth.

228 Uncleared debris from dying cells or aggregated proteins can be toxic and may

229 s, cells recycle nucleotides from the DNA of dying cells or from cellular material ingested through t

230 e, non-vesicular leakage, reverse transport, dying cells or glia.

231 s, but can also sense self-DNA released from dying cells or in neutrophil extracellular traps complex

232 Self-DNA (eg, released from dying cells or in neutrophil extracellular traps) and an

233 ory and cell death signaling pathways within dying cells orchestrate adaptive immunity.

234 ing of actin and myosin II that squeezes the dying cell out of the epithelial sheet.

235 ring of actin and myosin, which squeezes the dying cell out of the epithelium.

236 ontract an actomyosin ring that squeezes the dying cell out.

237 thelia maintain intact barriers by squeezing dying cells out using a process termed cell extrusion.

238 conduits through which toxic molecules from dying cells pass to and injure coupled neighbors.

239 Adaptive immune responses to Ags released by dying cells play a critical role in the development of a

240 Engulfment of dying cells plays an important role during animal develo

241 evated first during apoptosis, implying that dying cells poise to recover, even while under apoptotic

242 Dead and dying cells produce signals that can influence Ag proces

243 r synthetic TLR7/8 agonists contained within dying cells promote the conversion of monocytes to DCs w

244 Flu-infected dying cells promoted monocytes to become mature DCs and

245 port that LL37 can bind self-RNA released by dying cells, protect it from extracellular degradation,

246 We found that both surviving and dying cells reach similar levels of p53, indicating that

247 mes containing engulfed particles, including dying cells, recruit elements of the autophagy pathway t

248 e neurons with abnormal maturation and fewer dying cells relative to control mice.

249 mature IL-1beta and of the alarmin IL-1alpha Dying cells release IL-1alpha also, independently of the

250 Dead and dying cells release nucleic acids.

251 hat necrosis stimulates inflammation because dying cells release proinflammatory molecules that are r

252 s of the MPS and neighboring tissue cells in dying cell removal, and candidate molecules that might a

253 Dying cells represent a threat to the body that should b

254 , and immunologically silent disposal of the dying cells requires a coordinated orchestration of mult

255 the hypothesis that impaired PS exposure on dying cells results in defective macrophage programming,

256 e adherens junctions are disassembled as the dying cell retracts, and new contacts are formed between

257 is is a regulated form of necrosis, with the dying cell rupturing and releasing intracellular compone

258 roinflammatory properties to DNA released by dying cells, setting up a positive amplification loop be

259 er m2 resulted in 40% to 50% cell death with dying cells showing extensive tissue transglutaminase cr

260 c granulomas also contained large numbers of dying cells, some of which coexpressed the F4/80 macroph

261 Dying cells stimulate inflammation, and this response is

262 Activation of initiator caspases in the dying cells stimulates the production of hydrogen peroxi

263 pase substrate that is rapidly eliminated in dying cells, suggesting that ICD-1 apoptosis-suppressing

264 Activation of ERK, p38 and JNK in the dying cells suggests that an overly active MAPK signalin

265 und that microtubules in cells surrounding a dying cell target p115 RhoGEF to the actin cortex to con

266 Proinflammatory molecules released by dying cells, termed damage-associated molecular patterns

267 roliferating cells, but fewer proportions of dying cells, than did the CLL cells of TCL1-Tg mice.

268 faces death in the form of its own dead and dying cells that arise during normal tissue turnover, in

269 as a proinflammatory molecule released from dying cells that contributes significantly to the cell d

270 es a mechanism to explain cohort behavior of dying cells that is seen both in normal development and

271 ights into the molecular signals released by dying cells, the role of pattern recognition receptors,

272 of these new observations challenge the way dying cells themselves are viewed, as well as how health

273 us ligands that are released from uninfected dying cells, thereby activating immune responses against

274 RP) cation channel, CED-11, that acts in the dying cell to promote the increase in apoptotic cell ref

275 nuclear DNA-associated entities released by dying cells to induce type I IFN.

276 , we demonstrate that the signal produced by dying cells to initiate this process is sphingosine-1-ph

277 ARP-1 reduces GzmA-mediated death and drives dying cells to necrosis rather than apoptosis.

278 of caspase-9, Apaf-1, or caspase-3/7 causes dying cells to secrete IFN-beta.

279 he initiation of the release of signals from dying cells to stimulate melanoma tumor growth.

280 In the Drosophila wing imaginal disc, dying cells trigger compensatory proliferation through s

281 which cells undergo death determines whether dying cells trigger inflammatory responses or remain imm

282 ion of oxidized phospholipids, a hallmark of dying cells, triggering hyperactivation of dendritic cel

283 s of sterile inflammation, ATP released from dying cells triggers, through activation of the purinerg

284 ance is tightly linked to apoptosis and that dying cells use both recruitment and eat-me signals for

285 onsidered only a passive process of dead and dying cells, vascular calcification has now emerged as a

286 as damage-associated molecular patterns, by dying cells was not sufficient for CD8(+) T cell cross-p

287 7E11 as a marker of dying cells was studied by flow cytometry and microscopy

288 on of HMGB1, an established DAMP released by dying cells, was critical for tumor progression in an es

289 Ficolin-2 protein, which bound to dying cells, was detected in donor kidneys in a passenge

290 ein, factor H, and C1q share some ligands on dying cells, we showed that these three proteins did not

291 Approximately 52% of the dying cells were glia, and 48% were neurons.

292 , we asked whether MPs derived in vitro from dying cells were similar to those in maternal plasma.

293 n (DAMP), released from ischemic tissues and dying cells which, when crystalized, is able to activate

294 d cells might instead be glia, nonneural, or dying cells, which are irrelevant to direct neuronal sig

295 ient mice showed in vivo defects in clearing dying cells, which led to multiple organ damage indicati

296 homeostasis, some organs are able to replace dying cells with additional proliferation of surviving c

297 in released during tumor cell turnover or to dying cells with permeable membranes.

298 imilar responses were induced by loading the dying cells with the TLR7/8 ligand ssRNA, whereas dying

299 Phagocytes clear dying cells within an organism to prevent damaging infla

300 Dying cells within type A F. tularensis-infected tissues