ライフサイエンスコーパス: DR5

1 R-controlled activation of death receptor 5 (DR5).

2 ating transcription of the death receptor 5 (DR5).

3 Bcl-2 family members, and death receptor 5 (DR5).

4 tion of the synthetic auxin response element DR5.

5 TLs used the TRAIL cytotoxic pathway through DR5.

6 is signaling via the death receptors DR4 and DR5.

7 he isolated TM domain of the long isoform of DR5.

8 of the p53 target genes CDKN1A or TNFRSF10B/DR5.

9 sion of WOX5 and the auxin response reporter DR5.

10 for the cytokinin and auxin markers CRE1 and DR5.

11 s or B-Raf (V600E) reduced the expression of DR5.

12 vitro with comparable affinities to DR2 and DR5.

13 RAIL through the two death receptors DR4 and DR5.

14 ubiquitination and lysosomal degradation of DR5.

15 sis that was abrogated by siRNA silencing of DR5.

16 ugh the proapoptotic death receptors DR4 and DR5.

17 pression of both the TRAIL receptors DR4 and DR5.

18 dation of DR5, suggesting that it stabilizes DR5.

19 trimerizing its functional receptors DR4 or DR5.

20 omo-oligomerization and stability of DR4 and DR5.

21 h through binding to death receptors DR4 and DR5.

22 Death receptor 5 (DR5), a cell surface pro-apoptotic protein, triggers apo

23 Furthermore, we identified death receptor 5 (DR5), a member of tumour necrosis factor (TNF)-receptor

24 nexpected finding that for death receptor 5 (DR5), a receptor in the tumor necrosis factor receptor s

25 ular DR5 protein, driving ligand-independent DR5 activation and apoptosis engagement via caspase-8.

26 o2L/TRAIL; however, the mechanism underlying DR5 activation is unknown.

27 The resulting model of DR5 activation should revise the accepted architecture o

28 ave potential in sensitizing cancer cells to DR5 activation-based cancer therapy.

29 R5 expression impede cancer cell response to DR5 activation-induced apoptosis and activated immune ce

30 naling suppresses DR5 expression and impairs DR5 activation-induced apoptosis and T cell-mediated kil

31 b-AP15 on death receptor 5 (DR5) levels and DR5 activation-induced apoptosis as well as on understan

32 ion of DR5 expression and the enhancement of DR5 activation-induced apoptosis in Ras-mutant cancer ce

33 ts of B-Raf inhibition on DR5 expression and DR5 activation-induced apoptosis in Ras-mutant cancer ce

34 face DR5 levels, resulting in enhancement of DR5 activation-induced apoptosis.

35 leads to up-regulation of death receptor 5 (DR5), activation of caspase-8 and -3, cleavage of poly (

36 hrough this route, WFA acted as an effective DR5 activator capable of potentiating the biologic effec

37 vival advantages through altering DR4 and/or DR5 activity.

38 t human TRAIL (native TRAIL) and dimeric DR4/DR5 agonist monoclonal antibodies (mAbs) failed in multi

39 ury and apoptosis following treatment with a DR5 agonist; however, this injury was prevented by pre-t

40 of cancer cell lines highly sensitive to the DR5 agonistic antibody AMG655 have either Ras or B-Raf m

41 r apoptotic response induced by TRAIL or the DR5 agonistic antibody AMG655 or cell killing by activat

42 ed apoptosis when combined with TRAIL or the DR5 agonistic antibody AMG655; these effects are DR5-dep

43 ects the sensitivity of myeloma cells to the DR5 agonistic human antibody lexatumumab but not the DR4

44 recombinant human TRAIL and drozitumab (anti-DR5 agonistic mAb) were used to explicitly verify the co

45 pproved agent Nelfinavir in combination with DR5 agonists to induce apoptosis in human malignancies.

46 ergistic induction of TRAIL and its receptor DR5 along with a potent induction of cell death.

47 showed elevated levels of ERK, RSK, ELK1 and DR5 along with decreased expression of Ki67.

48 nds to and activates human death receptor 5 (DR5; also known as TRAIL receptor 2).

