ライフサイエンスコーパス: TRAIL

1 TRAIL continues to garner substantial interest as a reco

2 TRAIL deficiency and MID1 silencing with small interferi

3 TRAIL induces cell death through binding to death recept

4 TRAIL receptors facilitate induction of apoptosis for se

5 TRAIL regulates MID1 and TSLP, inflammation, fibrosis, s

6 TRAIL-DR-mediated ryanodine receptor activation and endo

7 TRAIL-R suppression in tumor cells impaired CCL2 product

8 elated apoptosis-inducing ligand receptor 3 (TRAIL-R3) in CSF allowed for reliable prediction of dise

9 nces in human foreskin fibroblasts and WI-38 TRAIL-resistant cells and marginally sensitive MRC-5 cel

10 elective, potent and secretable variant of a TRAIL, S-TRAIL, and show that these cells significantly

11 We previously identified TRAILshort, a TRAIL splice variant, in HIV-infected patients and chara

12 48a is down-regulated in cells with acquired TRAIL-resistance compared with TRAIL-sensitive cells.

13 such as AMG655 to introduce a highly active TRAIL-R2-agonistic therapy into the cancer clinic.

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

15 Interestingly, neutralizing antibody against TRAIL significantly reduced muXg induced OCL formation.

16 short is sufficient to protect cells against TRAIL-induced killing, whereas immunodepletion of TRAILs

17 nt of NSCLC explants with the targeted agent TRAIL revealed differential sensitivity with the majorit

18 ypothesized that vitamin D deficiency alters TRAIL protein levels in human breast milk and mammary ep

19 Although TRAIL is considered a potential anticancer agent, it enh

20 RAIL)-induced apoptosis by the ECD, although TRAIL is still able to bind to the receptor.

21 tant UMOD were susceptible to TNF-alpha- and TRAIL-mediated apoptosis due to increased expression of

22 We conclude that CST5, AXIN1 and TRAIL are worthy of further study in the context of a pr

23 Our results identified CST5, AXIN1 and TRAIL as novel early biomarkers of TBI.

24 AXIN1 and TRAIL were able to discriminate between TBI and HV at <1

25 re induced, in part, by IL-10, TGF-beta, and TRAIL.

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

27 c niche, via the recruitment of NK cells and TRAIL-dependent killing of melanoma cells by macrophages

28 Cell growth regulation by CM and TRAIL was associated with the modulation of p53/Mdm2, Er

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

30 ucing human transmembrane proteins, FasL and TRAIL, synthesized and displayed on oil drops induce apo

31 Evidence of both FasL and TRAIL-mediated signaling was seen after engagement of Ju

32 ects of the N-terminal gelsolin fragment and TRAIL.

33 ion of inflammatory cytokines, perforin, and TRAIL by HSPC-NK cells.

34 e demonstrate for the first time that PL and TRAIL exhibit a synergistic anti-cancer effect in cancer

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

36 s reported on the expression of TRAIL-Rs and TRAIL-induced apoptosis in cultured human MCs, which dep

37 study, we determined the ability of SAHA and TRAIL as single agents or in combination to inhibit the

38 that the combinatorial treatment of SAHA and TRAIL may target multiple pathways and serve as an effec

39 duce EoE in TRAIL-sufficient (wild-type) and TRAIL-deficient (TRAIL(-/-)) mice and targeted MID1 in t

40 y reduced in these tumors by 48h after Apo2L/TRAIL treatment.

41 atocytes were not killed by the AMG655-Apo2L/TRAIL combination, also not when further combined with b

42 d with E-selectin adhesion protein and Apo2L/TRAIL (TNF-related apoptosis-inducing ligand) apoptosis

43 In vivo, liposome-displayed Apo2L/TRAIL achieved markedly better exposure and antitumor ac

44 or liposomal approaches as well as for Apo2L/TRAIL and other clinically relevant TNF ligands.

45 lex, enabled by concomitant binding of Apo2L/TRAIL and AMG655 to TRAIL-R2.

