ライフサイエンスコーパス: death receptor

1 CD95/Fas is an apoptosis inducing death receptor.

2 the interactions between nanofibers and the death receptors.

3 may also be relevant to apoptosis induced by death receptors.

4 susceptible cancer cells by engaging cognate death receptors.

5 induce apoptosis exclusively via one of its death receptors.

6 cancer cells regulate cell surface levels of death receptors.

7 ated serial killing and only killed once via death receptors.

8 rate (ORR) for single-agent anti-programmed death receptor 1 (anti-PD-1) therapy is modest in patien

9 display of the exhaustion markers programmed death receptor 1 (PD-1) and lymphocyte activation gene 3

10 f pembrolizumab, a humanised anti-programmed death receptor 1 (PD-1) antibody, in patients with PD-L1

11 P = .05), a higher proportion of programmed death receptor 1 (PD-1) expressing memory CD4 T lymphocy

12 programmed death ligand 1 (PD-L1)/programmed death receptor 1 (PD-1) immune checkpoint were shown to

13 associated protein 4 (CTLA-4) and programmed death receptor 1 (PD-1) were ineffective in controlling

14 made clinically in inhibiting the programmed death receptor 1 (PD-1)/PD-L1 interaction to enhance T c

15 rogrammed death receptor 1 ligand/programmed death receptor 1 (PDL-1/PD-1) pathway plays an important

16 cy of pembrolizumab (an anti-programmed cell death receptor 1 [PD-1] antibody) in advanced solid tumo

17 V were characterized by increased programmed death receptor 1 expression and reduced ADCC activity at

18 restored ADCC ability and reduced programmed death receptor 1 expression.

19 The anti-programmed death receptor 1 inhibitor nivolumab previously showed a

20 The programmed death receptor 1 ligand/programmed death receptor 1 (PDL

21 d by an up-regulation of the programmed cell death receptor 1 on CD8(+) and CD4(+) T cells, indicativ

22 phalitis arising during anti-programmed cell death receptor 1 therapy in a patient with metastatic me

23 l benefit of nivolumab (anti-programmed cell death receptor 1) monotherapy beyond Response Evaluation

24 r of costimulation (ICOS) ligand, programmed death receptor 1-ligand 1 (PD1-L1), CxxxC chemokine rece

25 ns in close association with programmed cell death receptor 1-positive infiltrating lymphocytes.

26 ic checkpoint antibodies blocking programmed death receptor 1/programmed death ligand 1 (PD-L1) signa

27 6) interact with their receptors, programmed death receptor-1 (PD-1) and cytotoxic T-lymphocyte antig

28 y that blocks interaction between programmed death receptor-1 (PD-1) and its ligands (PD-L1, PD-L2).

29 rogrammed death ligand-1 receptor programmed death receptor-1 (PD-1) showed antitumor effects in trea

30 otype and decreased expression of programmed death receptor-1 (PD-1), in addition to an elevated effe

31 point blockade with antibodies to programmed death receptor-1 (PD-1).

32 ansmit pN forces through the programmed cell death receptor-1 (PD1), a major target in cancer immunot

33 idenced by absence of sex bias in programmed death receptor-1 and responses to IL-6, anti-IL-10, anti

34 antigen vaccine was combined with programmed death receptor-1 blockade in patients with advanced canc

35 ase clinical trials targeting the programmed death receptor-1/ligand-1 (PD-1/PD-L1) pathway to overco

36 The anti-programmed-death-receptor-1 (PD-1) antibody pembrolizumab has shown

37 TNF-like ligand 1 A (TL1A) and death receptor 3 (DR3) are a ligand-receptor pair involv

38 s is crucial for immune homeostasis; TNFSF15:death receptor 3 (DR3) contributions to PRR responses ha

39 -like cytokine 1A (TL1A) associates with the death receptor 3 (DR3) on activated lymphocytes and indu

40 tudy, we have established that expression of Death Receptor 3 (DR3), a member of the TNF superfamily,

41 In this study, we demonstrate that death receptor 3 (DR3), a member of the TNFR superfamily

42 The expression of death receptor 3 (DR3), a member of the tumor necrosis f

43 mphocytes that bear its functional receptor, death receptor 3 (DR3).

