ライフサイエンスコーパス: necroptosis

1 not result in enhanced production of IFN or necroptosis.

2 otif], an amyloid motif regulating mammalian necroptosis.

3 eakage of DNA into the cytosol, and eventual necroptosis.

4 131) abrogated MLKL degradation and restored necroptosis.

5 the inflammasome/pyroptosis, apoptosis, and necroptosis.

6 ockdown of newly synthesized sigma3 enhances necroptosis.

7 ) binds to the 4HB domain of MLKL to inhibit necroptosis.

8 caspase-8-mediated apoptosis and MLKL-driven necroptosis.

9 domain-like (MLKL) protein-dependent tubule necroptosis.

10 ent a mouse model with increased bone marrow necroptosis.

11 TRADD was suggested to also mediate necroptosis.

12 heart damage was due to pneumolysin-mediated necroptosis.

13 dependent apoptosis and RIPK3/MLKL-dependent necroptosis.

14 logously chlorinated derivative exerted only necroptosis.

15 regulates cell death via both apoptosis and necroptosis.

16 on and cell death induction by apoptosis and necroptosis.

17 ing the confounding impact of RIPK3-mediated necroptosis.

18 d macrophages, leading to host cell death by necroptosis.

19 d during IPD is due in part to cardiomyocyte necroptosis.

20 m is independent from TNFalpha-signaling and necroptosis.

21 tion of a necrotic form of cell death called necroptosis.

22 tcomes, such as inflammation, apoptosis, and necroptosis.

23 ent apoptosis and Ripk1-Ripk3-Mlkl-regulated necroptosis.

24 RIPK3 interaction, RIPK3 phosphorylation and necroptosis.

25 his does not lead to either translocation or necroptosis.

26 ction, leading to ceramidosome formation and necroptosis.

27 ve itself, other proteins or both to inhibit necroptosis.

28 s cells undergoing apoptosis versus necrosis/necroptosis.

29 ssary to inhibit an IFN-primed virus-induced necroptosis.

30 on of host cells with reovirus can result in necroptosis.

31 cular mechanisms and relevance to disease of necroptosis.

32 nt small molecular inhibitor of RIPK1-driven necroptosis.

33 tion of a necrotic form of cell death called necroptosis.

34 TAK1 promotes its interaction with RIPK3 and necroptosis.

35 hich infection with a dsRNA virus results in necroptosis.

36 ion of these death receptors can also induce necroptosis.

37 igger apoptosis that gives rise to secondary necroptosis.

38 -inflammatory roles and functions to prevent necroptosis.

39 dial survival and homeostasis by suppressing necroptosis.

40 sis or a regulated form of necrosis known as necroptosis.

41 rd an alternate and detrimental cell fate of necroptosis.

42 urs in several forms including apoptosis and necroptosis.

43 for TNF-induced RIP1-initiated apoptosis and necroptosis.

44 complex, LUBAC also restricts TRAIL-induced necroptosis.

45 rm of programmed necrotic cell death, termed necroptosis.

46 rotecting infected monocytes from undergoing necroptosis.

47 masome activation independent of its role in necroptosis.

48 to RIPK3-dependent TNF-induced apoptosis and necroptosis.

49 ng on whether cells die through apoptosis or necroptosis.

50 is by itself can limit IAV, without need for necroptosis.

51 nclusions: Pneumovirus infection induces AEC necroptosis.

52 DNA methylation of RIP1-dependent targets of necroptosis.

53 morphic in humans, is reversed by inhibiting necroptosis.

54 genes in Toll-like receptor 4 (TLR4)-induced necroptosis.

55 ich induced cell death through apoptosis and necroptosis.

56 ential to driving pyroptosis, apoptosis, and necroptosis.

57 tigate the interaction between apoptosis and necroptosis.

58 NA sensors induce apoptosis, pyroptosis, and necroptosis.

59 fficient both to degrade MLKL and to inhibit necroptosis.

60 findings define a specialized form of axonal necroptosis.

61 s, similarly to cell lysis in pyroptosis and necroptosis(3,4).

62 aspase-independent form of cell death termed necroptosis(4,5).

63 s thought to inhibit activation of RIPK3 and necroptosis(8).

