ライフサイエンスコーパス: cell death

1 inating in activity-dependent, non-apoptotic cell death.

2 parthanatos, or other forms of non-apoptotic cell death.

3 ) regulates nitric oxide (NO) metabolism and cell death.

4 d in protein quality control, signalling and cell death.

5 its mitochondrial Ca(2+) overload to prevent cell death.

6 is associated with significant neuroretinal cell death.

7 genomic instability and ultimately leads to cell death.

8 resistance leads ultimately to mycobacterial cell death.

9 er cells to doxorubicin leading to apoptotic cell death.

10 rleukin-6 (IL-6) and APRIL, to prevent their cell death.

11 hondria dynamics and protects from apoptotic cell death.

12 virus, but mass fluctuations continue until cell death.

13 which correlates with their ability to cause cell death.

14 mutant of OPTN but not E50K and M98K induced cell death.

15 d Nod2 primed T cells for activation-induced cell death.

16 GMP), accompanied by only modest endothelial cell death.

17 sed flies with higher bacterial load and gut cell death.

18 Pandemic IAV suppresses this immunogenic DC cell death.

19 vates ER stress pathways that promote acinar cell death.

20 n-dependent, oxidative form of non-apoptotic cell death.

21 r pathway for endogenous dsRNA that leads to cell death.

22 NMDA) receptors causes neurodegeneration and cell death.

23 ms that link these fusions to the control of cell death.

24 was common and did not necessarily result in cell death.

25 rmation with resistance to radiation induced cell death.

26 d facilitate live-cell imaging of pyroptotic cell death.

27 eptor 2 antagonism triggered synergistic AML cell death.

28 including chemotherapy aim to induce tumour cell death.

29 phylococcal alpha-toxin-induced keratinocyte cell death.

30 re and that lowering O-GlcNAcylation induces cell death.

31 hich then disrupts the bilayer, resulting in cell death.

32 ation of incomplete HIV transcripts triggers cell death.

33 reach the threshold for survival and lead to cell death.

34 Y silencing promotes genomic instability and cell death.

35 phorylation in mitochondrial dysfunction and cell death.

36 cts with SUG1 and induces caspase-8-mediated cell death.

37 h 3-methyladenine, increases mixture-induced cell death.

38 is inhibition to further ensure induction of cell death.

39 ates the probability, but not the timing, of cell death.

40 otein domain suppressed GH12 protein-induced cell death.

41 with GTPase signaling, calcium signaling and cell death.

42 activity to some degree without evidence of cell death.

43 function, causing hypertrophy and subsequent cell death.

44 the effects of PM10, causing DNA damage and cell death.

45 nflammatory cytokines, but also by promoting cell death.

46 ed to KA or NMDA appear to undergo apoptotic cell death.

47 lanoma behaved differently in the context of cell death.

48 This amount of heating alone did not cause cell death.

49 permatogonial death and reduces overall germ cell death.

50 in culture medium were sufficient to promote cell death.

51 activation of RIPK1 was sufficient to induce cell death.

52 intracellular calcium (Ca(2+)) over time and cell death.

53 Typhimurium infection, eventually leading to cell death.

54 ing transcription factor EB and, eventually, cell death.

55 the edibility of cells undergoing programmed cell death.

56 ial for Ca(2+) signaling, bioenergetics, and cell death.

57 As), are able to directly trigger macrophage cell death.

58 Non-Culturable (VBNC)-like state and not by cell death.

59 lar functions but can become toxic and cause cell death.

60 stretch damage induced shrunken neurites and cell death.

61 rom inhibiting DNA gyrase and thereby averts cell death.

62 rich for patient response to anti-programmed cell death 1 and anti-PD-L1 therapies.

63 n this study, we demonstrate that programmed cell death 1 ligand 2 (PD-L2) regulates the production o

64 To determine the efficacy of programmed cell death 1 receptor (PD-1) inhibitors in locally advan

65 cells, and relatively few PD-1+ (programmed cell death 1-positive) T cells, an immunophenotypic patt

66 oidy), which typically results in disease or cell death [1].

