ライフサイエンスコーパス: necroptosis

1 involving RIP3-dependent regulated necrosis (necroptosis).

2 s cells undergoing apoptosis versus necrosis/necroptosis.

3 h then disrupts cellular membranes to effect necroptosis.

4 lineage kinase domain-like (MLKL) leading to necroptosis.

5 othesis that neutrophils fed CA-MRSA undergo necroptosis.

6 cell susceptibility to SMAC mimetic-induced necroptosis.

7 T cells, A20 prevents kinase RIPK3-dependent necroptosis.

8 -lineage kinase domain-like (MLKL)-dependent necroptosis.

9 ion and a form of regulated necrosis, called necroptosis.

10 ecently recognized regulated necrosis termed necroptosis.

11 not its activity, is required for preventing necroptosis.

12 cing cell detachment and promoting apoptosis/necroptosis.

13 proteins forming functional amyloids during necroptosis.

14 ing and activity of IL-1beta released during necroptosis.

15 nt small molecular inhibitor of RIPK1-driven necroptosis.

16 ient colorectal cancer (CRC) by induction of necroptosis.

17 and aggregation of MLKL, the executioner of necroptosis.

18 rmally to multiple inducers of apoptosis and necroptosis.

19 or MLKL may exert functions independently of necroptosis.

20 Ripk1 is directly involved in apoptosis/necroptosis.

21 anced death, confirming it as RIP1-dependent necroptosis.

22 arts died as a result of pneumolysin-induced necroptosis.

23 tissue inflammation drives TNF-alpha-related necroptosis.

24 /threonine kinase with essential function in necroptosis.

25 in TMEV-infected BHK-21 cells, which undergo necroptosis.

26 d mixed lineage kinase-like (MLKL)-dependent necroptosis.

27 lineage kinase domain-like (MLKL) to induce necroptosis.

28 ts that increased cellular glucose may prime necroptosis.

29 structural changes in MLKL that culminate in necroptosis.

30 ctivity of the heterodimer, it might prevent necroptosis.

31 d fungal programmed cell death and mammalian necroptosis.

32 ions, is also a potent inducer of macrophage necroptosis.

33 TAK1 promotes its interaction with RIPK3 and necroptosis.

34 vel regulatory mechanism for RIPK3-dependent necroptosis.

35 tream signaling activators of RIP3-dependent necroptosis.

36 pendent apoptosis and/or RIPK1/MLKL-mediated necroptosis.

37 hich infection with a dsRNA virus results in necroptosis.

38 in TMEV-infected BHK-21 cells, which undergo necroptosis.

39 IPs and subsequent structural changes during necroptosis.

40 inflammation and protect from apoptosis and necroptosis.

41 spase-independent and kinase RIPK3-dependent necroptosis.

42 ial factor for TNF-, TLR3-, and TLR4-induced necroptosis.

43 cting serine-threonine kinase 1 and CRC cell necroptosis.

44 go spontaneous cell death, primarily through necroptosis.

45 ly adhere to the cell surface to induce cell necroptosis.

46 inducing RIPK1 kinase-dependent apoptosis or necroptosis.

47 ent cell death driven by ferroptosis but not necroptosis.

48 osis leads to a switch to the RIP1-dependent necroptosis.

49 e of miR-21 in acute pancreatitis injury and necroptosis.

50 romoted cell proliferation and resistance to necroptosis.

51 inhibits cell death mediated by RIPK3-driven necroptosis.

52 ion of these death receptors can also induce necroptosis.

53 pendent signal transduction to interrupt the necroptosis.

54 step in tumor necrosis factor (TNF)-induced necroptosis.

55 ryonic lethality as a result of uncontrolled necroptosis.

56 osis and RIPK1 kinase-dependent apoptosis or necroptosis.

57 diates acute inflammation through macrophage necroptosis.

58 igger apoptosis that gives rise to secondary necroptosis.

59 -inflammatory roles and functions to prevent necroptosis.

60 dial survival and homeostasis by suppressing necroptosis.

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

62 rd an alternate and detrimental cell fate of necroptosis.

63 urs in several forms including apoptosis and necroptosis.

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

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

66 complex, LUBAC also restricts TRAIL-induced necroptosis.