49 is-inducing TNFRs, such as death receptor 5 (DR5), although displaying impressive activities against

50 Structure determination of the Apo2L/TRAIL-DR5-AMG 655 ternary complex illustrates how higher order

51 rough ROS-ERK-CHOP-mediated up-regulation of DR5 and DR4 signaling, down-regulation of cell survival

52 and possibly its derivatives, can stabilize DR5 and increase functional cell surface DR5 levels, res

53 nduced strong upregulation of death receptor DR5 and its ligand TRAIL.

54 tudies showed an inverse correlation between DR5 and Ki67.

55 TNF ligand-receptor complexes, namely TRAIL-DR5 and LTalpha-TNFR1.

56 rmed to investigate the levels of TRAIL DR4, DR5 and OPG receptors generating promising insights on t

57 Activation of macrophages required DR5 and receptor-interacting protein kinase 1.

58 ted architecture of the functioning units of DR5 and the structurally homologous TNF receptor superfa

59 f HI, mRNA, and protein expression of TRAIL, DR5 and the TRAIL decoy receptors osteoprotegerin (OPG),

60 express elevated levels of Death Receptor 5 (DR5) and its downstream regulators/effectors FLIP, Caspa

61 lso independent of the Fas ligand-Fas, TRAIL-DR5, and canonical death pathways, indicating a novel me

62 ity of RAR-RXR bound to DR0 compared to DR2, DR5, and DR8 to mediate RA-dependent transcriptional act

63 the proapoptotic death receptors (DRs) DR4, DR5, and Fas was not affected by E6 suppression.

64 The death receptors (DRs), DR4, DR5, and Fas, transduce cell-extrinsic apoptotic signals

65 related apoptosis-inducing ligand (TRAIL)-R2/DR5, and several ligands of NK cells in GNMT(-/-) livers

66 critical to the therapeutic activity of anti-DR5 antibodies and, together with previous reports on ag

67 Anti-DR5 antibodies of the type currently in clinical trials

68 and tumor retention kinetics of an agonistic DR5 antibody in a brain tumor xenograft model, we utiliz

69 The anti-human DR5 antibody TRA-8 was efficacious in reducing the sever

70 , which were then treated with an anti-human DR5 antibody, TRA-8.

71 antibodies against TRAIL receptors (DR4 and DR5) are currently being created for clinical cancer the

72 We propose that cells can use DR5 as a late protein-folding checkpoint before committi

73 the ER-Golgi intermediate compartment, where DR5 assembles pro-apoptotic caspase 8-activating complex

74 r i.c. delivery of fluorescence-labeled anti-DR5 at different dosages.

75 P4) not only increased expression of Fas and DR5 at the mRNA and protein level, but also recapitulate

76 zed toward regions of high expression of the DR5 auxin-signaling reporter, which suggests that SoPIN1

77 edicted and verified the CaM-binding site in DR5 being (354)WEPLMRKLGL(363) that is located at the al

78 d by a higher activity of the auxin reporter DR5-beta-glucuronidase in lateral root apices.

79 Expression of the auxin-induced reporter (DR5-beta-glucuronidase) is reduced in initiating lateral

80 to the experimentally observed decreased CaM-DR5 binding by the point mutations of the key residues i

81 the further investigation of the role of CaM-DR5 binding in DR5-mediated DISC formation for apoptosis

82 poptosis also play an important role for CaM-DR5 binding.

83 controls the sensitivity of myeloma through DR5 but not DR4 and suggest that a subset of patients wi

84 the O-glycosylated death receptors (DR4 and DR5), but the sensitivity to TRAIL-induced apoptosis of

85 agement promoted apoptotic signaling via DR4/DR5, but not Fas.

86 to TRAIL by upregulating mRNA expression of DR5 by 60% in vitro.

87 n the DR5 gene was required for induction of DR5 by azadirone.

88 The induction of DR5 by rapalogs is mediated by the ER stress regulator a

89 Deletion of DR5 by siRNA significantly reduced the apoptosis induced

90 ion of TRAIL with death receptor 4 (DR4) and DR5 can trigger apoptotic cell death.

91 E-cadherin augmented DR4/DR5 clustering and assembly of the death-inducing signal

92 binding of ENb to EGFR which in turn induces DR5 clustering at the plasma membrane and thereby primes

93 However, we have recently shown that DR5 clusters are more than just randomly aggregated rece

94 rimarily in microglia and astroglia, whereas DR5 co-localized with neurons and OPCs in vivo.

