ライフサイエンスコーパス: death receptor

1 gand-independent cytotoxic signaling by this death receptor.

2 ygous mutations in the gene encoding the Fas death receptor.

3 induce apoptosis exclusively via one of its death receptors.

4 the interactions between nanofibers and the death receptors.

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

6 susceptible cancer cells by engaging cognate death receptors.

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

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

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

10 Programmed death receptor 1 (PD-1) is an important signaling molecu

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

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

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

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

15 ry signals from the high level of programmed death receptor 1 expression also seen at this phase of i

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

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

18 of the surface markers CXCR5 and programmed death receptor-1 (PD-1) and synthesis of IL-21, require

19 T-cell expression of programmed death receptor-1 (PD-1) down-regulates the immune respon

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

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

22 es suggest that the B7-H1 ligand, programmed death receptor-1 (PD-1), is also expressed on myeloid ce

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

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

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

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

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

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

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

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

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

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

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

34 uces apoptosis through its cognate receptors death receptor 4 (DR4) and death receptor 5 (DR5), prefe

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

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

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

38 The TRAIL receptor (TRAIL-R1; also known as death receptor 4) is a transmembrane receptor that media

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

40 surface expression of both TRAIL receptors, death receptors 4 and 5 (DR4 and -5).

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

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

43 Moreover, no significant increase in death receptor 5 (DR5) expression was seen in CD4(+) T c

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

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

46 or-related apoptosis-inducing ligand (TRAIL) death receptor 5 (DR5) is significantly elevated in pati

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

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

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

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

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

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

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

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

55 cognate receptors death receptor 4 (DR4) and death receptor 5 (DR5), preferentially in malignant cell

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

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

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

59 us protein (CHOP), Bcl-2 family members, and death receptor 5 (DR5).

60 l antibody that binds to and activates human death receptor 5 (DR5; also known as TRAIL receptor 2).

61 revealed that up-regulation of cell surface death receptor 5 levels by treatment with 7-ethyl-10-hyd

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

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

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

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

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

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

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

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

70 Here we show that death receptor 6 (DR6) is a negative regulator of oligod

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

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

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

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

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

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

77 e complex-dependent necroptosis that follows death receptor activation as well as a RIP3-dependent, R

78 Inhibition of death receptor activation should have important therapeu

79 Death receptor activation triggers recruitment of FADD,

80 he mitochondrial apoptotic program following death receptor activation.

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

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

83 Death receptor agonist therapies have exhibited limited

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

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

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

87 ropose that IGFBP-3R represents a novel cell death receptor and is essential for the IGFBP-3-induced

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

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

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

91 esearch was to determine the contribution of death receptor and mitochondrial pathways to apoptosis i

92 ternate form of death that can be induced by death receptors and is linked to autophagy.

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

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

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

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

97 Apoptosis can occur via extrinsic (death receptor) and/or intrinsic (mitochondrial) pathway

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

99 rms independently of TNF, CD95L/FASL, TRAIL, death-receptors, and mitochondrial pathways.

100 spase recruitment domain (ARC) inhibits both death receptor- and mitochondrial/ER-mediated pathways o

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

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

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

104 by activating caspase-8 independently of the death receptor apoptotic pathway.

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

106 Death receptors are essential for immune homeostasis, bu

107 Death receptors are members of the tumor necrosis factor

108 involving alpha2-6 sialylation of the TNFR1 death receptor by the ST6Gal-I sialyltransferase.

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

110 Ligation of these death receptors can also induce necroptosis.

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

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

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

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

115 The Fas death receptor (CD95) is expressed on macrophages, smoot

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

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

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

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

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

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

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

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

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

125 However, the role of TRADD in other death receptor (DR) signaling pathways, including DR3, h

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

127 DBA also induced both death receptor (DR)-5 and DR4.

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

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

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

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

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

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

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

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

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

137 e extrinsic pathway through the proapoptotic death receptors DR4 and DR5.

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

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

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

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

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

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

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

145 Death receptors (DRs) of the TNFR superfamily contribute

146 hat the death of cells following ligation of death receptors (DRs), a subfamily of cell surface molec

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

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

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

150 chotomy reflects differences in cell surface death receptor expression.

