ライフサイエンスコーパス: necrotic cell death

1 re leads to necroptosis, a regulated form of necrotic cell death.

2 ibly by suppressing JNK-dependent programmed necrotic cell death.

3 key RIP3 downstream component of TNF-induced necrotic cell death.

4 ich then induces plasma membrane rupture and necrotic cell death.

5 yers in COR signaling and disease-associated necrotic cell death.

6 (DISC) and is required for the induction of necrotic cell death.

7 s as the quintessential framework underlying necrotic cell death.

8 s ConA/GalN induced apoptosis in addition to necrotic cell death.

9 the mice were resistant to apoptotic but not necrotic cell death.

10 th, and JNK contributes to apoptotic but not necrotic cell death.

11 Infected memory CD4+ T cells underwent rapid necrotic cell death.

12 ucella mutants induce macrophage oncotic and necrotic cell death.

13 eregulation, the first irreversible stage of necrotic cell death.

14 g components plays a key role in TNF-induced necrotic cell death.

15 l death, while other proteases are active in necrotic cell death.

16 assay demonstrated that BopC is required for necrotic cell death.

17 ochondria, which resulted in reduced ATP and necrotic cell death.

18 t subsequently promotes oxidative damage and necrotic cell death.

19 , a structure involved in both apoptotic and necrotic cell death.

20 gainst the loss of DeltaPsim and resulted in necrotic cell death.

21 (especially S-nitrosothiols) and subsequent necrotic cell death.

22 ritical role in mediating both apoptotic and necrotic cell death.

23 PT has been implicated in both apoptotic and necrotic cell death.

24 c release and caspase 3 cleavage, as well as necrotic cell death.

25 protein inhibited the loss of DeltaPsim and necrotic cell death.

26 in mediating ROS accumulation in TNF-induced necrotic cell death.

27 droxyanisole efficiently blocked TNF-induced necrotic cell death.

28 pattern of cell destruction consistent with necrotic cell death.

29 gp96 are released from cells as a result of necrotic cell death.

30 of NAD+/ATP energy stores and ultimately to necrotic cell death.

31 of the signaling cascade of this TNF-induced necrotic cell death.

32 f intracellular ATP depletion, a hallmark of necrotic cell death.

33 ors did not significantly affect TNF-induced necrotic cell death.

34 icular myocardium through both apoptotic and necrotic cell death.

35 n cleaved substrate, a marker of excitotoxic/necrotic cell death.

36 enated were the same as those that underwent necrotic cell death.

37 e modulation of other types of apoptotic and necrotic cell death.

38 etes cellular NAD+ and ATP stores and causes necrotic cell death.

39 oxygen species production, and apoptotic and necrotic cell death.

40 (LCLs) that had been subject to apoptotic or necrotic cell death.

41 h, we propose that CD91 acts as a sensor for necrotic cell death.

42 ath that has been described as distinct from necrotic cell death.

43 and MeHg were found to induce apoptotic and necrotic cell death.

44 ding to disruption of the inner membrane and necrotic cell death.

45 gnal downstream events such as apoptosis and necrotic cell death.

46 creases in chromosomal damage, apoptosis and necrotic cell death.

47 otective in an ischemia model of excitotoxic/necrotic cell death.

48 cells prevents apoptotic cell death but not necrotic cell death.

49 recognized as a major cause of apoptotic or necrotic cell death.

50 processes which result in both apoptotic and necrotic cell death.

51 e event in apoptosis and also occurred after necrotic cell death.

52 the cell's earliest responses to inducers of necrotic cell death.

53 his swelling is, in many cases, a prelude to necrotic cell death.

54 -N-terminal kinase (JNK) pathway, leading to necrotic cell death.

55 ial Ca(2+) triggers mPTP opening, leading to necrotic cell death.

56 ndrial matrix Ca(2+) concentrations triggers necrotic cell death.

57 utophagic flux and resistance to Mtb induced necrotic cell death.

58 todynamic injury, resulting in predominantly necrotic cell death.

59 ve oxygen species production, culminating in necrotic cell death.

60 ction of reactive oxygen species and massive necrotic cell death.

61 ining uPAS cargo and leading to AIF-mediated necrotic cell death.

62 entiates MLKL phosphorylation/activation and necrotic cell death.

