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 TLs used the TRAIL cytotoxic pathway through DR5.

5 is signaling via the death receptors DR4 and DR5.

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

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

8 sion of WOX5 and the auxin response reporter DR5.

9 trimerizing its functional receptors DR4 or 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 sis that was abrogated by siRNA silencing of DR5.

15 ugh the proapoptotic death receptors DR4 and DR5.

16 pression of both the TRAIL receptors DR4 and DR5.

17 h through binding to death receptors DR4 and DR5.

18 dation of DR5, suggesting that it stabilizes DR5.

19 tion of the synthetic auxin response element DR5.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

45 Knockdown of DR5 and DR4 by small interfering RNA (SiRNA) reduced the

46 enhanced expression of death receptors (DRs) DR5 and DR4 in cancer cells.

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

48 We observed that DBA-induced induction of DR5 and DR4 was mediated through generation of reactive

49 n species- and ERK-mediated up-regulation of DR5 and DR4, down-regulation of cell survival proteins,

50 Thus, activated GLI genes repress DR5 and Fas expressions while upregulating Bcl-2 and PDG

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

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

53 tudies showed an inverse correlation between DR5 and Ki67.

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

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

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

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

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

59 ted celastrol-induced expression of CHOP and DR5, and consequent sensitization to TRAIL.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

76 axr1 auxin resistance, ectopically expressed DR5:beta-glucuronidase in developing embryos, and defect

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

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

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

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

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

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

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

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

85 Deletion of DR5 by siRNA significantly reduced the apoptosis induced

86 Ligation of DR5 by tumor necrosis factor (TNF)-related apoptosis-ind

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

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

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

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

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

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

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

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

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

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

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

98 4, Arg-359, Glu-355, Leu-363, and Glu-367 in DR5 death domain that are important for DR5 recruitment

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

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

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

102 655; these effects are DR5-dependent because DR5 deficiency abolished the ability of b-AP15 to enhanc

103 antitumor efficacy was documented after anti-DR5 delivery.

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

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

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

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

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

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

110 Although activated PDC killed the DR5-expressing HIV-infected Sup-T1 cell line, PDC did no

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

112 siRNA decreased the induction of DBA-induced DR5 expression and apoptosis.

113 silencing of CHOP abolished gossypol-induced DR5 expression and associated potentiation of apoptosis.

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

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

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

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

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

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

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

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

122 silencing of CHOP abolished the induction of DR5 expression by celastrol and associated enhancement o

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

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

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

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

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

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

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

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

131 ase (RSK)-dependent mechanism that regulates DR5 expression primarily using celecoxib as a DR5 induce

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

133 hat small molecules such as celecoxib induce DR5 expression through activating ERK/RSK signaling and

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

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

136 Furthermore, DR5 expression was increased whereas Bcl-2 (direct targe

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

138 ects on increasing DR5 promoter activity and DR5 expression, indicating that CHOP and Elk1 co-operati

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

140 F4 is involved in celecoxib-induced CHOP and DR5 expression.

141 duced apoptosis via epigenetic regulation of DR5 expression.

142 g that CHOP and Elk1 co-operatively regulate DR5 expression.

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

144 5 (DR5), whereas HOTAIR knockdown increased DR5 expression.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

187 R5 expression primarily using celecoxib as a DR5 inducer.

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

189 uction; gene silencing of ERK abolished both DR5 induction and potentiation of apoptosis by TRAIL.

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

191 nd Elk1-mediated mechanisms are critical for DR5 induction.

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

196 We show here that expression of TRAIL and DR5 is increased by Stx1 treatment.

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

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

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

200 Death receptor 5 (DR5) is a death domain-containing transmembrane receptor

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

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

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

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

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

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

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

225 CD8(+) T cells from AC-injected wild-type or Dr5(-/-) mice could transfer tolerance.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

242 AIL death receptors through the ROS-ERK-CHOP-DR5 pathway.

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

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

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

246 lk1 exhibited enhanced effects on increasing DR5 promoter activity and DR5 expression, indicating tha

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

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

252 hift studies demonstrated the existence of a DR5 RA response element upstream of Pitx2 that binds all

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

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

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

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

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

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

265 r binds to a retinoic acid response-element (DR5) site in the OLFM4 promoter and mediates all-trans-r

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

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

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

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

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

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

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

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

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

281 Ligated DR5 triggers recruitment of the proapoptotic proteins Bi

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

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

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

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

286 th an RSK2 inhibitor or RSK2 siRNA abrogated DR5 up-regulation by celecoxib as well as other agents.

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

288 de of ATF4 abrogated both CHOP induction and DR5 up-regulation, indicating that ATF4 is involved in c

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