ライフサイエンスコーパス: dead cell

1 ze with each other and with actin around the dead cell.

2 the endogenous rng gene in doubly mutant rne deaD cells.

3 ons of dividing, quiescent (nondividing) and dead cells.

4 onses, degrade lipoproteins, and phagocytose dead cells.

5 f fluorescein, and intracellular staining in dead cells.

6 ble for LAP induced by uptake of microbes or dead cells.

7 nt cell-associated Ags derived from captured dead cells.

8 end-point markers of assays for live versus dead cells.

9 specific to cell-associated Ags of captured dead cells.

10 ogous CD8(+) T cell responses against Ags of dead cells.

11 osis and impairing the subsequent removal of dead cells.

12 assays, as a marker distinguishing live from dead cells.

13 the contaminant is associated with permeable dead cells.

14 unction in the recognition and engulfment of dead cells.

15 g nonsporulating siblings and feeding on the dead cells.

16 e, OR), which differentiate between live and dead cells.

17 nd cell proliferation, presumably to replace dead cells.

18 nse against infection and for the removal of dead cells.

19 phagocytic cells recognize and engulf these dead cells.

20 with <2n DNA content and finally, dying and dead cells.

21 cellular matrix proteins, efficiently engulf dead cells.

22 the cytoplasm and of living cells nucleus of dead cells.

23 e Shh domain and a decrease in the number of dead cells.

24 olor fluorescent dye to distinguish live and dead cells.

25 ught to facilitate the recycling of DNA from dead cells.

26 odimer and calcein to discriminate live from dead cells.

27 epresent live, apoptotic, and late-apoptotic/dead cells.

28 radation of cells rather than recognition of dead cells.

29 which interacts with Annexin A1 (ANXA1) from dead cells.

30 cognize phosphatidylserine on the surface of dead cells.

31 es for efficient recycling of molecules from dead cells.

32 actively by living neurons and passively by dead cells.

33 ytes recognize phosphatidylserine exposed on dead cells.

34 d not internal P6 in membrane-compromised or dead cells.

35 f the kinase was also induced by exposure to dead cells.

36 important role in regulating the removal of dead cells.

37 9A) is a DC-restricted receptor that detects dead cells.

38 ignificant Tl accumulation by either live or dead cells.

39 cell lines also decreased the engulfment of dead cells.

40 e nutrients for growth and reproduction from dead cells.

41 h the limbal stroma containing live, but not dead, cells.

42 TPC reduced OGD-induced neuronal death (e.g. dead cells: 52.5 +/- 5.4% vs. 72.3 +/- 7.2% in the contr

43 educed TPC-induced neuronal protection (e.g. dead cells: 68.2 +/- 5.2% vs. 56.9 +/- 4.6% in vehicle+T

44 Dead cells accumulated in bone marrow from lupus patient

45 of self-RNA, but not self-DNA, released from dead cells accumulated in GCs drives enhanced GC respons

46 Consequently, in PSR-deficient mice, dead cells accumulated in the lung and brain, causing ab

47 f, spontaneously develops lesions containing dead cells, accumulates increased salicylic acid (SA) le

48 Dead cells accumulating in the tissues may contribute to

49 on in a static assay and a greater amount of dead-cell accumulation during biofilm maturation.

50 n mice led to the accumulation of unengulfed dead cells after MI, resulting in exacerbated inflammato

51 Dead cells also release danger signals that activate den

52 iding cells, and increases the percentage of dead cells among dividing T cells.

53 li that can induce inflammation-specifically dead cells and a variety of irritant particles, includin

54 monstrate that actin, presumably released by dead cells and abundant in infected sites, might be util

55 (MMP-9) and enhance macrophage clearance of dead cells and bacteria (GM-CSF).

56 ltures efficiently internalize material from dead cells and can cross-present exogenous antigens to C

57 DNA and by self-DNA, which is released from dead cells and complexes with antimicrobial peptides or

58 , the zones within solid tumors that contain dead cells and debris that will not be labeled by biored

59 hich surveil their surroundings for dying or dead cells and efficiently clear them in a quiescent man

60 tic carcinoma deposits in close proximity to dead cells and efficiently phagocytose tumour cells.

61 vested at days 0, 1, and 5 to count live and dead cells and intracellular mycobacteria.

62 are constructed on a cell sorter to exclude dead cells and lineage (CD45(+)Ter-119(+))-positive cell

63 ammatory reaction that clears the wound from dead cells and matrix debris, while activating reparativ

64 Inflammatory reaction clears dead cells and matrix debris, while prolongation or expa

65 infiltration and clearance of the wound from dead cells and matrix debris.