63 pecifically the role of Bax/Bak in regulated necrotic cell death.

64 mage in TEN through activation of programmed necrotic cell death.

65 X was accompanied by contractile failure and necrotic cell death.

66 ndrial calcium overload, MPTP formation, and necrotic cell death.

67 amics and participates in both apoptotic and necrotic cell death.

68 xygen species which can render apoptotic and necrotic cell death.

69 ependent mitochondrial swelling and restored necrotic cell death.

70 ing evidence regarding the immunogenicity of necrotic cell death.

71 stance to mitochondrial calcium overload and necrotic cell death.

72 dative stress and autophagic, apoptotic, and necrotic cell death.

73 promoters of necroptosis, a pro-inflammatory necrotic cell death.

74 water plays a critical role in apoptotic and necrotic cell death.

75 ractions between autophagy and apoptotic and necrotic cell death.

76 cate serglycin in promoting apoptotic versus necrotic cell death.

77 and nuclear DNA fragmentation, resulting in necrotic cell death.

78 oduction of interleukin-1beta and programmed necrotic cell death.

79 sing SV40 large T antigen completely rescued necrotic cell death.

80 APAP hepatotoxicity in humans, resulting in necrotic cell death.

81 tic of C. elegans programmed cell deaths and necrotic cell deaths.

82 eyond the simple view of 'apoptotic' versus 'necrotic' cell death.

83 a with the eukaryotic cell and was a form of necrotic cell death accompanied by osmotic lysis.

84 low toxicity and the absence of apoptotic or necrotic cell death after 24 or 48 h of incubation.

85 l permeability transition (MPT) can initiate necrotic cell death after reperfusion, but the MPT is al

86 ed molecular pattern that is released during necrotic cell death and also secreted from activated mac

87 eficient (PARP(-/-)) mice are protected from necrotic cell death and ATP depletion but not from apopt

88 ificantly affected the extent of UVA-induced necrotic cell death and ATP depletion in all the cell li

89 ore, hematoxylin and eosin staining revealed necrotic cell death and cell loss in Pgc-1(c) livers and

90 itizes cardiac myocytes to TNFalpha-mediated necrotic cell death and DOX cardiotoxicity.

91 echanism of IFN-induced RIP kinase-dependent necrotic cell death and identify FADD and caspases as ne

92 This is because (1) massive necrotic cell death and increased infiltration of leukoc

93 AKI is histologically characterized by necrotic cell death and inflammation.

94 The kinase RIPK3 is required to induce necrotic cell death and is strongly induced in cells iso

95 gether were almost completely protected from necrotic cell death and MD disease.

96 eptide cancer therapeutic because it induces necrotic cell death and not apoptosis, which is uncommon

97 an and deferoxamine to UW solution inhibited necrotic cell death and preserved mitochondrial structur

98 tion of phagocytosed Shigella led to massive necrotic cell death and release of the bacteria.

99 his swelling is, in many cases, a prelude to necrotic cell death and the dye trypan blue was used to

100 termined reduced cell proliferation, massive necrotic cell death, and fibrosis.

101 response (a-UPR) hyperactivation, long-term necrotic cell death, and release of damage-associated mo

102 actor receptor (TNFR) I mediates TNF-induced necrotic cell death, and that RIP, FADD, and TRAF2 are c

103 Cellular susceptibility to UVA-induced necrotic cell death appears to reflect the intracellular

104 mitochondrial respiratory chain defects and necrotic cell death are mutually dependent on and obliga

105 hanisms activated during the early stages of necrotic cell death are poorly characterized.

106 Apoptotic and necrotic cell death are well characterized and are influ

107 DNA damage-induced necrosis, thus assigning necrotic cell death as a form of "programmed cell death.

108 Myocardial infarction is a manifestation of necrotic cell death as a result of opening of the mitoch

109 The mechanism of neutrophil impairment was necrotic cell death as determined by morphological analy

110 hat RIPK1 is a key mediator of apoptotic and necrotic cell death as well as inflammatory pathways.

111 des new evidence that caspases contribute to necrotic cell death as well.

112 t attenuated all other parameters, including necrotic cell death, at 6 hours after APAP.

113 classification model specified apoptotic and necrotic cell death based on single cell Raman spectra.

