ライフサイエンスコーパス: cell death

1 commonly established ceramide functions (eg, cell death).

2 eading to the accumulation of DNA damage and cell death.

3 response, which, if not relieved, results in cell death.

4 to necroptosis, a regulated form of necrotic cell death.

5 rocyte loss, and subsequent retinal ganglion cell death.

6 he immune regulators IL6 and IL8 followed by cell death.

7 esulting in DNA damage-checkpoint arrest and cell death.

8 ria regulate ATP production, metabolism, and cell death.

9 loss of heterozygosity, genetic disease, or cell death.

10 to unregulated unfolded protein response and cell death.

11 ive burden that, if unchecked, would lead to cell death.

12 ing, oligomerization, and capacity to induce cell death.

13 nscription of tumor suppressors that promote cell death.

14 Factor Receptor (EGFR)-Akt axis, and finally cell death.

15 were found to induce apoptotic and necrotic cell death.

16 vation and subsequently prevented autophagic cell death.

17 these monobodies potently block necroptotic cell death.

18 tion of RIPK3 and CASP8 and sensitization to cell death.

19 s can lead to mismetallation of proteins and cell death.

20 ss-linking, resulting in conglomerations and cell death.

21 egrity, signaling, and cell proliferation to cell death.

22 uced G(2)/M arrest and augments TMZ-mediated cell death.

23 s associated with increased inflammation and cell death.

24 -alpha)-induced signalling and prevention of cell death.

25 thought to cause rod and cone photoreceptor cell death.

26 ol for assessing inflammasome activation and cell death.

27 f these intracellular parameters, leading to cell death.

28 h transient postnatal OTR expression without cell death.

29 ancer therapeutics and resulted in effective cell death.

30 ducts of energy metabolism which can lead to cell death.

31 hat proteasome inhibition is associated with cell death.

32 of reactive oxygen species that can lead to cell death.

33 m stores could avoid HlyA induced macrophage cell death.

34 n mouse neurons leads to widespread neuronal cell death.

35 at leads to MESN-subtype-dependent apoptotic cell death.

36 a(2+) taken up by mitochondria could lead to cell death.

37 cell surface may determine antibody-mediated cell death.

38 concentration and dosing kinetics, including cell death.

39 lases KDM6A (UTX) and KDM6B (JMJD3) leads to cell death.

40 ions in seed maturation and plant programmed cell death.

41 l differentiation combined with an increased cell death.

42 lla thereby amplifying its ability to elicit cell death.

43 on survival during developmentally-regulated cell death.

44 lyploidy protects against DNA damage-induced cell death.

45 to cleave gasdermin-D and induce pyroptotic cell death.

46 r ceramide, often linked to the induction to cell death.

47 or highly expressed, it can lead to unwanted cell death.

48 potent activator of proliferative arrest and cell death.

49 equently triggered AMPK-dependent autophagic cell death.

50 ization of the plasma membrane and bacterial cell death.

51 death into immunologically silent apoptotic cell death.

52 Asp-348 and Asp-387 during the execution of cell death.

53 lls housing symbiotic bacteria, during their cell death.

54 the doses that are not related to increased cell death.

55 ases melanoma cell proliferation and reduces cell death.

56 sd7c-KO brain exhibited hypoxia and neuronal cell death.

57 X family involvement in neurodevelopment and cell death.

58 aging, immunity, proteostasis and programmed cell death.

59 ed root meristematic cells from heat-induced cell death.

60 ty of mechanisms, including the induction of cell death.

61 attenuated cancer cell growth and eventually cell death.

62 alance in dopaminergic neurotransmission and cell death.

63 ere their numbers are adjusted by programmed cell death.

64 ecrosis factor production, and were prone to cell death.

65 r of necroptosis, a form of programmed lytic cell death.

66 dance of GSDMD were resistant to Tir-induced cell death.

67 sdermin D (GSDMD) cleavage drives pyroptotic cell death.

68 by Fenton reaction-mediated ferroptosis-like cell-death.

