ライフサイエンスコーパス: TRAIL receptor

1 icient mice and mice treated with a blocking TRAIL receptor.

2 nhanced in animals that received the soluble TRAIL receptor.

3 enhanced in animals treated with the soluble TRAIL receptor.

4 cific, as it could be inhibited with soluble TRAIL receptor.

5 f caspase 8 by increasing its recruitment to TRAIL receptors.

6 SRC, PI3K, G-protein-coupled receptors, and TRAIL receptors.

7 IL R2 (P < 0.01), but not TRAIL or the other TRAIL receptors.

8 ted apoptosis-inducing ligand (TRAIL) Apo-2L/TRAIL receptors.

9 urine TRAIL, suggesting that they are indeed TRAIL receptors.

10 protein that is most closely related to the TRAIL receptors.

11 sis and expression of the apoptosis-inducing TRAIL receptors.

12 tic of Fas, tumor necrosis factor, and human TRAIL receptors.

13 romosome 8p22-21, clustered with three other TRAIL receptors.

14 clustered with the genes encoding two other TRAIL receptors.

15 hereas curcumin enhanced the upregulation of TRAIL receptors.

16 affecting Bcl-2 family proteins and/or Apo2L/TRAIL receptors.

17 omas from apoptosis triggered through Fas or TRAIL receptors.

18 on and inducing tumour expression of Fas and TRAIL receptors.

19 y RNA interference depletion of TNFalpha and TRAIL receptors.

20 ng on agonistic monoclonal antibodies to the TRAIL receptors.

21 , tumor necrosis factor receptor-I, DR3, and TRAIL-receptors.

22 is factor-related apoptosis-inducing ligand (TRAIL) receptors.

23 , and TNF-related apoptosis-inducing ligand (TRAIL) receptors.

24 Agonistic anti-TRAIL receptor 1 and anti-TRAIL receptor 2 antibodies or

25 r members of the TNFR superfamily, including TRAIL receptor 1 and CD40, show similar homotypic associ

26 whereas only the RID protein is required for TRAIL receptor 1 downregulation.

27 po-2L/TRAIL receptors death receptor (DR) 4 (TRAIL receptor 1) or DR5 (TRAIL receptor 2), decoy recep

28 ctor (TNF) receptor superfamily, namely Fas, TRAIL receptor 1, and TRAIL receptor 2.

29 All of the cell lines expressed TRAIL receptor 1/death receptor 4 (TRAIL-R1/DR4) and TRA

30 nd Adriamycin) induced death receptors (DRs) TRAIL receptor 1/DR4 and TRAIL receptor 2/DR5, and succe

31 ial cells by up-regulating the expression of TRAIL receptors 1 and 2 in a CD36 and Jun NH(2)-terminal

32 show that TRAILshort binds preferentially to TRAIL receptors 1 and 2 with significantly reduced inter

33 ainst TNF-related apoptosis-inducing ligand (TRAIL) receptor 1 (mapatumumab) and TRAIL receptor 2 (le

34 iated apoptosis via up-regulation of surface TRAIL-receptor 1/receptor 2 (DR4/DR5) levels and to Fas

35 ination of triterpenoids and monoclonal anti-TRAIL receptor-1 (DR4) antibody also induces apoptosis o

36 x is sufficient to induce down-modulation of TRAIL receptor-1 and -2 from the cell surface and revers

37 man receptor for the cytotoxic ligand TRAIL (TRAIL receptor-1, designated DR4) was identified recentl

38 Here, we demonstrate that TRAIL receptor 2 (DR5) forms receptor dimers in a ligand

39 ligand (TRAIL) receptor 1 (mapatumumab) and TRAIL receptor 2 (lexatumumab) and small-molecule inhibi

40 The experiments reported here show that TRAIL receptor 2 (TR2) is cleared from the cell surface

41 receptor signaling, and by up-regulation of TRAIL receptor 2 (TRAIL-R2).