95 n (ECD) of long isoform of death receptor 5 (DR5) could block endogenous receptor assembly, mimicking

96 inant DR5-Fc chimera protein suggesting that DR5 cytotoxic signaling is ligand-independent.

97 tial distribution in the CaM-binding site in DR5 DD by the point mutations of W354A, E355K, R359A, L3

98 s of W354A, E355K, R359A, L363N, or E367K in DR5 DD could directly contribute to the experimentally o

99 y the point mutations of the key residues in DR5 DD.

100 oop between alpha2 helix and alpha3 helix of DR5 DD.

101 4, Arg-359, Glu-355, Leu-363, and Glu-367 in DR5 death domain that are important for DR5 recruitment

102 interaction of CaM with DR5 is localized at DR5 death domain.

103 king activation of caspase-8 by the TRAIL-R2/DR5 death receptor; notably, this activation was not dep

104 ctivity do not affect the function of DR4 or DR5 death receptors upon treatment with TRAIL, implicati

105 Here, we examined the contribution of DR5 death signaling to lipoapoptosis by free fatty acids

106 655; these effects are DR5-dependent because DR5 deficiency abolished the ability of b-AP15 to enhanc

107 antitumor efficacy was documented after anti-DR5 delivery.

108 cancer cell lines requires death receptor-5 (DR5)-dependent permeabilization of lysosomal membranes.

109 d cancer cells by driving their death due to DR5-dependent apoptosis through B-Raf inhibition.

110 agonistic antibody AMG655; these effects are DR5-dependent because DR5 deficiency abolished the abili

111 reactive T cells, thereby reducing GVHD in a DR5-dependent manner.

112 CTL resistance was due to DR5 downregulation and an inverted ratio of pro- to anti

113 strated that soluble ECD disrupts endogenous DR5-DR5 interactions.

114 sis in alpha-SMA(+ )MFBs through upregulated DR5 during its activation.

115 tein chains selectively bind to the purified DR5 ectodomain and induce its oligomerization.

116 Surprisingly, proteolytic removal of the DR5 ectodomain can fully activate downstream signaling i

117 eutrophil-derived TRAIL induces apoptosis of DR5-expressing macrophages, thus promoting early bacteri

118 termining the effects of B-Raf inhibition on DR5 expression and DR5 activation-induced apoptosis in R

119 S17 also up-regulated DR5 expression and DR5 knockdown partially reversed S17-

120 bition of B-Raf/MEK/ERK signaling suppresses DR5 expression and impairs DR5 activation-induced apopto

121 Silencing of p53 strongly decreased DR5 expression and induced resistance to nutlin-3a and l

122 n primary myeloma cells, nutlin-3a increased DR5 expression and lexatumumab efficiency but did not in

123 fect of B-Raf inhibition on the induction of DR5 expression and the enhancement of DR5 activation-ind

124 PLX4032 induces DR5 expression at transcriptional levels, largely due to

125 and Elk1 are required for celecoxib-induced DR5 expression based on promoter deletion and mutation a

126 demonstrated that both Ras and B-Raf induce DR5 expression by enforced expression of oncogenic Ras (

127 current study has demonstrated induction of DR5 expression by the oncogenic proteins Ras and B-Raf a

128 inhibition and the consequent suppression of DR5 expression impede cancer cell response to DR5 activa

129 significantly induces cell surface TRAIL and DR5 expression in both CSCs and non-CSCs.

130 We detected DR5 expression in ECs within tumors but not normal tissu

131 that Nelfinavir-induced ER stress modulates DR5 expression in human glioblastoma multiforme cells an

132 r disruption and antitumor activity required DR5 expression on tumor ECs but not malignant cells.

133 (melphalan) p53-inducing stresses increased DR5 expression only in TP53 wild-type cells and synergis

134 Silencing of CHOP or DR5 expression selectively prevented caspase activation,

135 rtantly, we have elucidated that Ras induces DR5 expression through co-activation of ERK/RSK and JNK

136 e further demonstrated that HOTAIR regulates DR5 expression via the epigenetic regulator enhancer of

137 of the presence of del17p; did not increase DR5 expression, arguing against an activation of p53 pat

138 a was related to a p53-dependent increase of DR5 expression.