69 heckpoint inhibitor targeting the programmed cell death 1 (PD-1) axis, has shown promising results fo

70 hat elucidated the biology of the programmed cell death 1 (PD-1), programmed cell death 1 ligand 1 (P

71 thermore, co-blockade of TIM3 and programmed cell death 1 (PD1) can result in tumour regression in pr

72 ligand 1 (PDL1) with its receptor programmed cell death 1 (PD1) inhibits T cell responses, and blocka

73 ustion features including reduced programmed cell death 1 expression and increased T-cell proliferati

74 e programmed cell death 1 (PD-1), programmed cell death 1 ligand 1 (PD-L1) and cytotoxic T lymphocyte

75 cally relevant targets, including programmed cell death 1 ligand 1 (PD-L1), in a STING-dependent mann

76 The interaction of programmed cell death 1 ligand 1 (PDL1) with its receptor programme

77 The programmed cell death 1 pathway as an important immune checkpoint h

78 ne therapy, such as with the anti-programmed cell death-1 (anti-PD-1) monoclonal antibody nivolumab,

79 cancers using immunotherapy with programmed cell death-1 (PD-1) checkpoint blockade.

80 mediated in part by expression of programmed cell death-1 (PD-1) encoded by the Pdcd1 gene.

81 Programmed cell death-1 (PD-1)/programmed death ligand-1 blockade m

82 ting in a distinct spatiotemporal pattern of cell death(7,8).

83 excess prooxidant loads leading to selective cell death, a therapeutically exploitable difference.

84 cipitates a pattern of neurodegeneration via cell death across disparate but linked brain regions may

85 Cell death after a delayed mitosis was rescued by inacti

86 ncreasing reactive iron, oxygen species, and cell death; an effect further potentiated by chemotherap

87 tes involution by exacerbating inflammation, cell death and adipocytes repopulation.

88 s the activation of NLR SUMM2 for initiating cell death and autoimmunity.

89 trapure flagellin from S Typhimurium induced cell death and cytokine secretion in THP-1 cells and pri

90 return, negatively regulates RPW8.1-mediated cell death and defense response via suppressing RPW8.1 e

91 6, ERF016 or ORA59 increases RPW8.1-mediated cell death and defense response.

92 (FTY720) attenuates psychosine-induced glial cell death and demyelination both in vitro and ex vivo m

93 ignaling negatively regulate RPW8.1-mediated cell death and disease resistance via suppressing RPW8.1

94 rative diseases, often resulting in neuronal cell death and functional impairment.

95 e evidence that cannabidiol (CBD) can induce cell death and increases the radiosensitivity of GBM by

96 crobiome contributes to cholestasis-mediated cell death and inflammation through mechanisms involving

97 roaches to dissect the roles of caspase-8 in cell death and inflammation.

98 Balanced regulation of cell death and inflammatory immune responses is essentia

99 ory step in signal transduction that impacts cell death and inflammatory signaling downstream of vari

100 induced phenotypic events, i.e. induction of cell death and inhibition of division, at a single-cell

101 In contrast, prevention of cell death and innate immunity after CI+Txp requires inh

102 n in PI(3)P-deficient P. falciparum precedes cell death and is reversible after withdrawal of the str

103 kinase RIPK3 is required to induce necrotic cell death and is strongly induced in cells isolated fro

104 We found that ferroptotic cell death and lipid peroxidation can be inhibited by tr

105 ed protective ER chaperones, and (3) greater cell death and liver injury.

106 during intracellular growth, leading to host cell death and loss of virulence.

107 ese structures in certain environments after cell death and lysis, magnetosome magnetite crystals con

108 sms through which PMNs directly induce tumor cell death and proliferation in vivo and suggest that th

109 is likely altered in these individuals, with cell death and skewed cellular composition playing signi

110 her sites of open chromatin, leading to germ cell death and sterility.

111 cascade, thereby changing a balance between cell death and survival.