44 Its known receptor is death receptor 3 (DR3).

45 Death receptor 3 (DR3, TNFRSF25), the closest family rel

46 Death receptor 3 (DR3; TNFRSF25) and its tumor necrosis

47 t tumor necrosis factor receptor superfamily death receptor 3 (TNFRSF25, DR3) and Fas receptors (Fas)

48 Intestinal fibroblasts express Death-receptor 3 (DR3; the only know receptor for TL1A)

49 immunoreactivity for activated caspase-3 and death receptor-3 in adulthood, suggesting an enduring at

50 The interaction of TRAIL with death receptor 4 (DR4) and DR5 can trigger apoptotic cel

51 ucing ligand wild type (rhTRAIL(WT)) and its death receptor 4 (DR4)-specific variant rhTRAIL(4C7) in

52 receptors (DcR1 and DcR2) co-expressed with death receptor 4 (DR4)/DR5 on the same cell can block th

53 is-inducing ligand (TRAIL) and its receptor, death receptor 4, sensitizing cells to an autocrine loop

54 Computational analysis identified the TRAIL Death Receptor-4 (DR4) as a potential novel miR-25 targe

55 ancreatic cancers express elevated levels of Death Receptor 5 (DR5) and its downstream regulators/eff

56 xtracellular domain (ECD) of long isoform of death receptor 5 (DR5) could block endogenous receptor a

57 poptosis through intracellular activation of death receptor 5 (DR5) independent of its canonical extr

58 Death receptor 5 (DR5) is a cell surface pro-apoptotic d

59 Death receptor 5 (DR5) is an apoptosis-inducing member o

60 studying the modulatory effects of b-AP15 on death receptor 5 (DR5) levels and DR5 activation-induced

61 The fatty acid palmitate can activate death receptor 5 (DR5) on hepatocytes, leading to their

62 These interactions were associated with death receptor 5 (DR5) up-regulation and caspase-8 activ

63 ults in activation of the FAS and TNFRSF10B (death receptor 5 (DR5)) promoters, increased Fas and DR5

64 Death receptor 5 (DR5), a cell surface pro-apoptotic pro

65 Furthermore, we identified death receptor 5 (DR5), a member of tumour necrosis fact

66 re, we report an unexpected finding that for death receptor 5 (DR5), a receptor in the tumor necrosis

67 tein (CHOP), which leads to up-regulation of death receptor 5 (DR5), activation of caspase-8 and -3,

68 ibodies to apoptosis-inducing TNFRs, such as death receptor 5 (DR5), although displaying impressive a

69 s-inducing ligand (TRAIL) with its receptor, death receptor 5 (DR5), leading to induction of apoptosi

70 hibited the expression of the TRAIL receptor death receptor 5 (DR5), whereas HOTAIR knockdown increas

71 ell-autonomous, UPR-controlled activation of death receptor 5 (DR5).

72 athways in upregulating transcription of the death receptor 5 (DR5).

73 Assembling oligomers for Death Receptor 5 stimulation, we probed multivalency eff

74 , the first direct biophysical evidence that Death Receptor 5 TM-dimers open in response to ligand bi

75 that activation of the apoptosis-initiating Death Receptor 5, as well as other structurally homologo

76 l tumor necrosis factor receptors, including Death Receptor 5, involves a scissorlike opening of the

77 s such as Fas ligand, its receptor (Fas) and death receptor 5, which are regulated by IRF-1.