139 5 (DR5), whereas HOTAIR knockdown increased DR5 expression.

140 duced apoptosis via epigenetic regulation of DR5 expression.

141 B-Raf/MEK/ERK signaling positively regulates DR5 expression.

142 no significant increase in death receptor 5 (DR5) expression was seen in CD4(+) T cells from viremic

143 olon cancer cells and xenografts through the DR5, FADD and caspase-8 axis, and is strongly enhanced b

144 d apoptosis-inducing ligand (TRAIL), TRAIL-R(DR5), Fas, and Fas ligand mRNAs and/or proteins, all det

145 not inhibited by a soluble human recombinant DR5-Fc chimera protein suggesting that DR5 cytotoxic sig

146 Upon ligand binding, DR5 forms large clusters within the plasma membrane that

147 Here, we demonstrate that TRAIL receptor 2 (DR5) forms receptor dimers in a ligand-dependent manner

148 nal factors CHOP, Elk1, and c-Jun to enhance DR5 gene transcription.

149 The CHOP binding site on the DR5 gene was required for induction of DR5 by azadirone.

150 s histone H3 lysine 27 trimethylation on the DR5 gene.

151 as revealed by significantly reduced DR5-GUS/DR5-GFP accumulation and compromised degradation of AXR3

152 However, detailed analyses of DR5:GFP and DR5:uidA activity in wild-type, pft1-2, and

153 Wild-type plants expressing auxin-responsive DR5:GFP or DR5:GUS reporters displayed intense signal in

154 ::PIN1::GFP (for green fluorescent protein), DR5:GFP, DR5:uidA, and BA3:uidA in pft1-2 mutants and in

155 ution of auxin in root tips as measured by a DR5::GFP reporter, and an altered pattern of cell divisi

156 auxin, and expression of the auxin reporter DR5::GFP was induced.

157 Reduced activity of the auxin-induced DR5-green fluorescent protein reporter suggests that aux

158 ent protein fluorescence signal encoded by a DR5:green fluorescent protein construct was measured in

159 roots developed fewer nodules, had decreased DR5-GUS activity associated with infection sites, and ha

160 In addition, the activity of the synthetic DR5-GUS auxin reporter was strongly reduced in mtlax2 ro

161 DR5-GUS, a reporter for auxin response, was preferential

162 mutant as revealed by significantly reduced DR5-GUS/DR5-GFP accumulation and compromised degradation

163 Expression of the DR5:GUS auxin reporter was also less effectively induced

164 lants expressing auxin-responsive DR5:GFP or DR5:GUS reporters displayed intense signal in lateral ne

165 expression of the auxin-response marker gene DR5::GUS did not increase in spa mutant seedlings expose

166 om activity of the auxin-responsive reporter DR5::GUS suggests that the dampening of auxin responses

167 Expression of the auxin reporter DR5::GUS was also higher in a tcp15 mutant than in a wil

168 , activity of the auxin-responsive reporters DR5::GUS, DR5::nYFP, and IAA2::GUS was reduced.

169 The proapoptotic death receptor DR5 has been studied extensively in cancer cells, but it

170 n function: auxin-responsive markers such as DR5 have a broader distribution along the distal petal m

171 mab and DOTA-conatumumab to Fc-coupled human DR5 (huTR2-Fc) was tested in a kinetic analysis assay, a

172 Results show that CaM directly binds to DR5 in a calcium dependent manner in breast cancer cells

173 the death receptors TRAILR1/DR4 and TRAILR2/DR5 in a wide range of cancers, while sparing normal cel

174 tissue remodeling and targeting upregulated DR5 in alpha-SMA(+) MFBs is a viable therapy for fibrosi

175 To quantify accumulation of anti-DR5 in brain tumors, we generated a dosage-response curv

176 TP53 wild-type myeloma cells overexpressed DR5 in correlation with sensitivity to lexatumumab.

177 increased DR5 levels including cell surface DR5 in different cancer cell lines with limited or no ef

178 vel crosstalk between WA, ERK/RSK, ELK1, and DR5 in HCC inhibition.