66 Recognition of microbial pathogens and dead cells and their phagocytic uptake by specialized im

67 educed neutrophilic inflammatory response to dead cells and tissue injury in vivo as well as greatly

68 mediators, while also promoting clearance of dead cells and tissue repair.

69 uired to initiate CD8(+) T cell responses to dead cells and to induce effective antitumor immune resp

70 eveloped to distinguish DNA from live versus dead cells and to separate extracellular from intracellu

71 lays preferential affinity for apoptotic and dead cells, and DS-stimulated cell cultures produce anti

72 n tissue healing, clearance of pathogens and dead cells, and initiation of adaptive immunity.

73 Mtb grew as a clump in dead cells, and macrophages which internalized dead infe

74 types allow the macrophage to engulf lipids, dead cells, and other substances perceived as danger sig

75 in mediating inflammation, the clearance of dead cells, and possibly resolution.

76 contrast is generated in the vicinity of the dead cells, and serves as an imaging marker for cell dea

77 tectable within 2 to 4 hours after uptake of dead cells, and that proteolysis by cathepsin D in an ac

78 death, the cells that sense and react to the dead cells, and the consequences of these fundamental el

79 The filamentation of the dead cells, and their protection by cell-permeable iron

80 genous porcine PBPC membranes (erythrocytes, dead cells, and/or platelets) to the purified fractions

81 required by DCs to cross-prime CTLs against dead cell antigens in mice.

82 thereby activating immune responses against dead-cell antigens.

83 Macroscopic patches of dead cells appeared 6 days after inoculation.

84 The number of dead cells appeared to be the same in all groups at each

85 In the wild-type embryo, these dead cells are rapidly engulfed and cleared by macrophag

86 Efferocytosis, the process by which dying or dead cells are removed by phagocytosis, has an important

87 y the p53/p21/bax/bcl-2 pathway and that the dead cells are replaced by hyperproliferative cells, lea

88 scopy, we recognized direct interaction with dead cells as an origin of autoantigenic association of

89 the outer leaflet of the plasma membrane of dead cells, as the ligands for CD300a.

90 gs such as immunization with antigen-bearing dead cells, as well as in highly immunogenic situations

91 he types of cell death were analyzed by Live/Dead cell assay, staining for active caspase 3, and sens

92 signal and potentiate cross-presentation of dead cell-associated antigens by DCs.

93 cells and facilitates cross-presentation of dead cell-associated antigens by dendritic cells.

94 rophages activate CD8 T cells in response to dead cell-associated antigens in lymph nodes and by tran

95 ss of DNGR-1-dependent cross-presentation of dead cell-associated antigens, formally demonstrating th

96 nner and that controls cross-presentation of dead cell-associated antigens.

97 nase Syk to promote DC cross-presentation of dead cell-associated antigens.

98 ficient priming of cytotoxic T cells against dead cell-associated antigens.

99 t specifically reduces cross-presentation of dead-cell-associated antigens in vitro and decreases the

100 is also essential for cross-presentation of dead-cell-associated antigens.

101 experiments showed that only permeabilized, dead cells avidly took up rSPARC into their nuclei.

102 nt methods that distinguish between live and dead cells based on membrane integrity, providing a high

103 er cells with 89.8 and 13.2% of the live and dead cells being deflected, respectively.

104 actual effects in terms of not only live and dead cells but also damaged cells.

105 that DNGR-1 did not mediate DC activation by dead cells but rather diverted necrotic cell cargo into

106 Phagocytic clearance not only disposes of dead cells but usually elicits an anti-inflammatory resp

107 which has been used to block phagocytosis of dead cells by concealing phosphatidylserine, efficiently

108 hat GDNF significantly reduced the number of dead cells by inhibiting apoptotic cell death.

109 ter apoptosis or necrosis, macrophages clear dead cells by phagocytosis.

110 s, indicating the inhibition is specific for dead cell cargo that is accompanied by viral or poly(I:C

111 blood DNA, the subsequent administration of dead cells caused no change in DNA levels.

112 and 7-day percentage (ratio of live cells to dead cells) cell viability was assessed with confocal mi

113 a stark contrast to the established model of dead cell clearance in multicellular organisms.

114 Previously, defects in dead cell clearance were linked to neurodegeneration, bu

115 lates functions like the interferon pathway, dead cell clearance, and antigen presentation.

