ライフサイエンスコーパス: corpse

1 that can be run at global scales (MIMICS and CORPSE).

2 crosis", derived from the Greek "nekros" for corpse.

3 step in apoptosis is engulfment of the cell corpse.

4 ge acquired during the effort to recover the corpse.

5 ell death (PCD) to produce a functional cell corpse.

6 rity followed by rapid shrinkage of the cell corpse.

7 phagocytes interpret the engulfed apoptotic corpse.

8 o act as a signal for engulfment of the cell corpse.

9 the ingestion of cholesterol-rich apoptotic corpses.

10 ryos contain many unusually large cell-death corpses.

11 programmed cell death or engulfment of cell corpses.

12 ents efficient engulfment of pharyngeal cell corpses.

13 robial pathogens, and apoptotic and necrotic corpses.

14 refractile bodies resembling irregular cell corpses.

15 phospholipid ligand on the surfaces of cell corpses.

16 the outcomes that are triggered by the cell corpses.

17 regions) led to no or fewer-than-normal cell corpses.

18 t six genes in the removal of apoptotic cell corpses.

19 ace phagocytic receptor that recognizes cell corpses.

20 mbranes and clusters around neighboring cell corpses.

21 ngulfing cells during the engulfment of cell corpses.

22 scent to Everest, is certainly littered with corpses.

23 nfirmed by the absence of signs of trauma on corpses.

24 tivity, and preferentially engulfed neuronal corpses.

25 pathogens transmissible through contact with corpses.

26 ility for inferring postmortem relocation of corpses.

27 of macrophages to remove bystander apoptotic corpses.

28 diators during the phagocytosis of apoptotic corpses.

29 more termites than retrieval of conspecific corpses.

30 T cell responses to antigens present in cell corpses.

31 ng the processing of ingested apoptotic cell corpses.

32 ls and signal efficient phagocytosis of cell corpses.

33 08 promotes the degradation of engulfed cell corpses.

34 crophages) for the efficient removal of cell corpses.

35 mal tissue cells can digest nearby apoptotic corpses(1-4).

36 er tissues from 27 Italian and United States corpses: 3.5-hour-old to 37-day-old.

37 rey and professional phagocytes to clear the corpse(6).

38 aridity (with little or no decomposition of corpses) a simple demographic model shows that dead indi

39 In 136 human forensic corpses, a post-mortem cardiac MR examination was carrie

40 ion of Atg1, in glia is sufficient to rescue corpse accumulation as well as neurodegeneration.

41 receptor Mertk is associated with apoptotic corpse accumulation in the testes and degeneration of ph

42 et al. show that swelling of nuclei in cell corpses activates eicosanoid signaling to recruit leukoc

43 endosperm (SE) retains nutrient-packed cell corpses after grain filling.

44 nty corpses (four female corpses and 16 male corpses; age range, 15-80 years), all of whom were repor

45 thologically (that is, necrotic vs apoptotic corpses) also are recognized by macrophages but do not d

46 Twenty corpses (four female corpses and 16 male corpses; age range, 15-80 years), al

47 ne distinct pathways for the phagocytosis of corpses and bacteria in Drosophila.

48 of DNGR-1 binds F-actin exposed by dead cell corpses and causes the receptor to signal and potentiate

49 required for digesting DNA of apoptotic cell corpses and dietary DNA, it is not required for viabilit

50 f DD1alpha thus prevents persistence of cell corpses and ensures efficient generation of precise immu

51 ment; rnp-8 null mutants have more germ cell corpses and fewer oocytes than normal.

52 ficient processing of the ingested apoptotic corpses and for successive efferocytosis.

53 ower survival, with many uncleared apoptotic corpses and inflammatory cytokines within the colonic ep

54 th lipids released by neighbouring apoptotic corpses and retinoids released by healthy counterparts.