78 Activation of death receptor-5 (DR5) leads to the formation of death i

79 poptosis of liver cancer cell lines requires death receptor-5 (DR5)-dependent permeabilization of lys

80 ng of the Amyloid Precursor Protein (APP) to Death Receptor 6 (DR6) and activation of a downstream ca

81 Recent studies implicate death receptor 6 (DR6) in an amyloid precursor protein (

82 Death receptor 6 (DR6) was recently shown to bind APP vi

83 Very recently, death receptor 6 (DR6) was shown to be involved in the n

84 We find that an orphan receptor, death receptor 6 (DR6), is required to drive axon degene

85 tracellular and extracellular space to drive death receptor 6 and calpain-dependent catastrophic dege

86 We also found that death receptor 6, but not p75 neurotrophic factor recept

87 a knock-out of the DR6 gene, which codes for Death Receptor 6.

88 released amyloid precursor protein (APP) and death receptor-6 (DR6) on MNs as the top predicted ligan

89 ys, the former is induced by the ligation of death receptors, a subset of the TNF receptor (TNFR) sup

90 Ligand binding to death receptors activates apoptosis in cancer cells.

91 y murine cytomegalovirus (MCMV) infection or death receptor activation and suppressed by the MCMV-enc

92 Inhibition of death receptor activation should have important therapeu

93 Death receptor activation triggers recruitment of FADD,

94 o explain cell decision making downstream of death receptor activation, we developed a semi-stochasti

95 he mitochondrial apoptotic program following death receptor activation.

96 We observed that death-receptor activation or starvation-induced metaboli

97 d suggests testable hypotheses to reconsider death receptor agonism as a therapeutic strategy.

98 Death receptor agonist therapies have exhibited limited

99 Genetic deletion of the death receptor agonists Fas ligand or TRAIL from the hem

100 ion to a multidrug resistance phenotype: ER, Death Receptor and epithelial to mesenchymal transition

101 m for molecular cross-talk between extrinsic death receptor and intrinsic mitochondrial apoptosis pat

102 eate an N-APP fragment that binds to the DR6 death receptor and mediates axon pruning and degeneratio

103 iscovered death repressor that inhibits both death receptor and mitochondrial apoptotic signaling.

104 f hepatocyte apoptosis by inhibition of both death receptor and mitochondrial death signaling.

105 inase/c-Jun N-terminal kinase and that other death receptors and activatory immune receptors were co-

106 The upregulation of death receptors and NKG2D ligands together on cells afte

107 ssential role in the signalling triggered by death receptors and pattern recognition receptors.

108 nase that mediates necroptosis downstream of death receptors and TLRs.

109 two death receptors or between either of the death receptors and TRAILR4.

110 property of antagonizing both the extrinsic (death receptor) and intrinsic (mitochondria/endoplasmic

111 of inter alia mitochondrial apoptotic genes, death receptors, and caspase enzymes, inducing DNA damag

112 d no role for regulatory T-cell-, programmed death receptor-, and transforming growth factor-beta-med

113 Lifeguard (LFG) is a death receptor antagonist mainly expressed in the nervou

114 immunotherapies such as anti-programmed cell death receptor antibody, cancer stem cell inhibitors, ta

115 regulate DR6 and TROY, indicating that these death receptors are downstream target genes of Wnt/beta-

116 Death receptors are known inducers of apoptosis and cell

117 Death receptors are members of the tumor necrosis factor

118 sis in HEK293T cells was mediated not by the death receptor but by the mitochondrial pathway, as demo

119 the tumor necrosis factor receptor 1 (TNFR1) death receptor by TNF induces either cell survival or ce

120 Ligation of these death receptors can also induce necroptosis.

121 These findings indicate that in the nucleus, death receptors can function as tumor promoters and migh

122 and IHC protein are increased for the entire death receptor cascade.