116 laque stability with a focus on induction of dead cell clearance, inhibition of protease activity, an

117 We conclude that autophagy contributes to dead-cell clearance during PCD by a mechanism that likel

118 covered by direct extraction of plasmid from dead cell colonies followed by plasmid transformation in

119 KO culture has a higher percentage of dead cells compared with both WT and overexpressing cell

120 Since dead cells constituted only 10% of the biofilm populatio

121 Accordingly, DCs that captured dead cells containing poly(I:C), or influenza virus, are

122 study, we find that human DCs that captured dead cells containing the TLR3 agonist poly(I:C) produce

123 ted samples by 893 h not seen in mineral and dead cell controls.

124 The CTLD of DNGR-1 binds F-actin exposed by dead cell corpses and causes the receptor to signal and

125 izing lactate dehydrogenase release and live/dead cell cytotoxicity assays, we found in different cel

126 -length AIM in facilitating the clearance of dead cell debris in injured kidney, which is a key respo

127 es to chemokines, injury-conditioned medium, dead cell debris, and high mobility group box chromosoma

128 ction in response to self-DNA, self-RNA, and dead cell debris.

129 body tissues, where they ingest and degrade dead cells, debris, and foreign material and orchestrate

130 pherical geometry that tracks the viable and dead cell densities and the concentration of DO within t

131 luorescence develops, rendering live but not dead cells detectable.

132 titration of monoclonal antibodies, use of a dead-cell discriminator and 'dump' channel, selection of

133 portant roles in cell survival, clearance of dead cells (efferocytosis), and suppression of inflammat

134 As with influenza virus, in PKCbetaII kinase-dead cells, EGF receptor was trapped in a late endosome

135 pacity of DCs to cross-present antigens from dead cells extends to the expansion of high affinity T c

136 The responsibility of handling these dead cells falls on phagocytes of the immune system, whi

137 istribution of proliferating, quiescent, and dead cells for different cellular characteristics.

138 ulation after excluding debris, doublets and dead cells from the analysis.

139 al ridges that run the length of the mature (dead) cell, gathering the cuticularized scale cell surfa

140 tricted antigen derived from both viable and dead cells haptenated with low and high levels of SMX-NO

141 Dead cells, however, did not contain inclusions of HTT,

142 nly partially blocks phagocytosis of already dead cells, implicating at least one additional receptor

143 The multiplex assay can detect 200 dead cells in a population of 10,000 viable cells.

144 s, we detect and separate a subpopulation of dead cells in an unsupervised manner and, in classifying

145 effect on growth and caused accumulation of dead cells in both pta and ackA mutants.

146 y determine the relative numbers of live and dead cells in culture by introducing a combination of tw

147 The cell-viability assay revealed very few dead cells in ex vivo corneal endothelium that overexpre

148 d to assess the results in terms of live and dead cells in the bulk liquid: standard viable plate cou

149 molecules responsible for the engulfment of dead cells in the infarcted area remain largely unknown.

150 infarction (MI) results in the generation of dead cells in the infarcted area.

151 Ratiometric measurement of viable and dead cells in the same sample provides an internal contr

152 and migrated through them, leaving trails of dead cells in their wake.

153 DCs that have captured poly(I:C)-containing dead cells, indicating the inhibition is specific for de

154 DCs that have captured poly(I:C)-containing dead cells, indicating the inhibition is specific for MH

155 cross-presentation of Ag associated with the dead cells induces CD8+ regulatory (or suppressor) T cel

156 The recognition and clearance of dead cells is a process that must occur efficiently to p

157 The efficient removal of dead cells is an important process in animal development

158 herefore, the consequence of phagocytosis of dead cells is strongly affected by those components of t

159 soluble cyt c extracted with detergent from dead cells, it appears to recognize cyt cbound in a dete

160 ronic smoke exposure increased the number of dead cells, lactate dehydrogenase release, and interleuk

161 ion of proliferating and quiescent cells and dead cell material (necrotic and apoptotic) within a mul

162 e suggests that PCD can be 'altruistic': the dead cells may directly or indirectly benefit survivors

163 filtrating leukocytes clear the infarct from dead cells, mediators repressing inflammation are releas

164 We found that dead cells not only released intracellular stores of uri

165 sed 24 h later by propidium iodide uptake in dead cell nuclei.

166 Considering a recent finding that, in dead cells, nucleoli were targeted by C1q and two nucleo

167 n of the percentages of live, apoptotic, and dead cells of the gp70(+) and gp70(-) thymic lymphocytes

168 ace are inactivated, resulting in a layer of dead cells on GO-TFC that limit biofilm formation.