55 al fingerprints for the presence of metazoan corpses and show that death cue sensing by AWB and ASH l

56 However, how dying cells, cell corpses and their liberated cytokines, chemokines and in

57 ed for efficient degradation of the engulfed corpse, and in the absence of LAP, engulfment of dead ce

58 tin reorganization around the apoptotic cell corpse, and that CED-1 and CED-6 colocalize with each ot

59 he information that can be passed on by cell corpses, and (c) the ways by which efferocyte population

60 e somatic tissues, excessive numbers of cell corpses, and profound defects in morphogenesis and diffe

61 ll programmed cell death is blocked and such corpses are absent.

62 ar and molecular mechanism by which neuronal corpses are culled during DRG development.

63 lls for the death of Minute neighbors, whose corpses are engulfed by wild-type cells.

64 How cell corpses are engulfed is largely unknown.

65 ey are so rapidly phagocytosed that very few corpses are ever seen in most embryonic tissues.

66 ndergoing pyroptosis, and whether pyroptotic corpses are immunogenic.

67 nct modes of recognition for these different corpses are linked to opposing responses from engulfing

68 Cell corpses are often engulfed by professional phagocytes su

69 Corpses are often recognized by a postmortem change in a

70 By 3 days postfertilization, most cell corpses are rapidly engulfed by macrophages.

71 During programmed cell death, cell corpses are rapidly engulfed.

72 How the massive numbers of corpses are removed is unknown.

73 Few apoptotic corpses are seen even in tissues with high cellular turn

74 The exposure to C. elegans corpses, as well as corpse lysates, activates sensory ne

75 apacity of these cells to cross-present cell corpse-associated antigens to MHC class I-restricted T c

76 binds dead-cell debris and facilitates XP of corpse-associated antigens.

77 tic material, may be compared with that of a corpse at a funeral: they provide the reason for the pro

78 on is indicative of the cellular status of a corpse at the time of death, a portion of which may repr

79 s dead cells accumulate in its way, forming "corpse barriers" that block further attacks.

80 d high level exposure (direct contact with a corpse, body fluids, or a case with diarrhoea, vomiting,

81 o some efferocytic macrophages carrying high corpse burden.

82 defective not only in the engulfment of cell corpses but also in the migrations of two specific gonad

83 tial for efficient phagocytosis of apoptotic corpses but was not required for the engulfment of bacte

84 tosis followed by programmed removal of cell corpses by blood phagocytes within approximately 1 day.

85 ognition and subsequent phagocytosis of cell corpses by engulfing cells.

86 gocytosis of axonal debris and neuronal cell corpses by glia.

87 ed host cells and then clearance of cellular corpses by macrophages.

88 bed despite engulfment of zooid-derived cell corpses by phagocytes.

89 r surface, which promotes the uptake of cell corpses by professional phagocytes and ultimately suppor

90 Apoptotic cell (AC) corpses can be taken up by certain types of dendritic ce

91 nally resolve their phagocytic cargo of cell corpses, cell debris, and pathogens.

92 Whether corpse clearance can be enhanced in vivo for potential b

93 Here, we investigate the mechanism of corpse clearance in the Drosophila melanogaster ovary, a

94 ese genes redundantly promote cell death and corpse clearance in the EAS, but are not required for SE

95 expressed on phagosomal surfaces during cell corpse clearance in the same time window as DYN-1.

96 and UNC-73 (the TRIO homolog) also regulate corpse clearance in vivo, upstream of CED-12.

97 nship between a find-me signal and efficient corpse clearance in vivo.

98 during cell death to facilitate efferocytic corpse clearance is not well understood.

99 New observations suggest that corpse clearance is tightly linked to apoptosis and that

100 emobilize stored nutrients through a complex corpse clearance process.

101 s tubulate into small vesicles to facilitate corpse clearance within 1.5 h.

102 observations, we suggest that efferocytosis (corpse clearance) could contribute to proper tissue clos

103 RL-8 reduces tubulation by kinesin-1, delays corpse clearance, and mislocalizes ARL-8 away from lysos

104 ytes via TTR-52 and CED-1 to facilitate cell corpse clearance.