42 Here, we show that a combination of a TRAIL receptor 2 agonist antibody, Lexatumumab, and 3TSR

43 DR5 (also called TRAIL receptor 2 and KILLER) is an apoptosis-inducing me

44 Agonistic anti-TRAIL receptor 1 and anti-TRAIL receptor 2 antibodies or combinations of both were

45 IFN stimulation caused a concomitant loss of TRAIL receptor 2 expression, which coincides with monocy

46 in the expression kinetics of caspase 3 and TRAIL receptor 2 were observed.

47 h receptor (DR) 4 (TRAIL receptor 1) or DR5 (TRAIL receptor 2), decoy receptor (DcR) 1 and DcR2, Flam

48 s human death receptor 5 (DR5; also known as TRAIL receptor 2).

49 perfamily, namely Fas, TRAIL receptor 1, and TRAIL receptor 2.

50 ath receptors (DRs) TRAIL receptor 1/DR4 and TRAIL receptor 2/DR5, and successive treatment with TRAI

51 is factor-related apoptosis-inducing ligand (TRAIL) receptor 2/DR5-mediated death pathway in human me

52 ile acids up-regulate death receptor 5 (DR5)/TRAIL-receptor 2 (TRAIL-R2) expression thereby sensitizi

53 DR5 (TNF-related apoptosis-inducing ligand [TRAIL] receptor 2), and anti-TRAIL and anti-DR5 antibodi

54 ion of two additional human TRAIL receptors, TRAIL receptor-2 and TRAIL receptor-3, that belong to th

55 Interestingly, TRAIL receptor-2 but not TRAIL receptor-3 contains a cyt

56 on is warranted into targeted therapy toward TRAIL receptor-2, to potentially bypass the adverse effe

57 euroblastoma cells to TRAIL by up-regulating TRAIL receptor-2/DR5/KILLER and Bid.

58 ificantly reduced interaction with the decoy TRAIL receptors 3 and 4.

59 Interestingly, TRAIL receptor-2 but not TRAIL receptor-3 contains a cytoplasmic "death domain" n

60 Because of its lack of a death domain, TRAIL receptor-3 is not capable of inducing apoptosis.

61 Thus, TRAIL receptor-3 may function as an antagonistic decoy r

62 human TRAIL receptors, TRAIL receptor-2 and TRAIL receptor-3, that belong to the tumor necrosis fact

63 Knockdown of TRAIL receptor 4 by RNA interference or ectopic expressi

64 ed apoptosis-inducing ligand (TRAIL) action, TRAIL receptor 4, and the down-regulation of Fas, the re

65 In these cells, the predominant effect of TRAIL receptor activation is the activation of nuclear f

66 ngs suggest that one should select drugs for TRAIL receptor agonist combination therapy based not jus

67 mma treatment alone or in combination with a TRAIL receptor agonist significantly decreased the incid

68 of metastatic disease and the combination of TRAIL receptor agonist therapy with IFNgamma-mediated im

69 Cells recovered from both TRAIL receptor agonist-treated and nontreated tumors wer

70 vivo growth favors TRAIL resistance but that TRAIL receptor agonists are active in Ewing's sarcoma fa

71 odies to TRAIL receptors, and small molecule TRAIL receptor agonists are in various stages of preclin

72 To determine the in vivo efficacy of TRAIL receptor agonists in Ewing's sarcoma family of tum

73 but did not increase the antitumor effect of TRAIL receptor agonists on primary tumors.

74 family of tumors and that the combination of TRAIL receptor agonists with IFNgamma is a potent regime

75 ittle or no toxicity to normal cells; hence, TRAIL-receptor agonists are currently undergoing clinica

76 ential implications for cancer therapy using TRAIL-receptor agonists.