46 ermore, covalent surface attachment of Apo2L/TRAIL onto liposomes--synthetic lipid-bilayer nanosphere

47 We found that a single dose of Apo2L/TRAIL resulted in a wave of apoptosis which reached a ma

48 n therapy such that an initial dose of Apo2L/TRAIL would precede administration of gemcitabine or oth

49 ially enhanced cytotoxicity of soluble Apo2L/TRAIL against diverse cancer cell lines.

50 These results suggest that Apo2L/TRAIL has a potential as a tumor priming agent and provi

51 y between AMG655 and non-tagged TRAIL (Apo2L/TRAIL) in killing cancer cells.

52 The synergy of AMG655 with Apo2L/TRAIL extended to primary ovarian cancer cells and was f

53 NK-cell depletion as well as TRAIL and NKG2D pathway blockade induced a significant i

54 g HOTAIR in TRAIL-sensitive cells attenuated TRAIL-induced apoptosis, and shRNA-mediated HOTAIR knock

55 centration suppressed the expression of both TRAIL alpha and beta proteins.

56 addition, responders had higher CD56(bright) TRAIL expression and interferon gamma production at end

57 e prostate cells sensitizes to cell death by TRAIL (TNF-related apoptosis-inducing ligand).

58 ished cellular apoptotic response induced by TRAIL or the DR5 agonistic antibody AMG655 or cell killi

59 ined the role of HOTAIR in pancreatic cancer TRAIL resistance and investigated the underlying molecul

60 cancer cells, whereas in resistant cancers, TRAIL/TRAIL-R can promote metastasis via Rac1 and PI3K.

61 K (NK1.1(+)CD3(-)) cells, defined as CD49a(+)TRAIL(+)CXCR6(+)DX5(-) cells in the mouse liver, constit

62 rement of AhR for the maintenance of CD49a(+)TRAIL(+)CXCR6(+)DX5(-) liver-resident NK cells and their

63 lular microenvironment and therefore confers TRAIL resistance not only on the cell which produces it,

64 ated complex I as well as of the cytoplasmic TRAIL-induced complex II In both of these complexes, HOI

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

66 -sufficient (wild-type) and TRAIL-deficient (TRAIL(-/-)) mice and targeted MID1 in the esophagus with

67 ers of magnitude superior to that of dimeric TRAIL-Fc, but also manifests more favorable pharmacokine

68 ed dephosphorylation and activation of Dyn1, TRAIL-DR endocytosis, and increased resistance to TRAIL-

69 ependent on the ubiquitously expressed Dyn2, TRAIL-induced DR endocytosis is selectively regulated by

70 afenib-induced ROS accumulation that enables TRAIL to activate caspase-8 in RCC.

71 nd engineered stem cells (SC) expressing ENb-TRAIL, we show that the treatment with synthetic extrace

72 racellular matrix (sECM) encapsulated SC-ENb-TRAIL alleviates tumor burden and significantly increase

73 function and FRET studies, we show that ENb-TRAIL blocks EGFR signalling via the binding of ENb to E

74 We show that ENb-TRAIL has therapeutic efficacy in tumor cells from diffe

75 ath receptor (DR) targeted ligand TRAIL (ENb-TRAIL).

76 feres with apoptosis induction by endogenous TRAIL, which could be expressed by immune cells.

77 Collectively, endogenous TRAIL/TRAIL-R-mediated CCL2 secretion promotes accumulat

78 ur data suggest that nanoparticle-engineered TRAIL-expressing hADSCs exhibit the therapeutically rele

79 By engineering TRAIL to escape binding by DcRs, we found that DcRs do n

80 y abolished the ability of b-AP15 to enhance TRAIL- or AMG655-induced apoptosis.

81 at the N-terminal gelsolin fragment enhances TRAIL-induced loss of cell viability by inhibiting phosp

82 ) display on the cell surface and in evading TRAIL-mediated apoptosis than was Ad26.

83 rrow of patients with mastocytosis expressed TRAIL-R1.

84 unknown, however, whether and to what extent TRAIL/TRAIL-R signaling in cancer cells can affect the i

85 was also independent of the Fas ligand-Fas, TRAIL-DR5, and canonical death pathways, indicating a no

86 Finally, TRAIL and CCL2 are co-regulated with MDSC/M2 markers in

87 rly ubiquitinated targets of LUBAC following TRAIL stimulation.