112 ism has a role in glucose starvation-induced cell death and that pharmacologic inhibition of glucose

113 caspase-dependent but caspase 3-independent cell death and that the mechanism of cell death depends

114 as aflatoxin B(1) (AFB(1)), induce apoptotic cell death and the resulting cell debris stimulates hepa

115 these organoids is associated with increased cell death and transcriptional dysregulation indicative

116 E-BP knockdown were resistant to BBR-induced cell death and were resensitized to BBR after pharmacolo

117 f the ISR transcriptional program, increased cell death, and defective AID expression.

118 d molecular players regulating developmental cell death, and discusses recent findings with which the

119 M vesicles (OMVs) to influence inflammation, cell death, and disease pathogenesis.

120 NA interference also leads to dwarfism, mild cell death, and enhanced resistance to M. oryzae in the

121 reticulum stress, mitochondrial dysfunction, cell death, and inflammation.

122 phodepletion, T cell priming via immunogenic cell death, and inflammation; all occur within the conte

123 a, diabetes incidence, hypoinsulinemia, beta-cell death, and loss of beta-cell mass observed in Ak li

124 2 double mutant exhibits strong dwarfism and cell death, and silencing of both genes via RNA interfer

125 B) signaling, cell proliferation, programmed cell death, and survival and is crucially involved in in

126 ltimately results in programmed execution of cell death, and the nature of this cell death is determi

127 y a pathogenic Cdkl5-Sox9 axis in epithelial cell-death, and support CDKL5 antagonism as a therapeuti

128 grity, recognition by cellular immunity, and cell death are all buffered by blocking stress signaling

129 se in vertebrates, the mechanisms leading to cell death are largely unexplored.

130 Metabolism and cell death are tightly linked in the phenomenon of ferro

131 were evaluated by immunoblotting, ELISA, and cell death assays, respectively.

132 is is an iron-dependent form of nonapoptotic cell death associated with oxidized polyunsaturated phos

133 nstrate that in vitro, hMGL-4.0 causes tumor cell death, associated with increased reactive oxygen sp

134 e pathogens often triggers a rapid localized cell death at the pathogen infection sites, termed the h

135 roliferation with no difference in apoptotic cell death between control and Ddr1(-/-) animals.

136 family member, and activation and adipocyte cell death both in vitro and in vivo Here, we found that

137 DDH cartilage, with no evidence of augmented cell death by activation of caspase 3.

138 Anti-apoptotic members suppress cell death by deploying a surface groove to capture the

139 in the management of solid tumors and induce cell death by forming intrastrand dinucleotide DNA adduc

140 ents oxidative stress-induced DNA damage and cell death by suppressing mitochondrial ROS production.

141 limiting the induction of a necrotic form of cell death called necroptosis.

142 g of Annexin V, demonstrates that programmed cell death can be promoted by the peptide assembly.

143 used chemotherapeutically to promote cancer cell death can have the opposite effect on wild-type epi

144 ght cancer hallmarks: apoptosis, cell cycle, cell death, cell motility, DNA repair, immune response,

145 cancer, such as inflammation, resistance to cell death, cellular proliferation, neurohormonal stress

146 TNF-alpha and IFN-gamma induced inflammatory cell death characterized by inflammatory cell death, PAN

147 Programmed cell death contributes to host defense against pathogens

148 ither restore cellular homeostasis or induce cell death depending on the insult.

149 pendent cell death and that the mechanism of cell death depends on the genetic composition of the hos

150 enomenon of ferroptosis, a form of regulated cell death driven by peroxidation of phospholipids.

151 Instead, they underwent local cell death due to excessive phagocytosis of lysosomes.

152 methods are limited by interior hypoxia and cell death due to insufficient surface diffusion, preven

153 metabolism, contributing to stationary phase cell death during exposure to weak acid stress.

154 terials is a promising approach for reducing cell death during gastrointestinal passage and controlli

155 n aggregation is a major driver of aging and cell death during growth arrest, and that coordinated ac

156 ogenesis by triggering T cell activation and cell death during viral spread.