114 to I/R increased reactive oxygen species and necrotic cell death, both of which were mitigated by ATF

115 to I/R increased reactive oxygen species and necrotic cell death, both of which were mitigated by ATF

116 Reperfusion with glycine alone prevented necrotic cell death but did not induce apoptosis and onl

117 APAP-induced phosphorylase a activation and necrotic cell death, but failed to inhibit phosphorylase

118 rned by signals associated with apoptotic or necrotic cell death, but is an intrinsic feature of the

119 herefore serine hydrolase inhibitors prevent necrotic cell death by blocking mitochondrial calcium up

120 -mediated proteolysis; caspases also subvert necrotic cell death by cleaving and inactivating poly AD

121 ion of PARP1 is known to be a major cause of necrotic cell death by depleting NAD(+) /ATP pools durin

122 so required for mitochondrial pore-dependent necrotic cell death by facilitating outer membrane perme

123 tuberculosis inhibits apoptosis and promotes necrotic cell death by inhibiting production of prostagl

124 have been shown to suppress cell damage and necrotic cell death by moderating the amount of labile i

125 psulotomy specimens most likely results from necrotic cell death caused by damage during or soon afte

126 To test if NF-kappaB can protect from necrotic cell death caused by high levels of molecular O

127 Ferroptosis is a distinct form of necrotic cell death caused by overwhelming lipid peroxid

128 In contrast, programmed necrotic cell death causes release of immunostimulatory

129 Necrotic lesions and necrotic cell death characterize severe autoimmune nephr

130 Ferroptosis is a mechanism of regulated necrotic cell death characterized by iron-dependent, lip

131 A rapid necrotic cell death, characterized by cell swelling and

132 scription and affected genes associated with necrotic cell death, chromosome condensation, and mRNA p

133 apoptotic-competent conditions or a type of necrotic cell death dependent on RIP1 kinase, termed nec

134 ctor, BopC, is required for the induction of necrotic cell death during Bordetella infection.

135 Necrotic cell death during Mycobacterium tuberculosis (M

136 urprised to find no evidence of apoptotic or necrotic cell death during stages of peak myofiber loss,

137 Necrotic cell death evoked by cytoplasmic Ca(2+) overloa

138 -associated caspase-8 activity and increased necrotic cell death following antigenic stimulation, imp

139 )C2] malate showed a significant increase in necrotic cell death following treatment in the ICB-sensi

140 rroptosis, a newly emerged form of regulated necrotic cell death, has been demonstrated to play an im

141 ntrations 12.5 ug/mL resulted in significant necrotic cell death in A549 and HaCaT cells, and caspase

142 Consistent with a role of necrotic cell death in adjuvant effects, Leu-Leu-OMe rep

143 g of CAPN5, has been shown to be involved in necrotic cell death in Caenorhabditis elegans.

144 )-NC(Ca-ATP) channel plays a central role in necrotic cell death in central nervous system (CNS) inju

145 te that the C-terminal domain of CpnT causes necrotic cell death in eukaryotic cells.

146 stem (TTSS) is required for the induction of necrotic cell death in infected mammalian cells.

147 Virulent M. tuberculosis strains induce necrotic cell death in macrophages by an obscure molecul

148 the mechanisms that lead to the induction of necrotic cell death in macrophages.

149 Moreover, necrotic cell death in Mtb-infected macrophage cultures

150 a CD44/ITGA4 containing complex and triggers necrotic cell death in multiple myeloma cell lines.

151 and neurobehavioral deficits; apoptotic and necrotic cell death in neurons were reduced by Rapamycin

152 d orchestrate the induction of apoptotic and necrotic cell death in neurons, a VDAC1siRNA and an acti

153 RPE is known to undergo necrotic cell death in response to oxidative stress.

154 sine triphosphate depletion, and the ensuing necrotic cell death in skin fibroblasts, and this effect

155 tal cytokeratin 18 suggested the presence of necrotic cell death in TASH and may be a useful serologi

156 e, Leu-Leu-OMe, mimics the alum-like form of necrotic cell death in terms of cathepsin dependence and

157 generating a photoacid, effectively induced necrotic cell death in the HCT 116 cells.

