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

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

4 important role in regulating the removal of dead cells.

5 9A) is a DC-restricted receptor that detects dead cells.

6 ignificant Tl accumulation by either live or dead cells.

7 cell lines also decreased the engulfment of dead cells.

8 e nutrients for growth and reproduction from dead cells.

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

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

11 onses, degrade lipoproteins, and phagocytose dead cells.

12 f fluorescein, and intracellular staining in dead cells.

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

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

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

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

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

18 osis and impairing the subsequent removal of dead cells.

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

20 the contaminant is associated with permeable dead cells.

21 olecular techniques to distinguish live from dead cells.

22 unction in the recognition and engulfment of dead cells.

23 g nonsporulating siblings and feeding on the dead cells.

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

25 nd cell proliferation, presumably to replace dead cells.

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

27 phagocytic cells recognize and engulf these dead cells.

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

29 minutes of injury, where they rapidly engulf dead cells.

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

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

32 olor fluorescent dye to distinguish live and dead cells.

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

34 odimer and calcein to discriminate live from dead cells.

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

36 espan was extended through the scavenging of dead cells.

37 eir ability to rapidly and efficiently clear dead cells.

38 imately 95% accuracy in identifying live and dead cells.

39 cilitating the non-inflammatory clearance of dead cells.

40 aureus, distinguishing living bacteria from dead cells.

41 ment, leading to significant accumulation of dead cells.

42 ter 5-FU treatment and elevates the ratio of dead cells.

43 es for efficient recycling of molecules from dead cells.

44 cellular matrix proteins, efficiently engulf dead cells.

45 radation of cells rather than recognition of dead cells.

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

47 cognize phosphatidylserine on the surface of dead cells.

48 actively by living neurons and passively by dead cells.

49 cell viability and the distribution of live/dead cells.

50 ytes recognize phosphatidylserine exposed on dead cells.

51 amyloid occurred in clustered capsules with dead cells.

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

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

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

55 nge, T6SS activity becomes self-limiting, as dead cells accumulate in its way, forming "corpse barrie

56 Dead cells accumulated in bone marrow from lupus patient

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

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

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

60 Dead cells accumulating in the tissues may contribute to

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

62 dead cells) across a wide linear range (10-1000 cells/mu

63 ows clear differentiation between living and dead cells after 3 h of inducing apoptosis.

64 distribution, resulting in a high number of dead cells after aPDT.

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

66 Dead cells also release danger signals that activate den

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

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

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

70 nesis and daily in adult organisms, clearing dead cells and associated cellular debris is important i

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

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

73 l for cell growth dependent on the uptake of dead cells and cell debris.

74 ophages, together referred to as MPhi, clear dead cells and cellular debris in the infarcted brain th

75 Microbial residues, composed of dead cells and cellular fragments, are major contributor

76 Accumulation of dead cells and cholesterol crystallization are hallmarks

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

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

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

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

81 g various types of cells, including live and dead cells and healthy and infected cells.

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

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

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

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

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

87 c mechanism responsible for the clearance of dead cells and the resolution of inflammation.

88 or role in the clearance of the infarct from dead cells and the subsequent stimulation of reparative

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

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

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

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

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

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

95 low biomass, discrimination between live and dead cells, and functional analysis.

96 g mediator production, impaired clearance of dead cells, and functional changes in immune cells that

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

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

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

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

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

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

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

104 llular matrix components, the elimination of dead cells, and the restoration of normal blood flow.

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

106 create volume differences between living and dead cells, and then, the differences were characterized

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

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

109 thereby activating immune responses against dead-cell antigens.

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

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

112 osis occurs within epithelia, the harmful or dead cells are apically extruded from tissues to maintai

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

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

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

116 general principle whereby signals within the dead cell as well as the environment are integrated by s

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

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

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

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

121 lines, quantified by flow cytometry and live/dead cell assays.

122 t types of microorganisms including live and dead cell assessments.

123 binding to F-actin and cross-presentation of dead cell-associated antigens by cDC1s.

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

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

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

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

128 n initiate adaptive immune responses against dead cell-associated antigens, provided that (1) said an

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

130 decreases induction of cross-presentation of dead cell-associated antigens.

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

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

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

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

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

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

137 ge error and standard deviation for live and dead cells being 7.61 2.01 and 5.78 1.13, respectively.

