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 step in apoptosis is engulfment of the cell corpse.

3 ge acquired during the effort to recover the corpse.

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

5 rity followed by rapid shrinkage of the cell corpse.

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

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

8 programmed cell death or engulfment of cell corpses.

9 ents efficient engulfment of pharyngeal cell corpses.

10 robial pathogens, and apoptotic and necrotic corpses.

11 refractile bodies resembling irregular cell corpses.

12 phospholipid ligand on the surfaces of cell corpses.

13 the outcomes that are triggered by the cell corpses.

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

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

16 ace phagocytic receptor that recognizes cell corpses.

17 mbranes and clusters around neighboring cell corpses.

18 ngulfing cells during the engulfment of cell corpses.

19 diators during the phagocytosis of apoptotic corpses.

20 more termites than retrieval of conspecific corpses.

21 T cell responses to antigens present in cell corpses.

22 scent to Everest, is certainly littered with corpses.

23 ng the processing of ingested apoptotic cell corpses.

24 ls and signal efficient phagocytosis of cell corpses.

25 08 promotes the degradation of engulfed cell corpses.

26 crophages) for the efficient removal of cell corpses.

27 the ingestion of cholesterol-rich apoptotic corpses.

28 ryos contain many unusually large cell-death corpses.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

49 How cell corpses are engulfed is largely unknown.

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

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

52 Cell corpses are often engulfed by professional phagocytes su

53 Corpses are often recognized by a postmortem change in a

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

76 Vertebrate corpse decomposition provides an important stage in nutr

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

101 rged macrophages carrying multiple apoptotic corpses form.

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

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

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

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

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

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

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

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

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

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

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

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

114 mal degradation in phagocytosis of apoptotic corpses in vivo.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

132 Corpses of the congeneric species, Reticulitermes virgin

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

174 Reticulitermes flavipes responded to corpses within minutes of death.

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