179 ndependent of p53 because UA induced DR4 and DR5 in HCT116 p53(-/-) cells.

180 Nonetheless, a role for TRAIL and/or DR5 in mediating lipoapoptotic pathways is unexplored.

181 misfolded proteins can directly engage with DR5 in the ER-Golgi intermediate compartment, where DR5

182 red free DOX does not effectively upregulate DR5 in tumor tissues nor demonstrate synergy with TRAILP

183 umumab is a potential PET tracer for imaging DR5 in tumors and may be useful for measuring on-target

184 eled conatumumab as a PET tracer for imaging DR5 in tumors.

185 factor-1(ELK1) and Death Receptor protein-5 (DR5) in HCC.

186 f death receptors (DRs) (TNFR1, Fas, DR4 and DR5) in iPS-derived cardiomyocytes at both protein and m

187 ntracellular activation of death receptor 5 (DR5) independent of its canonical extracellular ligand A

188 Lipids, which stimulate DR5, induce release of hepatocyte EVs, which activate an

189 rization inhibitors similarly attenuated DR4/DR5-induced apoptosis.

190 ompetitive mTOR/PI3K inhibitors also promote DR5 induction and FADD-dependent apoptosis in colon canc

191 tor induction was not cell type-specific, as DR5 induction was observed in other cell types.

192 Thus, DR5 integrates opposing UPR signals to couple ER stress

193 on of PDCA-1+ cells or interruption of TRAIL-DR5 interaction protects infected 129 mice.

194 In this study, we characterized CaM and DR5 interactions in breast cancer cells with integrated

195 lded proteins can act as ligands to activate DR5 intracellularly and promote apoptosis.

196 Binding and clustering of the DR5 is a prerequisite for efficient apoptosis initiation

197 x illustrates how higher order clustering of DR5 is achieved when both agents are combined.

198 eric structure of two functional isoforms of DR5 is indistinguishable.

199 The direct interaction of CaM with DR5 is localized at DR5 death domain.

200 Death receptor 5 (DR5) is a cell surface pro-apoptotic death receptor for

201 Death receptor 5 (DR5) is an apoptosis-inducing member of the tumor necros

202 is-inducing ligand (TRAIL) death receptor 5 (DR5) is significantly elevated in patients with nonalcoh

203 S17 also up-regulated DR5 expression and DR5 knockdown partially reversed S17-induced apoptosis,

204 Overexpression of Akt, DR5 knockdown, and Foxo3a knockdown rescues ONC201/TIC10

205 (TRAIL) with its receptor, death receptor 5 (DR5), leading to induction of apoptosis, offers a promis

206 Activation of death receptor-5 (DR5) leads to the formation of death inducing signaling

207 inhibited ERK1/2 phosphorylation and reduced DR5 levels in both human thyroid cancer and melanoma cel

208 Treatment with b-AP15 potently increased DR5 levels including cell surface DR5 in different cance

209 ize DR5 and increase functional cell surface DR5 levels, resulting in enhancement of DR5 activation-i

210 atory effects of b-AP15 on death receptor 5 (DR5) levels and DR5 activation-induced apoptosis as well

211 -bearing mice with an oligomeric form of the DR5 ligand Apo2L/TRAIL induced apoptosis in tumor ECs, c

212 by palmitate transcriptionally up-regulates DR5, likely resulting in ligand-independent cytotoxic si

213 ion in Huh-7 human hepatoma cells leading to DR5 localization into lipid rafts, cell surface receptor

214 eutic application of TRAIL or agonistic anti-DR5 mAb (MD5-1) dramatically improved survival of S. pne

215 pact of B-Raf or MEK inhibition on TRAIL- or DR5-mediated anticancer therapy and on TRAIL/DR5-mediate

216 levels displayed greater sensitivity to DR4/DR5-mediated apoptosis.

217 Calmodulin (CaM) has been shown to regulate DR5-mediated apoptotic signaling, however, its mechanism

218 w insights into potential roles of RNF183 in DR5-mediated caspase activation in IBD pathogenesis.