77 TRAIL receptors also activate the protein kinase JNK.

78 tors of TRAIL, including recombinant soluble TRAIL receptors and a neutralizing antibody against TRAI

79 with IFNgamma increased tumor expression of TRAIL receptors and caspase 8, but did not increase the

80 ch as agonistic monoclonal antibodies to the TRAIL receptors and recombinant TRAIL, are being develop

81 ced apoptosis, even though the expression of TRAIL receptors and several apoptosis-associated molecul

82 creased the expression of the death-inducing TRAIL receptors and, concomitantly, decreased the intrac

83 is factor-related apoptosis-inducing ligand (TRAIL) receptors and suppresses TRAIL-induced apoptosis.

84 known TNF-related apoptosis-inducing ligand (TRAIL) receptors and tested on a panel of human melanoma

85 is factor-related apoptosis-inducing ligand (TRAIL) receptors and triggers apoptosis on ligation with

86 alian TNF-related apoptosis-inducing ligand [TRAIL] receptors) and with viral superinfection leading

87 protein-dependent expression of DR5, a major TRAIL receptor, and reduces the levels of cellular FLICE

88 pressed lesser amounts of the death-inducing TRAIL receptors, and greater amounts of survivin, an inh

89 (TRAIL), agonistic monoclonal antibodies to TRAIL receptors, and small molecule TRAIL receptor agoni

90 in of TNF-related apoptosis-inducing ligand (TRAIL) receptors, and is required for TRAIL-induced apop

91 Several novel drugs targeting TRAIL receptors are currently in clinical trials.

92 se findings, along with our observation that TRAIL receptors are expressed in RCC tumor tissue, sugge

93 FADD(-/-) MEF cells stably transfected with TRAIL receptors are resistant to TRAIL-mediated cell dea

94 This article examines the TRAIL receptors as potential targets for activating the

95 The status of the TRAIL receptors (assessed by immunoblotting and flow cyt

96 in-containing molecule, was recruited to the TRAIL receptor-associated signaling complex.

97 ock reovirus-induced apoptosis by preventing TRAIL-receptor binding.

98 un phosphorylation, is inhibited by blocking TRAIL/receptor binding, suggesting that apoptosis and c-

99 Anti-TRAIL antibody and soluble TRAIL receptors block reovirus-induced apoptosis by prev

100 ted apoptosis was TRAIL specific, as soluble TRAIL receptor blocked target cell death.

101 s inducing ligand (TRAIL) and death-inducing TRAIL receptors, but blockade of TRAIL:TRAIL receptor in

102 Upregulation of TRAIL receptor by the combination was also observed in t

103 nt evidence suggests that TNFR-1 and Fas and TRAIL receptors can also trigger an alternative form of

104 ot changed in the resistant cells, including TRAIL receptors, cFLIP, Bax, Bid, or IAP proteins.

105 We show that TRADD is recruited to the TRAIL-receptor complex, and RIP1 recruitment is mediated

106 her members of the TNF receptor superfamily, TRAIL receptors contain a pre-ligand binding assembly do

107 EC were found to contain significantly fewer TRAIL receptors DcR1 and DcR2 which are not capable of c

108 Two additional TRAIL receptors (DcR1 and DcR2) do not transmit an apopt

109 Dox up-regulated the expression of the TRAIL receptor death receptor 5 (DR5) and synergisticall

110 R expression inhibited the expression of the TRAIL receptor death receptor 5 (DR5), whereas HOTAIR kn

111 tes a novel cross-talk mechanism between the TRAIL receptor death signaling pathway and the mitochond

112 r to correlate with the levels of the Apo-2L/TRAIL receptors death receptor (DR) 4 (TRAIL receptor 1)

113 Despite the expression of TRAIL receptors death receptor 4 and death receptor 5, p

114 nding analysis using the TRAIL protein and a TRAIL receptor (death receptor 5) revealed that both the

115 L and amiloride did not change the levels of TRAIL receptors (death receptor (DR)4, DR5, and DcR2 (de

116 Our aims were to determine which TRAIL receptor, death receptor (DR) 4 or DR5, mediates l

117 induced the cell surface expression of both TRAIL receptors, death receptors 4 and 5 (DR4 and -5).