88 A functional inhibitory role for TRAIL-R3/4 was revealed by shRNA knockdown and mAb block

89 that TRAIL-triggered cytokine secretion from TRAIL-resistant cancer cells is FADD dependent and ident

90 Furthermore, TRAIL potentiated doxorubicin-induced decrease in beatin

91 ose inverse ex vivo correlation between hHSC TRAIL-R4 expression and susceptibility to apoptosis unde

92 sequential administration of a tumor-homing TRAIL sensitizer and long-acting TRAILPEG.

93 However, TRAIL has the capacity to bind to regulatory receptors i

94 rimer-Tag) to the C-terminus of mature human TRAIL leads to a disulfide bond-linked homotrimer which

95 pite initial promise, both recombinant human TRAIL (native TRAIL) and dimeric DR4/DR5 agonist monoclo

96 However, recombinant human TRAIL demonstrates limited therapeutic efficacy in clini

97 e therapeutic potential of recombinant human TRAIL in experimental rheumatoid arthritis (RA) models.

98 asured in serum before treatment (MIG, IL22, TRAIL, APRIL, VEGF, IL3, TWEAK, SCF, IL21), identified p

99 Importantly, TRAIL-overexpressing hADSCs inhibited GBM growth, extend

100 studies indicate the involvement of AMPK in TRAIL-TZD-mediated apoptosis and beta-catenin cleavage a

101 g IFN-free therapy, suggesting a decrease in TRAIL-mediated killing by NK cells.

102 LP reconstituted hallmark features of EoE in TRAIL(-/-) mice and recombinant TRAIL induced esophageal

103 used Aspergillus fumigatus to induce EoE in TRAIL-sufficient (wild-type) and TRAIL-deficient (TRAIL(

104 Overexpressing HOTAIR in TRAIL-sensitive cells attenuated TRAIL-induced apoptosis

105 caspase-8 activation have been implicated in TRAIL-induced NF-kappaB activation; however, the underly

106 osis, and shRNA-mediated HOTAIR knockdown in TRAIL-resistant PANC-1 cells sensitized them to TRAIL-in

107 ear factor kappaB activation were reduced in TRAIL(-/-) mice, whereas protein phosphatase 2Ac levels

108 RAIL-R, a consequence of del(8p), results in TRAIL insensitivity, which may contribute to ibrutinib r

109 y epithelial cell-derived factors, including TRAIL and MID1, which promote TH 2 cell development via

110 resistance to cancer therapeutics, including TRAIL, in multiresistant cancers such as RCC.

111 itionally, normal fibroblasts had incomplete TRAIL-induced caspase-8 activation compared with cancer

112 Increased TRAIL expression additionally involved the NF-kappaB and

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

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

115 The MMP12 CTD initiates TRAIL-mediated tumor cell death through its conserved SR

116 is unknown whether this was due to intrinsic TRAIL resistance within primary human cancers or insuffi

117 combinant isoleucine-zipper-tagged TRAIL (iz-TRAIL).

118 ha-oriented side chain are superior to known TRAIL-sensitizing withanolides belonging to withaferin A

119 ENb) and death receptor (DR) targeted ligand TRAIL (ENb-TRAIL).

120 is factor-related apoptosis-inducing ligand (TRAIL) and 5-fluorouracil.

121 is factor-related apoptosis-inducing ligand (TRAIL) and by visualizing and quantifying extracellular

122 is factor-related apoptosis-inducing ligand (TRAIL) and its receptor, death receptor 4, sensitizing c

123 is factor-related apoptosis-inducing ligand (TRAIL) as drug-delivery vehicles for targeting and eradi

124 ly member 10A/10B apoptosis-inducing ligand (TRAIL) based pro-apoptotic therapies that induce death r

125 is factor-related apoptosis-inducing ligand (TRAIL) can induce apoptosis in tumor cells including bre

126 with TNF-related apoptosis-inducing ligand (TRAIL) for markedly enhanced induction of apoptosis in V

127 is factor-related apoptosis inducing ligand (TRAIL) has attracted great interest as a cancer therapy

128 is factor-related apoptosis inducing ligand (TRAIL) has been implicated in cellular growth/apoptosis,

129 is factor-related apoptosis inducing ligand (TRAIL) has been shown to increase osteoclastogenesis.