64 ive oxygen species were sufficient to induce necroptosis, a caspase-independent mechanism of host cel

65 Necroptosis, a cell death pathway mediated by the RIPK1-

66 MLKL is the essential effector of necroptosis, a form of programmed lytic cell death.

67 Paneth cells and displayed TNFalpha-mediated necroptosis, a form of programmed necrosis.

68 expected role of TAM kinases as promoters of necroptosis, a pro-inflammatory necrotic cell death.

69 Necroptosis, a programmed form of necrosis, is executed

70 al and genetic approaches, we tested whether necroptosis, a regulated cell-death mechanism implicated

71 pore) and that opening of this pore leads to necroptosis, a regulated form of necrotic cell death.

72 ces sex-dependent RD primarily by triggering necroptosis and activating an inflammatory response that

73 itiated RIPK3-dependent parallel pathways of necroptosis and apoptosis in infected cells.

74 ng complex II and subsequent RIPK1-dependent necroptosis and apoptosis were inhibited.

75 e myocardium and induces cardiac injury with necroptosis and apoptosis, followed by cardiac scarring

76 iled to trigger ICD-linked responses such as necroptosis and autophagy.

77 k1(K612R/K612R) mutation sensitizes cells to necroptosis and caspase-1 activation in response to TLRs

78 l lethality arising from both RIPK3-mediated necroptosis and FADD/caspase-8-driven apoptosis.

79 e oxygen species, resulting in resistance to necroptosis and ferroptosis.

80 terized by hypersensitivity to apoptosis and necroptosis and increased inflammatory response in perip

81 nd TNF production contribute to heme-induced necroptosis and inflammasome activation; however, the ro

82 RIP1 kinase regulates necroptosis and inflammation and may play an important r

83 RIP1 regulates necroptosis and inflammation and may play an important r

84 isease and as a tumour suppressor, regulates necroptosis and inflammation by regulating necrosome for

85 from alkylation-induced RD, showing reduced necroptosis and inflammation compared to males.

86 action motif (RHIM), triggers ZBP1-dependent necroptosis and inflammation in mice(15,16).

87 cleic acids by ZBP1 triggers RIPK3-dependent necroptosis and inflammation, which could underlie the d

88 serve as an important mechanism to fine-tune necroptosis and inflammation.

89 ing kinase involved in regulating apoptosis, necroptosis and inflammation.

90 on of RIPK1 controls TNF-mediated apoptosis, necroptosis and inflammatory pathways(1).

91 sinic:polycytidylic acid (poly(I:C))-induced necroptosis and inflammatory signalling.

92 anisms of phosphatidylserine exposure during necroptosis and its role in the recognition of necroptot

93 ll established, the regulatory mechanisms of necroptosis and its significance in the pathogenesis of

94 s of cell death such as necrosis, apoptosis, necroptosis and pyroptosis.

95 ed factor 2 (Traf2) in regulating myocardial necroptosis and remodeling using genetic mouse models.

96 after PS exposure can reverse the process of necroptosis and restore cell viability.

97 of Atg16l1 and Zbp1 accelerated LPS-mediated necroptosis and sepsis in mice.

98 IPK1 in keratinocytes induces ZBP1-dependent necroptosis and skin inflammation.

99 ated that PPARalpha mediates RIPK3-dependent necroptosis and that this pathway plays a central role i

100 We also discuss the inhibitors of necroptosis and the ways these inhibitors have been used

101 TRADD fails to rescue Fadd(-/-) embryos from necroptosis, and ablation of TRADD rescues Ripk1(-/-) mi

102 vation triggers inflammation and pyroptosis, necroptosis, and apoptosis (PANoptosis) by activating re

103 igate the relative importance of pyroptosis, necroptosis, and apoptosis during Salmonella infection,

104 g markedly decreased cell viability, induced necroptosis, and delayed culture wound closing in three

105 ation of EIF2A, increased levels of IRGM and necroptosis, and increased release of nuclear DAMPs comp

106 itively and negatively regulating apoptosis, necroptosis, and inflammation.