158 All treatments prevented alcohol-induced necrotic cell death in the liver.

159 hat activate PPARalpha, leading to increased necrotic cell death in the lung which correlates with th

160 e, network analysis indicated an increase in necrotic cell death in the lungs of superinfected mice c

161 n of the suicide program of myocytes exceeds necrotic cell death in the pathologic heart of ischemic

162 s oxidative burst, mitochondrial damage, and necrotic cell death in TSC-deficient cells in a highly s

163 Heat shock proteins inhibit apoptotic and necrotic cell death in various cell types.

164 fication and discrimination of apoptotic and necrotic cell death in vitro is challenging.

165 xposure leads to immediate, target-selective necrotic cell death in vitro.

166 annexin V can be used to image apoptotic and necrotic cell death in vivo.

167 eases (HD) selectively induces a new form of necrotic cell death, in which endoplasmic reticulum (ER)

168 The phenotype of necrotic cell death induced by a mitochondrial electron

169 ess both mec-4(d)-induced cell death and the necrotic cell death induced by expression of a constitut

170 Depletion of ALKBH7 suppresses necrotic cell death induced by numerous alkylating and o

171 alpain proteases, which are activated during necrotic cell death induced by severe heat shock.

172 Programmed necrotic cell death induced by the tumor necrosis factor

173 ELLigence technology and AFM have shown that necrotic cell death induced the expansion of the cell ad

174 In one form of programmed necrotic cell death, induced by cytotoxic alkylating age

175 ERK inhibition generates both apoptotic and necrotic cell death-inducing pathways.

176 BNIP3 has been linked to both apoptotic and necrotic cell death involving mitochondrial permeability

177 Together our findings suggest that necrotic cell death is a powerful mediator of a Th2-asso

178 n tumor-bearing mice developing regions with necrotic cell death is demonstrated.

179 gical and genetic analyses revealed that the necrotic cell death is distinct from the RIP1/3 pathway-

180 onfirming that protection from apoptotic and necrotic cell death is independent of the stage of hiber

181 How it is released from chromatin during necrotic cell death is not known.

182 Necroptosis, a form of programmed necrotic cell death, is a gatekeeper of host defense aga

183 the CNS to apoptosis and a form of regulated necrotic cell death known as necroptosis that is mediate

184 When compounds 1-11 were tested for necrotic cell death (LDH release test) nitrones 1-3, 6,

185 Ferroptosis is an iron-dependent form of necrotic cell death marked by oxidative damage to phosph

186 Pyroptosis is a mechanism of programmed, necrotic cell death mediated by gasdermins, a family of

187 ion and p38 MAPK inhibition to abrogation of necrotic cell death mediated by mitochondrial membrane p

188 tion with RBCs, lung ECs underwent regulated necrotic cell death (necroptosis) and released the essen

189 re we identify a distinct, ferroptotic-like, necrotic cell death occurring in vivo during wounding of

190 very high concentrations, leukotoxin caused necrotic cell death of bovine peripheral leukocytes.

191 orticosteroids such as dexamethasone inhibit necrotic cell death of cells infected with Mycobacterium

192 Ultrastructural analysis confirmed necrotic cell death of EBOV-infected cells.

193 te that the intracellular LIP and subsequent necrotic cell death of human skin fibroblasts is signifi

194 t the host inflammatory response and lead to necrotic cell death of infected macrophages.

195 exacerbated ATP depletion, cytotoxicity, and necrotic cell death of LLCPK(1) cells subjected to hypox

196 In contrast, necrotic cell death of macrophages infected with rough B

197 ic ischemia followed by reperfusion leads to necrotic cell death (oncosis), which often occurs within

198 rane potential, leading to ATP depletion and necrotic cell death or to cytochrome c release and apopt

199 oxic molecules to trigger cell cycle arrest, necrotic cell death, or apoptosis.

200 mpound 1 concentration-dependently inhibited necrotic cell death pathway activation and 2.5 mM compou

201 chondrial membrane potential (DeltaPsim) and necrotic cell death pathway activation.

202 th, suggesting that NF-kappaB suppresses the necrotic cell death pathway.

203 ce, generated within intestinal cells by the necrotic cell death pathway.

204 ometric analyses indicate both apoptotic and necrotic cell death pathways.