67 Programmed cell death-1 (PD-1) is an inhibitory receptor with an es

68 Programmed cell death-1 (PD-1)-targeted therapies enhance T cell re

69 Programmed cell death-1 mRNA expression was increased in tissue hom

70 The anti-Programmed cells Death-1 was stopped and a topical corticosteroid t

71 ensitivity for detecting low levels of tumor cell death (2%-5%).

72 bserved that 6-ETI induces ATP depletion and cell death accompanied by S phase arrest and DNA damage

73 s of the small peptide derivatives result in cell death, accompanying significant rearrangement of cy

74 lation, accompanied by excessive necroptotic cell death and a reduced number of secretory epithelial

75 This safe antibacterial dye induces cell death and apoptosis in several glioma cell lines, t

76 anticancer drug targets because they control cell death and are structurally and functionally differe

77 eroxisomes during final stages of programmed cell death and can be used as a marker of this stage.

78 1 GapmeR significantly increased OGD-induced cell death and Caspase 3 activity in BMECs.

79 uce oxidative stress and are associated with cell death and chronic diseases in organisms.

80 ical prosurvival protein for preventing beta-cell death and clarify the mechanisms behind its downreg

81 vation, neutrophil accumulation, endothelial cell death and desquamation, and mural thrombosis.

82 l infection, this response can contribute to cell death and disease.

83 dothyronamine (T1AM), on cell proliferation, cell death and DNA damage was studied in two ovarian can

84 Cigarette smoke promotes cell death and features of pancreatitis in EtOH-sensitiz

85 irth may be an important trigger of neuronal cell death and identify transient cell groups that may u

86 evaluate biochemical changes associated with cell death and impacts on the cell cycle in three dinofl

87 These findings imply that MDA5-induced cell death and inflammation in the pancreas facilitate p

88 (G158A) mutant failed to suppress pyroptotic cell death and inflammatory responses.

89 a pathogen sensor and a central regulator of cell death and inflammatory responses.

90 interaction motifs (RHIM) play a key role in cell death and inflammatory signalling(1-3).

91 l ROS, as well as increased differentiation, cell death and mtDNA damage.

92 es were decoded via separate measurements of cell death and other antiproliferative effects, gaining

93 1, VdEG1 and VdEG3 acted as PAMPs to trigger cell death and PAMP-triggered immunity (PTI) independent

94 on products can mediate tissue inflammation, cell death and profibrotic signalling.

95 These cells undergo cell death and replacement (turnover) throughout life in

96 agy response and dictate the balance between cell death and survival following loss of cell-matrix co

97 ant for suppression of a caspase-independent cell death and the long-term survival of FA-treated cell

98 re we investigated the mechanisms of splenic cell death and their relationship to control of parasite

99 Eliminating PEPD causes cell death and tumor regression due to p53 activation.

100 help to identify tumour subsets that undergo cell death and tumour regression upon inhibition of CDK4

101 Here we show that ischemic cell death and uptake of cell debris by macrophages in t

102 n is a major susceptibility factor for tumor cell death and, as such, constitutes a potential biomark

103 ding sustained proliferation, suppression of cell death, and altered metabolism.

104 n tissues, where it regulates bioenergetics, cell death, and Ca(2+) signal transduction.

105 regulation of genes involved in Fas-mediated cell death, and Erdr1 fails to induce apoptosis in Fas-d

106 he cellular oxidative environment and induce cell death, and hence could serve as novel therapeutics.

107 ociated exaggerated inflammasome activation, cell death, and IL-18 secretion, suggesting that restori

108 reby protecting tumour cells from MYC-driven cell death, and indeed, MYC selects for this pathway in

109 shown to prevent B cell activation, increase cell death, and induce tolerance in vivo.