107 TNFalpha promotes necroptosis, and its expression is facilitated by mitoge

108 ough initiation of apoptosis, suppression of necroptosis, and modulation of cell death-independent si

109 upregulation of IL-33, an alarmin linked to necroptosis, and other chemokines and cytokines and prev

110 ing for overt damage, immunofluorescence for necroptosis, and Sirius red/fast green staining for coll

111 ock-down of RIPK3, a second key regulator of necroptosis, and the downstream effector MLKL (Mixed Lin

112 Here, we studied the involvement of necroptosis (another programmed cell death process) and

113 ase-8-dependent apoptosis and MLKL-dependent necroptosis are inhibited.

114 Neuroinflammation and necroptosis are major contributors to neurodegenerative

115 pes of necrotic death such as pyroptosis and necroptosis are mediated by active mechanisms of executi

116 We also demonstrate that apoptosis and necroptosis are mutually exclusive fates in IAV-infected

117 Apoptosis and necroptosis are two regulated cell death mechanisms; how

118 demonstrate infected monocytes also initiate necroptosis as a "trap door" death pathway in response t

119 The identification of necroptosis as a key mechanism for axonal degeneration i

120 This work highlights necroptosis as a possible preferred ICD form over apopto

121 ve damage marker), and overexpression of the necroptosis-associated genes Rip1 and Rip3 The activity

122 Here, we report an antiviral necroptosis-based genetic screen to identify novel host

123 ty transition-related regulated necrosis and necroptosis both contribute to oxalate-induced AKI, iden

124 caspase cleavage of RIPK1 not only inhibits necroptosis but also maintains inflammatory homeostasis

125 y to RIPK1 activation-mediated apoptosis and necroptosis, but also induction of pro-inflammatory cyto

126 ex (DISC) and the RIPoptosome, also initiate necroptosis by building filamentous scaffolds that lead

127 at the AMPK-Parkin axis negatively regulates necroptosis by inhibiting RIPK1-RIPK3 complex formation;

128 in mu1 negatively regulates reovirus-induced necroptosis by limiting RNA synthesis.

129 Induction of necroptosis by mammalian reovirus requires both type I i

130 RIPK3 induces necroptosis by phosphorylating MLKL, which then induces

131 The sigma3 protein limits the induction of necroptosis by preventing excessive production of interf

132 vous system independently of its function in necroptosis by promoting itaconate production in infecte

133 Defective autophagy enhanced necroptosis by Tumor necrosis factor (TNF) and Toll-like

134 nstration that neuroinflammatory signals and necroptosis can act locally in the axon to stimulate SAR

135 lternative pathway of controlled cell death, necroptosis can be triggered by tumor necrosis factor vi

136 of the action of ESCRT-III, cells undergoing necroptosis can express chemokines and other regulatory

137 ovoked by inhibition of caspase activity and necroptosis cascades.

138 The necroptosis cell death pathway has been implicated in ho

139 pseudokinase is the terminal effector in the necroptosis cell death pathway.

140 ins unknown.Objectives: To determine whether necroptosis contributes to RSV bronchiolitis pathogenesi

141 However, whether necroptosis, conventionally considered a fail-safe cell

142 cal analysis demonstrated that inhibition of necroptosis delays not only the morphological degenerati

143 ing protein (RIP) kinase 3 (RIPK3)-dependent necroptosis directs inflammation and tissue injury, as w

144 TKO] mice) leads to unrestrained bone marrow necroptosis driven by increased Rip1 kinase (Ripk1).

145 functional RIPK1 kinase activity-independent necroptosis driven by the RIPK3-MLKL pathway in TAK1-def

146 m in vertebrates is programmed necrosis, or "necroptosis", driven by receptor-interacting protein kin

147 ient in IAV-activated apoptosis to show that necroptosis drives robust antiviral immune responses and

148 mouse developed LPR disease, removal of the necroptosis effector Mlkl from Caspase-8(D387A/D387A) mi

149 ivities of both RIPK1 and RIPK3, but not the necroptosis effector protein, MLKL.

150 2-deficient cells became highly sensitive to necroptosis even at low TNFalpha levels.

151 nic TLR4 signaling, WT cells did not undergo necroptosis, even when MK2 was disabled.

152 her forms of regulated cell death, including necroptosis, ferroptosis and pyroptosis.