130 TNF-related apoptosis-inducing ligand (TRAIL) has been shown to induce apoptosis in malignant c

131 is factor-related apoptosis-inducing ligand (TRAIL) induces apoptosis in cancer cells while sparing n

132 is factor-related apoptosis-inducing ligand (TRAIL) is a death ligand cytokine known for its cytotoxi

133 TNF-related apoptosis-inducing ligand (TRAIL) is a death ligand that can induce apoptosis in ce

134 TNF-related apoptosis-inducing ligand (TRAIL) is a potential cancer therapy that selectively ta

135 tor (TNF)-related apoptosis-inducing ligand (TRAIL) is known for specifically killing cancer cells, w

136 is factor-related apoptosis-inducing ligand (TRAIL) or aggregation.

137 TNF-related apoptosis-inducing ligand (TRAIL) promotes inflammation through upregulation of the

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

139 TNF-alpha related apoptosis-inducing ligand (TRAIL) selectively kills tumor cells, without damaging n

140 TNF-related apoptosis-inducing ligand (TRAIL) was initially described to induce apoptosis of tu

141 is factor-related apoptosis-inducing ligand (TRAIL) with its receptor, death receptor 5 (DR5), leadin

142 is factor-related apoptosis-inducing ligand (TRAIL), a cytokine known to induce apoptosis specificall

143 on of TNF-related apoptosis-inducing ligand (TRAIL), CD38, and Ki67 that significantly declined upon

144 ls of TNF-related apoptosis inducing ligand (TRAIL), compared with patients who failed to control HCV

145 tor (TNF)-related apoptosis-inducing ligand (TRAIL), thereby promoting viral persistence.

146 on of TNF-related apoptosis-inducing ligand (TRAIL)-induced apoptosis by the ECD, although TRAIL is s

147 ivate TNF-related apoptosis-inducing ligand (TRAIL)-induced apoptosis have shown promising efficacy,

148 is factor-related apoptosis-inducing ligand (TRAIL)-induced apoptosis in cancer cells.

149 is factor-related apoptosis-inducing ligand (TRAIL)-induced apoptosis, and knockdown of CAS renders c

150 phage TNF-related apoptosis-inducing ligand (TRAIL).

151 uding TNF-related apoptosis-inducing ligand (TRAIL).

152 uding TNF-related apoptosis inducing ligand (TRAIL).

153 TNF-related apoptosis-inducing ligand (TRAIL/Apo2L) has long been considered a tantalizing targ

154 is-factor-related apoptosis-inducing ligand, TRAIL) and an intracellular-acting small-molecule drug (

155 Both diffused through the endothelium, LUV-TRAIL being more efficient in killing tumour cells, show

156 e that vitamin D status in mothers modulates TRAIL expression in breast milk, which may have implicat

157 hat iNSC delivery of the anticancer molecule TRAIL decreases the growth of established solid and diff

158 s, such as CD49a, and the effector molecules TRAIL and CD73.

159 ere we identify cancer cell-expressed murine TRAIL-R, whose main function ascribed so far has been th

160 vity and receptor binding kinetics as native TRAIL in vitro which are 4-5 orders of magnitude superio

161 en due to rapid systemic clearance of native TRAIL and poor apoptosis-inducing potency of dimeric ago

162 dynamic profiles in vivo than that of native TRAIL.

163 romise, both recombinant human TRAIL (native TRAIL) and dimeric DR4/DR5 agonist monoclonal antibodies

164 iable levels of TRAIL-R2/3/4 (but negligible TRAIL-R1) ex vivo and after activation.

165 ncreases the cancer-cell-killing activity of TRAIL-R2-specific antibodies in vivo.