151 tudies, we show that EDD1 and GRHL2 suppress death-receptor expression, and that EDD1 expression is e

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

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

154 Fas is a member of the death receptor family.

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

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

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

158 The death receptor Fas is a critical mediator of the extrins

159 The death receptor Fas is critical for bacterial clearance a

160 ated human FOXP3+ T cells are protected from death receptor Fas-mediated apoptosis.

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

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

163 Herein we identify the death receptor, Fas (CD95), as an ST6Gal-I substrate, an

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

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

166 FADD is a common adaptor shared by several death receptors for signalling apoptosis through recruit

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

168 finding establishes a new paradigm by which death receptor function is impaired for the self-protect

169 34767) in the core promoter of the CD95 cell death receptor gene in 708 subjects with acute myeloid l

170 Here we report a new cell death receptor, IGFBP-3R, that is a single-span membrane

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

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

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

174 nger RNA (mRNA) levels for death ligands and death receptors in hepatocytes, as well as decreased cas

175 During apoptotic signaling induced by death receptors including Fas, FADD is required for the

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

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

178 s 8q22-amplified breast cancer cell lines to death receptor induced apoptosis.

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

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

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

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

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

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

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

186 d the resistance of pancreatic tumors to Fas death receptor-induced apoptosis, we investigated the mo

187 ong these, caspase-8 (Casp8) is critical for death receptor-induced apoptosis.

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

189 alogous to the RIP1-RIP3 complex controlling death receptor-induced necroptosis.

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

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

192 ndrial perturbation to amplify a more modest death receptor-initiated signal.

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

194 ndrome (ALPS), caused by mutation of the Fas death receptor, is massive lymphadenopathy from aberrant

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

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

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

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

199 ults demonstrate a direct role for RASSF5 in death receptor ligand-mediated apoptosis and provide fur

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

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

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

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

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

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

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

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

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

209 , enhanced tumor cell apoptosis initiated by death receptor ligation, and inhibited intracranial glio

210 stically different from those activated upon death receptor ligation.

211 nd FLIP orchestrate apoptosis in response to death receptor ligation.

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

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

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

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

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

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

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

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

220 eas, and lung cancer cell lines resistant to death receptor-mediated apoptosis.

221 Upregulated pathways included death receptor-mediated caspase cascade, mitochondrial d

222 trate that syndecan plays a negative role in death receptor-mediated cell death, suggesting potential

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

239 tion with M51R VSV, indicating that both the death receptor pathway and mitochondrial pathways are im

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

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

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

243 y protein (c-FLIP), a major regulator of the death receptor pathway of apoptosis.

244 The death receptor pathway was significantly altered, blocki

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

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

247 ells are p53-dependent activation of the DR4 death receptor pathway, caspase 8-mediated cleavage of B

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

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

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

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

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

253 ikely activates an apoptotic program via the death-receptor pathway.

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

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

256 ity to apoptosis via either mitochondrial or death receptor pathways, by a JNK-dependent mechanism.

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

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

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

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

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

264 Altered death receptor signaling and resistance to subsequent ap

265 gh which the regulatory effects of c-FLIP on death receptor signaling are controlled by GSK3, which c

266 therapeutic agents that enhance proapoptotic death receptor signaling by causing cellular degradation

267 Death receptor signaling has been classified as type I o

268 pancreatic cells to apoptosis induced by Fas-death receptor signaling may provide molecular insights

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

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

273 -negative FADD (to abrogate Fas/DR5-mediated death receptor signaling) and/or Bcl-2 (to block mitocho

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 we used a pooled shRNA screen to interrogate death receptor signaling.

279 icient to prevent necroptosis in the face of death receptor signaling.

280 expression wherein LGP2 operated to regulate death-receptor signaling and imparted sensitivity to CD9

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

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

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

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

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

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

287 SHP is a pivotal cell death receptor that targets mitochondria, where it binds

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

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

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

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

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

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

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

295 ity do not affect the function of DR4 or DR5 death receptors upon treatment with TRAIL, implicating a

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

297 f cell survival proteins and upregulation of death receptors via activation of ROS and CHOP mediated

298 cell survival proteins and up-regulation of death receptors via the ROS-mediated up-regulation of CH

299 Because p53 directly modulates expression of death receptors, we investigated here whether p53 can mo

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