157 Ferroptosis, a novel mode of cell death elicited by iron-dependent phospholipid perox

158 for detection of chromatin condensation and cell death, enabling studies of viral plaque formation w

159 ents an ancient transkingdom relationship of cell death execution modules involved in organismal defe

160 P3 inflammasome components or the downstream cell death executioner gasdermin D (GSDMD) led to an ini

161 min D (GSDMD) led to an initial reduction in cell death followed by a robust increase in the incidenc

162 ibitors unique to necroptotic proteins, this cell death has been found to occur in virtually all tiss

163 like protein Cf-2, triggering hypersensitive cell death (HR) and disease resistance.

164 Immunogenic cell death (ICD) is a way of reengaging the tumor-specif

165 rug-induced cell death, known as immunogenic cell death (ICD), can propagate antitumoral immunity to

166 dow combines the complex interplay of cancer cell death, immune activity, emergence of chemoresistanc

167 Caspases regulate cell death, immune responses, and homeostasis.

168 s to its antiapoptotic function, and induces cell death in a Bok-dependent manner.

169 Recombinant TNFalpha induced MDSC cell death in a dose- and RIP1-dependent manner.

170 2) accumulation, defense gene expression and cell death in Arabidopsis, all of which constitute a hal

171 eralasertib), in vitro, leading to selective cell death in ATM-deficient cells.

172 he ability of mCD40L to also directly induce cell death in CD40-expressing carcinomas, subsequently r

173 Neutrophil extracellular traps cell death in CRSwNP was associated with bacterial colon

174 unction and epithelial integrity, and spared cell death in crypt base columnar cells compared to TAI-

175 r-13 plays a major role in the regulation of cell death in developing avian B cells.

176 aggregates, ultimately inducing immunogenic cell death in dMMR cancer cells.

177 ombined PI3K/mTORi and CHK1i induces greater cell death in HGSOC cells and in vivo models by causing

178 signaling pathways and promotes accelerated cell death in HSV-infected cells.

179 h mutant huntingtin (mHTT) leads to neuronal cell death in Huntington's disease (HD) are not fully un

180 rs, increased dramatically cIN BAX-dependent cell death in mice.

181 cell stress to protect against pathological cell death in multiple diseases.

182 ption-replication conflicts, DNA damage, and cell death in oncogenic cells.

183 CMV induces autophagy to prevent necroptotic cell death in order to ensure the survival of infected m

184 from cellular stores may also play a role in cell death in other neurologic conditions.

185 cells in the G(2)/M phase (89%); 2) induces cell death in PC3 cells even after the removal of the co

186 eptors are able to induce either survival or cell death in presence or absence of their ligand, respe

187 The detection of cell death in some EAS cells together with an accumulati

188 sion leads to a growth advantage and induces cell death in surrounding cells.

189 ced during influenza virus infection induces cell death in the form of pyroptosis, apoptosis, and nec

190 k analysis indicated an increase in necrotic cell death in the lungs of superinfected mice compared t

191 X protein had no effect on BAX activation or cell death in the nutrient-replete state.

192 rmatitis pathology of cpdm mice and mediated cell death in the skin.

193 ne to undergo neutrophil extracellular traps cell death in the tissue of patients with severe type 2

194 iated AKI in vivo and cisplatin-induced RTEC cell death in vitro Importantly, aggravation of cisplati

195 ) dysregulation has been linked to neuronal cell death, including in hereditary retinal degeneration

196 utation carrier tend to be more sensitive to cell death induced by chromium (Cr) and nickel (Ni) expo

197 Our data suggest that the mechanism of cell death induced by CX-5461 is critical for rational c

198 Cell death induced by nuclear MLKL was a potent activato

199 Transfer of GNLY, but not other cell death-inducing cytotoxic granule proteins, strongly

200 erestingly, this phenotype was not caused by cell death induction or senescence.

201 can influence cellular processes, including cell death, inflammation, and immune responses, and ther

202 Cell death, inflammation, and tuft cell markers were dow

203 Necroptosis is a proinflammatory form of cell death instigated by pore-forming toxins such as S.

204 n D function convert inflammatory pyroptotic cell death into immunologically silent apoptotic cell de

205 Regulation of apoptotic cell death is an important component in the coral stress

206 cution of cell death, and the nature of this cell death is determined by the specific caspases involv

207 on, we show that glucose deprivation-induced cell death is driven not by the lack of glucose, but rat

208 , 2) occur intracellularly, and 3) for which cell death is not the dominant outcome.