166 MC-specific deletion of TRAIL-R was associated with a slight, but significant in

167 idence for the in vivo antitumor efficacy of TRAIL being proportional to systemic drug exposure and s

168 bing osteoclast formation, the expression of TRAIL in human milk as a function of vitamin D status in

169 In addition, the expression of TRAIL on NK cells was reduced during IFN-free therapy, s

170 Recent studies reported on the expression of TRAIL-Rs and TRAIL-induced apoptosis in cultured human M

171 t fusion proteins in which a soluble form of TRAIL, FasL or CD40L is genetically fused to a high-affi

172 inical-grade non-tagged recombinant forms of TRAIL, such as dulanermin, could be combined with antibo

173 this, we evaluated two drug formulations of TRAIL (TNF-related apoptosis inducing ligand): soluble a

174 IV-1 proviral DNA, and higher frequencies of TRAIL(+) NK cells.

175 also explored the expression and function of TRAIL-Rs in cultured murine and human MCs upon activatio

176 Activation of KIT regulates the function of TRAIL-Rs in MCs.

177 Haploinsufficiency of TRAIL-R, a consequence of del(8p), results in TRAIL inse

178 We sought to further define the impact of TRAIL-Rs on MCs in vivo and in vitro.

179 Therefore, inhibition of TRAIL expression could be an effective countermeasure fo

180 mutagenesis to prove that the inhibition of TRAIL-induced apoptosis by the ECD predominantly comes f

181 Repetitive injection of TRAIL-overexpressing hADSCs significantly prolonged anim

182 with MC-specific and ubiquitous knockout of TRAIL-R.

183 in D deficient mothers showed high levels of TRAIL (alpha and beta) proteins compared to milk from vi

184 y screening that muXg induces high levels of TRAIL expression in murine preosteoclast cells in the ab

185 ifferent donors expressed variable levels of TRAIL-R2/3/4 (but negligible TRAIL-R1) ex vivo and after

186 4, sensitizing cells to an autocrine loop of TRAIL-mediated cell death.

187 The apoptotic potential of TRAIL-R2 on hHSC was confirmed by lentiviral-mediated kn

188 amino acid residues 1-70) in the presence of TRAIL impairs cell viability of TRAIL resistant transfor

189 reased IL-6 levels, suppressed production of TRAIL, and reduced infiltration of polymorphonuclear cel

190 AMPKalpha1 expression showed a reduction of TRAIL-TZD-induced apoptosis, further confirming the part

191 transfection led to robust up-regulation of TRAIL in hADSCs, and that TRAIL-expressing hADSCs induce

192 ere IFNalpha induces macrophage secretion of TRAIL that causes endocytosis of Na,K-ATPase by the alve

193 presence of TRAIL impairs cell viability of TRAIL resistant transformed human hepatocytes (HepG2).

194 sis of hHSC in response to both oligomerised TRAIL and NK cells.

195 L- or DR5-mediated anticancer therapy and on TRAIL/DR5-mediated immune-clearance of cancer cells.

196 ults support a causative effect of HOTAIR on TRAIL sensitivity.

197 egative impact of B-Raf or MEK inhibition on TRAIL- or DR5-mediated anticancer therapy and on TRAIL/D

198 with recombinant TRAIL (Apo2L/Dulanermin) or TRAIL-R2-specific antibodies, such as conatumumab (AMG65

199 ligands TNF-alpha (Tumor Necrosis Factor) or TRAIL (TNF-Related Apoptosis-Inducing Ligand); is an ext

200 determined the different effects of SAHA or TRAIL alone and combining SAHA with TRAIL on the express

201 nstrate that the distinct effects of SAHA or TRAIL individually and in combination on the proliferati

202 lar mechanisms may facilitate either SAHA or TRAIL targeted use and the selection of suitable combina

203 lines to cell death by agonists TNFalpha or TRAIL and inhibited cIAP1>XIAP>IAP2.

204 unction may represent a strategy to overcome TRAIL resistance in pancreatic cancer.

205 y demonstrates a unique approach to overcome TRAIL-based therapy drawbacks using sequential administr

206 Here we demonstrate that sorafenib overcomes TRAIL resistance in RCC by a mechanism that does not rel

207 el paradigm for understanding and overcoming TRAIL resistance, in particular how HIV-infected cells e

208 dministering a potent, long-acting PEGylated TRAIL (TRAILPEG) is profoundly anti-rheumatic against tw

209 Contrary to its role in preventing TRAIL-induced RIPK1-independent apoptosis, HOIP presence

210 KK complex to complex I, LUBAC also promotes TRAIL-induced activation of NF-kappaB and, consequently,

211 tes as a carrier for the anti-cancer protein TRAIL could be an effective tool to directly target circ

212 firmed our hypothesis that membrane-proximal TRAIL species lack the capacity to physically engage the

213 ed apoptosis-inducing ligand-death receptor (TRAIL-DR) complexes in several cancer cells.