105 on should be considered whenever exposure to corpses contributes to epidemic propagation.

106 to maximize extraction of antigens from cell corpses, coupling DNGR-1 function to its cellular locali

107 Vertebrate corpse decomposition provides an important stage in nutr

108 underlying phagocyte arm extension and cell corpse degradation is not well understood.

109 totic cells successively, and to process the corpse-derived cellular material.

110 longed, frustrated phagocytosis and frequent corpse disintegration.

111 y, and results in delayed appearance of cell corpses during development in C. elegans.

112 h remodel synapses and engulf apoptotic cell corpses during development, but whether unique molecular

113 sly normal, but exhibit fewer apoptotic cell corpses during development.

114 ne ced-8 lead to the late appearance of cell corpses during embryonic development in C. elegans.

115 atures of coordinated clearance of apoptotic corpses during embryonic development.

116 ne ced-7 functions in the engulfment of cell corpses during programmed cell death.

117 Specifically, we identify two classes of corpse: early deaths with a swollen pharynx (which we ca

118 moting the internalization of apoptotic cell corpses; ELMO and Dock180 function together as a guanine

119 we show that macrophages, within minutes of corpse encounter, use transcriptional pause/release to u

120 CED-12 acts in engulfing cells for cell corpse engulfment and interacts physically with CED-5, w

121 Here, we show that apoptotic corpse engulfment by Drosophila macrophages is an essent

122 rter transgene was used that highlights cell corpse engulfment by fluorescence microscopy.

123 with apoptotic cells and which promotes cell-corpse engulfment by phagocytes.

124 rtebrate chordate Botryllus schlosseri, cell corpse engulfment by phagocytic cells is the recurrent m

125 e lacking atg5 display a defect in apoptotic corpse engulfment during embryonic development.

126 dox-sensitive transcription factor Nrf2 upon corpse engulfment during immune surveillance, downstream

127 that the molecular mechanism underlying cell corpse engulfment during programmed cell death may be co

128 spases, the BH3-only protein CED-13, and PCD corpse engulfment factors, are required in C. elegans to

129 apoptotic cells, ced-8 is important for cell corpse engulfment in C. elegans.

130 that ced-5, a gene that is required for cell-corpse engulfment in the nematode Caenorhabditis elegans

131 ysis places epn-1 and chc-1 in the same cell-corpse engulfment pathway as ced-1, ced-6 and dyn-1.

132 In C. elegans, PSR-1 acts in the same cell corpse engulfment pathway mediated by intracellular sign

133 an active process of cell assassination and corpse engulfment, and also roles for Myc and the Warts/

134 a receptor required for macrophage-mediated corpse engulfment, causes similar CNS defects.

135 legans homolog of PSR, is important for cell corpse engulfment.

136 adation did not occur in the absence of cell-corpse engulfment.

137 Without Rac1, residual milk and cell corpses flood the ductal network, causing gross dilation

138 rged macrophages carrying multiple apoptotic corpses form.

139 n the degradation of DNA from apoptotic cell corpses formed in the process of normal mammalian develo

140 Twenty corpses (four female corpses and 16 male corpses; age ra

141 -sectional study of the sampling of 27 human corpses from criminal cases with postmortem intervals be

142 ytic macrophages and the removal of cellular corpses from injury sites.

143 these flies to connect sites between which a corpse had been moved even in the absence of overall geo

144 pathway controlling the removal of apoptotic corpses has now been identified in the nematode.

145 n of live cell material and the rejection of corpses illuminate a stark contrast to the established m

146 creen for mutants containing refractile cell corpses in a C. elegans strain in which all programmed c

147 ds that the surrounding cells clear away the corpses in a manner appropriate to the type of cell deat

148 own about clearance of neuronal and synaptic corpses in AD and other neurodegenerative diseases.