123 Viral infection rapidly induces death receptor CD95 (Fas) expression by dendritic cells

124 s, GEM and OXP upregulated expression of the death receptor CD95 (fas) on live cells even at sub-cyto

125 IFNs, which together increase expression of death receptor CD95 on ILC3s and thereby promote subsequ

126 individuals expressed increased surface Fas death receptor (CD95) and programmed death-1, but simila

127 PD-1, CTLA-4, and the apoptosis-inducing Fas death receptor) compared with their lower-avidity CD4 co

128 ntial TRAIL responses involves clustering of death receptor complexes by E-cadherin and the actin cyt

129 anism that indicates how host CD95 prototype death receptor controls the life cycle of gammaherpesvir

130 Fas is a cell surface death receptor critical for immune regulation.

131 Using the death receptor deficient (Fas(lpr)) lupus-prone mouse, w

132 o functionally compromise the RASSF1A/MOAP-1 death receptor-dependent pathway and drive tumorigenesis

133 ugh activation of caspase-8, suggesting that death receptor-dependent pathways are involved.

134 The limonoid induced expression of death receptor (DR) 5 and DR4 but did not affect express

135 Death receptor (DR) ligands such as tumor necrosis facto

136 receptor (EGFR) targeted nanobody (ENb) and death receptor (DR) targeted ligand TRAIL (ENb-TRAIL).

137 In this study, we identified death receptor (DR)-induced apoptosis as a pathway that

138 Although both splice variants regulate death receptor (DR)-induced apoptosis by CASP8, the spec

139 c Inhibitory Molecule (FAIM-L) protects from death receptor (DR)-induced apoptosis, yet its mechanism

140 ancer therapy because it selectively induces death receptor (DR)-mediated apoptosis in cancer cells w

141 In this study, we developed death receptor (DR)4/5-reporters that offer an imaging-b

142 RAIL) and agonistic antibodies against TRAIL death receptors (DR) kill tumor cells while causing virt

143 elated apoptosis-inducing ligand receptor 1 (death receptor [DR]4).

144 TRAIL induces cell death through binding to death receptors DR4 and DR5.

145 ively attenuated apoptosis signaling via the death receptors DR4 and DR5.

146 cells are sensitive to TRAIL through the two death receptors DR4 and DR5.

147 ells by signaling through the O-glycosylated death receptors (DR4 and DR5), but the sensitivity to TR

148 prevented FFC-induced strong upregulation of death receptor DR5 and its ligand TRAIL.

149 The proapoptotic death receptor DR5 has been studied extensively in cance

150 These findings define a role for death receptors DR6 and TROY in CNS-specific vascular de

151 significantly upregulated the expression of death receptors (DRs) (TNFR1, Fas, DR4 and DR5) in iPS-d

152 Cell surface expression of the proapoptotic death receptors (DRs) DR4, DR5, and Fas was not affected

153 We hypothesized that downmodulation of death receptors (DRs) in addition to aberrant apoptotic

154 Death receptors (DRs) of the TNFR superfamily contribute

155 The death receptors (DRs), DR4, DR5, and Fas, transduce cell

156 in transformed cells expressing its cognate death receptors (DRs).

157 ce apoptosis in cells expressing its cognate death receptors (DRs).

158 at c-Jun N-terminal kinase (JNK) and the Fas death receptor each play a role in neuronal apoptosis oc

159 Death receptor expression varied across genetic subtypes

160 ucing ligand, or CD95 ligand or knockdown of death receptors fail to rescue BV6/dexamethasone-induced

161 der pathological conditions, upregulation of death receptor family ligands, such as tumour necrosis f

162 TNFRSF21, is a relatively new member of the death receptor family, and it was found that DR6 induces

163 Fas is a member of the death receptor family.

164 demonstrated that S-glutathionylation of the death receptor Fas (Fas-SSG) amplifies apoptosis.

165 that D-cyclins repress the expression of the death receptor Fas and its ligand, FasL.

166 The death receptor Fas and its physiological ligand (FasL) r

167 also demonstrate the requirement of the cell death receptor Fas for LtxA-mediated cell death in T lym

168 The death receptor Fas is critical for bacterial clearance a

169 FasL, expressed by CD4(+) T cells, activated death receptor Fas signaling in MPs, resulting in caspas

170 Mutations in the death receptor FAS(1,2) or its ligand FASL(3) cause auto

171 cues the apoptosis of T lymphocytes when the death receptor Fas/CD95 is dysfunctional.