153 he activation of RIPK1 sequentially promotes necroptosis followed by apoptosis in a temporally specif

154 oid arthritis underwent a GM-CSF-independent necroptosis following CD44 ligation; this effect was als

155 f IFN to control innate immune signaling and necroptosis following infection through a mechanism that

156 on cycle that contribute to the induction of necroptosis following infection with an RNA virus.IMPORT

157 Instead, this increase in necroptosis following sigma3 knockdown is accompanied by

158 encoded cell-death suppressors revealed that necroptosis functions as a trap door to eliminate virall

159 one of the genes of interest, the apoptosis/necroptosis gene RIPK3, show disturbed bone micro-archit

160 f pyroptosis, caspase-8-driven apoptosis, or necroptosis had minor impact on Salmonella control.

161 Inhibition of necroptosis had no effect on neutrophil trafficking in c

162 c cell-death and highlight diseases in which necroptosis has been found to play a role.

163 However, while necroptosis has been shown to contribute to antiviral im

164 RIPK3, a key mediator of necroptosis, has been implicated in the host defense aga

165 gulated cell death, including pyroptosis and necroptosis, have been described.

166 MLKL is the final executioner of canonical necroptosis; however, in axonal necroptosis, MLKL does n

167 RIPK1 and RIPK3 are key mediators of necroptosis; however, new findings support their role in

168 ponses by promoting apoptosis and inhibiting necroptosis in B cells.

169 ssions offer an understanding of the role of necroptosis in diseases and will foster efforts to pharm

170 alpha domains were required for ZBP1-induced necroptosis in fibroblasts that were treated with caspas

171 Thus, we demonstrate that dysregulated necroptosis in hematopoiesis promotes bone marrow progen

172 tion and reduced hyperphosphorylated Tau and necroptosis in HFD-fed rats.

173 que to HSCs, highlight an important role for necroptosis in HSC killing, and establish TNF-alpha as a

174 se domain-like pseudokinase (MLKL)-dependent necroptosis in infected cells.

175 cytomegalovirus triggers both apoptosis and necroptosis in infected cells; however, encoded inhibito

176 ptotic cell death in HeLa cells but enhances necroptosis in L929 cells.

177 aspase-8 activation may go hand-in-hand with necroptosis in macrophages, and revises current understa

178 or-interacting protein (RIP) kinase-mediated necroptosis in macrophages.

179 es that have recently been found to activate necroptosis in many of the cell types they infect.

180 syndrome (MDS), and we demonstrate increased necroptosis in MDS bone marrow.

181 our results demonstrate the critical role of necroptosis in mediating neurovascular damage and hypope

182 agues implicate Rip1 kinase (Ripk1)-mediated necroptosis in myelodysplastic syndrome (MDS)-like disea

183 raf2 deletion, validating a critical role of necroptosis in regulating pathological remodeling and he

184 nflammation, caspase-dependent apoptosis, or necroptosis in response to extracellular stimuli.

185 se domain-like protein)-dependent programmed necroptosis in response to sterile ligands such as oxidi

186 cing ZBP1 expression by interferons triggers necroptosis in RIPK1-deficient keratinocytes, and epider

187 Thus, ZBP1 drives necroptosis in the absence of the RIPK1-RHIM, but suppre

188 intains the intestinal barrier by inhibiting necroptosis in the epithelium.

189 Review, we outline the evidence implicating necroptosis in these neurological diseases and suggest t

190 tes that are cleaved by caspase-8 to prevent necroptosis in vivo have not been defined.

191 lead to cell death, including apoptosis and necroptosis, in both RIPK1-dependent and RIPK1-independe

192 form of regulated necrosis is represented by necroptosis, in which the receptor-interacting protein k

193 asp1(-/-)Casp11(-/-) mice, indicating that a necroptosis-independent function of RIPK3 also contribut

194 restingly, this flavanone compound: inhibits necroptosis induced by death receptors ligands TNF-alpha

195 ear cells to RIPK1 activation, apoptosis and necroptosis induced by TNF.