67 rm of programmed necrotic cell death, termed necroptosis.

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

69 induce RIPK1-kinase-dependent apoptosis and necroptosis.

70 K-1 or MLKL, and therefore was distinct from necroptosis.

71 dsRNA) within infected cells is required for necroptosis.

72 cular mechanisms and relevance to disease of necroptosis.

73 3 protein prevents DAI-mediated induction of necroptosis.

74 two different stages of infection to induce necroptosis.

75 nd the mechanism by which caspase-8 inhibits necroptosis.

76 ls fed CA-MRSA and attributed the process to necroptosis.

77 ey components of the molecular machinery for necroptosis.

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

79 However, the contribution of necroptosis, a caspase-independent pathway of cell death

80 nteracting protein kinase 3 (RIPK3) mediates necroptosis, a form of programmed cell death that promot

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

82 PK3 and its substrate MLKL are essential for necroptosis, a lytic cell death proposed to cause inflam

83 effectively kill cancer cells by triggering necroptosis, a non-apoptotic form of cell death.

84 Necroptosis, a programmed form of necrosis, is executed

85 Necroptosis, a regulated form of necrotic cell death, re

86 RIPK-1 figures prominently in necroptosis, a specific form of programmed cell death de

87 ion of IRGM1 (or IRGM) induced cell death by necroptosis, accompanied by release of damage-associated

88 h nec-1s, strongly suggesting that increased necroptosis accounts for exacerbation of this injury in

89 Furthermore, we observed that lowering necroptosis activation reduced cell loss in a mouse mode

90 current study is to test whether perturbing necroptosis affects progression of existing aneurysm usi

91 dy, we report that human neutrophils undergo necroptosis after exposure to GM-CSF followed by the lig

92 Human CMV blocks TNF-induced necroptosis after RIP3 activation and phosphorylation of

93 hrough dsRNA-dependent RLR receptor-mediated necroptosis against infections from different classes of

94 The induction of necroptosis also requires late stages of reovirus infect

95 However, whether inhibition of necroptosis ameliorates atherosclerosis is largely unkno

96 (also known as DAI or DLM-1), which induces necroptosis, an inflammatory form of cell death.

97 view, we discuss the molecular mechanisms of necroptosis and analyze the effect of inhibiting necropt

98 Necroptosis and apoptosis were detected in the myocardiu

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

100 influence immunity, we established models of necroptosis and apoptosis, in which dying cells are gene

101 acid binding are resistant to IAV-triggered necroptosis and apoptosis.

102 resistance to RIPK1-dependent apoptosis and necroptosis and are also partially protected against RIP

103 V activates parallel pathways of MLKL-driven necroptosis and FADD-mediated apoptosis, with the former

104 lineage kinase domain-like protein (MLKL) in necroptosis and gasdermin-D in pyroptosis] were recently

105 d to function downstream of RIPK3 to promote necroptosis and IL-1beta secretion.

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

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

108 ng molecule that induced RIP1/PARP1-mediated necroptosis and inhibited tumor growth.

109 nature illustrates the cooperative nature of necroptosis and innate inflammatory signaling pathways i

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

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

112 romote apoptosis or cytokine expression in a necroptosis and kinase-independent manner.

113 ron antiviral responses of infected cells to necroptosis and leads to rapid death of the virus-infect

114 est that miRNAs are critical participants in necroptosis and miR-21 enhances cellular necrosis by neg

115 s previously implicated in the regulation of necroptosis and pathologic tissue injury, in directing I

116 IRGM regulates necroptosis and release of DAMPs to induce gastrointesti

117 Although necroptosis and release of danger molecule high-mobility

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

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

120 s the plasma membrane, and may also apply to necroptosis and some forms of nonprogrammed necrosis.

121 Necroptosis and subsequent danger signal release is a no

122 lytic cell death pathways of pyroptosis and necroptosis and their implications in inflammation and c

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

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

125 pathologies via the induction of apoptosis, necroptosis, and nuclear factor-kappaB-driven inflammati

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

127 bserved following virus infection-apoptosis, necroptosis, and pyroptosis.

128 ever, the biological consequences of chronic necroptosis are unknown.