172 Here, we show that the Fas cell surface death receptor (Fas/CD95/Apo-1) regulates hepatic mitoch

173 ceptor has primarily been characterized as a death receptor for its ability to induce neuronal apopto

174 ptor 5 (DR5) is a cell surface pro-apoptotic death receptor for tumor necrosis factor-related apoptos

175 g a subset of integrins and the cell-surface death receptor FS-7-associated surface antigen.

176 proliferative syndrome (ALPS), defective Fas death receptor function causes lymphadenomegaly/splenome

177 34767) in the core promoter of the CD95 cell death receptor gene in 708 subjects with acute myeloid l

178 Increased expression of death receptor, immune costimulatory molecules, and Ad-I

179 3B and the FAS (first apoptosis signal) cell death receptor in FRLE cells.

180 NFRSF6) is a prototypical apoptosis-inducing death receptor in the tumor necrosis factor receptor (TN

181 These data demonstrate that the induction of death receptors in cardiomyocytes is likely a critical m

182 how that the AICD in TCReng CD4 T cells is a death receptor-independent process and that JNK and p53

183 Jun-NH2-terminal kinase (JNK)-dependent, but death receptor-independent way (2).

184 ase-8 signaling at a point of convergence of death receptor-induced apoptosis and perforin/granzyme-d

185 ed to protect virally infected cells against death receptor-induced apoptosis and to activate the NF-

186 ed to protect virally infected cells against death receptor-induced apoptosis by interfering with cas

187 ppaB to the protective effect of K13 against death receptor-induced apoptosis is not clear.

188 terial infection, NleB1/NleB(CR) antagonizes death receptor-induced apoptosis of infected cells by mo

189 y protein (c-FLIP) promotes cell survival in death receptor-induced apoptosis pathway in T lymphocyte

190 ppaB to the protective effect of K13 against death receptor-induced apoptosis remains to be determine

191 Caspase 8, the initiator caspase for death receptor-induced apoptosis, functions as a negativ

192 -inducing signaling complex (DISC) initiates death receptor-induced apoptosis.

193 iral immune functions, but rather because of death-receptor-induced programmed necrosis of airway epi

194 Of these factors, we show that death receptor inhibitor cellular caspase 8 (FLICE)-like

195 Furthermore, these two death receptors interact both genetically and physically

196 Besides causing necroptotic cell death, receptor-interacting protein kinase 3 (RIPK3) has

197 CD20 occupancy, and the relative efficacy of death receptor isoforms.

198 of the immuno-modulatory molecule programmed death receptor ligand 1 (PD-L1).

199 enes that modify FOXO activation of TRAIL, a death receptor ligand capable of inducing extrinsic apop

200 xposure of early activation antigen CD69 and death receptor ligand TRAIL, as well as interferon-gamma

201 Importantly, activation of IRF5 by the death receptor ligand tumor necrosis factor-related apop

202 that neutrophil-dependent expression of the death-receptor ligand FasL by iNKT cells was needed to r

203 del explains how alterations in the level of death receptor-ligand complexes, their clustering proper

204 Cisplatin in combination with death receptor ligands enhanced caspase-8 and caspase-3

205 CSC viability, CSC frequency, expression of death receptor ligands, and tumor burden.

206 ndependently of autocrine/paracrine loops of death receptor ligands, because blocking antibodies for

207 d extrinsically and required the presence of death receptor ligands, such as tumor necrosis factor-al

208 ne compound: inhibits necroptosis induced by death receptors ligands TNF-alpha (Tumor Necrosis Factor

209 heterodimerize with caspase-8 independent of death receptor ligation and activate caspase-8 via an ac

210 preciated to govern both apoptosis following death receptor ligation and cell survival and growth via

211 uction of apoptotic caspases was mediated by death receptor ligation and was detectable after 45 minu

212 stically different from those activated upon death receptor ligation.

213 by down-regulating FLIP, a key modulator of death receptor-mediated activation of caspase-8.