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

139 y distinguishing not only between viable and dead cells but also between dormant and actively growing

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

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

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

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

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

145 Efferocytosis, the phagocytic removal of dead cells by microglia and macrophages, was recently re

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

147 ould consist of only healthy viable cells as dead cells can confound the analysis.

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

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

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

151 ntenance of tissue homeostasis by scavenging dead cells, cell debris and lipoprotein aggregates via p

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

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

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

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

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

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

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

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

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

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

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

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

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

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

166 y credited to myeloid cells interacting with dead cell debris in the infarct zone(1,2).

167 trate that tubular cells exposed apically to dead cell debris secrete high levels of GM-CSF and induc

168 nes and growth factors, and they phagocytose dead cell debris, a process that is critical for resolut

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

170 By removing the dead cell debris, it can increase the live cell percenta

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

172 also known as CLEC9A), a receptor that binds dead-cell debris and facilitates XP of corpse-associated

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

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

175 ator of Clec9A and the cross-presentation of dead cell-derived antigens by mouse dendritic cells.

176 ll receptor Clec9A facilitates processing of dead cell-derived antigens for cross-presentation and th

177 of dendritic cell (DC), which cross-present dead cell-derived antigens.

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

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

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

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

182 ingle cell PD resulted in parallel events of dead cell exfoliation and migration of intact neighbouri

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

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

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

186 etacaspase 9 (AtMC9) plays roles in clearing dead cells, forming xylem vessels, and regulating immuni

187 mic processes to chase and capture migrating dead cell fragments using a "lazy" search strategy.

188 r-ligand interactions to clear pathogens and dead cells from a host.

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

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

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

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

193 o their role as danger signals released from dead cells, IL-1 family cytokines can be secreted in the

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

195 ocytosis, a process whereby phagocytes clear dead cells in a noninflammatory manner.

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

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

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

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

200 membranes is needed not only for identifying dead cells in culture, but also for imaging membrane bar

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

202 is a dye that distinguishes between live and dead cells in molecular assays like the Polymerase Chain

203 s TAZ, Notch, and hedgehog; how clearance of dead cells in NASH via efferocytosis may affect inflamma

204 ts exhibit growth defects and an increase in dead cells in root meristems after CPT treatment demonst

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

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

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

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

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

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

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

212 sequently, necrotic environment (hypoxia and dead cells) induced a cluster of complement 1q-positive

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

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

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

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

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

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

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

220 ual macrophages allow for optimal removal of dead cell material and pathogens in tissues.

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

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

223 on between treatment and cell type (live vs. dead cells/medium-no cells) was observed.

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

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

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

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

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

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

230 arly all SPMs is to enhance the clearance of dead cells or efferocytosis.

231 her microbes adhering to particles were live/dead cells or inert particles.

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

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

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

235 These dead cells persist in the brain throughout the lifespan

236 o statistically distinguish between live and dead cell populations.

237 This prevented phagocytic removal of dead cells, prevented maturation of monocyte-derived mac

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

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

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

241 to dying tumor cells through upregulation of dead-cell receptors and synergizes with Flt3L to promote

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

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

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

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

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

247 es and cancer, recognises F-actin exposed on dead cell remnants and promotes cross-presentation of as

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

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

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

251 Dead cells, ROS, embryos, and unfertilized eggs laid by

252 racy of 87.5-93.8%, indicating that live and dead cell samples could be well-recognized with the cons

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

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

255 ctate dehydrogenase cytotoxicity assay, live-dead cell staining and transmission electron microscopy

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

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

258 toGater harmonizes different measurements of dead cells such as Sytox and CFUs.

259 se, or other proteins released by damaged or dead cells, suggesting active transport through a Golgi-

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

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

262 n proposed as a method to eliminate dying or dead cells that accumulate and contribute to diseases su

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

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

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

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

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

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

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

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

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

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

273 r, Clec9A interactions are altered following dead cell uptake to favor antigen presentation.

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

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

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

277 at time, the discrimination between live and dead cells was attributed to dielectrophoretic effects.

278 The confluence of live and dead cells was measured every three hours over four days

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

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

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

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

283 Live and dead cells were accurately classified in more than 90% o

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

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

286 oral administration, since a minor number of dead cells were found in red color under a fluorescent m

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

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

289 In 2-4 h, dead cells were labeled with propidium.

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

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

292 Dead cells were observed to have significantly lower die

293 Subsequently, live and dead cells were successfully separated experimentally in

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

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

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

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

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

299 to heat or radiation: heated spheroids shed dead cells within four days of heating and displayed fas

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