110 sm is independent of explosive cell lysis or cell death, and the release of DNA is confined to a disc

111 rkers of inflammation, oxidative stress, and cell death, and transcriptomic analysis identified numer

112 y processes such as cell-fate specification, cell death, and transdifferentiation throughout post-emb

113 igger ferroptosis instead of another form of cell death, and whether this process could be adaptive i

114 g cellular stress, and increasing programmed cell death (apoptosis) in the tissues required for neuru

115 om cells or to selectively induce programmed cell death (apoptosis) or uncontrolled cell death (necro

116 Three regulatory events were investigated: cell death (apoptosis), neutrophil influx and cytokine/c

117 ntral role in the early stages of programmed cell death (apoptosis).

118 egulated "effector" genes that contribute to cell death, as well as genes that affect the sensitivity

119 We focus on the hippocampus neuronal cell death, as well as the potential link between LSD1 a

120 and immunohistochemistry, proliferation, and cell death assays to identify new neurons.

121 transcription polymerase chain reaction, and cell death assays.

122 osis has been implicated in the pathological cell death associated with degenerative diseases (i.e.,

123 oroidal neovascularisation and photoreceptor cell death associated with severe visual loss.

124 hways, including chromatin modifications and cell death-associated pathways.

125 Pano caused cell death at significantly higher rates compared to rep

126 elial cell division is controlled to balance cell death at the steady state.

127 which autophagy promotes caspase-independent cell death, ATG16L1 maintains the intestinal barrier by

128 We recently created a "cell death atlas," using the detection of activated casp

129 arizing cytokine production, and significant cell death, BCG induced a robust adult-like maturation p

130 However, they also cause non-oxidative cell death because anaerobic bacteria are also killed.

131 Side-by-side comparisons confirmed massive cell death, before synaptogenesis, within 1-4 DIV upon l

132 3) suppresses cell proliferation and induces cell death better than either single agent in several pr

133 re able to induce efficient apoptotic cancer cell death both in vitro and in vivo through tumor-speci

134 creased reactive oxygen species and necrotic cell death, both of which were mitigated by ATF6 overexp

135 uced oxygen, nutrients or chemically induced cell death, but the mechanisms driving this evolution ar

136 Thus, Drp1 deSUMOylation promotes cell death by enhancing Mff-mediated mitochondrial recru

137 ional NMDAR in non-neuronal cells results in cell death by excitotoxicity, hindering the development

138 Entosis, or cell death by invading another cell, is typical for tumo

139 a o mature IL-1beta causing inflammation and cell death by pyroptosis.

140 4a inhibited cancer cell growth and induced cell death by various mechanisms.

141 cently described distinct form of programmed cell death called NETosis.

142 popolysaccharides), which leads to premature cell death, callose deposition, or phloem protein accumu

143 g units, these results provide evidence that cell death can be sensed through measurements of cell-ge

144 l be more effective at slowing photoreceptor cell death caused by elevated cGMP.

145 erium modulates the cell cycle and programed cell death, contributing to periodontal lesion worsening

146 Further, molecules involved in cell death decisions also moonlight as critical nodes in

147 , triggering constitutive caspase-8-mediated cell death dependent on FADD but independent of Ser(533)

148 ggers cellular apoptotic pathways, increases cell death, diminishes autophagy, and reduces cancer for

149 Further studies revealed that the mode of cell death does not fall into one of the canonical categ

150 This form of cell death does not share morphological, biochemical, or

151 ment with anle138b leads to massive melanoma cell death due to a major dysregulation of autophagy, su

152 Transient activation of apoptotic cell death during early age correlated well with the dif

153 es in pre-rRNA level, ER stress markers, and cell death during glucose deprivation, which could be re

154 ell receptor (TCR) signaling largely induces cell death during thymocyte development, whereas weak TC

155 h increased M. tuberculosis Ag-induced CD4 T cell death ex vivo, indicating a possible mechanism cont

156 er a strategy designed to interfere with the cell death-facilitating properties of Kv2.1, specificall

157 ells to CQ, resulting in increased apoptotic cell death following treatment.

158 RI is hallmarked by inflammation, and hence, cell-death forms disjunct from immunologically silent ap

159 ed pronounced resistance to early or delayed cell death from hypoxia or hypoxia-ischemia.