214 Integral in the regulation and initiation of death receptor-mediated activation of programmed cell de

215 c-FLIP can inhibit death receptor-mediated apoptosis by competing with casp

216 ed Fas and FasL, initiated mitochondria- and death receptor-mediated apoptosis pathway.

217 nzyme inhibitory protein) is an inhibitor of death receptor-mediated apoptosis that is up-regulated i

218 where it functions as the apical protease in death receptor-mediated apoptosis triggered via the deat

219 Caspase-8, a central initiator of death receptor-mediated apoptosis, for example, is frequ

220 gnaling complex (DISC) is a critical step in death receptor-mediated apoptosis, yet the mechanisms un

221 ecting mTORC2 signaling to the regulation of death receptor-mediated apoptosis.

222 mitochondrial apoptotic pathway but not the death receptor-mediated apoptotic pathway.

223 This demonstrates that GrzB and death receptor-mediated cytotoxicity are differentially

224 Ezh2 accelerated effector Th cell death via death receptor-mediated extrinsic and intrinsic apoptoti

225 Caspase-8 activation can be triggered by death receptor-mediated formation of the death-inducing

226 eath in their first killing events to a slow death receptor-mediated killing during subsequent tumor

227 Our results document a critical role for death receptor-mediated LSEC injury and show the first e

228 Caspase 8 (Casp8) is essential for death-receptor-mediated apoptosis activity and therefore

229 tumour suppressor genes associated with the death-receptor-mediated intrinsic apoptosis pathway, and

230 athway triggered by SFV does neither involve death receptors nor the classical MAVS effectors TNFR-as

231 activation of caspase-8 by the TRAIL-R2/DR5 death receptor; notably, this activation was not depende

232 Apoptosis can be induced by either death receptors on the plasma membrane (extrinsic pathwa

233 Loss-of-function mutations in the Fas death receptor or its ligand result in a lymphoprolifera

234 ell death that can be observed downstream of death receptor or pattern recognition receptor signaling

235 DNA damage, but not upon stimulation of the death receptor or stress-induced pathways.

236 DAI to signal for necroptosis in response to death receptor or Toll-like receptor stimulation, pathog

237 nd heterophilic interactions between the two death receptors or between either of the death receptors

238 ponse to induction of extrinsic apoptosis by death receptors or intrinsic apoptosis by chemotherapeut

239 role of diphthamide in modulating NF-kappaB, death receptor, or apoptosis pathways.

240 In AUD hippocampus, ligand-death receptor pairs, i.e., TL1A-DR3 and FasL-Fas, were

241 ernate death pathway triggered by TNF family death receptors, pathogen sensors, IFNRs, Ag-specific TC

242 an T cells (Jurkats) expressing a functional death receptor pathway (WT) and a corresponding Fas-asso

243 eals that all of the major components of the death receptor pathway are present in coral with high-pr

244 ts establish activation of ER stress and the death receptor pathway as a novel anticancer mechanism o

245 We determined that the TNFR1 death receptor pathway is involved in axotomy-induced FM

246 xp requires inhibition of both the extrinsic death receptor pathway via TNFR1 and caspase-8 and inhib

247 The death receptor pathway was significantly altered, blocki

248 h two major pathways, the extrinsic pathway (death receptor pathway) and the intrinsic pathway (the m

249 (TNFRSF/TNFSF) are central mediators of the death receptor pathway, and the predicted proteome of Ac

250 Caspase-8, an executioner enzyme in the death receptor pathway, was shown to initiate apoptosis

251 in cells committed to die via the extrinsic death receptor pathway.

252 SL) and subsequent apoptosis through the FAS death receptor pathway.

253 g that coral AdTNF1 activates the H. sapiens death receptor pathway.

254 can be partially rescued by blockade of this death receptor pathway.