196 MOC activities, as we created interferon- or necroptosis-inducing myddosomes, inflammasomes that indu

197 Ponatinib, a necroptosis-inhibiting and Food and Drug Administration-

198 Necroptosis-inhibiting drugs may lessen organ damage dur

199 In conclusion, necroptosis inhibition directly improved cognition in pr

200 Necroptosis inhibition in early life ameliorated asthma

201 Adjunct necroptosis inhibition reduced the number of S. pneumoni

202 K1-induced oxidative stress upon caspase and necroptosis inhibition to further ensure induction of ce

203 Recently, necrostatin-1 (nec-1), a necroptosis inhibitor, showed beneficial effects in brai

204 Necroptosis inhibitors may be a viable adjunct therapy.

205 Necroptosis is a cell death pathway involved in inflamma

206 Necroptosis is a form of cell death that can be observed

207 Necroptosis is a form of programmed cell death defined b

208 Necroptosis is a form of regulated necrosis that is impl

209 Necroptosis is a highly inflammatory form of programmed

210 Necroptosis is a physiological cell suicide mechanism in

211 Necroptosis is a proinflammatory form of cell death inst

212 amage-associated molecular patterns and that necroptosis is active in advanced atherosclerotic plaque

213 Necroptosis is an alternative form of cell death trigger

214 Thus, necroptosis is an independent, "stand-alone" cell death

215 me" signals that are a feature of apoptosis, necroptosis is considered to be inflammatory.

216 xecuted by the activation of caspases, while necroptosis is dependent on the receptor interacting pro

217 from perinatal lethality when RIPK3-mediated necroptosis is disabled.

218 TNF receptor 1 (TNFR1)-induced necroptosis is known to require the formation of a RIPK1

219 characterized, the mechanism that tunes down necroptosis is largely unknown.

220 Necroptosis is mediated by RIPK1, RIPK3, and MLKL kinase

221 Necroptosis is one the best-characterized forms of regul

222 ic homeostasis of biasing cell death fate to necroptosis is substantial and poorly understood.

223 and the IAP ubiquitin ligases, how and when necroptosis is triggered in physiological settings are o

224 Although the activation of necroptosis is well characterized, the mechanism that tu

225 rogrammed cell death (pyroptosis, apoptosis, necroptosis) is an integral part of host defense against

226 e Kinase domain-Like (MLKL), a key player in necroptosis, is a multi-domain protein with an N-termina

227 Inhibition of necroptosis may be a viable strategy to limit the severi

228 se mouse genetic studies reveal that chronic necroptosis may underlie human fibrotic and autoimmune d

229 t studies indicate FADD suppresses embryonic necroptosis mediated by RIPK1.

230 h receptors such as TNFR1(1), and suppresses necroptosis mediated by the kinase RIPK3 and the pseudok

231 ation of RIPK1 and blocks both apoptosis and necroptosis mediated by TNFR1 signaling.

232 of canonical necroptosis; however, in axonal necroptosis, MLKL does not directly trigger degeneration

233 Here, we show that, during necroptosis, MLKL-dependent calcium (Ca(2+)) influx and

234 Thus, cells undergoing necroptosis need to overcome these independent suppressi

235 Of note, necroptosis occurred only in the absence of TTP and was

236 ylase AAG did not exhibit alkylation-induced necroptosis or inflammation.

237 emonstrate that pharmacologically inhibiting necroptosis or interferon signaling protects human organ

238 egulates various cellular processes, such as necroptosis or stem cell niche signaling.

239 athways including pyroptosis, apoptosis, and necroptosis (PANoptosis) and plays an essential role in

240 me activation and pyroptosis, apoptosis, and necroptosis (PANoptosis) that could be targeted for trea

241 th in the form of pyroptosis, apoptosis, and necroptosis (PANoptosis).

242 th in the form of pyroptosis, apoptosis, and necroptosis (PANoptosis).

243 genetic similarities with classic necrosis, necroptosis, parthanatos, or other forms of non-apoptoti

244 The extrinsic apoptosis and necroptosis pathways regulate each other and their balan

245 crystals trigger inflammation and renal cell necroptosis, processes that involve TNF receptor (TNFR)

246 Necroptosis promotes further cell death and neuroinflamm

247 d cell death have been identified, including necroptosis, pyroptosis, and autophagic cell death.

248 four types of active cell death (apoptosis, necroptosis, pyroptosis, and ferroptosis) mainly in mamm

249 pendent gene program that primarily prevents necroptosis rather than apoptosis, induces immunomodulat

250 We report here that TNFalpha-RIP1-mediated necroptosis regulates accumulation of MDSCs.

251 and DHA downregulated protein expressions of necroptosis related signals including tumor necrosis fac

252 otein distribution, and protein abundance of necroptosis related signals were determined.