209 Thus, cell death is often closely associated with the inductio

210 Necroptotic cell death is potently immunogenic and limits IAV spread

211 yelinating diseases in which oligodendrocyte cell-death is one of the pathological features.

212 As a cell undergoes apoptotic cell death, it experiences changes in morphology and ion

213 Yet, a mode of drug-induced cell death, known as immunogenic cell death (ICD), can p

214 f the commonly assessed biomarker programmed cell death ligand 1 (PD-L1) nor tumor mutational burden

215 S-986192, an adnectin-based human programmed cell death ligand 1 (PD-L1) tracer, was developed to non

216 necroptosis is an independent, "stand-alone" cell death mechanism that fully compensates for the abse

217 enotoxic agents, but rather are induced from cell death nucleases and are not fundamental to the mech

218 rasite antigen that initiates apoptosis-like cell death of parasites, adding fascinating insight into

219 Apoptotic cell death of the treated HeLa and BE(2)-C cells was dem

220 s influences the decision between initiating cell death or cell survival pathways.

221 cts of metabolic stress predominate and beta cell death or dysfunction occurs.

222 s beta-cell replication without induction of cell death or loss of insulin secretion, suggesting that

223 th fetal and adult life without induction of cell death or proplatelet formation.

224 s that NPR1 is centrally integrated into the cell death or survival decisions in plant immunity by mo

225 by inducing oxidative stress or ferroptotic cell death, or may be related to an inflammatory respons

226 significantly affecting cell proliferation, cell death, or UPR induction in murine myeloblast 32D an

227 hich bypasses the diffusion limit to prevent cell death over long-term cultures.

228 und to be effective in apoptotic-induced GBM cell death (over 90%) within 48 h of treatment.

229 ory cell death characterized by inflammatory cell death, PANoptosis.

230 Necroptosis is a cell death pathway involved in inflammation and disease.

231 is the terminal effector in the necroptosis cell death pathway.

232 However, the specific cell death pathways and key upstream sensors activated i

233 cisplatin must target molecules that control cell death pathways in the oocytes of primordial follicl

234 pase-6 promotes the activation of programmed cell death pathways including pyroptosis, apoptosis, and

235 Here, we provide an overview of nonapoptotic cell death pathways induced by DNA damage and discuss th

236 ogens use many strategies to manipulate host cell death pathways to facilitate their survival and dis

237 o oxidative stress, inflammation, myocardial cell death pathways, and neurohumoral mechanisms, are ad

238 save cellular energy and activate programmed cell death pathways, in the absence of glucose.

239 he activation status of the inflammasome and cell death pathways.

240 es, are also key regulators of mitochondrial cell death pathways.

241 by extracellular matrix (ECM) and programmed cell death (PCD) along the embryonic midline.

242 ruction of the bacterial chromosome, causing cell death prior to completion of phage replication.

243 This programmed cell death process is mediated by several signalling pat

244 ving rise to physical observables during the cell death process.

245 AX activation and induction of the intrinsic cell death program.

246 patients newly treated with anti-programmed cell death protein 1 (PD-1) agents (nivolumab or pembrol

247 s the immune checkpoint receptors programmed cell death protein 1 (PD-1) and cytotoxic T lymphocyte-a

248 ning CAR T cells, rhesusized anti-programmed cell death protein 1 (PD-1) antibody was administered to

249 Programmed cell death protein 1 (PD-1) has become one of the most i

250 Finally, the combination of anti-programmed cell death protein 1 with CCR2i considerably increased t

251 Innate immune-mediated programmed cell death (pyroptosis, apoptosis, necroptosis) is an in

252 1beta and IL-18 and induces the inflammatory cell death, pyroptosis, via gasdermin D.

253 delivery to decreased ceramide levels, lower cell death rates, and changes in the composition of the

254 to environmental stresses undergo regulated cell death (RCD) when homeostatic programs fail to maint

255 Oligomers of RCD-1 were associated with the cell death reaction, further supporting the evolutionary

256 y repressing estrogen signaling and inducing cell death related pathways.