255 D1 mice and investigated gene expression for death receptor pathways after target disconnection by ax

256 he expression of IL-33 and its regulation by death receptor pathways was investigated after the induc

257 ide gene enhancer in B cells (NF-kappaB) and death-receptor pathways without crossing lethal threshol

258 Recent studies indicate programmed cell death receptor (PD)-1 plays a significant role in the de

259 NF-related apoptosis-inducing ligand (TRAIL) death receptors, promoting early-phase replication.

260 of ETS-like transcription factor-1(ELK1) and Death Receptor protein-5 (DR5) in HCC.

261 nd functional assays, suggest that following death receptor recruitment, the FADD DED preferentially

262 diverse subcellular compartments, including death receptor regulation, modulation of endoplasmic ret

263 Here, we investigated the role of death receptor resistance in breast cancer progression.

264 Stimulation of death receptors results in the formation of intracellula

265 eal a role of GALE-mediated NS regulation in death receptor signaling and may have implications for t

266 e decisions following TLR signaling parallel death receptor signaling and rely on caspase 8 to suppre

267 Altered death receptor signaling and resistance to subsequent ap

268 These results implicate death receptor signaling as an important mediator of can

269 is largely independent of autophagy or major death receptor signaling pathways and demonstrated that

270 e predicted structural conservation of other death receptor signaling proteins, led us to wonder what

271 CRISPR screens identified death receptor signaling through FADD and TNFRSF10B (TRA

272 ASM has been implicated in CD95 death receptor signaling under certain stress conditions

273 Inhibition studies identified so-called death receptor signaling with activation of caspase-8 an

274 own-regulation of c-FLIP, a key inhibitor of death receptor signaling, and by up-regulation of TRAIL

275 lar pathogens, DNA damage-induced apoptosis, death receptor signaling, and macrophage polarization.

276 Independent of death receptor signaling, mitochondria sense apoptotic s

277 ell death pathways reminiscent of TNF family death receptor signaling.

278 Cytosolic caspase-8 is a mediator of death receptor signaling.

279 L) based pro-apoptotic therapies that induce death receptor signalling within the metastatic tumour c

280 revealed a more significant upregulation of death receptor signalling, driven by H5N1 than with H5N8

281 Previously, we have designed death receptor-specific TRAIL variants that induce apopt

282 optotic pathway is initiated by cell surface death receptors such as Fas.

283 functions: it mediates apoptosis induced by death receptors such as TNFR1(1), and suppresses necropt

284 ition by the T cell receptor (TCR) or from a death receptor, such as tumor necrosis factor receptor 1

285 TNF-alpha receptor 1, an important membrane death receptor that mediates both programmed apoptosis a

286 containing granzyme B (GrzB) or by engaging death receptors that initiate caspase cascades.

287 as validated using the structures of the Fas death receptor, the HIV-1 gp41 fusion protein, the influ

288 uggesting a reduction of signaling competent death receptors through formation heteromeric receptor c

289 s through alpha2,6-linked sialylation of the death receptor TNFR1 in many cell types.

290 due to increased expression and activity of death receptors TNFR1 and Fas.

291 e, other than FasL, known to require the Fas death receptor to initiate cell death.

292 High-level expression of the TRAIL death receptor TRAIL-R2 is found to be a hallmark of T c

293 eam of TNF-related apoptosis-inducing ligand-death receptor (TRAIL-DR) complexes in several cancer ce

294 of the TNF-related apoptosis-inducing ligand death receptors (TRAIL-DR), we show that TRAIL-DR signal

295 Activation of the death receptors TRAILR1 and TRAILR2 can lead to apoptosi

296 sis selectively via its interaction with the death receptors TRAILR1/DR4 and TRAILR2/DR5 in a wide ra

297 vive treatment with agonists of two distinct death receptors, tumor necrosis factor-related apoptosis

298 gh multiple ROS-dependent actions, including death receptor up-regulation, extrinsic apoptotic pathwa

299 CD95 (APO-1/Fas) is a death receptor used by immune cells to kill cancer cells

300 pathway activates caspases via cell-surface death receptors, which respond to cognate death ligands