160 of spectral analysis to oncosis or ischemic cell death had not previously been studied.

161 fects of XLP-2 and VEO-IBD XIAP mutations on cell death have been inconsistent.

162 leavage products of HuR are known to promote cell death; however, the underlying molecular mechanisms

163 ure of the nuclear envelope that can lead to cell death, if not prevented or healed within an appropr

164 We compared the predictive power of cell death imaging using (99m)Tc-duramycin with the curr

165 Pyroptosis is a form of cell death important in defenses against pathogens that

166 an antagonistic anti-PD-1 antibody increased cell death in 3D spheroids and extended survival of MDA-

167 nked hits protected against alphaSyn-induced cell death in a human neuronal PD model.

168 was found to enter intact cells and induced cell death in a process that was preceded by mitochondri

169 SNRK also decreases cardiac cell death in a UCP3-dependent manner.

170 quired to combat the induction of programmed cell death in a variety of distinct cell types.

171 hich are emerging as mediators of programmed cell death in a variety of processes that regulate cellu

172 de inhibitor simvastatin induced significant cell death in a wide range of human tumor cell lines, in

173 eactive oxygen species (ROS), p53 levels and cell death in androgen-deprived CRPC cells.

174 ed for ETI and containment of stress-induced cell death in Arabidopsis.

175 in D and the VDR in modulating autophagy and cell death in both the normal mammary gland and BC cells

176 The importance of cell death in brain development has long been appreciate

177 erstanding of mechanisms and consequences of cell death in complex organisms is the inability to indu

178 suppresses E2F1 and c-Myc levels and causes cell death in EBNA1-induced B cell lymphomas.

179 spectively, showed a significant increase in cell death in F0 mutants compared to controls.

180 analogue HNG protects from stressor-induced cell death in fibroblasts, cardiomyoblasts, neuronal cel

181 regulates immune and susceptible Programmed cell death in immunity transforming Ca(2+) signals into

182 se-independent fashion, but also exacerbated cell death in induced pluripotent stem cell-derived prim

183 Injection of TNF greatly increased levels of cell death in intestinal tissue of cIAP1-null mice, comp

184 This review will focus on the role of cell death in maintenance of T-cell homeostasis and outl

185 -induced liver dysfunction, inflammation and cell death in mice and pigs.

186 d that (i) NSAID Indomethacin induces robust cell death in primary patient-derived platinum-sensitive

187 hological changes associated with pyroptotic cell death in real time.

188 by executing either apoptotic or necroptotic cell death in response to infection.

189 ns execute inflammasome-dependent pyroptotic cell death in response to multiple stimuli and allow for

190 ith DLK to activate downstream signaling and cell death in RGCs, including in a mouse model of optic

191 Knockdown of GP130 or IL-2Rgamma induced cell death in selected JAK inhibitor-sensitive cells.

192 t activation, S-phase cell cycle arrest, and cell death in sensitive breast cancer cell lines.

193 accumulation of reactive oxygen species and cell death in the absence of p53.

194 es, but success is limited by extensive beta-cell death in the immediate posttransplant period and im

195 sation of cerebral blood flow (CBF) leads to cell death in the infarct core, but tissue surrounding t

196 al, anoikis resistance and induced apoptotic cell death in therapy-resistant EOC cells.

197 clear architecture, and activated programmed cell death, in D. citri midgut cells.

198 ignaling by anisomycin resulted in increased cell death independent of HIV reactivation.

199 However, 4a was found to induce cell death independent of ROS generation, and unlike man

200 al and physiological changes associated with cell death induced by algicidal bacteria.

201 er cells often acquire capabilities to evade cell death induced by current chemotherapeutic treatment

202 form demands a thorough understanding of how cell death induced in the context of infection influence

203 rmation of a single, compact speck and rapid cell-death induction in vivo requires a full-length ASC.

204 fy the HA genomic segment as the mediator of cell death inhibition.

205 Cell death introduces alterations in cell morphology and

206 cleotide accumulation during regulated tumor cell death involves interplay between ATP/AMP efflux pat

207 s role in signaling to SI-induced programmed cell death involving a DEVDase.