214 s activation of the CD19 and TRAIL receptor (TRAIL-R) apoptosis signaling pathways.

215 nt agonistic activity of the TRAIL-receptor (TRAIL-R)-targeting drugs.

216 related apoptosis-inducing ligand receptors (TRAIL-Rs) are preferentially expressed on neoplastic cel

217 al roles for the regulatory TRAIL receptors (TRAIL-R3/4) in a physiological setting.

218 es of EoE in TRAIL(-/-) mice and recombinant TRAIL induced esophageal TSLP expression in vivo in the

219 affected apoptosis induction by recombinant TRAIL.

220 ents responded to treatment with recombinant TRAIL (Apo2L/Dulanermin) or TRAIL-R2-specific antibodies

221 Here, we show that DcRs also regulate TRAIL sensitivity at a supracellular level and thus repr

222 Consistently, vitamin D regulated TRAIL mRNA expression in HME-1 cells.

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

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

225 on of TRAILshort with a specific Ab restores TRAIL sensitivity.

226 LKL-containing complex, LUBAC also restricts TRAIL-induced necroptosis.

227 The resulting TRAIL-Trimer not only retains similar bioactivity and re

228 x virus thymidine kinase, into therapeutic S-TRAIL secreting stem cells allowed their eradication pos

229 potent and secretable variant of a TRAIL, S-TRAIL, and show that these cells significantly suppresse

230 3-36 and compared their ability to sensitize TRAIL-mediated apoptosis in a panel of renal carcinoma c

231 Recombinant soluble TRAIL and agonistic antibodies against TRAIL receptors (

232 ecently developed the genetically stabilized TRAIL platform TR3 in efforts to improve the limitations

233 ovel small molecule that not only stimulates TRAIL-induced apoptosis in cancer cells, but may also pr

234 being a dominant negative ligand to subvert TRAIL-mediated killing.

235 oxo3a and significantly induces cell surface TRAIL and DR5 expression in both CSCs and non-CSCs.

236 riking synergy between AMG655 and non-tagged TRAIL (Apo2L/TRAIL) in killing cancer cells.

237 active recombinant isoleucine-zipper-tagged TRAIL (iz-TRAIL).

238 t up-regulation of TRAIL in hADSCs, and that TRAIL-expressing hADSCs induced tumor-specific apoptosis

239 We find that TRAIL induces up-regulation of CAS in a posttranscriptio

240 We hypothesize that TRAIL may play an important role in muXg enhanced OCL di

241 These results indicate that TRAIL signaling plays an important role in the muXg incr

242 We observed that TRAIL-resistant pancreatic cancer cells had higher level

243 We show that TRAIL stimulation activates ryanodine receptor-mediated

244 Here we show that TRAIL-triggered cytokine secretion from TRAIL-resistant

245 The TRAIL pathway can mediate apoptosis of hepatic stellate

246 The TRAIL-expressing platelets were demonstrated to kill can

247 i-CSC effect is significantly blocked by the TRAIL sequestering antibody RIK-2.

248 ected cells escape immune elimination by the TRAIL:TRAILshort receptor axis.

249 Hence, LUBAC controls the TRAIL signalling outcome from complex I and II, two plat

250 cer cells is FADD dependent and identify the TRAIL-induced secretome to drive monocyte polarization t

251 ls (0.5 to 5 nM) significantly increased the TRAIL alpha but no change in beta expression.

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

253 iciency was due to enhanced formation of the TRAIL death-inducing signalling complex, enabled by conc

254 201/TIC10 is a small-molecule inducer of the TRAIL gene under current investigation as a novel antica

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

256 Inhibition of the TRAIL signaling pathway has been shown to improve lung i

257 Here, we show that LUBAC forms part of the TRAIL-R-associated complex I as well as of the cytoplasm

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

259 mor-supportive immune-modulatory role of the TRAIL/TRAIL-R system in cancer biology.