118 e presence of mRNA encoding the "protective" TRAIL receptors did not correspond to resistance or sens

119 orylated MADD can directly interact with the TRAIL receptor DR4 thereby preventing Fas-associated dea

120 Activating TRAIL receptors DR4 and DR5 were expressed in all normal

121 nd 8, c-Flip or FADD, but elevates levels of TRAIL receptors DR4 and DR5.

122 d death domain (FADD), and links FADD to the TRAIL receptors DR4 and DR5.

123 uced the cell surface expression of both the TRAIL receptors DR4 and DR5.

124 tein c-FLIP(L), and up-regulate cell surface TRAIL receptors DR4 and DR5.

125 l-XL protected against overexpression of the TRAIL receptors DR4 and KILLER/DR5.

126 d the TNF-related apoptosis-inducing ligand (TRAIL) receptors DR4 and DR5 induce apoptosis by recruit

127 is factor-related apoptosis-inducing ligand (TRAIL) receptors DR4 and DR5.

128 luble TRAIL and agonistic antibodies against TRAIL receptors (DR4 and DR5) are currently being create

129 ted mRNAs encoding TRAIL as well as the four TRAIL receptors (DR4, DR5, DcR1/TRID, DcR2/TRUNDD) in hu

130 had no effect on the expression of the other TRAIL receptor, DR4.

131 c agents upregulated expression of the Apo2L/TRAIL receptor DR5 and the Bax homolog Bak in Baxminus s

132 uced apoptosis by inducing clustering of the TRAIL receptor DR5 at the cell surface and the redistrib

133 ly, stable expression of a dominant negative TRAIL receptor DR5 partially blocks IFN-induced cell dea

134 DCs that lack expression of TRAIL receptor DR5 were less susceptible to NK cell-medi

135 PL resulted in the upregulation of TRAIL receptor DR5, which potentiated TRAIL-induced apop

136 caspase-8 but up-regulated the levels of the TRAIL receptor DR5.

137 lt of radiation-induced up-regulation of the TRAIL-receptor DR5.

138 influenza-specific CD8(+) T cells, and high TRAIL receptor (DR5) expression occurs selectively on in

139 in surface heparan sulfate or a reduction in TRAIL receptor endocytosis.

140 the balance of death-inducing and regulatory TRAIL receptors expressed on hepatocytes.

141 uveal melanoma metastases were examined for TRAIL receptor expression by flow cytometry.

142 nd regulation of TRAIL-induced apoptosis and TRAIL receptor expression in human RCC cell lines and pa

143 Bortezomib up-regulated TRAIL receptor expression on quiescent CD34(+) CML cells

144 oincided with a selective down-regulation of TRAIL receptor expression on tumor cells.

145 Specific TRAIL receptor expression was determined by RT-PCR, and

146 TRAIL receptors facilitate induction of apoptosis for se

147 TRAIL-R3, a new member of the TRAIL receptor family, has been cloned and characterized

148 A fourth member of the emerging TRAIL receptor family, TRAIL-R4, has been cloned and cha

149 ain (FADD), decoy receptor 2 (DcR2), soluble TRAIL receptor fusion proteins (DR-4 and DR-5) and thymi

150 This is the first report describing a mouse TRAIL receptor gene and also demonstrating that the p53-

151 es found in the first introns of other three TRAIL receptor genes.

152 Its expression, like the other three TRAIL receptors (i.e., DR4, DR5, and DcR1), is regulated

153 the inhibition of NF-kappaB and induction of TRAIL receptors in bladder cancer cells.

154 the use of specific therapeutic agonists of TRAIL receptors in people whose tumors harbor somatic DR

155 to thymocytes, there is no up-regulation of TRAIL receptors in peripheral T cells on activation, whi

156 ith a detectable change in the expression of TRAIL receptors in reovirus-infected cells.