129 ced PCD due to hyperglycemia was specific to necroptosis as extrinsic apoptosis was inhibited by expo

130 consistently suggested RLR receptor-mediated necroptosis as the underlying mechanism of infected cell

131 es identified RIPK3, an essential kinase for necroptosis, as having a key role in inhibiting acute my

132 expression of RIP3, the master regulator of necroptosis, as well as phosphorylated mixed lineage kin

133 of poly(ADP ribose)polymerase-1 (PARP-1), or necroptosis, assessed by levels of phosphorylated mixed

134 required to prevent TNF-induced apoptosis or necroptosis but is necessary for the transcriptional pro

135 Dendritic cell necrosis was not due to necroptosis but was dependent of the presence of circula

136 s distinct from the RIP1/3 pathway-dependent necroptosis, but mediated by a functional deficiency of

137 observed in the FADD-deficient cells during necroptosis, but not during apoptotic activation of Panx

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

139 ovoked by inhibition of caspase activity and necroptosis cascades.

140 Nonetheless, it has already been shown that necroptosis contributes to cellular demise in various pa

141 dels, suggesting that inflammation caused by necroptosis contributes to tissue damage and that inhibi

142 itions, accumulating evidence indicates that necroptosis-deficient cancer cells are poorly immunogeni

143 In 293T cells, induction of necroptosis depended on expression of RIPK3 as well as t

144 activities in either inducing or preventing necroptosis, depending on the host species.

145 Hyperglycemic enhancement of necroptosis depends upon glycolysis with AGEs and ROS pl

146 K3 and MLKL are dispensable, indicating that necroptosis does not contribute to APAP-induced necrosis

147 1 (RIPK1) is a critical kinase that mediates necroptosis downstream of death receptors and TLRs.

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

149 induces cell death via parallel pathways of necroptosis, driven by the pseudokinase MLKL, and apopto

150 cal for preventing ZBP1/RIPK3/MLKL-dependent necroptosis during development.

151 ne CMV M45 mutant virus drives virus-induced necroptosis during nonproductive infection of RIP3-expre

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

153 Strikingly, induction of apoptosis and necroptosis effectors was sharply decreased in the absen

154 Absence of RIP3, a key mediator of necroptosis, exacerbated HFD-induced liver injury, assoc

155 However, the events that drive necroptosis execution downstream of IFN-I and RIP signal

156 Apoptosis, pyroptosis, pyronecrosis, necroptosis, ferroptosis, and parthanatos were excluded

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

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

159 Triggering necroptosis has become especially important in experimen

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

161 Intriguingly, many of the signal adaptors of necroptosis have dual functions in innate immune signali

162 chanisms that underlie distinct instances of necroptosis have just begun to emerge.

163 fections, or the T cell receptor can trigger necroptosis if the activity of the protease caspase-8 is

164 on degeneration by inducing inflammation and necroptosis in a manner dependent on receptor-interactin

165 are only beginning to appreciate the role of necroptosis in different pathological conditions, includ

166 at MLKL is an essential effector of aberrant necroptosis in embryos caused by loss of Caspase-8 or FA

167 eptor-interacting protein 3 (RIP3)-dependent necroptosis in erythroid precursor cells.

168 optosis and analyze the effect of inhibiting necroptosis in experimental models of critical illnesses

169 rinsic apoptosis in control Jurkat cells and necroptosis in FADD-deficient cells; treatment of both l

170 (ICP6 and ICP10, respectively) also prevent necroptosis in human cells by inhibiting the interaction

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

172 ar pathway that leads to cellular stress and necroptosis in macrophages challenged with a super-low d

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

174 TLR4 and the NLRP3 inflammasome, as well as necroptosis in macrophages.

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

176 There are many potential inducers of necroptosis in PDA, including ligation of tumour necrosi

177 to hyperglycemic levels of glucose enhances necroptosis in primary red blood cells (RBCs), Jurkat T

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

179 m adaptors RIPK1, TRIF, or DAI to signal for necroptosis in response to death receptor or Toll-like r

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

181 The molecular mechanisms that regulate necroptosis in the heart and its physiological relevance

182 egeneration, energy failure, DNA damage, and necroptosis in the retinas of WT mice.