169 magnetic radiation, and detect both live and dead cells online to score cell viability.

170 ither phosphatidylserine (PtdSer)-displaying dead cells or PtdSer-containing liposomes.

171 erentiate into a variety of cells to replace dead cells or to repair damaged tissues.

172 did not affect the viability of CE cells (15 dead cells per 600 cells).

173 These dead cells persist in the brain throughout the lifespan

174 o statistically distinguish between live and dead cell populations.

175 propidium monoazide to distinguish live from dead cells prior to DNA extraction, and 16S rRNA gene py

176 s a result of limited growth and division of dead cells produced by guillotining.

177 ME-ECTs displayed the lowest dead cell ratio (p < 0.001) and matured into 0.5 mm diam

178 It is currently unknown how DNGR-1 couples dead cell recognition to cross-priming.

179 responsible for the elimination of microbes, dead cells, redundant synapses, protein aggregates, and

180 to baseline, whereas, levels in nonadherent dead cells remained high.

181 ns contain small pools of lipid droplets and dead cell remnants (extracellular lipid) in addition to

182 lpha+ subset of dendritic cells phagocytoses dead cell remnants and cross-primes CD8+ T cells against

183 of radiosensitivity, tumor repopulation, and dead-cell resolving on the analysis of tumor volume regr

184 predictor (P = 0.001) and 89% vs. 57% using dead-cell resolving time (T(1/2) < 22 days versus T(1/2)

185 se, and in the absence of LAP, engulfment of dead cells results in increased production of proinflamm

186 SYTOX Green is generally considered a dead cell stain because it is not able to cross the memb

187 s, whereas histochemical observations with a dead cell stain were carried out on one of them.

188 firmed by fluorescence microscopy after live/dead cell staining of the bacteria in the measured biofi

189 Other molecules released by dead cells stimulate the generation of mediators from ex

190 these cells also sense uric acid crystals in dead cells, suggesting that the immune system is conscio

191 yielded more metabolically active and fewer dead cells than control suspensions.

192 microfluidic technique to separate live and dead cells that exploits differences in cellular stiffne

193 r patterns (DAMPs) are molecules released by dead cells that trigger sterile inflammation and, in ver

194 f the tumors, the fraction of clonogenically dead cells that was microscopically apparent, including

195 tibody that does not distinguish viable from dead cells, the phage selectivity in cell recognition mi

196 als (SC) turnover time x the ratio of living/dead cells, then compartmental turnover times are unequa

197 efferocytosis, the recognition and uptake of dead cells, thereby tricking neighboring cells into taki

198 From this we concluded that the ability of dead cells to bind to heparan sulfate proteoglycans on t

199 subpopulation uses the nutrients released by dead cells to grow.

200 actors that can stimulate the replacement of dead cells to the promotion of tissue repair or tissue r

201 The contribution of both living and dead cells to water storage can be derived from rehydrat

202 The ratio of live/dead cells varied in different size-fractions, and the p

203 Binding of dead cells via receptors present on the macrophage surfa

204 MTS assay cytotoxicity assay and live-dead cell viability test were conducted on J774A.1 cells

205 RI technique to distinguish between live and dead cells was next evaluated using MRI phantoms, and in

206 roscopy demonstrated that heparin binding to dead cells was restricted to 1 or 2 small domains on the

207 ked when the heparin-binding capacity of the dead cells was saturated by the addition of pentosan pol

208 surfaces require direct CNT-microbe contact, dead cells were able to shield living cells from the cyt

209 anical insult and found that the majority of dead cells were apoptotic.

210 allogeneic cells were tested to determine if dead cells were capable of inducing tolerance.

211 y in situ or after recovery from leaves, and dead cells were identified as those that were stained wi

212 as the electrokinetic mobilities of live and dead cells were indistinguishable.

213 ize grafts were 15 per high power field, and dead cells were less than 1 per high power field, indica

214 undant, but not on ED 4, when only scattered dead cells were observed histologically.

215 Dead cells were observed to have significantly lower die

216 e inflammatory cascade clears the wound from dead cells, whereas stimulating matrix degradation and c

217 cannot differentiate between the viable and dead cells which may overestimate the risk of infections

218 les flushing away of unaggregated (including dead) cells while viable spheroids remain inside microwe

219 ropose that the association of antigens from dead cells with DS is a possible origin of autoantigens

220 discrimination of viable and VBNC cells from dead cells, with high sensitivity.

221 aining revealed that KB1050 accumulated more dead cells within the biofilm population relative to UAM