205 The necrotic cell death phenomenon was independent of cultur

206 et-rich microthrombi (CD61) and induction of necrotic cell death [phosphorylated mixed lineage kinase

207 strate that PARP-1 activation and consequent necrotic cell death play an important role in the pathog

208 This activity may account for the necrotic cell death precipitated by these pathogens.

209 physiological (apoptotic) and pathological (necrotic) cell deaths reflects mechanistic differences i

210 cellular molecules associated with regulated necrotic cell death, replicating the characteristics of

211 Necroptosis, a regulated form of necrotic cell death, requires the activation of the RIP3

212 ms and demonstrate circadian phase-dependent necrotic cell death responses to Clostridium difficile t

213 and human enteroids demonstrate anti-phasic necrotic cell death responses to TcdB.

214 organism-specific, circadian phase-dependent necrotic cell death responses, and lay a foundation for

215 disruption of Rac1 abolishes clock-dependent necrotic cell death responses.

216 Ad5 activation of NLRP3 also induces necrotic cell death, resulting in the release of the pro

217 n regulation, triggers a lysosomal-dependent necrotic cell death routine.

218 predominance of ultrastructural features of necrotic cell death suggest a switch from apoptosis to n

219 ibitors of NF-kappaB facilitated TNF-induced necrotic cell death, suggesting that NF-kappaB suppresse

220 nvolves a newly described form of programmed necrotic cell death, termed necroptosis.

221 ating and suppressing two regulated forms of necrotic cell death, termed pyroptosis and necroptosis,

222 s are much more susceptible to apoptotic and necrotic cell death than CNS microglia, which is mirrore

223 Here, we show that HopG1 triggers necrotic cell death that enables the growth of adapted a

224 Ferroptosis is a regulated form of necrotic cell death that is caused by the accumulation o

225 l injury, there is an immediate induction of necrotic cell death that is seen only in GAG-depleted ex

226 s is a regulated caspase-independent form of necrotic cell death that results in an inflammatory phen

227 n, and peroxynitirte), induced apoptotic and necrotic cell death that was RONS-mediated (cell death p

228 on, lactate dehydrogenase (LDH) release, and necrotic cell death that were blocked by cyclosporin A (

229 ar NAD(+) depletion, subsequently preventing necrotic cell death that would otherwise occur due to PA

230 Interestingly, during TNF-induced necrotic cell death, the cellular ROS level was signific

231 Apart from regulating necrotic cell death, the physiologic function of the MPT

232 mitochondrial respiratory chain defects and necrotic cell death to the BH3-only protein Bcl-2-like 1

233 It appears that the necrotic cell death triggered by BopC occurs prior to th

234 intestinal Caco-2 cells undergo nonapoptotic necrotic cell death triggered by inositol 1,4,5-trisphos

235 To identify the factor(s) involved in necrotic cell death, type III-secreted proteins from B.

236 amage caused by UVA to mitochondria leads to necrotic cell death via adenosine triphosphate depletion

237 Until recently, necrotic cell death was believed to result from injuries

238 ed, particularly in T cells, and the rate of necrotic cell death was increased in patients with SLE.

239 At higher concentrations of methamphetamine, necrotic cell death was observed.

240 cluding apoptosis, which relies on caspases, necrotic cell death, which depends on receptor-interacti

241 (TG) have been used to study the process of necrotic cell death, which involves mitochondria in the

242 iving increased generation of superoxide and necrotic cell death, which was rescued by genetic inhibi

243 ffect of purines, hypoxanthine has prevented necrotic cell death while increasing caspase activity an

244 lin showed enhanced apoptosis, yet decreased necrotic cell death with associated increased caspase-3

245 ConA alone induced primarily necrotic cell death with no caspase activation, whereas

246 Simple stress or necrotic cell death with subsequent release of damage-as

247 Thus, Clec2d binds to histones released upon necrotic cell death, with functional consequences to inf

248 icin concentrations >/=10 micromol/L induced necrotic cell death within 24 hours, with no changes cha

249 IFN-beta, and the cultures underwent massive necrotic cell death within 3 d.

250 n either case, activated glia caused 75-100% necrotic cell death within 48 hr, which was completely p

251 ed pancreatic acinar mitochondria and caused necrotic cell death without affecting the initial [Ca(2+

252 Necrotic cell death yields the release of cellular compo