219 iption factor, reduced DR5 up-regulation and DR5-mediated caspase-8 activation upon palmitate treatme

220 n of dominant-negative FADD (to abrogate Fas/DR5-mediated death receptor signaling) and/or Bcl-2 (to

221 Conversely, EMT attenuated DR4/DR5-mediated DISC formation and caspase-8 stimulation.

222 estigation of the role of CaM-DR5 binding in DR5-mediated DISC formation for apoptosis in breast canc

223 esult in uncontrolled inflammation and TRAIL-DR5-mediated epithelial cell death, which may explain mo

224 DR5-mediated anticancer therapy and on TRAIL/DR5-mediated immune-clearance of cancer cells.

225 ed in draining lymph nodes in TRAIL(-/-) and DR5(-/-) mice compared with that of wild-type mice.

226 Unlike wild-type mice, Trail(-/-) or Dr5(-/-) mice did not develop tolerance to Ag injected i

227 In contrast, CLP-treated Trail(-/-) and Dr5(-/-) mice were better able to control the secondary

228 beta (RARbeta) binding to a direct repeat 5 (DR5) motif.

229 fatty acid palmitate induces an increase in DR5 mRNA and protein expression in Huh-7 human hepatoma

230 e UPR sensor IRE1alpha transiently catalyzed DR5 mRNA decay, which allowed time for adaptation.

231 ceptor 5 (DR5)) promoters, increased Fas and DR5 mRNA, and elevated cell surface expression of these

232 The complex relationships among DR5 network formation, transmembrane helix dimerization,

233 n in cells does not inhibit the formation of DR5 networks.

234 of the auxin-responsive reporters DR5::GUS, DR5::nYFP, and IAA2::GUS was reduced.

235 D predominantly comes from the disruption of DR5 oligomerization and not ligand sequestration.

236 on of NK activation ligands MICA/B, Fas, and DR5 on CSCs.

237 es expression of the death-inducing receptor DR5 on lung epithelia and its ligand TRAIL on inflammato

238 R2) co-expressed with death receptor 4 (DR4)/DR5 on the same cell can block the transmission of the a

239 cid palmitate can activate death receptor 5 (DR5) on hepatocytes, leading to their death, but little

240 tment significantly induced mRNAs for TRAIL, DR5, OPG, and mDcTRAILR2 in primary neurons and of TRAIL

241 The expression of TRAIL, DR5, OPG, and mDcTRAILR2 was significantly increased aft

242 Likewise, knockdown of DR5 or caspase-8 expression by shRNA technology attenuat

243 ddition, key molecules involved in the TRAIL/DR5 pathway during DC/NK cell interactions were determin

244 Aberrant expression of PINFORMED1, DR5, PLETHORA1, PLETHORA2 and WUSCHEL-LIKE HOMEOBOX5 wer

245 acidic cluster sorting protein-2 (PACS-2) to DR5-positive endosomes in Huh-7 cells where it forms an

246 death receptor 4 (DR4) and death receptor 5 (DR5), preferentially in malignant cells.

247 LFS at auxin response maxima sites using the DR5 promoter fails to fully rescue lfs plants, suggestin

248 Using the synthetic auxin-responsive DR5 promoter in soybean (Glycine max), we show that ther

249 of the FAS and TNFRSF10B (death receptor 5 (DR5)) promoters, increased Fas and DR5 mRNA, and elevate

250 DR5 promotes TNF-related apoptosis inducing ligand (TRAI

251 potentiated in HT-29 tumors by upregulating DR5 protein expression by 70% and initiating both extrin

252 Persistent ER stress built up intracellular DR5 protein, driving ligand-independent DR5 activation a

253 ition of cross-priming, and cross-linking of DR5 receptor led to reduced generation of MHC class I-Ag

254 ed to ER stress-induced up-regulation of the DR5 receptor.