149 argely responsible for the clearance of cell corpses in Drosophila melanogaster and mammalian systems

150 CED-1 failed to cluster around cell corpses in mutants defective in the engulfment gene ced-

151 ent manner as measured by counting apoptotic corpses in the nematode germ line.

152 a defect in the clearance of apoptotic cell corpses in vha-12 null mutants.

153 mal degradation in phagocytosis of apoptotic corpses in vivo.

154 consequence of recognition of the apoptotic corpse, independent of subsequent engulfment and soluble

155 The modulatory activity of the corpse is manifest as an immediate-early inhibition of p

156 The removal of apoptotic cell corpses is important for maintaining homeostasis.

157 e that macrophage-mediated clearance of cell corpses is required for proper morphogenesis of the Dros

158 removal of both apoptotic and necrotic cell corpses is required for the full cell-killing effect of

159 pment and viability, because undigested cell corpses lead to lesions throughout the body.

160 e exposure to C. elegans corpses, as well as corpse lysates, activates sensory neurons AWB and ASH, t

161 That the characteristic cell corpse morphology is also induced in Arabidopsis and tob

162 (approximately 50 kb) DNA fragments and cell corpse morphology--including cell shrinkage, plasma memb

163 istic practices such as secondary interment, corpse mutilation and ritualized witch executions might

164 e is extensive apoptosis, and these neuronal corpses need to be cleared to prevent an inflammatory re

165 liferation, indicating that the reduced cell corpse number is not a direct result of premature embryo

166 This reduction in corpse number is not caused by reduced apoptosis, but in

167 , probably explaining the diminution in cell corpse number; however, others have little effect on cel

168 process of degradation of the DNA of a cell corpse occurs in at least three distinct steps and requi

169 have been observed using tools to clean the corpse of a deceased group member.

170 cellular machinery promoting phagocytosis of corpses of apoptotic cells is well conserved from worms

171 eration research, which is littered with the corpses of studies that reported regeneration that later

172 Corpses of the congeneric species, Reticulitermes virgin

173 g the resolution phase of inflammation, the 'corpses' of apoptotic leukocytes are gradually cleared b

174 mbly during decomposition of mouse and human corpses on different soil substrates.

175 ironment in search of pathogens or apoptotic corpses or debris.

176 Certain fly larvae can infest corpses or the wounds of live hosts.

177 the chloride-sensing pathway (and not due to corpse overload or poor degradation), including the chlo

178 Our data indicate that corpses persist because of defective degradation of cell

179 Our data indicate that corpses persist because of defective phagosome maturatio

180 omes specifically resulting in specific cell corpse/phagocyte interactions (phagocytic synapses) that

181 posing components of the conserved apoptotic corpse phagocytosis machinery.

182 DOCK180, which acts with CED-10 Rac in cell-corpse phagocytosis, acted with MIG-2 but not CED-10 in

183 ntrast, ced-10 is uniquely required for cell-corpse phagocytosis, and mig-2 and rac-2 have only subtl

184 g and cell migration but did not affect cell-corpse phagocytosis.

185 An investigation of this corpse phenotype revealed that it results from a reversa

186 The corpse plant (Amorphophallus titanum) is so named becaus

187 are few recorded occurrences of this type of corpse preparation for a large number of archaeological

188 role in development, and the removal of cell corpses presents an important challenge for the developi

189 or Draper as well as other components in the corpse processing machinery.

190 er maturing phagosomes, supporting defective corpse processing.

191 acrophage genes involved in cytoskeleton and corpse processing.

192 This defect is due to persistence of cell corpses, rather than impairment of PCD.

193 that the ABC transporter CED-7 promotes cell corpse recognition by CED-1, possibly by exposing a phos

194 pose that phagocytosis is not merely passive corpse removal but has an active role in maintaining neu

195 Thus, genes that mediate corpse removal can also function to actively kill cells.

196 At least seven corpse removal genes in nematodes have mammalian equival

197 e the primary phagocytic cells for apoptotic corpse removal in developing mouse dorsal root ganglia (

198 difficult to track cell death and subsequent corpse removal in vivo.