183 and polyinosinic-polycytidylic acid-induced necroptosis in vitro, and Ripk1(D138N/D138N) mice are pr

184 t RARgamma has a similar role in TNF-induced necroptosis in vivo.

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

186 ing serine-threonine kinase 1, a mediator of necroptosis, in CRC cells.

187 on Thr231 and Ser232, which is a hallmark of necroptosis, in the skin and thymus.

188 Downstream effector pathways of necroptosis include formation of advanced glycation end

189 he caspase-8-binding domain, which unleashes necroptosis independent of RHIM function.

190 Unlike necroptosis induced by classical TNF-like cytokines, nec

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

192 Importantly, human CMV is shown to block necroptosis induced by either TNF or M45 mutant murine C

193 than either apoptosis induced by DeltaM36 or necroptosis induced by M45mutRHIM virus.

194 sis induced by classical TNF-like cytokines, necroptosis induced by proteasome inhibitors does not re

195 Our work describes parallel networks of necroptosis-induced CXCL1 and Mincle signalling that pro

196 act RIP1/RIP3 signalling depended in part on necroptosis-induced expression of the chemokine attracta

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

198 Furthermore, the necroptosis inhibitor necrostatin-1 but not the pan-casp

199 Necroptosis is a cell death pathway regulated by the rec

200 Necroptosis is a form of cell death associated with infl

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

202 Programmed necrosis or necroptosis is a form of nonapoptotic cell death driven

203 Necroptosis is a form of programmed cell death defined b

204 Necroptosis is a form of programmed necrosis that is reg

205 Necroptosis is a form of regulated cell death that criti

206 Necroptosis is a highly inflammatory form of programmed

207 Thus, necroptosis is a human host defense pathway against two

208 Necroptosis is a physiological cell suicide mechanism in

209 Necroptosis is a programmed cell death pathway that has

210 Necroptosis is a recently identified form of cell death

211 Necroptosis is a regulated form of necrosis, with the dy

212 Necroptosis is a regulated, nonapoptotic form of cell de

213 Necroptosis is a RIP1-dependent programmed cell death (P

214 Necroptosis is an alternate programmed cell death pathwa

215 by RIPK1 and RIPK3 with the possibility that necroptosis is but one mechanism by which these kinases

216 Necroptosis is characterized by rapid permeabilization o

217 Necroptosis is considered to be complementary to the cla

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

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

220 Necroptosis is driven by two serine threonine kinases, R

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

222 Necroptosis is mediated by the kinase activities of rece

223 IP 3 (RIPK3) driving extrinsic apoptosis and necroptosis is not fully understood.

224 We confirmed that necroptosis is not involved in APAP toxicity by using mi

225 Necroptosis is one the best-characterized forms of regul

226 Indeed, necroptosis is triggered by caspase inhibition to ensure

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

228 Future studies will show whether necroptosis is truly a better strategy to overcome apopt

229 ction has been extensively investigated, how necroptosis is unleashed following virus infection is un

230 optosis, mitochondria-mediated necrosis, and necroptosis, is critically involved in ischemic cardiac

231 r-interacting protein (RIP) kinase-dependent necroptosis, is upregulated and activated in human autoi

232 regulator of cellular death by apoptosis and necroptosis; its importance in development is exemplifie

233 optosis inducers FADD and caspase 8, and the necroptosis kinases receptor interacting protein kinase

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

235 ulted in increased protein expression of the necroptosis mediators receptor-interacting protein kinas

236 tosis, suggesting that systemic targeting of necroptosis might be associated with the risk of promoti

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

238 between ANCA-induced neutrophil activation, necroptosis, NETs, the AP, and endothelial damage.

239 isingly, this death occurs primarily through necroptosis, not apoptosis, due to assembly of the necro

240 In this study, we demonstrated that necroptosis occurred in clinical atherosclerotic samples

241 mmation through release of HMGB1 and induces necroptosis of lung EC.

242 e we interrogate the consequences of chronic necroptosis on immune homeostasis by deleting Ripk1 in m

243 herefore, we examined the impact of heme and necroptosis on Leishmania replication.