260 Its gene therapy with the TRAIL suicide gene effectively induces apoptosis of HeLa

261 7 cells in inflamed arthritic joints through TRAIL-induced apoptosis while increasing anti-inflammato

262 ion of ILC-associated IL7R (CD127), TNFSF10 (TRAIL), KIT (CD117), IL2RA (CD25), CD27, CXCR3, DPP4 (CD

263 ystem to regulate the expression of TNFSF10 (TRAIL) in the context of glioma therapy and found that i

264 omitant binding of Apo2L/TRAIL and AMG655 to TRAIL-R2.

265 d expression of miR-148a sensitized cells to TRAIL and reduced lung tumorigenesis in vitro and in viv

266 the resistance of pancreatic cancer cells to TRAIL-induced apoptosis via epigenetic regulation of DR5

267 has been shown to sensitize cancer cells to TRAIL-induced apoptosis, in particular by down-regulatio

268 appaB and AP-1 sites and sensitized cells to TRAIL-induced apoptosis.

269 ic compounds for sensitizers of RCC cells to TRAIL-mediated apoptosis led to identification of the 17

270 efficacy in clinical trials, possibly due to TRAIL-resistance of primary cancers and its inherent sho

271 ctivity and sensitized normal fibroblasts to TRAIL-mediated apoptosis.

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

273 modified to enhance sensitization of RCCs to TRAIL-mediated apoptosis, thereby assisting development

274 However, resistance to TRAIL and other targeted therapies is an important issue

275 -DR endocytosis, and increased resistance to TRAIL-induced apoptosis.

276 egulation of caspase-8 confers resistance to TRAIL-induced cell death in normal cells through blockad

277 e cancer cells have developed resistances to TRAIL which limits anticancer potential.

278 but many pancreatic cancers are resistant to TRAIL therapy.

279 ne MCs from wild-type mice were resistant to TRAIL-induced apoptosis, SCF-stimulated MCs underwent ap

280 knockdown of CAS renders cells resistant to TRAIL.

281 , including lung cancer, remain resistant to TRAIL.

282 lated MCs underwent apoptosis in response to TRAIL.

283 g KIT mutations also promoted sensitivity to TRAIL-mediated apoptosis in human MCs.

284 n also resulted in greater susceptibility to TRAIL-induced cell death, consistent with its proapoptot

285 IL-resistant PANC-1 cells sensitized them to TRAIL-induced apoptosis.

286 d cancer cells to PLX4032 sensitizes them to TRAIL-induced apoptosis; this is also a c-Raf/MEK/ERK-de

287 ich the microenvironment can diminish tumour TRAIL sensitivity.

288 le living cells or population of cells, upon TRAIL stimulation.

289 Instead CXCR6+ NK could upregulate TRAIL, a key death ligand in hepatitis pathogenesis.

290 s (PBMCs) from patients with SVR upregulated TRAIL, as well as IFN-gamma and the chemokines CXCL9 and

291 higher levels of HOTAIR expression, whereas TRAIL-sensitive pancreatic cancer cells had lower HOTAIR

292 lin peptide1-70 alone or in combination with TRAIL, induced inhibition of Akt phosphorylation and key

293 ively augmented apoptosis when combined with TRAIL or the DR5 agonistic antibody AMG655; these effect

294 d enhances its activation when combined with TRAIL, but not alone.

295 with acquired TRAIL-resistance compared with TRAIL-sensitive cells.

296 rginally sensitive MRC-5 cells compared with TRAIL-sensitive human lung and colon cancer cells.

297 mechanisms of combining HDAC inhibitors with TRAIL in the treatment of breast cancer are poorly under

298 SAHA or TRAIL alone and combining SAHA with TRAIL on the expression of a number of apoptosis-related

299 re, we reasoned that PL would synergize with TRAIL to stimulate potent apoptosis in cancer cells.

300 ompared with C4-2-DN cells when treated with TRAIL-TZD, thus suggesting that C4-2-DN cells were more