208 Cell death is a perpetual feature of tissue microenviron

209 Cell death is also required for removal of infected, dam

210 Cell death is an important target for imaging the early

211 Precise control of cell death is crucial for tissue homeostasis.

212 it may contribute to the execution of wheat cell death, it is also likely to have an important secon

213 advanced solid tumours expressing programmed cell death ligand 1 (PD-L1) and report here on the inter

214 Programmed cell death ligand 1 (PD-L1) is part of an immune checkpo

215 Drug Administration (FDA) detect programmed cell death ligand 1 (PD-L1) to enrich for patient respon

216 amma and sensitize tumors to PD-1/programmed cell death ligand 1 blockade-induced rejection.

217 ngs suggest that components of the classical cell death machinery also have important non-cell-death

218 ared light and convert it into heat, causing cell death mainly by apoptosis and/or necrosis.

219 NPs suggests the mechanisms and kinetics of cell death may be influenced by nano-scale metal oxide m

220 rgoing apoptosis, suggesting that programmed cell death may limit viral dissemination in the brain an

221 assay gives morphological information about cell death mechanism.

222 vival but can enhance cell survival in other cell-death mutants, indicating that ced-11 facilitates t

223 of skin, undergoing an alternative route of cell death, namely cornification rather than apoptosis.

224 ammed cell death (apoptosis) or uncontrolled cell death (necrosis).

225 protein kinase 1 (RIPK1), a key regulator of cell death, NF-kappaB, and MAPK signaling.

226 cell death machinery also have important non-cell-death (non-apoptotic) functions in flies, nematodes

227 l death through mitotic catastrophe and that cell death occurred also from interphase.

228 Programmed cell death occurs in a highly reproducible manner during

229 context for the argument that apoptotic-like cell death occurs in plants.

230 k of quantitative data defining exactly when cell death occurs.

231 n MCF-7 breast carcinoma cells, which caused cell death of cancer cells followed by phagocytosis of c

232 istant plants contain the infection by rapid cell death of the infected area through the hypersensiti

233 patterning, vascular development, programmed cell death, organ abscission, senescence, and plant resp

234 While ATP depletion led to cell death, over-acetylated tubulin led to inhibition of

235 e we identified a previously uncharacterized cell death pathway regulated by TAK1, which is unexpecte

236 n root cells, HS triggered an iron-dependent cell death pathway that was characterized by depletion o

237 id not activate the apoptotic or necroptotic cell death pathway.

238 nzymatic activation of the caspase dependent cell death pathway.

239 ubtilis and discuss how the use of regulated cell death pathways during bacterial development may hel

240 sensing to trigger activation of programmed cell death pathways during IAV infection.

241 y reveals the effect of antiviral programmed cell death pathways on inflammation, shows that caspase-

242 Understanding the implications of distinct cell death pathways will help in the development of ther

243 trongly implicate two distinct cGMP-mediated cell death pathways, and suggest that therapeutic design

244 fication that regulates immune signaling and cell death pathways, notably tumor necrosis factor recep

245 s infection induces activation of programmed cell death pathways.

246 in, such as what initiates or terminates the cell death period.

247 The rapid cell death phenotype was reproducible in in vitro cultur

248 nd used this system to characterize NOD2 and cell death phenotypes driven by XIAP.

249 hypertrophic chondrocytes undergo programmed cell death prior to bone formation.

250 eutrophil extracellular traps, a specialized cell death process in which DNA-based structures contain

251 Blocking programmed cell death protein (PD)-1 signaling, which mediates T ce

252 ints, such as the one mediated by programmed cell death protein 1 (PD-1) and its ligand PD-L1, have b

253 Signaling between programmed cell death protein 1 (PD-1) and the PD-1 ligands (PD-L1,

254 T cells expressing a low level of programmed cell death protein 1 and a high level of OX40 were assoc

255 ars, it has been established that programmed cell death protein ligand 1 (PD-L1)-mediated inhibition

256 In plants, regulated cell death (RCD) plays critical roles during development

257 fficacy of pembrolizumab (an anti-programmed cell death receptor 1 [PD-1] antibody) in advanced solid

258 CRK28-mediated cell death required the common receptor-like protein kin

259 , this same molecular treatment enhanced the cell death response to high-frequency electric fields (

260 nd M45 in blocking apoptotic and necroptotic cell death responses.