199 ehavioural tasks they perform, assuming more corpse removal tasks, particularly infected corpse remov

200 al challenge in understanding how defects in corpse removal translate into diseased states is the ide

201 corpse removal tasks, particularly infected corpse removal, and reducing their efforts in foraging a

202 We propose that during cell corpse removal, dynamin's self-assembly and GTP hydrolys

203 ally downstream of these proteins to mediate corpse removal, functionally linking the two engulfment

204 gulfing cells to control locomotion and cell corpse removal, respectively, indicating that unc-108 ha

205 d-10 (rac) downstream of ced-2 (crk) in cell corpse removal.

206 ND-1 and its partner CCZ-1 as new factors in corpse removal.

207 and rapid post-mortem clearance of cellular corpses represent a physical defense mechanism restricti

208 hich encodes a receptor that recognizes cell corpses, rescues the cell-killing defects of ced-1 mutan

209 ure of macrophages to dispose of cancer cell corpses, resulting in a pro-inflammatory tumor microenvi

210 revent macrophages from removing neighboring corpses, revealing a new mechanism by which senescence m

211 ell death, which accounts for the extra cell corpses seen in pag-3 mutants.

212 as been implicated in the engulfment of cell corpses, suggesting that CED-7 and ABC1 may be functiona

213 al efferocytosis of SARS-CoV-2-infected cell corpses suppresses macrophage anti-inflammation and effi

214 bial eukaryotic ecology within a decomposing corpse system and suggest that microbial community data

215 hree unique regions), showed unusually large corpses that were, in some cases, attributable to extrem

216 ss-of-function phenotype of Ad-infected cell corpses that, in contrast to cells infected with wt Ad14

217 ronted with high rates of emerging apoptotic corpses, the macrophages displayed heterogeneity in engu

218 tic cells using macrophages, plants use cell corpses throughout development and disassemble cells in

219 Recent news headlines claimed that corpses thrown into Syrian streets are causing cutaneous

220 of cell debris may go beyond merely removing corpses to actively promoting regeneration in developmen

221 own previously that the ability of apoptotic corpses to be recognized by macrophages and to modulate

222 pt their transcription to achieve continuous corpse uptake is incompletely understood.

223 ulted in a significant increase in apoptotic corpse uptake per phagocyte, whereas the loss of SLC12A4

224 TIM-4 lacking its cytoplasmic tail promoted corpse uptake via PtdSer recognition.

225 ocyte, whereas the loss of SLC12A4 inhibited corpse uptake.

226 sively engulf and process multiple apoptotic corpses via efferocytosis to achieve tissue homeostasis(

227 The burial task associated with congeneric corpses was coupled with colony defence and involved ten

228 ng apoptotic cells, and phagocytosis of cell corpses was mediated by the binding of adiponectin to ca

229 om wild type in the temporal pattern of cell corpses was observed, indicating that much of the genome

230 least 16 unique regions), an excess of cell corpses was observed.

231 rare ritual in the Imperial Roman times when corpses were more often cremated.

232 The developmental stage at which the extra corpses were observed varied among the class III deficie

233 elegans, results in supernumerary apoptotic corpses, whereas its overexpression is sufficient to inh

234 tion ensure efficient and rapid clearance of corpses wherever death is encountered within the varied

235 dertaking behaviour depends on the origin of corpses which is associated with different types of risk

236 to the pathological accumulation of necrotic corpses, which induce an inflammatory response that init

237 optotic cell rupture, to crown the resultant corpse with filopodia.

238 upon direct contact of the virally infected corpses with responder macrophages.

239 Reticulitermes flavipes responded to corpses within minutes of death.

240 uring this death phase called takeover, cell corpses within the dying organism are engulfed by circul