253 osis may further worsen the damage, although necroptosis-related proteins may have additional roles i

254 Induction of cell death by necroptosis requires production of interferon.

255 We find that necroptosis requires sensing of the genomic RNA within i

256 Induction of cell death by necroptosis requires the detection of viral gene product

257 Necroptosis requires the translocation of the pseudokina

258 We demonstrate that deregulated necroptosis results in systemic inflammation, tissue fib

259 odes of programmed cell death, apoptosis and necroptosis, share molecular machinery but diverge in ou

260 AM kinases are promoters of pro-inflammatory necroptosis, shedding light on the biological complexity

261 thway activation, the precise checkpoints in necroptosis signaling are still unclear.

262 Necroptosis signaling pathway plays a critical role in i

263 e epithelial cells through modulation of the necroptosis signaling pathway.

264 , which is associated with inhibition of the necroptosis signaling pathway.

265 ses showed was crucial for reconstitution of necroptosis signaling.

266 ect point of input from TAM kinases into the necroptosis signaling.

267 and inhibited downstream innate immunity and necroptosis signaling.

268 date the mechanisms by which Traf2 regulates necroptosis signaling.

269 caspase-dependent apoptosis but increases in necroptosis signaling.

270 362A) die as embryos owing to MLKL-dependent necroptosis, similar to caspase-8-deficient mice.

271 nd the requirement of RIPK1/3/MLKL-dependent necroptosis, specifically in the bone marrow-derived com

272 ases RIPK1 and RIPK3 play important roles in necroptosis that are closely linked to the inflammatory

273 rm of regulated necrotic cell death known as necroptosis that is mediated by receptor-interacting pro

274 masome activation/pyroptosis, apoptosis, and necroptosis; the specific ligand for ZBP1 activation rem

275 a countermeasure to prevent the execution of necroptosis, thereby promoting the continued survival of

276 n addition to their roles in stress-mediated necroptosis, these ceramide-enriched pores also regulate

277 nstrate that axonal degeneration proceeds by necroptosis, thus defining a novel mechanistic framework

278 suppressor of RIPK1, and the transition from necroptosis to apoptosis.

279 he relative contributions of ferroptosis and necroptosis to folic acid (FA)-induced AKI in mice.

280 schemia/reperfusion insult rapidly activates necroptosis to promote cerebral hemorrhage and neuroinfl

281 ecreased TNFalpha-induced and RIP1-dependent necroptosis to sustain survival and accumulation.

282 The benefits of necroptosis to the host, however, may sometimes be outwe

283 n Z-DNA/RNA binding in ZBP1's ZBDs prevented necroptosis upon infection with mouse cytomegalovirus.

284 Blocking necroptosis using mixed lineage kinase domain-like defic

285 channel 1a (ASIC1a) mediates acidic neuronal necroptosis via recruiting receptor-interacting protein

286 Necroptosis was blocked using pharmacological inhibitors

287 Necroptosis was determined via viability assays and immu

288 e-protein kinase (RIP)-3-mediated intestinal necroptosis was linked to increased mitotic cell cycle a

289 TNF-mediated necroptosis was mediated by RIPK1 kinase activity, where

290 eath pathways and that upon knockout of AH1, necroptosis was more immunogenic than apoptosis in a pro

291 pif and Mlkl or pharmaceutical inhibition of necroptosis was partially redundant, implying interlinke

292 (MLKL), a key terminal mediator of cellular necroptosis, was rapidly and persistently degraded by th

293 racts with mu1, also functions in regulating necroptosis, we used small interfering RNA (siRNA)-media

294 o receptor-interacting protein kinase-driven necroptosis, whereas unregulated cell death like acciden

295 sis takes place through RIPK3-MLKL-dependent necroptosis, which can be counterregulated by autophagy.

296 uired for signaling in cells that results in necroptosis, which is also dependent on tumor necrosis f

297 this review, we focus on how pyroptosis and necroptosis, which release potent immune cytokines such

298 e mode of action toward both ferroptosis and necroptosis, while the analogously chlorinated derivativ

299 ular cascades regulating both pyroptosis and necroptosis will yield even more targets to treat diseas

300 a suggest that pharmacological inhibition of necroptosis with Nec-1s stabilizes pre-existing aneurysm