157 RAIL-R3 is unique when compared to the other TRAIL receptors in that it lacks a cytoplasmic domain an

158 g protein, mediates cell death involving the TRAIL receptors in the hepatic stellate cell line, LX2.

159 These findings suggest that TRAIL receptors induce apoptosis, NF-kappaB and JNK acti

160 duced by gossypol treatment was critical for TRAIL receptor induction and apoptosis potentiation.

161 ation was also required for gossypol-induced TRAIL receptor induction; gene silencing of ERK abolishe

162 a receptor or TNF receptor-1, but not Fas or TRAIL receptors, inhibits the cytopathicity and replicat

163 ucing TRAIL receptors, but blockade of TRAIL:TRAIL receptor interaction does not alter HIV-induced ce

164 In summary, we propose a model of TRAIL receptor interference driven by PLAD-mediated form

165 ential, initiates apoptosis by re-organizing TRAIL receptors into large clusters, although the struct

166 mechanism by which FADD is recruited to the TRAIL receptors is not clear.

167 re the cloning of the mouse homologue of the TRAIL receptor KILLER/DR5 (MK).

168 directed at proapoptotic p53 targets reveal TRAIL receptor KILLER/DR5 contributes significantly to T

169 utation occurs in head/neck and lung cancer (TRAIL receptor KILLER/DR5) and in lpr mice (Fas).

170 Hepatocytes from murine TRAIL receptor knock-out mice (DR(-/-)) displayed reduce

171 TRAIL receptors ligation in PC3 activated caspases -2, -

172 is factor-related apoptosis-inducing ligand (TRAIL) receptor ligation.

173 hibition in combination with agonists of the TRAIL receptor may provide an enhanced therapeutic index

174 s factor receptor apoptosis-inducing ligand (TRAIL) receptors mediate anoikis in human CRC cells.

175 identify a mechanism for viral modulation of TRAIL receptor-mediated apoptosis and suggest the E3 pro

176 gents with DR-activating modalities, such as TRAIL receptor monoclonal antibodies, may benefit patien

177 Unlike the only other known murine TRAIL receptor mTRAILR2, however, neither mTNFRH2 nor mT

178 We have identified a fifth TRAIL receptor, namely osteoprotegerin (OPG), a secreted

179 be attributed to an increased expression of TRAIL receptor O-glycosylation enzyme in syndecan-1-defi

180 Still, the stoichiometry of TRAIL receptor oligomers as well as the issue of whether

181 ing ligand (TRAIL) and of the death-inducing TRAIL receptors on neutrophils, which confers an acquire

182 The expression of TRAIL and TRAIL receptors on RA SF lymphocytes and monocyte/macrop

183 is factor-related apoptosis-inducing ligand (TRAIL) receptors on uveal melanoma cells and metastases

184 is did not correlate with mRNA expression of TRAIL receptors or cellular FLICE-like inhibitory protei

185 is did not correlate with mRNA expression of TRAIL receptors or cFLIP.

186 Degradation of Fas and TRAIL receptors protects Ad-infected cells from apoptosi

187 Expression of the activating TRAIL receptors R1 and R2 was detected by flow cytometry

188 activated and activated M1-D cells expressed TRAIL receptors (R1 and R2), but only activated cells we

189 could interact with thyroid follicular cell TRAIL receptors, RNase protection assays were used to de

190 revented by Fas-Ig fusion protein or soluble TRAIL receptor (sDR5), respectively.