257 isruption of the early coordinated non-lytic cell death response, ultimately supports the inflammator

258 Cell death resulted from the recruitment of 53BP1 to DNA

259 Apoptosis, a conserved form of programmed cell death, shows interspecies differences that may refl

260 pic brain slices we found that D(1)R-induced cell death signaling and neuronal degeneration, are miti

261 s led to a refined view of how NF-kappaB and cell death signaling are interlinked and how they regula

262 blocking the cytokine-mediated inflammatory cell death signaling pathway identified here may benefit

263 apoptosis owing to concomitant activation of cell death signalling pathways; these cells are poised t

264 es an iron- and ROS-dependent, GPX4 mediated cell death, suggesting ferroptosis as a major mechanism.

265 and led to impaired microglia physiology and cell death, suggestive of a mechanistic convergence betw

266 unchecked inflammation that causes neuronal cell death, systemic stress, and lethal immunodepression

267 n, and a cancer-protective form of regulated cell death termed ferroptosis, all depend on iron metabo

268 sis, a caspase-independent mechanism of host cell death that failed to eradicate S. aureus and instea

269 T cells in the tumor experience substantial cell death that is in part mediated by IFN-independent a

270 Ferroptosis is a regulated form of cell death that occurs when phospholipids with polyunsat

271 eceptors are known inducers of apoptosis and cell death that recruit death domain (DD) proteins FADD

272 ptosis is a more recently recognized form of cell death that relies on iron-mediated oxidative damage

273 ve well-understood consequences that lead to cell death, the disease association of several rhodopsin

274 hat genes related to cell cycle, DNA repair, cell death, the IGF1 pathway, and immunity are under inc

275 After cell death, these crystals are trapped into sediments th

276 Apoptosis induces cell death through mitochondrial outer membrane permeabi

277 in NUP98-PHF23 expressing AML cells leads to cell death through necrotic and late apoptosis pathways.

278 n, pancreatic, and lung cell lines triggered cell death through PTCH proapoptotic signaling.

279 l death was via lysosome-mediated programmed cell death through upregulation of cathepsin B, Tnf and

280 of genetic lesions drives the activation of cell death to eliminate cells with defective genome.

281 importance in proliferation, apoptosis, and cell death ultimately renders them hot targets in cancer

282 HPV16 E7-expressing cells are sensitized to cell death under conditions of metabolic stress, which i

283 s mutants that trigger antiviral necroptotic cell death upon early viral gene expression.

284 nfolded protein response (UPR) signaling and cell death upon ER stress induction.

285 utrophils can undergo a nonapoptotic type of cell death using components of the necroptotic pathway,

286 the most upstream enzyme, EBP, led to cancer cell death via depletion of downstream sterols, an obser

287 ed as a critical factor for immune-initiated cell death via ferroptosis.

288 RSV-induced epithelial cell death was associated with increased phosphorylated

289 This cell death was attenuated by knockdown or inhibition of

290 In vitro, cell death was induced in more than 80% of the cells and

291 cytes repopulation, estrogen-induced mammary cell death was via lysosome-mediated programmed cell dea

292 ecrosome signaling, cytokine production, and cell death were evaluated by immunoblotting, ELISA, and

293 and wild-type cINs during the period of cIN cell death were indistinguishable.

294 genes associated with defense and programmed cell death were strongly activated, including a suite of

295 cer and lung metastasis by triggering cancer cell death when netrin-1 is lowly expressed.

296 le exocytosis, in developmentally programmed cell death when the predominant pro-apoptotic caspase CE

297 red immunity (ETI) often leads to programmed cell death, which is restricted by NPR1, an activator of

298 ells to limit cytolytic function and promote cell death, which ultimately leads to fewer T(RM) cells

299 ry, and confirmed the spatial correlation of cell death with ferumoxytol distribution.

300 omas (HCCs) are treated by inducing ischemic cell death with transarterial embolization (TAE) or tran