244 fferent from activated T cells, there was no necroptosis or increase in reactive oxygen species in c-

245 Decoupling NF-kappaB signaling from necroptosis or inflammatory apoptosis reduced priming ef

246 n the other hand, inhibition of parthanatos, necroptosis, or apoptosis did not change cocaine cytotox

247 Necroptosis, or programmed necrosis, contributes to the

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

249 domain like (MLKL), two core proteins of the necroptosis pathway, blocks crystal cytotoxicity.

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

251 The effector of necroptosis, phosphorylated mixed-lineage kinase domain-

252 Programmed necrosis (necroptosis) plays an important role in development, tis

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

254 Another type of programmed cell death is necroptosis (programmed necrosis), but its role in pancr

255 Necroptosis promotes inflammation through leakage of cel

256 e emerged, including immunogenic cell death, necroptosis, pyroptosis, and netosis that interweave dif

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

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

259 n this review, we discuss recent advances in necroptosis research and the functional consequences of

260 1 or RIPK1, key mediators of parthanatos and necroptosis, respectively, did not prevent cocaine-induc

261 f necrotic cell death, termed pyroptosis and necroptosis, respectively.

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

263 of MLKL, the cell death-execution protein in necroptosis, revealing a transkingdom evolutionary relat

264 stinct alternative mechanisms of cell death: necroptosis, RIPK1-independent and -dependent apoptosis.

265 ote three distinct mechanisms of cell death: necroptosis, RIPK1-independent and dependent apoptosis.

266 Necroptosis signaling is modulated by the kinase RIPK1 a

267 date the mechanisms by which Traf2 regulates necroptosis signaling.

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

269 , IE1-regulated viral gene product acts on a necroptosis step that follows MLKL phosphorylation prior

270 that selectively kill motor neurons through necroptosis, suggesting a new therapeutic avenue.

271 by identifying mechanisms to counterbalance necroptosis, sustain plasma membrane integrity, and prol

272 ich cells are extraordinarily susceptible to necroptosis, that local glucose levels alter the balance

273 that following LPS treatment, or LPS-induced necroptosis, the TLR adaptor protein TRIF and inhibitor

274 viral RNA are required for the induction of necroptosis, they are not sufficient.

275 events including inflammation, apoptosis and necroptosis through different signaling complexes.

276 h interaction with mitochondria, the role of necroptosis through receptor-interacting proteins 1 and

277 Finally, therapeutic blockade of necroptosis through TNFalpha or RIPK1 inhibition amelior

278 CRD increases intestinal necroptosis, thus rendering the gut epithelium more susc

279 anisms, RDA, RIPK1-independent apoptosis and necroptosis.TNFalpha can promote three distinct mechanis

280 dicate that ALA-SDT mediates the switch from necroptosis to apoptosis by activating the caspase-3 and

281 ls, which is responsible for the switch from necroptosis to apoptosis.

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

283 All these steps are required for necroptosis to occur.

284 Intact ZBP1-ZBDs were also required for necroptosis triggered by ectopic expression of ZBP1 and

285 enal tubules do not undergo sensitization to necroptosis upon genetic ablation of either FADD or casp

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

287 otein kinase 1 (RIPK1) induces apoptosis and necroptosis via kinase-dependent mechanisms and exhibits

288 We found that necroptosis was activated in postmortem human AD brains,

289 ished an in vitro necroptotic model in which necroptosis was induced in THP-1-derived foam cells by s

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

291 During programmed necroptosis, we observed frequent cell-cell transfer of

292 atin-1, an inhibitor of programmed necrosis (necroptosis), which occurs in renal tubular cells during

293 neumolysin kills infiltrated macrophages via necroptosis, which alters the immune response.

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

295 est understood form of regulated necrosis is necroptosis, which is transduced by the kinase activitie

296 caspase 8 by glutathionylation, resulting in necroptosis, which occurs independently of tumor necrosi

297 ated sonodynamic therapy (ALA-SDT) inhibited necroptosis while promoting apoptosis.

298 Blocking necroptosis with catalytically inactive RIPK3(D161N), RH

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

300 ineage domain-like protein (MLKL), targeting necroptosis with the RIPK1 inhibitor necrostatin-1 or ge