261 Because pyroptosis (ie, cell death resulting from inflammasome activation) is ty

262 d death (CWID) and TCR restimulation induced cell death (RICD).

263 sclerosis-associated mutant, E478G, induced cell death selectively in 661W cells.

264 eting of receptor-mediated proliferation and cell death signaling pathways in different tumor types a

265 e zipper kinase (DLK) has been implicated in cell death signaling secondary to axonal damage in retin

266 ectral signatures unique to various modes of cell death, such as cells undergoing apoptosis versus ne

267 ion of murine cytomegalovirus (MCMV)-encoded cell-death suppressors revealed that necroptosis functio

268 e release is the hallmark of a novel form of cell death termed pyroptosis.

269 Necroptosis is a form of cell death that can be observed downstream of death rece

270 Ferroptosis is a form of programmed cell death that is pathogenic to several acute and chron

271 is a highly inflammatory form of programmed cell death that results from MLKL-mediated disruption of

272 secreted from cells undergoing nonprogrammed cell death that signal tissue and cell damage.

273 h, can reduce protein synthesis and initiate cell death through induction of pro-apoptotic pathways.

274 The MMP12 CTD initiates TRAIL-mediated tumor cell death through its conserved SR20 peptide.

275 arrest and segregation abnormalities lead to cell death through mitotic catastrophe and that cell dea

276 aired nuclear localization of TRADD triggers cell death through the persistent activation of JNK and

277 herapeutic strategies tailored to manipulate cell death to limit T-cell survival (eg, autoimmunity an

278 lial cell division must be tightly linked to cell death to preserve barrier function and prevent tumo

279 um, there was a trend for elevated apoptotic cell death under most irradiation conditions; however, D

280 ting gammaH2AX and 53BP1 foci, and augmented cell death upon oxidative telomeric DNA damage.

281 ms whereby trimethoprim treatment results in cell death, using Escherichia coli as the model organism

282 Simvastatin induced apoptotic cell death via the intrinsic apoptotic pathway.

283 cible gene I (RIG-I) initiates ZBP1-mediated cell death via the RIG-I-MAVS-IFN-beta signaling axis.

284 Induction of cell death was cell autonomous and required RNA synthesi

285 Moreover, effector-induced host cell death was dependent on NbBAK1 and NbSOBIR1.

286 Autophagy was monitored biochemically and cell death was measured using multiple assays.

287 TEM cell death was prevented with neutralizing anti-IL-2 Ab

288 actors leading to Mtb proliferation and host cell death, we used live cell imaging to track Mtb infec

289 ion or ultrastructural features of apoptotic cell death were observed.

290 halamus, and found that the highest rates of cell death were seen at the earliest postnatal ages in m

291 lation, ABC-transporter gene expression, and cell death were used to select a suitable glyphosate con

292 erchlorates to cause a 10.8-fold increase in cell death when compared to cells exposed to UV radiatio

293 SsCP1 could induce significant cell death when expressed in Nicotiana benthamiana.

294 35.2, but not XBAT35.1, was found to trigger cell death when overexpressed in tobacco (Nicotiana bent

295 Therefore, loss of TAK1 elicits noncanonical cell death which is mediated by RIPK1-induced oxidative

296 host complex resulted in increased cancerous cell death while noncancerous control cells were unaffec

297 interaction or not with DNA as the cause of cell death, while dimeric Ru(ii) polypyridyl complexes a

298 Programmed cell death widely but heterogeneously affects the develo

299 Caspase-1-mediated cell death with accompanying cytokine release is the hal

300 bited increased susceptibility and apoptotic cell death with oxidative stress.