191 Although Huh-7 cells express both TRAIL receptors, short hairpin RNA silencing of DR5 but

192 The Fas/tumor necrosis factor (TNF)/TRAIL receptors signal death through a cytoplasmic death

193 suggesting a previously unreported role for TRAIL receptor signaling in mediating DXR-induced hair l

194 -Ala-Asp (VAD), indicating the presence of a TRAIL receptor signaling pathway similar to that identif

195 ever, when combined with agonists of the DR5/TRAIL receptor, siRNAs directed against the UbcH10 trans

196 In contrast, TRAIL receptors stably transfected into heterozygous FAD

197 distinct from those of the known human decoy TRAIL receptors, suggesting that the presence of TRAIL d

198 bination treatments with cytotoxic drugs and TRAIL receptor-targeted agents do not provide additional

199 is factor-related apoptosis-inducing ligand (TRAIL) receptor-targeted agents as antitumor drugs is th

200 he mAb permitted a precise evaluation of the TRAIL receptors that induce apoptosis (TRAIL-R1 and -R2)

201 optosis (TRAIL-R1 and -R2) compared with the TRAIL receptors that potentially regulate TRAIL-mediated

202 Although human colon carcinomas express TRAIL receptors, they can also demonstrate TRAIL resista

203 NOD mice received an injection of a soluble TRAIL receptor to block TRAIL function.

204 ave dissected the contribution of regulatory TRAIL receptors to apoptosis resistance in primary human

205 elective targeting of the two death-inducing TRAIL receptors to maximise efficacy.

206 The potential for these inhibitory TRAIL receptors to protect hHSC from apoptosis opens new

207 CD95, TNF-related apoptosis-inducing ligand (TRAIL) receptors, Toll-like receptors, reactive oxygen s

208 L path is because of a loss of cell membrane TRAIL receptors (TR1/TR2) not only in cell lines but in

209 and simultaneous activation of the CD19 and TRAIL receptor (TRAIL-R) apoptosis signaling pathways.

210 emonstrate a role for the apoptosis-inducing TRAIL receptor (TRAIL-R) as a metastasis suppressor.

211 ion and IFN-gamma also reciprocally modulate TRAIL receptor (TRAIL-R) expression.

212 TRAIL receptor (TRAIL-R) signaling has been implicated i

213 (TRAIL), TNF-alpha converting enzyme (TACE), TRAIL receptor (TRAIL-R)2, TNFR-related death receptor (

214 The TRAIL receptor (TRAIL-R1; also known as death receptor 4

215 Ligand-induced translocation of TRAIL receptors (TRAIL-R) 1 and 2 (also called DR4 and D

216 edundant functional roles for the regulatory TRAIL receptors (TRAIL-R3/4) in a physiological setting.

217 Therefore, we analyzed how TRAIL-receptor (TRAIL-R) costimulation is modulating TCR

218 rs or insufficient agonistic activity of the TRAIL-receptor (TRAIL-R)-targeting drugs.

219 e the identification of two additional human TRAIL receptors, TRAIL receptor-2 and TRAIL receptor-3,

220 Low levels of the death-inducing TRAIL receptors, TRAIL-R1 and TRAIL-R2 but not the putat

221 The TRAIL-receptor/TRAIL system originally described to indu

222 r-related apoptosis-inducing ligand (TRAIL), TRAIL receptor (TRAILR) 1, and TRAILR2 and down-regulati

223 Two additional TRAIL receptors, TRID/DcR1 and DcR2, lack functional dea

224 aled that TRAIL-R2 and TRAIL-R3 are the main TRAIL-receptors used by NB cells.

225 tudy, we demonstrate that a functional Apo2L/TRAIL receptor was necessary for the induction of cell d

226 Using a soluble TRAIL receptor, we examined the consequences of TRAIL bl

227 mRNA molecules encoding TRAIL receptors were constitutively expressed by osteobl

228 Two additional TRAIL receptors were identified.

229 nd those cell lines expressing low levels of TRAIL receptor, were resistant to apoptosis induced by t

230 2, Stat3 and NF-kappaB) affects TNF, Fas and TRAIL receptors, which play important roles in acquiring

231 Targeting TRAIL receptors with either recombinant TRAIL or agonist

232 onist decoy receptor (designated as TRID for TRAIL receptor without an intracellular domain) that may