255 7 in DR5 death domain that are important for DR5 recruitment of FADD and caspase-8 for DISC formation

256 ings warrant further study on the biology of DR5 regulation by Ras and B-Raf, which may provide new i

257 negative (c-IAP-2 and Bcl-xL) and positive (DR5) regulators were potential incriminators partly regu

258 ence of an asymmetric auxin response using a DR5 reporter and observe morphological asymmetries in yo

259 Analysis of a DR5 reporter transgenic line further suggested that cyto

260 E-cadherin bound specifically to ligated DR4/DR5, requiring extracellular cadherin domain 1 and calci

261 ptors (TRAIL-R) 1 and 2 (also called DR4 and DR5, respectively) into lipid raft membrane microdomains

262 The results suggest that CHOP-DR5 signaling and calpain activation differentially cont

263 Here, we uncover a role for DR5 signaling in tumor endothelial cells (ECs).

264 was reduced by inactivating mediators of the DR5 signaling pathway or rho-associated, coiled-coil-con

265 We investigated whether lipid-induced DR5 signaling results in the release of extracellular ve

266 We show that a DR5-specific variant (rhTRAIL D269H/E195R) displays a si

267 AP15 substantially slowed the degradation of DR5, suggesting that it stabilizes DR5.

268 of Ras or B-Raf mutations on the outcome of DR5-targeted cancer therapy.

269 ients with multiple myeloma may benefit from DR5 therapy.

270 Targeting DR5 to induce breast cancer apoptosis is a promising str

271 to explicitly verify the contribution of the DR5/TRAIL pathway in killing melanomas.

272 duced inflammatory responses were blunted in DR5/TRAIL-R null animals.

273 ER stressors induced DR5 transcription via the UPR mediator CHOP; however, th

274 largely due to enhancing CHOP/Elk1-mediated DR5 transcription.

275 In human/mouse DR5-transgenic LysM.Cre mice, transgenic DR5 was restric

276 A human/mouse-chimeric DR5-transgenic mouse, under the regulation of a mouse 3-

277 In human/mouse DR5-transgenic Ubc.Cre mice with CIA, transgenic DR5 was

278 and experiments in synthetic vesicles on the DR5 transmembrane dimer suggest that dimerization is fac

279 s necessary for the covalent dimerization of DR5 transmembrane domains.

280 brane itself plays an active role in driving DR5 transmembrane helix interactions or in the formation

281 Thus, RNF183 promoted not only DR5 transport to lysosomes but also TRAIL-induced caspas

282 recruitment to lysosomes suggests that TRAIL/DR5 triggers endosomal PACS-2 to recruit Bim and Bax to

283 Ligated DR5 triggers recruitment of the proapoptotic proteins Bi

284 However, detailed analyses of DR5:GFP and DR5:uidA activity in wild-type, pft1-2, and 35S:PFT1 see

285 FP (for green fluorescent protein), DR5:GFP, DR5:uidA, and BA3:uidA in pft1-2 mutants and in 35S:PFT1

286 ved through expression of the auxin reporter DR5::uidA transgene.

287 tress-mediated transcription factor, reduced DR5 up-regulation and DR5-mediated caspase-8 activation

288 d)porphyrin chloride blocked ROS generation, DR5 up-regulation, caspase-8 activation, DNA damage, and

289 tions were associated with death receptor 5 (DR5) up-regulation and caspase-8 activation, whereas cel

290 alling in stromal cells abolishes epithelial DR5 upregulation and apoptosis, reducing host susceptibi

291 ted that the B-Raf inhibitor PLX4032 induces DR5 upregulation exclusively in Ras-mutant cancer cells;

292 ociated with activation of the ERK/RSK axis, DR5 upregulation, and elevated nuclear accumulation of E

293 transgenic Ubc.Cre mice with CIA, transgenic DR5 was most highly expressed on CD11b+ macrophages, wit

294 use DR5-transgenic LysM.Cre mice, transgenic DR5 was restrictively expressed on macrophages.

295 parated by 1, 2, or 5 nucleotides (DR1, DR2, DR5), we show that in mouse embryoid bodies or F9 embryo

296 DCs that lack expression of TRAIL receptor DR5 were less susceptible to NK cell-mediated inhibition

297 sion of the TRAIL receptor death receptor 5 (DR5), whereas HOTAIR knockdown increased DR5 expression.

298 sulted in the upregulation of TRAIL receptor DR5, which potentiated TRAIL-induced apoptosis in cancer

299 lfs meristems and TIBA-pin apices activated DR5:YFP expression with similar kinetics; however, only

300 on of the auxin reporters pPIN1:PIN1:GFP and DR5:YFP Upon auxin microapplication, both lfs meristems